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INTRODUCTION TO PARASITOLOGY

Parasitology is the science that deals with the study of living

organism that depends on another organism for the purpose of
procuring food and securing protection. These organisms which are
usually smaller and weaker than the other organism are known as
parasites. Parasites are organisms that obtain its food and shelter
from another organism and derive all the benefits from the association.
The organism that provides physical protection and nourishment to the
parasites is known as host.

Types of host:
1. Final or Definitive host - harbors the adult/sexual stage of the
parasites Ex. Man,Dog,Cat

2. Intermediate host - harbors part or all the larval stages of the

parasites
a. First intermediate host - harbors the early larval stages
of the parasites Ex. snail
b. Second intermediate host - harbors the infective larval
stage of the parasite Ex. Fish, vegetables

3. Reservoir host - other animals that harbors the same species as

that of man. These hosts ensures the continuity
of the life cycle of the parasites and act as
additional source of infection Ex. Rodents,pig

4. Paratenic host - harbors the parasite in an arrested state of

development. However, the parasite is
capable of continuing its life cycle in a
suitable host Ex. Fresh water prawn, crab

HOST – PARASITE RELATIONSHIP

In general, parasitism includes any association in which an

organism depends upon another organism for its existence. This type
of association is far from a rare or unusual condition. More important
parasitism is not an abnormal condition nor it is necessarily a
pathogenic one. Host-Parasite association maybe temporary or a
permanent one. Parasitism is a process by which one organism, the
parasite, living for or part of its life cycle on or within another, the host,
obtains its energy or sustenance from the latter while producing effects
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that range from no demonstrable effect to severe pathology and death.

Within the great range of interorganismal relationships, all of which can
be combined under the term symbiosis, mutualism and commensalism.
Symbiosis is a close association between two organisms that is
permanent wherein one can not exist independently. On the other
hand, mutualism is an association that is beneficial to both the
parasites and the host in which one can still survive even without the
other. In commensalism only the parasite benefit from the association
while the host is unaffected.

PARASITIC INFECTION AND DISEASE

Infection connotes a “take” in which the infective agent becomes

established in the host. Infection is associated with endoparasitism
that is the dwelling and feeding of a parasite within a host. On the
other hand infestation is associated with ectoparasitism.

The distinction between parasitic infection and parasitic disease

is an important demonstration of the often- ignored truism that in most
instances infection is a necessary but not a sufficient cause of disease.
In parasitic infection, the host usually shows mild symptoms and
suffers a little damage. On the other hand, in parasitic disease, the host
develops pathologic changes and exhibit symptoms of varying degree.
In parasitic diseases, there maybe initial toxic manifestations, high
fever , evidence of inflammation, generalized or localized pain and
other physical signs of disease.

FACTORS AFFECTING TRANSMISSION OF PARASITES

1. the source of infection

2. an effective mode of transmission and portal of entry
3. the presence of a susceptible host
4. successful entry of the infective stage of the parasite

SOURCES OF EXPOSURE TO INFECTION

Based on sources of exposure to infection, parasites maybe

classified as follows:

1. Soil-Transmitted Group (STH- Soil Transmitted Helminths)

These parasites require further development in the soil
before they become infective. Soil polluted with human
excreta is usually responsible for exposure to infection with
Ascaris lumbricoides, Trichuris trichiura,Hookworms, etc.
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2. Snail-Transmitted Group
These groups requires further development within the
body of snail which serve as their intermediate host before
they can become infective. Ex. flukes(Trematodes)

3. Arthropod-Transmitted Group
Some specie of insects act as vectors of parasitic
diseases such as mosquitoes, sandfly and Tsetse fly

Vectors are organisms that transmit parasites to man and

may serve as intermediate host or definitive host to some
parasite. There are two types of vectors:
a. Biological vector - essential in the life cycle
Ex. Anopheles
b. Mechanical/Phoretic vector – not essential in the life
cycle
Parasites such as Plasmodium and Filarial worms(e.g.
Wuchereria bancrofti) require vector.

4. Animal/Food-Transmitted Group
These groups requires further development in the flesh
of some animals that man consume. Raw pork maybe source
of infection with Trichinella spiralis and Taenia solium while
raw beef maybe source of Taenia saginata.

5. Contact-Transmitted Group
Person to person transmission, wherein the parasites
require no further development and are readily infective like
Enterobius vermicularis and Trichomonas vaginalis.

6. One’s self (autoinfection)

In this case, the infected person is his own source of re-
exposure. There are two types of autoinfection, external and
internal. Examples of parasite that can be acquired through
autoinfection are Enterobius vermicularis and Strongyloides
stercoralis.

PORTAL OF ENTRY AND MODE OF TRANSMISSION

1. Mouth
This is the common portal of entry of most intestinal
parasites. Parasite can enter the host’s body through
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a. ingestion of the infective stage

Ex. cyst of Entamoeba histolytica,embryonated egg of Ascaris
lumbricoides and Trichuris trichiura
b. intimate oral contact/kissing Ex. Trichomonas tenax

2. Skin
Some parasites enter the body of the host through the ff:
a. active larval penetration/skin penetration
Ex. Hookworms,Strongyloides,Schistosomes
b. bite of arthropod vector
Ex. Plasmodium and Wuchereria

3. Others
a. Genitals
Parasites are acquired through sexual intercourse.
Ex. Trichomonas vaginalis, Entamoeba histolytica

b. Nose/Intranasal cavity
Parasite are acquired through inhalation.
Ex. Enterobius vermicularis, Naegleria

c. Transplacental
Parasites cross the placental barrier.
Ex. Toxoplasma gondii

CLINICAL INCUBATION PERIOD AND BIOLOGICAL INCUBATION PERIOD

Once the parasites has successfully entered the body of the

host,characteristically it is carried or actively migrates to a location
where it matures and produces progeny. Signs and symptoms will
not be immediately manifested by the individual after the process of
inoculation(exposure), although there are some infected individual that
do not show any signs and symptoms and are known as carrier. The
interval between exposure to the parasites and the appearance of the
earliest signs and symptoms is referred to as Clinical Incubation
Period. On the other hand, the development of the parasite in a
particular host and demonstration of the stages of the parasites in the
different specimens is known as Biological Incubation Period or
Prepatent Period.

LIFE CYCLE

Life cycle is the development of a parasite which involves the

survival and development in the external environment and in one or
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more hosts. The life cycle of a parasite maybe simple or complicated

and can be divided into three major groups: (1)those with definitive
host and without intermediate host (2)those with definitive host and
one intermediate host and (3)those with definitive host and with two
intermediate hosts.
Parasites having no intermediate host are transmitted directly
from man to man(or animal to animal),usually through fecally
contaminated food or water. Parasite requiring intermediate host/s
usually select a large mammals, crustaceans,insect vectors,fish or
vegetable to complete their life cycle.

DIAGNOSIS
Diagnosis of parasitic infection or diseases has two methods of
approach:
1. Clinical Diagnosis
This method of diagnosis is based on the recognition of
the characteristic signs and symptoms of the infection of
disease.
2 Laboratory diagnosis
This method is based on the identification of the
parasites in the different specimens.
TREATMENT
The successful treatment of the infected patient includes use of
chemotherapeutic agents, surgical intervention and adequate nutrition
to build up general resistance.The following points must be considered
before proceeding with the treatment:
a. severity, duration and intensity of infection and the probability
of
reinfection
b. efficacy, availability, toxicity and acceptability of the treatment
EPIDEMIOLOGY
Epidemiology is the body of knowledge that concerns diseases
in human population or communities rather than in individuals. It may
include the study of the manifestations of any diseases, which happens
to attack groups of individual at any time. It is also concerned with the
relationships of various factors and conditions, which determine
frequencies and distribution of an infectious process, a disease or a
physiological state in a human community.
Distribution of Diseases
1. Endemic - when a disease in human population maintains a
relatively steady, moderate level
2. Epidemic - if there is a sharp rise in the incidence or an
out- break of considerable intensity occurs
3. Hyperendemic- if the prevalence of a disease in a community is high
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4. Sporadic - if it appears only occasionally in one or at

most few members of a community
5. Pandemic - the disease covers extensive area of the
world
PREVENTION AND CONTROL
The prevention of parasitic disease depends upon the erection of
barriers to the spread of parasites through the practical application of
biologic and epidemiological knowledge. The control of parasitic
diseases includes the following procedures:
1. reduction of the sources of infection in human beings by
therapeutic measures
2. education in personal prophylaxis to prevent dissemination of
infection and to reduce opportunities for exposure
3. sanitary control of water, food and proper waste disposal
4. destruction or control of reservoir hosts and vectors
5. erection of biologic barriers to the transmission of parasites
CLASSIFICATION OF PARASITES
A. According to habitat
1. Endoparasite - those that live within the body of the host
2. Ectoparasite - those that live outside or on the surface
of the body of the host
B. According to its effects to the host
1. Pathogenic - cause injury by its mechanical,
traumatic or toxic activities
2. Non-pathogenic - derives benefits from the host without
causing any considerable damage or harm
C. According to mode of living
1. Obligate - takes up a permanent residence and is
completely dependent upon its host for
existence throughout its life
2. Facultative - capable of leading both free and parasitic
existence under favorable or appropriate
circumstances
3. Incidental - one that establishes itself in a host in
which it does not ordinarily lives
4. Temporary - free living during part of existence and
seeks only its host intermittently to obtain
nourishment
5. Permanent - remains on or in the body of the host
from early life to maturity
6. Spurious or - one which parasitizes other hosts and
Coprozoic recovered in a living or dead state from
human excreta; no further development
and do not cause injury or damage
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ACTIVITY SHEET NO. 1

NAME_________________________________SEC_____DATE______

1. Discuss zoonosis and enumerate the type of zoonosis.

2. Explain the concept of binomial nomenclature in the

classification of parasites.

3. Differentiate external autoinfection from internal autoinfection

and cite examples.
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CLASSIFICATION OF PARASITES OF MEDICAL IMPORTANCE

METAZOA

_______________________________________
 
Nemathelminthes Platyhelminthes
(Roundworms) (Flatworms)

________________
 
Cestodea Trematodea
(tapeworms) (flukes)

PROTOZOA

_____________________________
 
Sarcomatigophora Sporozoa
 
Mastigophora Coccidia
Sarcodina Haemosporina
Toxoplasmea
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PHYLUM NEMATODA( THE TRUE ROUNDWORMS)

The nematodes include numerous free living and parasitic
species. There are about 500,000 species of nematodes and 10,000 of
these have been described. The free-living forms are widely distributed
in water and soil, while the parasitic species live in plants, mollusk,
annelids, arthropod and vertebrates.

Morphology and general characteristics

The adult nematode is unsegmented, elongated, cylindrical
worm. The species parasitic in human range in length, from 2mm to
more than a meter. The sexes are separate (dioecious). The male is
smaller than female and the posterior portion of male is curved or
coiled.

The supporting body wall consists of the following

1. an outer, hyaline, non-cellular cuticle with three main
layers:(a)cortical layer, which is the outermost layer
composed of collagen and cuticulin; (b)homogenous
matrix,the middle layer and (3)the fibrous layer
2. a subcuticular epithelium or hypodermis which is
responsible for secretion of the cuticle
3. layer of muscle cell or somatic musculature, wherein
there are two types of muscle cells (a) platymyarian
muscle cells and (2) coelomyarian muscle cells

All of the viscera including the digestive system, excretory

system and the reproductive system are suspended in a body cavity
known as pseudocele or pseudocoelum. This body cavity is lined with
a delicate connective tissue and a single layer of muscle cells. The
fluid of pseudocele known as hemolymph contains hemoglobin,
glucose, proteins, salts and vitamins and fulfills the function of the
blood. The body wall and the hemolymph serve as hydroskeleton of
nematodes which maintains body shape, aids in locomotion and in
some nematodes maintains its position in the host.

Digestive System
The adult worm has a complete digestive tract. It is a simple tube
extending from the mouth to the anus, which opens on the ventral
surface and a short distance from the posterior extremity.
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1. Mouth- located at the anterior end; maybe equipped with

hooks,teeth, plates and other structures for the
purpose of abrasion, attachment and sensory
response

2. Buccal cavity - tubular or funnel-shaped, which in some

species is expanded for sucking purposes

3. Esophagus - a muscular tube that pumps food posteriorly

into the intestine; characteristically varies in
size, shape and structures which are useful for
species identification
Types of esophagus:
1. Filariform - simple, long and slender; seen in
Strongyloides
2. Rhabditiform - divided into distal corpus, an isthmus and
an esophageal bulb; seen in Enterobius
3. Spiruroid - anterior portion muscular, posterior
glandular; seen in Filarial worms
4.Strongyliform - short, muscular with a waist, seen in
Ancylostoma
5. Stichosoma - long, thin, capillary-like lined with
esophageal gland cells known as
stichocytes or stichosomes seen in
Trichuris, Capillaria and Trichinella

Filariform Rhabditiform Spiruroid Strongyliform Stichosoma

4. Intestine/Midgut - a flattened tube with a wide lumen that

follows a straight course from the
esophagus to the rectum; wall is lined with
a single layer of columnar cells with
microvilli. This absorbs nutrients and
probably plays a role in the excretion of
nitrogenous waste products.
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5. Rectum - in female, the intestine leads into a short

rectum lined with cuticle; in male it joins
with the genital duct to form a common
cloaca, which opens through the anus.
Around the anal orifice are papillae, the
number and pattern of which aid in the
identification of the specie. Defecation
occurs when the anus is dilated and the
pseudocele pressure forces the feces out.

Nervous system
The nervous system consists of a dorsal, a ventral and a four
lateral longitudinal trunks with transverse commissures. The most
important commissure is the CIRCUM-ESOPHAGEAL RING
COMMISSURE, which constitutes the nerve center. Nerve endings
terminate in all of the important organs and in the integument,
especially in sensory papillae. Sensory organs like papillae, amphids
and phasmids maybe present.

PAPILLAE are minute inflations of the cuticle, which function as

tactile receptors. The paired minute chemoreceptor organs located in
the cephalic or cervical region of all nematodes are known as
AMPHIDS. On the other hand, a pair of minute lateral post anal or
caudal chemoreceptor organ present in some specie of nematodes
without caudal glands is known as PHASMIDS.

Excretory system
The excretory system consists of two lateral canals that lie in the
lateral longitudinal cords of hypodermis. Near the anterior end of the
body, the lateral canals join in a bridge from which the terminal ducts
leads to a ventral pore in the region of the esophagus.

Reproductive system
The male reproductive organs are situated in the posterior third
of the body as a single coiled or convoluted tube, the various parts of
which are differentiated as testis, vas deferens, seminal vesicle and
ejaculatory duct. Accessory copulatory apparatus consists of one or
two ensheathed copulatory spicules which are sclerotizations of the
cuticle arising from the dorsal wall of cloaca. This spicules maybe
short or long and use for attachment of the male to the female during
copulation. In some species, a wing like appendage or copulatory
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bursa/bursa copulatrix maybe present. Nematodes spermatozoa are

stored in the seminal vesicle.

The female reproductive system may either be a single or

bifurcated tube, differentiated into ovary, oviduct, seminal receptacle,
uterus, ovijector, vagina and a vulva that opens to the exterior. The
ovum passes from the ovary into the oviduct(fallopian tube) where it is
fertilized.

The female adult maybe classified into (a)oviparous, in which

eggs are oviposited and the embryo develops outside the maternal
body as in Ascaris, Trichuris; (b)viviparous or larviparous,where the
adult female gives birth to a larva as in Trichinella spiralis and Filarial
worms and (c)parthenogenetic where the female can produce viable
eggs without being fertilized by the male worms as in Strongyloides
stercoralis.

Ovum

The daily output of a gravid female may range from 20 to 200,000

eggs. The egg consists of a multinucleated mass of protoplasm
usually containing yolk granules. The egg shell may consists of three
layers:

1. vitelline membrane - formed immediately after

(fertilization membrane) sperm penetration;waxy,
colorless and lipoidal in nature

2. chorionic or true shell - a secretory product of the egg;

chitinous in nature and synthe-
sized from glycogen and
ovarian nitrogen

3. albuminous layer - outermost layer;has a tanning

action
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MALE NEMATODE

FEMALE NEMATODE
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DIGESTIVE SYSTEM NERVOUS SYSTEM

EXCRETORY SYSTEM
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Development of Nematodes (Life Cycle)

Parasitic nematodes pass through simple or complex life cycle
both within and outside the body of a host. Nematodes have five
successive fundamental stages, four(4)larval stages and the adult, with
growth and a molt of cuticle(ecdysis) between two stages.

There are two types of life cycle observed in nematodes:

1. Direct - require a definitive host but does not
(Homogonic) require an intermediate host; from the egg
stage it develop into the infective stage
Nematodes with only one host are
homoxenous

2. Indirect - it require both a definitive host and one or

(Heterogenic) two intermediate hosts for the development
into infective stage
Nematodes with more than one host are
heteroxenous

Transmission to a new host depends upon the ingestion of the

infective stage, skin penetration of the infective larval stage, the bite of
infected arthropod or inhalation of the infective stage. The location or
habitat of the adult parasite in the host, to a large extent, governs the
escape of the eggs and the character of the life cycle. When the habitat
of the parasites is in the intestinal tract, the eggs or larvae leave the
host via the feces. When its habitat is elsewhere in the body, there are
other avenues of escape like in urine, sputum, blood and tissue. Lymph
or tissue fluids.

Life span
The life span of nematodes varies wherein some has a life span
of one month, some may live for 12 months and there are also some
which survive for at least 14 years. Nematodes, with few exceptions do
not multiply in humans, thus differentiating them from many other
pathogenic organisms.
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Pathogenicity
The effect of parasitic nematodes upon the host depends upon
the species and location of the parasite. Since nematodes rarely
multiply in humans, the number of parasites present or the intensity of
infection is a critical factor in determining the amount of damage to the
host. The local reactions to adult worms in the intestine are generally
minimal; there maybe some local irritation, some degree of invasion of
the intestinal wall or mucosal damage from blood sucking.

The signs and symptoms of roundworm infection include the

following: passage of worm by mouth, rectum, or, with certain species
(particularly dracunculosis), through skin ulcers; worm eggs may also
be passed in feces ,abdominal cramps, loss of appetite,diarrhea or
constipation,flatulence ,weight loss ,anemia, cough, chest pain, or
difficultly breathing ,nausea and vomiting,fever ,skin lesions, rashes,
hives, itching ,muscle aches ,swelling of lymph nodes ,visual
impairment with certain species (particularly onchocerciasis)

The risk factors for roundworm infection include: living in or visiting

a warm, tropical climate ;poor sanitation, poor personal hygiene,
crowded conditions, such as day care or institutional settings,
compromised immune system,malnutrition ,eating undercooked meat
from carnivorous animals ,eating dirt or clay (children and especially
boys tend to become infected this way),contact with animal feces and
multiple insect bites
Diagnosis:
Diagnosing roundworm infection involves identifying the species
of worm causing the infection. If a worm passes through the mouth or
rectum, it should be brought to the physician for analysis and
identification. Other steps in diagnosis may include: Physical exam ,
Stool and urine samples – identify microorganisms in the stool and
urine ,Blood tests – detect infection in the blood ,Muscle and/or skin
biopsy – reveals infections that affect the muscle and/or skin ,
Ultrasound – reveals worms in lymph nodes ,X ray – reveals large
worms in abdominal region ,Sampling of contents of small intestine
may reveal presence of roundworms ,Tape test – used particularly for
pinworm infections; physician applies cellulose acetate tape to the skin
around the anal region, removes the tape, and then examines it for
pinworm under a microscope.
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CLASSIFICATION OF MEDICALLY SIGNIFICANT NEMATODES

I Based on the presence or absence of caudal chemoreceptor

organ

A. Class Enoplea ( Class Adenophorea; Class Aphasmidea)

- without caudal chemoreceptor organ(phasmids)
- provided with caudal glands

1. Trichuris trichiura
2. Trichinella spiralis
3. Capillaria philippinensis

B. Class Rhabditea ( Class Secernentia; Class Phasmidea)

- with caudal chemoreceptor organ(phasmids)
- without caudal glands

1. Ascaris lumbricoides
2. Strongyloides stercoralis
3. Enterobius vermicularis
4. Angiostrongylus cantonensis
5. Filarial worms
6. Hookworms
7. Dracunculus medinensis

II Based on Habitat

A. Intestinal nematodes
a. Those that inhabit the small intestine
1. Ascaris lumbricoides
2. Capillaria philippinensis
3. Hookworms
4. Strongyloides stercoralis
b. Those that inhabit the large intestine
1. Trichuris trichiura
2. Enterobius vermicularis

B. Extra-Intestinal Nematodes
1. Trichinella spiralis - muscles
2. Filarial worms - lymphatic, tissue
3. Dracunculus medinensis - tissue
4. Angiostrongylus cantonensis - brain
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Ascaris lumbricoides
Common name : Giant intestinal roundworm
Disease : Human Ascariasis

Morphology :

A. Adult

Ascaris lumbricoides is the largest and most common

Nematode of man, male measuring 15 – 30 cm by 3 mm, whereas the
female measures 20 – 45 cm by 5 mm. The large creamy white or
pinkish worm is cylindrical, elongated, tapering gradually at the
anterior end. The diagnostic features of adult Ascaris are:

a. smooth finely striated cuticle with a faint

longitudinal white lateral lines which is seen as
a whitish streak along the entire length of the
body
b. terminal mouth with trilobate lips and a small
triangular buccal cavity

The male has a ventrally curved papillated posterior

extremity with two copulatory spicules. The female on the other hand,
has a paired reproductive organs in the posterior two thirds of the
female and in the anterior and middle third of female is a depression
around the worm where the vagina is located.

B. Ova
There are two types of Ascaris egg that maybe
recovered in the stool, namely:
1. Fertilized eggs - broadly ovoid, golden brown in color,
measures 45 – 75 micron by 35 – 45 micron, with thick
transparent shell which is made up of three layers:
a. vitelline membrane – an inner non permeable, lipoidal layer
b. glycogen membrane – thick, transparent middle layer
c. albuminous/mammilary coat – outermost layer
Inside the egg is a mass of organized, fine granules. This ova
single-celled when freshly expelled; need period of
embryonation in soil
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2. Unfertilized egg - generally larger, longer, elongated or

sometimes irregular in shape measuring 88 – 94 microns. The
egg shell consists of only two layers, a relatively thinner
glycogen membrane and an irregular coating of albuminous
layer. The vitelline layer is absent in infertile eggs.Inside the
egg shell are disorganized highly refractile granules which are
coarse and of various sizes. Unfertilized eggs will not undergo
any further development in the soil.

Occasionally, mammilary coat maybe absent or removed in some eggs

and they are referred to as “decorticated”, while eggs with albuminous
layer are referred to as “corticated”.

Life cycle:
The adult worm normally inhabits the lumen of the small
intestine. They obtain their nourishment from the semi-digested food of
the host. The unsegmented eggs or fertilized eggs are passed out in the
feces and if defecation is done directly in the soil, rapid development of
the eggs takes place and in about two to three weeks, third stage
larvae after two molts are formed within the egg shell and this is the
embryonated egg, the infective stage of Ascaris lumbricoides. These
eggs will never hatch in soil and the only mode of transmission is
ingestion of this embryonated egg. When this fully embryonated eggs
are swallowed, the larvae hatch in the upper small intestine which
penetrate the intestinal wall to reach the venules or lymphatics,
entering the blood circulation. In the portal circulation, the larvae pass
to the heart and lungs. The larvae reach the lungs 1 – 7 days after
ingestion. Since they are 0.02 mm in diameter and the pulmonary
capillaries are only 0.01 mm in diameter, they break out of the
capillaries into the alveoli. After growth and essential development in
the lungs, they migrate or are carried by the bronchioles to the bronchi,
ascend to the trachea to the glottis and pass down the esophagus to
the small intestine. On arrival in the small intestine they undergo a
fourth molt. Ovipositing female develop in about 2 to 2 ½ months after
infection and they live from 12 to 18 months. A female worm has a
productive daily out-put of 200,000.
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Adult in small intestine

⇗ ⇘
larvae ascend respiratory eggs pass out in the
tree and swallowed,descend feces
to S.I. to mature ⇩
⇧ in soil,embryonation
larvae reach the heart and of fertilized eggs in
lungs, molt twice 1 – 2 weeks
⇧ ⇩
in small intestine, eggs hatch ⇦ fully embryonated eggs
and larvae penetrate the ingested by man
mucosa and enter the blood
circulation

Pathology:
The pathology of Ascaris lumbricoides maybe grouped into
those caused by the larval stage and those caused by the adult:

a. Pathology due to larval migration

Larval migration to the lungs can produce pneumonitis
resembling an asthmatic attack accompanied by marked eosinophilia
(Ascaris pneumonitis of Loeffler’s syndrome). The clinical
manifestations are asthmatic type of respiration, cough, urticaria, rash,
edema of the lips and eosinophilia.
Occasionally, ectopic larva may initiate granulomatous
reactions in organs like the brain, spinal cord and kidneys.

b. Pathology due to the adult worm

The adult worm usually feeds on the intestinal contents,
the liquid nutrients. Small numbers of adult worms in the intestine (10 –
20 worms) may not show symptoms and go unnoticed by the host.
Symptoms such as abdominal pain, diarrhea, nausea and loss of
appetite maybe experienced by the host.

Serious and sometime fatal effects of Ascariasis are due to

the erratic migration of the adult worms. They maybe regurgitated and
vomited and may escape through the nostrils. Vomited Ascaris may
pass the larynx and may lead to suffocation or may reach the lungs and
produce pulmonary gangrene or may enter the eustachian
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tube and provoke otitis media. Fever and certain drugs are the two of
the causative factors of Ascaris migration.

The adult may invade the bile duct, gall bladder, liver and
appendix. They may occlude the ampulla of vater and cause acute
hemorrhagic pancreatitis. The worm may penetrate the intestinal wall,
migrate into the peritoneal cavity and produce peritonitis. Some worms
may become entangled resulting in intestinal obstruction.

Even when the worms cause little or no traumatic damage,

the by-product of living or dead worms may rarely produce marked
toxic manifestations such as edema of the face and urticaria,
accompanied by loss of appetite and weight.

Diagnosis:
Diagnosis is made by finding the eggs in the feces, fertilized or
unfertilized by performing Direct Fecal Smear, kato-thick, kato-katz or
concentration technique.

Stool examination may give a negative finding in the following

conditions:
a. when the patient is actually free from Ascaris infection
b. worms are still immature in the lumen
c. during larval migration
d. when only male worms are present in the intestine
Ascaris-specific antibodies can be detected by Ascaris-specific
peptides in dot EIA, a method with satisfactory sensitivity and
specificity for helminth diagnosis.

Treatment:
Piperazine citrate, pyrantel pamoate, mebendazole, albendazole,
levimazole can be used to treat Ascariasis. Piperazine and Pyrantel
pamoate are used these days because these drugs have a
neuromuscular blocking effect on the parasite causing paralysis.

Epidemilogy:
Ascaris lumbricoides is a prominent parasite in both temperate
and tropical zones, but it is common in warm countries and prevalent
where sanitation is poor.
 22

22

Ascariasis occur at all ages, but it is more prevalent in the 5 – 9

year old group, in pre-school and young children who are frequently
exposed to contaminated soil. Infected small children provide the chief
source of soil contamination by their promiscuous defecation in
dooryards and earthen-floored houses, where the resistant eggs remain
viable for long periods.

The infective eggs are transmitted hand-to-mouth by children

who come in contact with contaminated soil directly through playthings
or through dirt-eating. Extensive use of night soil as fertilizers accounts
for infection in all ages.

Ascaris eggs are susceptible to desiccation. A moist, loose soil with

moderate shade provides a suitable environment. Dryness is
unfavorable for survival and eggs are destroyed by direct sunlight
within 15 hours and are killed at temperature above 40ºC. Eggs are
resistant to chemical disinfectant and can withstand temporary
immersion in strong chemicals. Ascaris eggs in soil may survive for a
year or two in temperate climate and probably only a few weeks in
tropical countries.

Ascariasis is the most common helminth infection worldwide

with an estimated 1 billion individuals infected. In the Philippines, the
prevalence ranges from 80 – 90 % in rural areas and in poor and slum
sections of towns and cities.

Domestic pigs are susceptible to infection with human Ascariasis

thus serve as a significant reservoir host since human can acquire
infection with pig Ascaris, Ascaris suum.

Prevention and Control:

There are two methods used in the control of Ascariasis, either
mass treatment or selective treatment. Mass treatment although ideal
may not be practical because of the high costs of antihelminthiases.
Selective treatment refers to treating only a group usually those found
positive for eggs after stool examination.

For the preventive aspect, health education, sanitary disposal of

human excreta, proper personal hygiene, refrain from using human
excreta as fertilizer and thorough cooking of food.
 23

23

Ascaris lateral lines Ascaris trilobate lips

Male copulatory spicule

 24

24

Ascaris fertilized egg Ascaris fertilized egg

(corticated) (decorticated)

Ascaris unfertilized egg Ascaris unfertilized egg

(corticated) (decorticated)

Ascaris embryonated egg

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Toxocara canis and Toxocara cati

Common name : Dog ascaris and Cat ascaris
Disease : Toxocariasis or Visceral Larva Migrans

Toxocara canis and Toxocara cati are Ascaris worms naturally

parasitic in the intestines of dogs and cats that accidentally infect
human, an abberant host, producing a disease called visceral larval
migrans (VLM) or toxocariasis. VLM is a clinical syndrome resulting
from the invasion of human visceral organs by nematode larvae of the
genus Toxocara.

Life cycle:
In dogs and cats, the worm exhibit the same life cycle as the
human Ascaris. The adult female worms are 10 – 12 cm in length and
pass numerous eggs into their host’s feces. In moist soil, the eggs
become embryonated in several weeks. When ingested by dogs and
cats, the larvae hatch in the small intestine, migrate to the intestinal
mucosa and by way of blood stream reach the liver, lungs, bronchial
tree and trachea, swallowed again and mature in the small intestine of
these animals.

The embryonated eggs on the other hand, when ingested by

human, larvae will hatch and can not follow its normal course of
development as seen in their natural hosts. The larvae penetrate the
intestinal mucosa and are carried by the blood stream to the liver,
lungs and other organs. Here they wander for weeks and months or
become dormant and they do not develop beyond the migrating larval
forms.

Pathology:
Larval migration may produce hemorhage, necrosis and granuloma at
the site. Eosinophilia, liver damage, pulmonary inflammation and ocular
problems have also been observed. A number of children have exhibit
anemia accompanied by a high WBC count.
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26

Diagnosis:
The diagnosis of toxocariasis in human is usually established on
clinical grounds with triad of marked eosinophilia, hepatomegaly and
hyperglobulinemia. Examination of stool from infected patients is not
useful because egg-laying adults are not present. However,
examination of fecal material from infected pets often supports the
diagnosis.

Treatment:
Because the clinical course of VLM is so variable, it is very
difficult to evaluate efficacy of any treatment. In addition, since the
infection is usually self-limited, only severe cases need to be treated.
Thiabendazole appears to shorten the course of the disease.

Epidemiology:
Wherever infected dogs and cats are present, the eggs are threat
to human. This is especially true for children who are exposed to
contaminated soil and who tend to put objects in their mouth.

Prevention and control:

Small children should be protected against contact with infected
dogs and cats. Animal under six(6)months should be dewormed with
piperazine every month and older one every two(2)months. Worms
passed, as a result of treatment should be destroyed. Dogs and cats’
stools passed in children’s play areas should be buried and sandboxes,
which offer an attractive defecating area to cats, should be covered
when not in use. There is no satisfactory chemical for killing the eggs
in soil.
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ACTIVITY SHEET NO. 2

NAME______________________________SEC_____DATE_______

1. Explain why failure to demonstrate the characteristic Ascaris

eggs in the feces does not rule out Ascariasis?

2. Give other nematodes, aside from Toxocara, that can cause

Visceral larval migrans.

3. Explain why migration of adult Ascaris cause serious and fatal

effects?
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Trichuris trichiura
Common name : Whipworm
Disease : Trichuriasis

Morphology:
A. Adult

The human whipworm lives attached to the wall of the caecum.

Man is the principal host of Trichuris, but it has also been reported in
monkeys and hogs.

The adult worm is flesh colored or pinkish and the anterior is

characteristically attenuated, whiplike while posterior end is more
robust. Three fifths of the body is traverse by a narrow esophagus
resembling a string of beads while two fifths contains the intestine and
a set of reproductive organs. Female is slightly larger than male and
measures 3.5 to 5 cm in length with a straight posterior end. On the
other hand, the male measures 3 to 4.5 cm in length and has its
posterior and coiled through 360º or more, with a sheathed single
spicule.

B. Ova
The eggs measures 50 – 54 by 22 – 23 microns and are discharge
in the stool in the unsegmented stage. The egg is characteristically
barrel shaped/lemon shaped/football shaped or Japanese lantern in
appearance with prominent bipolar plugs on both ends. The shell is
rather thick and composed of three layers, with yellowish outer layer
and a transparent inner layer. Embryonation of eggs takes place in soil,
where the first stage larvae is formed in three weeks.

Life cycle:
The adult worm inhabits the caecum. The fertilized eggs are
unsegmented when passed out in the feces. Embryonation takes place
in the soil, where an unhatched, first stage larvae is produced in 3
weeks in a favorable environment. When the fully embryonated egg is
ingested by man, the activated larvae escapes from the weakened egg
shell in the upper small intestine and penetrate the intestinal wall,
where it remains for 3 to 10 days, then passes down to the caecum to
transform into adult. The development period from the ingestion of
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eggs to ovipositing adult worms covers about 30 to 90 days. The

number of eggs produced per day by a female has been establishing at
3,000 to 10,000. Its life span is 4 to 6 years.

Adult worm attached

to the walls of caecum
⇗ ⇘
larvae hatch in eggs passed out
intestine in the feces
⇧ ⇩
embryonated eggs ⇦ in soil, eggs embryonate
ingested by man in 2 – 3 weeks

Pathology:
Light infections usually do not give rise to recognizable clinical
manifestations and the presence of the parasite is discovered only on
routine stool examination.

Patient with heavy Trichuriasis, the worms maybe found throughout the
colon and rectum. The characteristic clinical picture include frequent
small blood-streaked diarrheic stool, abdominal pain and tenderness,
nausea and vomiting, anemia(hypochromic anemia), weight loss and
rectal prolapse.

Diagnosis:
Diagnosis is made by stool examination using DFS or Kato-thick,
kato-katz or concentration technique to demonstrate the characteristic
barrel-shaped ova.

Treatment:
Albendazole, Mebendazole, Pyrantel pamoate are the drug of choice in
the treatment of Trichuriasis.
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Epidemiology:
The prevalence of Trichuris infection is high but its intensity is
usually light. The prevalence ranging as high as 80% in certain tropical
countries. The prevalence rate of Trichuriasis in the Philippines ranges
from 80 to 90%. It is more common in warm, moist region of the world.
Its distribution is coextensive with that of Ascaris lumbricoides. The
highest incidence is found in regions of heavy rainfall, subtropical
climate and highly polluted soil. It has been observed that Trichuris
eggs in the soil are less resistant to adverse conditions than Ascaris
eggs.

Children are more frequently infected than adults. The heaviest

infections are in young children, who live largely at ground level,
habitually contaminate the soil and pick up infection from polluted
dooryards. Infection results from the ingestion of embryonated eggs
via hands, food or drink that have been contaminated directly by
infested soil or indirectly by playthings, domestic animals or dust.

Prevention and Control:

Infection maybe prevented by:
1. treatment of infected individuals
2. sanitary disposal of human feces
3. washing of hands before meals
4. proper instruction to children on sanitation and proper personal
hygiene
5. thorough washing and cooking of food
6. avoid using human excreta as fertilizer
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Trichuris trichiura Trichuris trichiura

Female male

Trichuris trichiura ova

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ACTIVITY SHEET NO. 3

NAME_____________________________SEC______DATE________

1. What are the differences and similarities in the life cycle of

Ascaris lumbricoides and Trichuris trichiura?

2. Why do patient with large number of Trichuris may suffer

anemia?

3. Explain why rectal prolapse in possible in case of heavy

Trichuriasis?
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HOOKWORMS

Necator americanus
Common name: New World Hookworm, American Hookworm
Disease : Necatoriasis, Uncinariasis, Tropical anemia
“Laziness”

Ancylostoma duodenale
Common name: Old World Hookworm
Disease : Ancylostomiasis, Miner’s anemia

Ancylostoma braziliense
Common name: Cat Hookworm
Disease : Cutaneous Larva Migrans, Creeping eruption

Ancylostoma caninum
Common name: Dog Hookworm
Disease : Cutaneous larva Migrans, Creeping eruption

Morphology:
A. Adult
Ancylostoma duodenale adult is relatively stout, the body
contour tends to follow the general body curvature of the body hence it
looks like a letter “C”. The large buccal capsule is equipped with two
pairs of ventral teeth almost similar in size. The male worms have a
fan-like organelle at the posterior portion known as copulatory bursa or
bursa copulatrix, which is short and broad with a tripartite or tridigitate
dorsal ray and with a pair of simple, long, bristle-like copulatory
spicule, plain and free at the tip.

Necator americanus adult is small and has a tendency to

go against the general body curvature at the anterior end hence a hook
is formed (S shaped). The buccal capsule is provided with a pair of
semi-lunar cutting plates. Located near the lateral margin of the buccal
capsule is a long cephalic or amphidial gland which secretes a potent
anticoagulant, that promote the flow of any blood or tissue fluids drawn
into the buccal capsule. The bursa copulatrix is longer than broad with
a bidigitate or bipartite dorsal ray and a long, slender copulatory
spicules that are fused at the tip to form a delicate barb.
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34

One of the smaller species of hookworms, Ancylostoma braziliense

possesses a pair of large teeth and a pair of inconspicuous median
teeth in the buccal capsule. The bursa copulatrix is almost as broad as
long and is supported by relatively short lateral rays.

Ancylostoma caninum is a common parasite of dogs. They have

a wide buccal capsule bearing three pairs of ventral teeth. The cephalic
or amphidial gland of the worm secretes an anticoagulant that delays
coagulation of blood. Long, moderately slender rays support the male
bursa.

B. Larvae
1. Rhabditiform larvae ( 1st stage larvae)
This larvae hatches in 24 – 48 hours. This is short,stout
with a long, narrow buccal chamber and a flask-shaped muscular
or bulbous esophagus and an inconspicuous genital
primordium. The mouth is open and they feed on bacteria and
organic matter present in the soil or feces, hence they are
considered as the feeding stage of Hookworm.

2. Filariform larvae ( 3rd stage larvae)

This develops in the soil within 5 – 8 days. This larvae
grows longer and slender with a pointed posterior end. The
mouth closes, the esophagus elongates and has a protective
sheath as covering. This is the non-feeding stage and the
infective stage of hookworm.

C. Eggs
The eggs are ovoidal, thin-shelled and colorless, measures
56 – 60 by 34 – 40 microns. It is unsegmented at oviposition and
usually in 2 – 8 cell stages of cell division in fresh feces.

Life cycle of human hookworms:

The adult worm inhabits the small intestine and is attached into
the intestinal mucosa by the use of their tooth-like processes. The adult
worms feed on lymph, RBC and plasma. The fertilized eggs are passed
out in the feces. The eggs mature rapidly in a moist, warm soil and
produce the rhabditiform larvae in 1 – 2 days. The rhabditiform larvae
molt twice in 7 – 10 days and transform into non-feeding filariform
larvae, which is infective to man. The active filariform larvae, which
frequent the upper half-inch of soil and project from surface, on
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35

contact with exposed human skin, usually the feet, secure lodgment in
the hair follicles or scaling fragments of the epidermis and penetrate
down to the deeper portion of the corium or to the subcutaneous tissue
where some of them enter the superficial venules. The larvae enter the
lymphatics or venules and are carried in the blood into the heart, to the
lungs, where because of their size, they are unable to pass the capillary
barrier and therefore break out of the capillaries into the alveoli. They
ascend the bronchi and trachea, finally swallowed and pass down to
the intestines. This larval heart and lung migration takes about 1 week.
During this period, the larvae undergo a third molt and acquire a
temporary buccal capsule, which enables the adolescent worm to feed.
After a fourth molt at about the thirteenth day, they acquire the adult
characteristics and mature egg laying females are produced in 5 – 6
weeks after infection. The life span of the worms is from 2 – 13 years.
Ancylostoma duodenale female produces 30,000 eggs daily while
Necator americanus female produces 9,000 eggs daily. Rarely, infection
by Ancylostoma duodenale through ingestion of filariform larvae which
will develop into adult worms without the lung passage.

Adults in small intestine

⇗ ⇘
Esophagus eggs passed out in feces
⇧ ⇩
Swallowed in soil; eggs liberate
⇧ Rhabditiform larvae(1-2 days)
Trachea ⇩
⇧ in 5-8 days, larvae transform
Lungs into filariform larvae
⇧ ⇩
Enters the blood ⇦ filariform larvae penetrate
circulation skin of man

Life cycle of animal hookworms:

The adult worms of animal hookworms inhabit the intestine of
cats and dogs. Eggs are passed out in the feces into the soil. In the
soil, the eggs will transform into rhabditiform larvae and finally into
infective filariform larvae. The larvae may penetrate the skin of the
animal hosts and will develop into adult. On the other hand, filariform
larvae can penetrate the skin of man but fail to complete their
development in this incompatible host.
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Pathology:
A. Pathology due to the larval stages
1. Ground itch or Dew itch
Percutaneous entry of the infective filariform larvae is
often characterized by an itching sensation or dermatitis. Itching
is often severe and it is known as “ground itch” or “dew itch”, as
it is related to contact with soil, especially on a dewy morning.
Within several hours, allergic reactions to the worms or their
products causes pruritus, erythematosus papular rash that may
become vesicular. Scratching may lead to secondary bacterial
infection.

2. Pulmonary lesion (Wakana Disease)

Wakana disease is a syndrome caused by the massive
pulmonary migration of larval stages of hookworms. This maybe
due to allergic reaction to the migrating larvae and may produce
symptoms similar to Ascaris pneumonitis.

3. Creeping eruption or cutaneous larva migrans

Creeping eruption is a dermatitis characterized by
serpiginous intracutaneous lesions caused by migration of the
filariform larvae or nematode larvae that normally do not infect
the human host like A. caninum and A. braziliense. The infective
larval stage can enter the human skin but can not pass below the
stratum germinativum producing instead a serpiginous tunnel in
this stratum. There will be no further development in human host,
the larvae remain trapped in the skin of the wrong host for
weeks or months, wandering through subcutaneous tissue. The
larvae move at a rate of several millimeters to a few centimeters
per day.

B. Pathology due to adult worms

1. Hookworm anemia
Adult worms suck the host’s blood and mucosal
substances. An anticoagulant secretion facilitates blood sucking.
Another factor that should be considered is the presence of
bleeding raw areas of mucosa left by the adult worms when they
transfer to a new site. The blood picture is “Microcytic hypo-
chronic anemia”. The signs and symptoms of chronic infection
are those of profound iron deficiency anemia. The essential
damage produced in intestinal hookworm infection is
hemorrhage from the intestinal wall.
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2. Hypoalbuminemia
There is a low level of albumin due to combined loss of
blood, lymph and protein.

Diagnosis:
Final diagnosis for hookworm infection is made by finding the
characteristic eggs in the feces usually by performing DFS. In light
infection, concentration technique maybe required such as Zinc Sulfate
Floatation and Formalin Ether Concentration, to recover the eggs. On
prolonged standing, 24 hours, the eggs may hatch and liberate the
rhabditiform larvae, which should be differentiated from those of S.
stercoralis. The collection of larvae from eggs hatched on filter paper
strips with one immersed in water (Harada-Mori) is reported to give a
high percentage of positive findings. Eggs counting methods such as
Stoll Egg Count and Kato thick smear, are useful in surveys. Hookworm
larvae can be recovered from soil by Baermann Funnel Method and by
the Damp Gauze Pad method of Beaver.

The diagnosis of creeping eruption is based on the clinical

appearance of the tunnels and a history of contact with dogs and cats
and soil. Occassionally, larvae are recovered in skin biopsy or
following freezing of the skin.

Treatment:
The current drugs of choice are mebendazole, albendazole and
flubendazole. Mebendazole and Albendazole are both benzimidazole
derivatives that block the uptake of glucose by most intestinal and
tissue nematodes. If significant anemia is present, the first
consideration is the treatment of anemia. Iron therapy is indicated to
raise hemoglobin level to normal. Thiabendazole, either topical or
systematic has been successful for creeping eruption.

Epidemilogy:
The prevalence of hookworm infection depends on:

1. the continous presence of infection in the human population,

2. defecation habits ensuring the eggs are deposited in favorable
locations for extrinsic development of parasites,
3. favorable environmental conditions and
4. opportunity of the filariform larvae to infect humans
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Factors determining the geographic distribution prevalence of

the two common species of human hookworms:

1. temperature
2. pattern of rainfall
3. burying action of dung beetles

In the Philippines, the overall prevalence rate of hookworm

infection is about 5 – 45 % wherein the dominant specie is Necator
americanus.

The eggs and developmental stages of N. americanus are more

tolerant of high temperature than those of A. duodenale. The eggs and
developing larvae of A. duodenale are able to tolerate low temperature
that retards the development of Necator. Hookworm larvae move very
little horizontally but can migrate upward as much as one meter. The
infective filariform larvae are usually sheathed though at times it may
exsheath. Improper disposal and use of human feces as fertilizer are
the chief sources of infection in areas where individuals walk
barefooted.

The larvae of A. duodenale has been observed to exhibit a

dormant phase in man, migrating to the intestine before becoming
quiescent, others probably rest in muscles before migrating to the
lungs and onward to the intestine. This larval latency complicates
treatment and control of A. duodenale since dormant nematode larvae
are more resistant to antihelminthic and may resume development at a
later date.

Prevention and Control:

Prevention and control of hookworm infection involves the
following:

1. proper personal hygiene

2. sanitary disposal of human excreta
3. wearing of shoes and slippers to avoid skin contact with
filariform larvae in contaminated soil
4. treatment of infected individuals
5. mass treatment when incidence is greater than 50%
6. correction of anemia by giving adequate diet and iron therapy
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Hookworm Rhabditiform larvae Hookworm filariform larvae

Hookworm ova
 40

40

BUCCAL CAPSULE OF HOOKWORM

Necator americanus Ancylostoma duodenale

Ancylostoma caninum Ancylostoma braziliense

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Strongyloides stercoralis

Common name : Threadworm

Disease : Strongyloidiasis, Cochin-China Diarrhea

Strongyloides stercoralis is known for its extra ordinary

conditions. It is the most documented facultative parasite capable of
leading both a free living and parasitic existence. People are the
principal host of S. stercoralis, but dogs and monkeys have a similar
parasite. Similar specie, Strongyloides fuellerborni, can infect higher
primates and humans.

Morphology:
A. Adult
The parasitic female measuring up to 2 – 7 mm in length
and 30 – 4 um in width, is small, colorless, semi-transparent filiform
nematode with a finely striated cuticle. It has a short buccal cavity and
a long, slender cylindrical esophagus extending through the anterior
third or two-fifths of the body. In the parasitic phase, no male form of
this parasite has been reliably identified, possibly because it is not
essential in the life cycle of the parasite; the parasitic female being
parthenogenetic is capable of self-fertilization without the participation
of the male.

The free-living female is shorter than the parasitic female

but is stouter and with a double bulbed muscular esophageal pharynx.
The free-living female is broadly fusiform, smaller than the female, with
pointed tail that is curved ventrad.

B. Larvae

1. Rhabditiform larva
This larva has a short buccal cavity, muscular elongated
esophagus with a pyriform posterior bulb and a relatively
conspicuous genital primordium. This is passed out in the feces.

2. Filariform larva
This is a long, delicate larvae with a long esophagus and
with a forked or notched tail.
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C. Eggs
The paired uteri of the parasitic female contain a single
file of thin-shelled, transparent, partially embryonated eggs which are
squarish resembling “Chinese lantern”. These eggs are seldom seen in
the feces.

Life cycle:
Parasitic female are most frequently found in the duodenum and
jejunum, penetrating the mucosa of the intestinal villi, where they
burrow in serpentine channels in the mucosa, depositing eggs and
securing nourishment. The eggs of the parasitic female are deposited
in the intestinal mucosa. They hatch into rhabditiform larvae that
penetrate the glandular epithelium and passed out in the feces.

This parasite has three types of life cycle:

1. Direct cycle
After a short feeding stage of 2 – 3 days in the soil, the
rhabditiform larvae transform into filariform larvae. On contact
with skin of man, the filariform larvae enter the venous
circulation, pass through the heart and are carried to the lungs.
In the lungs, they break out of pulmonary capillaries into the
alveoli and migrate to the pharynx, glottis and are swallowed and
reach the upper part of the small intestine, where they develop
into adult. Mature ovipositing females develop in about 28 days
after the initial infection.

2. Indirect cycle
In this cycle, the rhabditiform larvae develop into sexually
mature free living females and males. After fertilization, the free
living female produced partially embryonated eggs, which
complete their development in few hours and hatch into
rhabditiform larvae. These larvae may repeat the free living
generation or under certain conditions, these larvae
metamorphose into the infective filariform larvae. The indirect
phase appears to be associated with the optimal environment
conditions for the free living existence in tropical countries.

3. Autoinfection
At times the larvae may develop rapidly into the filariform
larvae while en transit down the bowel. They may establish a
developmental cycle within the host by penetrating the mucosa
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of the lower portion of the ileum and colon, enter the blood
stream, undergo a heart and lung phase, then return to the
intestine and mature in the mucosa. At other, filariform larvae
are passed in freshly evacuated stool. Upon contact with the
perianal skin, such larvae cause re-infection.

Parasitic female in ⇨ Eggs deposited in ⇨ Rhabditiform larva

small intestine of man intestinal mucosa hatch from eggs
⇧ ⇙ ⇩ ⇩
esophagus Autoinfection Direct Indirect
⇧ ⇩ cycle cycle
swallowed in s.i., rhabdi- ⇩ ⇩
⇧ tiform larvae Rhabditiform larvae passed
pharynx transform into out in feces into the soil
⇧ filariform Ι ⇩
trachea larvae Ι free living
⇧ ⇩ Ι adults(F & M)
alveoli penetrate Ι ⇩
⇩ intestinal mucosa Ι eggs
lungs Ι Ι ⇩
⇧ Ι Ι Rhabditiform
⇧ Ι Ι larvae
⇧ ⇩ ⇩ ⇩
heart ⇦ blood stream ⇦ penetrate the ⇦ Filariform larvae
skin of man

Pathology:
In great majority of cases of Strongyloidiasis, infections are light
and go unnoticed by their human hosts, as they produce no significant
symptoms. The only objectively discerned abnormality is peripheral
esoniophilia.
The types of diseases caused by Strongyloides maybe classified
as cutaneous, pulmonary and intestinal:
1. Cutaneous infection
The initial penetration of the skin by the filariform larvae of
Strongyloides provokes little or no reaction, although if the
number of larvae is usually large, there maybe pruritus and
erythema at the site of penetration. In highly sensitized
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individuals(repeatedly infected), an allergic response to the

penetrating larvae may develop. The larva may not be successful
in promptly carrying out their pulmonary migration, instead they
may migrate in the skin causing a type of creeping eruption or
larva migrans characterized by a rapidly progressing linear
urticarial lesion termed as larva currens(racing larva).
2. Pulmonary infection
Pneumonitis may develop as a result of larval migration to
the lungs.
3. Intestinal infection
In heavy infection, the mucosa maybe honeycombed by
the adult worms and larvae and sloughing of extensive patches
may occur. Long- standing and heavy infections result in weight
loss and chronic dysentery accompanied by malabsorption and
steatorrhea.

Diagnosis:
The presence of the characteristic rhabditiform larvae in feces is
diagnostic. Harada-Mori is used to recover the larvae. Three stool
samples, one per day for 3 days are recommended because S.
stercoralis larvae may occur in “showers”, with as many present one
day and few or none the next day. The duodenal fluid collected via
aspiration or string test should be examined if feces are negative. The
duodenal fluid gives a slightly higher positive finding. Eggs can only be
obtained by drastic purge or duodenal intubation. Serological
procedures such as ELISA and IHA are also available.

Treatment:
The drug of choice is albendazole and thiabendazole.

Epidemiology:
S. stercoralis is especially prevalent in the tropical and
subtropical areas where warm, moisture and lack of sanitation favor its
free-living existence.

Prevention and control:

Improved sanitation, proper personal hygiene and prompt
treatment of existing infections and use of shoes and slippers to avoid
contact with contaminated soil are good preventive measures.
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Strongyloides stercoralis Strongyloides stercoralis

Rhabditiform larva filariform larva
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ACTIVITY SHEET NO. 4

NAME_____________________________SEC______DATE_______

1. Differentiate the infection due to larval stage of hookworm

from the infection due to the larval stage of Strongyloides.

2. What is the characteristic appearance of the intestinal mucosa

In Strongyloidiasis and what bring about this appearance?

3. Discuss the similarities and differences in the life cycle of

Hookworm and Strongyloides.
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Enterobius vermicularis
Common name : Pinworm or Seatworm
Disease : Enterobiasis or Oxyuriasis

Morphology:
A. Adult

The adults are small, whitish or brownish in color. The

male measures 2 – 5 mm in length, the tail or posterior end is strongly
curved and a single copulatory spicule is present. The adult female
measures 8 – 13 mm in length and has a long pointed tail. The uteri of
the gravid female are distended with eggs. The diagnostic features of
adult Enterobius are:
1. a pair of lateral cuticular wing-like expansion at the
anterior end known as “ cephalic alae”

2. a distinct or prominent esophageal bulb

Eggs:

Eggs are elongated measuring 50 – 60 by 20 – 30 microns;

wherein the ventral side is flattened thus the appearance is similar to
letter “D” or characteristically lopsided in appearance. There are two
eggshell layers, an outer thick hyaline albuminous membrane and an
inner embryonic, lipoidal membrane. The eggs are fully embryonated
when laid and will mature within six hours after oviposition of gravid
female and these are already infective. A gravid female may oviposit
4,672 to 16,888 eggs per day. Eggs are resistant to disinfectant and
under cool, moist condition may remain viable for 13 days.

Life cycle:
Man is the only known host of Enterobius vermicularis. The adult
worm inhabits the caecum of the large intestine with the head attached
to the intestinal wall. Immature female and male occasionally maybe
found in the rectum and lower part of the colon. At times, the worms
may travel upward to the stomach, esophagus and nose. In gravid
female, the uteri become packed with eggs and the body becomes
distended, which makes the female release its hold on the intestinal
wall and migrate to the perianal and perianal regions, where eggs are
expel in masses by the contraction of the uterus and vagina under
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48

the stimulus of lower temperature and aerobic environment. The female

usually dies after oviposition.

The eggs laid on the perianal region become fully mature within
six hours and are readily infective. Upon ingestion of these eggs, larvae
hatch in the duodenum, the liberated rhabditiform larvae molt twice
before reaching adolescence in the jejunum and upper ileum, pass
down into the caecum and develop into adult worms in 2 – 3 weeks to 2
months. Under optimum condition eggs remain viable up to 13 days.

Male and female

Adults in caecum
⇗ ⇘
migrate to its final gravid female migrates
habitat in the to the perianal region
large intestine to deposit embryonated eggs
⇧ ⇩
larvae hatch in ova are infective to man 6 hrs.
the duodenum after deposition
⇖ ⇙
Ova are ingested or
inhaled by man

Pathology:
Many children and adults show no recognizable symptoms and
usually serve only as carriers. At the site of attachment, there maybe
minute ulcerations or abscesses especially in the cecal mucosa. The
most significant pathologic conditions are produced by migrating
gravid female wherein the migration of the famle from the caecum to
the perianal region to oviposit cause crawling sensation. During this
period, there maybe intense itching in the perianal region or pruritus
ani which will result to scratching of the itchy area until it is scrarified.
Pruritus ani more often may give rise to hemmorrhage, eczema and
pyogenic infection of the anal and perianal region.

A number of signs and symptoms has been attributed to the

presence of pinworm like poor appetite, disturbed sleep, insomnia,
weight loss, irritability, grinding of teeth, nausea and vomiting, but
these symptoms are often difficult to establish its correlation with
pinworm infection.
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49

Migrating worms may enter the appendix and produce

appendicitis. In female patients the migrating worm may oviposit in the
genital causing vulvovaginitis with mucoid vaginal discharge or may
enter the reproductive tract up to the fallopian tubes and either become
encysted or produce symptoms of salphingitis.

Diagnosis:
Pinworm infection is suspected in individual that shows perianal
itching, insomnia and restlessness. Diagnosis is made by finding the
characteristic eggs using Graham Scotch tape anal swab technique. In
only about 5% infected patients are eggs found in the feces. The
sample should be collected soon after the patient awakens in the
morning and before he takes a bath or defecates, since oviposition
usually takes place at night. Repeated examinations on 7 consecutive
days are necessary before the patient is considered free from infection.

Occasionally, adult worms maybe seen crawling from the anus at

night, after the child has been put to sleep. In such cases, the worms
should be placed in alcohol and brought to the laboratory for
identification.

Treatment:
The infection is self-limited and in the absence of reinfection,
ceases without treatment.

Albendazole, mebendazole and pyrantel pamoate are effective

against infection with pinworm. To avoid reinfection in the family since
it is easily spread within the family, hence it is termed a “familial
disease”; it is customary to treat the entire family simultaneously.

Epidemiology:
Enterobius vermicularis occur worldwide, but it is more common
in the temperate and cold regions because of less frequent bathing and
infrequent changing of clothes. In moist tropics, where infants and
young children are essentially unclothed, oxyuriasis is less prevalent
than in cooler climates where person to person spread is greatest in
crowded conditions such as in day care centers, schools and mental
institutions. Although this parasite is more prevalent in the lower
economic group, it is not uncommon in the well-to-do and highly
educated elite group and even in the seats of the mighty. Enterobiasis
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is a group infection and is more common in infected families or in

asylums.

In the Philippines, it is 29% among school children from

exclusive private schools and 56% from those coming from public
schools. Studies conducted in the Philippines showed that eggs were
collected from under fingernails and fingertips.

The most common of transmission are:

1. hand to mouth transmission from scratching the perianal folds in
response to irritation by the migrating egg laying female worms
2. inhalation of airborne eggs from dust
3. autoinfection through the anus
In retroinfection, the fully embryonated eggs hatched in
The perianal region and the larvae migrate into the rectum and
large intestine. Autoinfection is responsible for continued
existence of infection in infected individuals.

Prevention and control:

Proper personal hygiene especially hand washing before and
after meals and cutting of fingernails. Things used by infected
individuals like clothes and bedlinens should be sterilized by boiling.
General cleanliness in the house should always be practice. When one
member of the family or institution proved positive for Enterobiasis, all
members should be treated irregardless of whether each one has been
examined by perianal swab or not.
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Enterobius vermicularis Enterobius vermicularis

Female Male
0

Enterobius vermicularis ova

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ACTIVITY SHEET NO. 5

NAME______________________________SEC_________DATE_______
1. Why is Enterobius also referred to as “society worm”?

2. How does autoinfection in case of oxyuriasis takes place?

3. What are the factors responsible for oviposition of gravid

female at the perianal region at night ?

4. What main morphological features will differentiate adult

Enterobius from other nematodes?
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Capillaria philippinensis

Common name : Pudoc worm

Disease : Intestinal Capillariasis, Pudoc’s disease

Morphology:
A. Adult

Capillaria philippinensis are very tiny worms, the male

measures 2.13 to 3.17 mm in length with an extra ordinary long, smooth
spicular sheath. The female measures 2.5 to 4.3 mm in length, the
anterior portion contains the esophagus and the stichosomes; the
posterior portion contains the intestine and the reproductive organs.
There are two types of Capillaria female:

a. Typical female - 8 – 10 eggs in the uterus

(oviparous) arranged in a single row; gives
rise to typical Capillaria egg

b. Atypical female - 40 – 45 eggs in the uterus

(larviparous) arranged in 2 – 3 rows;hatch
while still in the uterus

B. Eggs

There are two types of Capillaria eggs:

1. Typical Capillaria egg - produced by typical Capillaria

female; yellow in color, moderately thick, with striated egg
shell with flattened bipolar plugs, measure 42 by 20
microns, characteristically with indentation in the middle
thus peanut-shaped and are usually in the single or two
segmented stage of development

2. Atypical Capillaria egg - produced by typical female, thin-

shelled without bipolar plugs and multisegmented or
embryonated. These eggs hatch while still in utero into the
first stage larvae
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Life cycle:
Capillaria philippinensis adult lives burrowed into the mucosa of
the small intestine, predominantly in the jejunum, with both ends free.
Typical and atypical females produced eggs and larvae. Eggs are
passed out in the feces, embryonate in water 3 – 9 days and when
ingested by fresh water fish which serve as intermediate host, hatch
and develop into adult in three weeks time producing first generation
female which gives birth to larvae. These larvae grow into adult within
two weeks and the female of these generations produced the typical
Capillaria eggs. The presence of atypical female producing larvae
accounts for the internal multiplication of the parasites inside the
intestine.

Male and atypical female

worms in small intestine
⇗ ⇧ ⇘
man ingests raw in 2 or more weeks, 2nd
fish harboring the generation larvae develop
infective larvae into male worms and
⇧ typical female
embryonated eggs ⇩
ingested by fresh eggs laid by typical
water fish female worms
⇖ ⇙
Eggs passed out in water,
embryonate in 3 – 5 days

Pathology:
The clinical manifestations of the disease are extreme and
persistent diarrhea that may lead to dehydration, rapid weight loss,
abdominal pain, gurgling of stomach (borborygmus), muscle wasting,
anorexia, vomiting and edema. There is malabsorption of fats and
sugar (intestinal malabsorption) and low plasma levels of Potassium,
Calcium, carotene and total protein. If the disease is not treated
immediately severe manifestations of the disease may develop like
hypotension and cardiac failure and may lead to the death of the
patient.
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Diagnosis:
The specimen of choice is stool. DFS, conc. technique like AECT,
FECT reveal eggs and larvae and sometimes even adult worms.

Treatment:
Mebendazole and Albendazole are the drug of choice. In severe
cases with electrolyte and protein loss, electrolyte replacement should
be given to the patients.

Epidemiology:

The first case of human infection with Capillaria philippinensis

occurred in 1963 from Ilocos Norte and since then, there have been
2,000 confirmed cases and 108 deaths. There are more reported cases
of male infection than female with ratio of 2:1. Man acquires the
parasite by ingestion of raw or insufficiently cooked fish harboring the
infective stage. In the Philippines, transparent fishes like bagsang,
bagsit and ipon may harbor the parasite. Capillaria philippinensis is a
parasite of fish-eating birds and there is a fish-bird cycle in nature
ensuring the continuity of its life cycle. The ability to infect fish-eating
birds suggest that this parasite maybe widely distributed throughout
Asia and possibly elsewhere.

The provinces endemic in the Philippines are Ilocos Norte, Ilocos

Sur, Cagayan, La Union, Pangasinan, Zambales, Agusan del Norte and
Leyte.

Prevention and control:

Since infection is acquired by eating raw or improperly cooked
fish, fish should be thoroughly cooked to prevent disease in man.
Proper sanitary practices should also be practice. All infected
individuals should be treated immediately and feces should be
disposed properly.
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Capillaria philippinensis Capillaria philippinensis

Female Male

Typical Capillaria philippinensis ova

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ACTIVITY SHEET NO. 6

NAME_____________________________SEC_________DATE_______

1. Explain the fish – bird cycle of Capillaria.

2. What are the similarities and differences in the life cycle of

Trichuris and Capillaria?

3. What is responsible for internal multiplication in Capillariasis?

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Trichinella spiralis
Common name : Trichina worm
Disease : Trichinosis, Trichiniasis

Morphology:
A. Adult

Adult worm is minute, whitish in color with the anterior

End of the body consisting of esophagus filled with stichosomes. The
male measures 1.5 by 0.04 mm with a single testis located near the
posterior end. The female measures 3.5 mm by 0.06 mm with a single
ovary located at the very posterior part of the body. The female is
viviparous or larviparous and is capable of producing 1,500 larvae.

B. Larvae

The larvae measures 80 – 120 microns by 5.6 microns at

birth but reaches the size of 900 - 1,300 microns by 35 - 40 microns
after it enters a striated muscle. It has a spear-like burrowing anterior
tip. The mature encysted larva has a digestive tract similar to that of the
adult and although the reproductive organs are not fully developed
differentiation of sexes is often possible.

Life cycle:
Human infection with T. spiralis is an accidental occurrence because
this parasite is primarily a parasite of carnivarous and omnivorous
animals like hogs, rats, bears, foxes, dogs and cats. The same animal
acts as final and intermediate host, harboring the adult parasite
temporarily and the larvae for a longer period. In order to complete the
life cycle flesh containing the mature encysted larva must be ingested
by another host. Hence, trichinosis in humans becomes a “dead end
alley” infection. Adult birds may temporarily harbor the adult parasite,
but the larvae do not encyst in the muscles.

When the infective larvae are ingested by humans, usually in

pork, they pass to the upper small intestine, where the capsules are
digested and the larva released in a few hours. The liberated larvae
immediately invade the intestinal mucosa. They become mature worms
in 18 – 24 hours, wherein the sexes maybe differentiated. After
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59

fertilization, the male is dislodged from the mucosa and carried out of
the intestine, although they sometimes remain there for several days.
The female increases in size and in about 48 hours, burrows deeply into
the intestinal mucosa, from the duodenum to the caecum. On the fifth
day, the viviparous female begins to deposit larvae into the mucosa
and sometimes directly into the lymphatics and mesenteric lymph
nodes, from which they reach the thoracic duct and enter the blood
stream and are distributed and carried to the different parts of the body.
Larvae maybe lodged in various foci including the brain, myocardium
and body cavities. They are capable of encysting and developing only
in striated muscles. Among the muscles heavily parasitized are
diaphragm, masseteric, intercostal, laryngeal, lingual, extraocular,
nuchal, pectoral, deltoid, gluteus, biceps and gastrocnemius. The
larvae are mostly liberated within 4 – 16 weeks, but production
continues with lessened intensity as long as the female worms remain
in the intestine. The adult female dies after passing her larvae and then
is digested or passed out in the intestine. The life cycle of the worm
terminates in the musculature of humans where the larvae eventually
die and calcify.

Encysted larvae in
muscles of pig
⇘
ingestion of improperly
DEAD END CYCLE cooked infected pork
⇧ ⇩
encyst in striated infected flesh is digested
muscles by gastric juice, the larvae
⇧ ⇩
larvae enter the adults in the duodenum
circulation ⇙
⇖
larviparous female burrows
into mucosa and deposit
larvae

Pathology:
The variability and severity of the clinical symptoms depend
upon the number of worms, the size and the age of the patient, the
tissues invaded and the general resistance of the patient.
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Except for the early intestinal lesions caused by the adult worms,
pathology is concerned with the presence of the larvae in the muscles
and vital organs. Five larvae/gram of muscle could result to death.

The disease is commonly divided into three phases

corresponding to the periods of:

1. Incubation and intestinal invasion

Symptoms include diarrhea or constipation, vomiting,
abdominal cramps, malaise and nausea.

2. larval migration and muscle invasion

The typical signs and symptoms are fever, facial edema,
urticaria, pain and swelling and weakness. In severe cases, there
maybe splenomegaly, gastric and intestinal hemorrhages.

3. encystment and encapsulation

This is the convalescent stage, wherein fever, weakness,
pain and other symptoms start to disappear. Full recovery is
expected since trichinosis is a self-limiting disease.

Diagnosis:
1. Muscle biopsy - demonstration of the encysted larvae
2. Serological tests - CFT, ELISA, BFT (Bentonite
Flocculation Test), Bachmann
intradermal test using antigen prepared
from T. spiralis diluted 1:5,000 or
1:10,000.
Reaction is observed after 30 mins.
Positive result is a blanched wheal
surrounded by an area of erythema
4. Beck’s Xenodiagnosis - make use of experimental animals like
Albino rats

Treatment:
Thiabendazole maybe given during the first week of infection to
expel the adult worm from the gastrointestinal tract. This drug has no
effect on migrating larvae and may proved to be useless two weeks
after exposure. Mebendazole is larvicidal when given at 2o mg per kg
body weight 6 hourly for 10 to 14 days.
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Patients with symptomatic trichinosis should be confined to bed

and given general supportive treatment. Salicylates are usually enough
to relieve headache and muscular pain. Fluids and electrolytes balance
should be watched since impaired capillary permeability can lead to
general edema and later mobilization of fluid.

Epidemiology:
Prevalence of trichinosis in humans is associated with
consumption of pork and pork products, hence this is common in pork-
eating countries like Europe and United States than in tropics and the
Orient.

Trichinosis is a zoonosis. Man acquires the infection from

inadequately cooked or improperly processed infected lean pork or
bear meat. Two hosts are required to complete the life cycle. There are
two maintenance cycle:
a. pig to pig
b. rat to rat

Prevention and control:

The general public should be continuously informed through
educational campaigns regarding pork and bear transmission. It is
recommended that meat be cooked at 77ºC ( 177ºF). Freezing is another
way to kill larvae. Storage at -15ºC for 20 days or -30ºC for six days is
effective. Smoking, salting or drying of meat are not effective.
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Trichinella spiralis Trichinella spiralis

Female Male

Trichinella spiralis larva

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ACTIVITY SHEET NO. 7

NAME_______________________________SEC_____DATE_______

1. Discuss the method of Xenodiagnosis used for identification

of Trichinella spiralis.

2. Explain the dead end cycle if Trichinella spiralis is

Ingested by man.
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Filarial worms

Introduction and general morphology:

The slender filarial worms of the Superfamily Filariodiae are
slender arthropod-transmitted parasites of the circulatory and
lymphatic systems, muscles, connective tissues or serous cavities of
vertebrate hosts.
The filiform white worms range from 2 to 50 cm in length, the
female being twice the size of the male. The simple mouth is usually
without definite lips and the buccal cavity is inconspicuous. The
esophagus is cylindrical, has no cardiac bulbus and is usually of the
spiruroid type. The male is provided with two copulatory spicules.
The viviparous female gives birth to pre-larval microfilaria which
are unique because they are less differentiated than the first stage
larvae of other nematodes. Microfilaria is a highly motile, snake-like
organism consisting of dark staining nuclei occupying almost the
entire width of the body; the column of nuclei may serve as an
anatomical landmarks used in differentiating species. Absence or
presence of nuclei at the tip of the tail varies in different species. The
microfilaria maybe classified based on the presence or absence of
embryonic sheath. A sheath is a delicate, close fitting membrane that is
derived from the original eggshell and is only detectable as it projects
beyond the head or the tail portion. Microfilaria maybe (a)sheathed,
provided with embryonic sheath or (b)unsheathed, without the
embryonic sheath. The microfilaria of different species differs in
morphology, location in the host and the type of periodicity.

Microfilarial Periodicity
Periodicity refers to the rhythmical appearance of microfilaria in
the peripheral blood circulation and this varies with species. Some
exhibit nocturnal periodicity, wherein the microfilaria is found chiefly at
night, numbers are high during a four (4) hour period at midnight (10
PM to 2 AM) and scanty or absent during the daylight hours. In diurnal
periodicity, the number of microfilaria is high during daylight hours
between 10 AM to 2 PM. In some regions of the world, some species
exhibit modified periodicity, hence subperiodic. When the microfilaria
are continuously present in the blood circulation during the day and
night but with an increase in numbers during daytime, it is designated
as subperiodic diurnal. If the increase in number occur during night
time, it is subperiodic nocturnal. Knowledge of microfilaria periodicity
is important in determining the proper or best time for specimen
collection for laboratory identification of the parasites.
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MICROFILARIA

Characteristics of head and tail ends of Microfilaria

W. bancrofti B. malayi L. loa

O. volvulus M. perstans M. streptocerca M. ozzardi

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Life cycle:
The life cycle of filarial worms in general, involves:

1. The ingestion of microfilaria from the blood or tissues by a

blood sucking insect

2. The development of the microfilaria in the arthropod vector

through two distinct larval stages (1st and 2nd stages) before
reaching the infective stage which is the third stage filariform
larva

3. The transfer of the infective larva to the skin of a new host

by insect bite

4. The development and maturation of the larva at its selection

site

Microfilaria
(blood/tissues)
⇗ ⇘
Development into sucked/ingested by
Adult at it's selective blood sucking
site ( habitat) insect/s
⇧ ⇩
infected insect bite ⇦ development of microfilaria
a susceptible host in blood sucking insects
(L1,L2 and L3→infective stage)
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Medically Significant Species:

The principal species parasitic in humans are:

(1) Wuchereria bancrofti

Habitat : lower lymphatics
Microfilaria : sheathed, nocturnal periodicity
Distribution : Tropics and Sub-tropics

(2) Brugia malayi

Habitat : upper lymphatics
Microfilaria : sheathed, nocturnal periodicity
Distribution : Eastern Asia,India,Southwestern Pacific

(3) Loa loa

Habitat : Cutaneous and subcutaneous tissues
Microfilaria : sheathed, diurnal periodicity
Distribution : Tropical Africa

(4) Mansonella(Dipetalomena) perstans

Habitat : body cavities
Microfilaria : unsheathed, non- periodic
Distribution : Tropical Africa and Tropical South America

(5) Mansonella streptocerca

Habitat : skin and subcutaneous tissues
Microfilaria : unsheathed, non- periodic
Distribution : Tropical Africa

(6) Mansonella ozzardi

Habitat : subcutaneous tissues, possibly body cavity
Microfilaria : unsheathed, non- periodic
Distribution : Tropical America

(7) Onchocerca volvulus

Habitat : subcutaneous tissues
Microfilaria : unsheathed, present in cutaneous lymphatics
Distribution : Tropical Africa, North Yemen, Mexico, Brazil,
Guatemala, Venezuela, Columbia, Ecuador
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Wuchereria bancrofti
Common name : Bancroft’s filarial worm
Disease : Bancroftian filariasis, Wucheriasis,
Elephantiasis

Morphology:
The worm being a tissue invading nematode is found inhabiting
the lymph vessels and lymph glands of the vertebrate host. The adult
worms are long, creamy white, filiform in shape, tapering at both ends
and with a smooth cuticula. The male measures about 2 to 4 cm in
length and the female 8 to 10 cm in length.

The microfilaria, actively moving about through the lymph or

blood measures 244 to 296 micron in length by 7.5 to 10 micron in
diameter and are enclosed in hyaline sheath which is much longer than
the larva itself. The columns of dark staining nuclei are in 2 to 3 rows
and distinctly conspicuous and discrete when stained with vital dyes.
The excretory cell near the excretory pore is small while the G cells
located toward the posterior end are small, similar in size and usually
flat on one side. The tail is tapering to a delicate point with no terminal
nuclei. The microfilaria has several curvatures and has a graceful
appearance. It exhibits nocturnal periodicity, except the South Pacific
type, which is subperiodic. Animal experimentation showed that the
microfilaria is concentrated in the small blood vessels of the lungs
during the day and is liberated into the peripheral circulation at night.
The stimuli that send microfilaria from the lungs and other tissues into
the circulating blood and later back into the tissues are essentially
unknown. Body temperature and oxygen tension has been proposed as
factors that determine the circadian rhythm. Reversing the period of
sleep and activity of the host can reverse the periodicity of W. bancrofti
microfilaria.

Life cycle:
Adult worms are found tightly coiled in nodular dilations of the
lymphatic vessels, most frequently in the varises of the lymphatic
vessels of the lower extremities, the groin glands and epididymis in
male and the labial glands in female. If both sexes are present within
the same site, mating could take place with the production of
microfilaria. If not, infection exists but detection proved to be very
difficult because of the absence of microfilaria. The adult female, once
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fertilized, gives birth to prelarval microfilaria which eventually find their

way into the blood circulation where they are sucked by appropriate
mosquito vector while taking a blood meal. On arrival in the stomach of
the vector, microfilaria losses their sheath and migrate into the thoracic
muscles where they undergo two ecdysis to develop into the filariform
larva (3rd stage larvae), which is the infective stage to the human host.
From the thoracic muscles, the filariform larva migrate toward the head
and proboscis of the mosquito and during blood meal are deposited at
the vicinity of the bite wound and penetrate the broken skin or pores of
the human skin. After gaining access into the body of the human host,
from the skin they pass through peripheral lymphatics, in which they
migrate and grow, then settle down in certain lymphatic vessels
retrograde to lymph nodes, grow to maturity and mate. Maturation
takes about 12 to 18 months and the length of life in the human host is
considered to be about 5 years. Humanity is the only known definitive
host of W. bancrofti.

Pathology:
Filarial symptoms are caused mainly by the adult worms. These
adults maybe living, dead or degenerating. Microfilaria apparently
causes less pathology although they have been associated with
Tropical Pulmonary Eosinophilia (TPE), granuloma of the spleen and
allergic reactions following their destruction by drugs. TPE is a classic
example of occult filariasis in which classical clinical manifestations
are not present and microfilaria are not found in the blood but maybe
found in the tissues. The adult worms lying in the dilated lymphatics or
in the sinuses of the two lymph nodes, provoke a pseudotubercular
granulomatous reaction which becomes more pronounced on their
death. It results to occlusion of the small lymphatics and narrowing of
the larger ones, which may give way to edema, vascular and lymphatic
hyperplasia, fibrosis and caesation. Prolonged obstruction of the lymph
glands will eventually lead to marked fibrosis giving rise to
elephantiasis, the degenerating worms being absorbed and replaced by
hyalinized or even calcified scar tissues. The most commonly
encountered clinical manifestations are hydrocoele and chylocoele with
accompanying enlargement of the inguinal and lymph nodes and
elephantiasis of the scrotum and vulva. Enlargement of the genitals and
lower lymphatics are common.
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Diagnosis:

Laboratory diagnosis of bancroft’s filariasis is based on the

demonstration of microfilaria in the blood. Microfilaria of W. bancrofti
exhibits nocturnal periodicity chiefly present in the blood during the
night from 8:00 PM to 4:00 AM. The best time to collect blood specimen
is during the peak hours, which is between 10 PM to 2 AM. Most
commonly used method for diagnosis is the preparation of thick blood
smear about the size of 25 centavo coin (2 thick smear/slide)
dehemoglobinized and stained with Giemsa or Wright’s or Delafield’s
Hematoxylin stain. Dehemoglobinization is necessary before staining
the blood smear and this is accomplished by immersing the smear in
distilled water for a few minutes until the color of the smear turns into
white. Wet smear may also be done by placing one drop of blood in a
slide and adding one drop of acetic acid in order to lyze the RBC.
Movement of the microfilaria is observed in this method. Heparizined
capillary method is also useful in the diagnosis. These is done by filling
up the heparinized tube with blood, then centrifuge and get the buffy
coat and place it in a slide and stain with Giemsa or Wright’s. If
negative in these methods, concentration methods maybe useful such
as Knott’s concentration and the Millipore or Membrane Titration
method. In Knott’s concentration technique, acetic acid and Formalin
are used. Aside from blood, urine and scrotal fluid can also be used in
the laboratory diagnosis of this infection.

In many chronic infections, microfilaria may not be demonstrated

in the peripheral blood because of the following factors:

1. low intensity of infection

2. dead worms
3. obstructed lymphatics

Treatment:

The drug of choice for treating active cases of Bancroft’s

filariasis is Diethylcarbamazine(DEC).
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Epidemiology:
The disease has a worldwide distribution in tropical and
subtropical countries. At least 48 species of mosquitoes including
Aedes, Anopheles, Culex and Mansonia are natural or experimental
vectors. The prevalence of filariasis is correlated with the density of
population and poor sanitation, since mosquito vectors breed mainly in
water contaminated with sewage and decaying organic matter. The
principal vector in the Western hemisphere is Culex quinquefasciatus
and in the South pacific, Aedes polynesiensis. The former is a night-
biting, sylvatic, non-domesticated mosquito.

In the Philippines, there are two types of Bancroftian filariasis

namely, the urban type which is most prevalent in abaca raising areas
of the country and the rural type prevailing rather away from the
houses towards the mountains and hills. In urban type, the mosquito
vector is Aedes poecilus, which breeds in the water, accumulated in the
axils of abaca and banana plants. In the rural type, the vector is
Anopheles minismus flavorostris, a night biting mosquito that breeds
in mountain streams.

The provinces endemic for W. bancrofti are the ff.: Romblon,

Camarines Sur and Norte, Albay, Sorsogon, Mindoro, Quezon, Masbate,
Samar, Leyte, Bohol, All provinces in Mindanao, Palawan, Sulu and Mt.
Province (Bondoc)

Prevention and control:

Education regarding filarial infections, control of mosquito

vector, use of protective clothings and insect repellants and treatment
of infections to prevent further transmission are essential in the
prevention and control of bancroftian filariasis.
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Brugia malayi

Common name : Malayan filarial worm

Disease : Malayan filariasis

Morphology:
The adult B. malayi bears a general resemblance to those of W.
bancrofti; they are delicate, whitish, thread like filaria that live in dilated
lymphatics. The male measures 13 to 23 mm in length, the female 43 to
55 mm in length.

The microfilaria measure 177 to 230 micron in length, are

enclosed in a sheath, have angular curvature with secondary kinks. The
column of nuclei is in two rows and is indistinct or confluent. The
excretory cell is large and the G cells are larger than those of W.
bancrofti and are ovoidal in shape. The most distinguishing
characteristic of the microfilaria of B. malayi is the presence of two
discrete nuclei at the tip of the tail. In the peripheral blood of patients,
microfilaria exhibit nocturnal periodicity although in some areas like
Malaysia, Thailand, Java, Southern Vietnam, Sumatra and the
Philippines, it is subperiodic nocturnal.

Life cycle:
Humanity is usually the only definitive host, but there is another
variety of B. malayi that infect monkeys and felines. The worm has
basically the same life cycle as W. bancrofti except for the mosquito
vector. The intermediate hosts are mosquitoes belonging to genera
Mansonia, Anopheles, Aedes and Armigeres.

Pathology:
The pathogenic mechanism of human filariasis due to B. malayi
are essentially the same as those of W. bancrofti except that the
deformity produce in infected cases is not as severe as in the latter.
Malayan filariasis is characterized by superficial lymphadepathy and
high eosinophilia (7 – 20%).
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Diagnosis:

Laboratory diagnosis is made by identification of microfilaria in

the blood. Microfilaria have a subperiodic periodicity and although they
are also present during the day, the best time to collect blood specimen
should be during the night where they are present in greater number in
the peripheral blood circulation. Laboratory methods used for W.
bancrofti also apply to B. malayi. The knotting of microfilaria, an agonal
phenomenon during drying of the films maybe prevented by adding
chloroform or methanol to the blood.

Treatment:
Diethlycarbamazine is the drug of choice.

Epidemiology:
B. malayi is primarily present in India, Thailand, Vietnam, Sri
Lanka, Indonesia, Philippines, China, Korea and small focus in Japan.
Animal reservoir such as cats and monkeys are recognized. The typical
vector is Mansonia but in Japan, Korea and coastal China, it is Aedes
togoi. Mansonia is most prevalent in low regions, where numerous
ponds are infested with water plants of the genus Pistia, which are
essential for the breeding of these mosquitoes.

In the Philippines, B. malayi was found to be restricted to areas

of fresh water swamps, whereas W. bancrofti has a wider distribution.
There seems to be only one type of malayan filariasis in the Philippines
with modified periodicity (subperiodic nocturnal). The mosquito vectors
are Mansonia bonneae, which breeds in fresh water swamps and
Mansonia uniformis, which breeds in rice fields.

The province endemic for malayan filariasis are:

1. Palawan 3. Agusan
2. Sulu (Bongao in Tawi-tawi 4. Eastern Samar

Prevention and control:

The prevention and control is similar to W. bancrofti.
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Wuchereria bancrofti microfilaria

Brugia malayi microfilaria

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ACTIVITY SHEET NO. 8

NAME_______________________________SEC____DATE__________

1. If you get a negative laboratory result in diagnosis of filariasis,

does it indicate the absence of infection? Why?

2. Explain why dehemoglobinization of blood smear is necessary

before the staining procedure?

3. Does enlargement of the scrotum and elephantiasis specific or

diagnostic of filariasis?
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Loa loa
Common name : African eyeworm, loa worm
Disease : Loiasis, Calabar or fugitive swellings

Morphology:
The adult is a cylindrical, thread-like worms, inhabit the
subcutaneous tissue. Male measure 30 to 34 mm in length, female
measures 40 to 70 mm in length.

The microfilaria is sheathed, has diurnal periodicity and

measures 250 to 300 microns in length and 6 to 8 microns in width. The
sheath stains poorly in ordinary blood films and is usually overlooked.
The excretory cells and G cells are similar as in microfilaria of B.
malayi. The tail is tapering gradually, caudal nuclei continuous with
those of the trunk. General appearance is similar to the microfilaria of
B. malayi. The optimum site for the microfilaria during their non-
circulation phase is the lung; they appear only in the peripheral blood
during the day.

Life cycle:
Humans and possibly monkeys are the only definitive hosts. The
intermediate hosts are certain day biting flies of the Genus Chrysops,
the mango flies (primarily C. silacea and C. dimidiata). The ingested
microfilaria passes through a cyclic development in these flies in 10 –
12 days. A person when bitten by the infected fly is infected with the
microfilaria released from the proboscis of the fly to the skin near the
bite wound. Within an hour the larva penetrate the subcutaneous tissue
and muscular tissues, where they become adult worms in about 12
months. The adult worms may live for 17 years or more.

Pathology:
The adult worms normally live in the subcutaneous tissue
through which they migrate back and fourth provoking a temporary
inflammatory reaction known as “fugitive” or “Calabar” swellings
regarded as local reactions to sudden liberation of the worm’s
metabolites.
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Adults are particularly troublesome when passing in the orbital

conjunctiva or across the bridge of the nose. Under the conjunctiva, it
can produce irritation, edema of the eyelids and impaired vision. In
Uganda, there are three types of ocular manifestations, namely:

(1) conjunctiva granulomata - present as non-painful, itchy

solitary of small yellow nodules about 2 mm in length
(2) painless edema of the eyelids known as “bung eye”
(3) protopsis - edema of the orbital cellular tissue which is
also called “bug eye” or “bulge eye”

Diagnosis:
It can be specifically diagnosed from identification of microfilaria
in the peripheral blood during the day, or by removal of the adult
worms from the skin of the conjunctiva.

Treatment:
The surgical removal of adult when accessible is an accepted
method of treatment. A favorable time is during their migration across
the nose of conjunctiva. Chemotherapy with diethylcarbamazine is
effective but several courses of treatment maybe needed.

Epidemilogy:
Loa loa is confined to the equatorial rain forest of Africa and is
endemic in Tropical West Africa, the Congo basin and parts of Nigeria.
Infection is most prevalent in small settlements situated in or at the
margin of the forests and is favored by the presence of rubber
plantations.

Prevention and control:

Education regarding the infections and its vectors, especially for
persons entering the known endemic areas is essential. Protection
from fly bites along with treatment of cases is also helpful in reducing
the incidence of the infection. However, the presence of disease in
animal reservoir (monkeys) limits the feasibility of controlling the
disease.
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Onchocerca volvulus
Common name : Convoluted filaria
Disease : Onchocerciasis, River blindness

Morphology:
The adult worms are commonly located in nodules in
subcutaneous connective tissue usually encapsulated in fibrous
tumors. The living worms are white, opalescent and transparent with
distinct transverse striations of the cuticula. The worms are filiform and
blunt at both ends. They are characteristically coiled within the
nodules. Male measures 19 to 42 mm in length; female measures 33.5
to 50 mm in length.

The female give birth to unsheathed microfilaria which are

typically found in the lymphatics of connective tissues and cutaneous
layers in the vicinity of the parent worm, as well as in the stratum
germinativum and corneal conjunctiva, rarely in blood or internal
organs. Microfilaria measures 315 to 360 by 6 microns, the anterior and
posterior ends being nuclei free.

Life cycle:
Humanity is the only definitive host. The non-sheathed
microfilaria when ingested by Simulium or black fly during feeding
undergo metamorphosis in the thoracic muscles of the vector and
transform into 3rd stage filariform larva which is the infective stage to
the definitive host. The mature larva which then migrate to the
proboscis of the infected fly and when the fly bites, larva escape to the
skin of the new host and penetrate the bite wound. The larvae migrate
from the skin to the subcutaneous tissues and become adult worms.
Adult may live for 15 years and are capable of producing microfilaria for
at least 9 to 10 years.

Pathology:
The usual clinical manifestations of the disease are fever,
eosinophilia and urticaria. As the worm mature, mate and begin
producing microfilaria, the subcutaneous nodules begin to appear and
can occur on any part of the body. These nodules are most dangerous
when present on the head and the neck because the microfilaria may
migrate to the eyes and cause severe tissue damage leading to
blindness.
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A number of skin conditions are related to the presence of this

parasite including pruritus, hyperkeratosis, myxedematous thickening
and hanging groin wherein the nodules are located near the genitalia.

Diagnosis:
The method of choice is aseptic removal of skin snip of the
subcutaneous nodules and the microscopic examination of this tissue
in a cover-slipped drop of saline to detect the presence of unsheathed
microfilaria. O. volvulus microfilaria are not found in blood specimen
but maybe found in urine specimens because nodules are often located
near the genitalia.

Treatment:
Surgical removal of the encapsulated nodule is often performed
to remove the adult worms and stop production of microfilaria. In
addition, treatment with DEC followed by Suramin is recommended
with an alternative drug mebendazole.

Epidemiology:
O. volvulus is endemic in many parts of Africa especially in the
Congo basin and Volta River basin. In America, it occurs in many parts
of Central and South American countries. Several species of the black
fly genus Simulium serve as vectors, but none so appropriately named
as principal vector except Simulium damnosum (the damned black fly).
The disease is confined to neighborhood of rapidly flowing streams
where the black flies or buffalo gnats breed.

There is greater prevalence of infection in men than in women

because of greater occupational exposure. It has been shown by
studies in endemic areas in Africa that 50% of men will be totally blind
before they reach 50 years of age. This account for the common term
“river blindness” applied to the development of onchocercosis.

Prevention and control:

Education regarding the disease and its black fly transmission is
essential. Protection from black bites by use of protective clothing,
screens and insect repellants, as well as prompt diagnosis and
treatment of infections are critical.
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Mansonella species
Filarial infections caused by Mansonella species are less
important than those previously discussed. All of the species produce
non-sheathed microfilaria in blood and subcutaneous tissue and all are
transmitted by biting midges (Culicoides). Infection caused by these
species can be treated with DEC as for previous filarial infections.
Species identification can be accomplished with blood smear, noting
the structure of microfilaria.

Mansonella perstans
Common name : Persistent filaria
Disease : Dipetalonemiasis
Habitat : body cavities, commonly peritoneal cavity and
Pleural cavity

Morphology:
The adults are creamy white, elongated, cylindrical with smooth
cuticle and bluntly rounded anterior and posterior end curved ventrally
in both sexes. The male measures 45 mm by 60 microns while the
female measures 70 to 80 by 120 microns. The microfilaria appears in
the blood both day and night (non-periodic) with nuclei extending up to
the tip of the blunt tail.

Mansonella ozzardi
Common name : Ozzard’s filaria
Disease : Mansonelliasis or Ozzard’s filariasis
Habitat : body cavities

Morphology:
The female measures 65 to 81 mm in length and 0.21 to 0.25 mm
in diameter. The male species are known only from a posterior segment
33-mm in length and 0.2 mm in diameter. The whole male worm has not
yet been seen. The non-periodic microfilaria which is unsheathed
somewhat resembles that of M. perstans in size but differs in the
appearance of the tail, which tapers to a thin filament, contains a
column of 4 to 6 ovoid or bar-like nuclei and the tail itself beyond the
nuclei is somewhat basophilic.
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Mansonella streptocerca

Morphology:
The non-sheathed microfilaria measures 180 to 240 microns. The
cephalic space is slightly longer than wide and the first 4 to 5 nuclei are
elongated and tend to be quadrate, arranged in a single column of 9 to
12 which extend to the rip of the tail. When fixed, the microfilaria is
relatively straight except at the posterior end which, is strongly bent in
a shepherd’s crool curve.

Epidemiology:
Human infection is produced by bites of infected Culicoides
which, breed in jungles and swamps. The infective stage is filariform
larva. Man is the final host and some of the monkeys in Africa and
South America have been found as reservoir hosts.
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Angiostrongylus cantonensis
Common name : Rat lungworm or Rodent lungworm
Disease : Angiostrongyliodiasis or Eosinophilic
Meningoencephalitis in man
Habitat : lungs of rats

Morphology:
The adults are filiform having a length of 17 to 25 mm. The female
measures 21 to 25 mm in length by 0.30 to 0.36 mm in diameter. The
female is characterized by having a “barber’s pole” appearance due to
the looping of milky white uterine tubules around the blood filled
intestine. The posterior end is shaped somewhat like a bluntly ending
horn. The male measures 15.9 to 19 mm in length by 0.26 mm in
diameter. The male has a well-developed caudal bursa which, is kidney-
shaped and single lobed.

The eggs are elongated, ovoidal with a delicate hyaline shell and
measure 46 to 48 by 86 to 74 microns.

Life cycle:
The adult inhabits the pulmonary arteries of rats. The gravid
female discharges eggs into the pulmonary vessels. These eggs
develop and their larvae break into the respiratory tract, migrate up the
trachea, are swallowed and pass out in the rat’s feces. The larvae may
either be eaten or penetrate molluscan intermediate host, snails of the
genus Achatina and Pila, as well as Planaria and fresh water prawns.
The larvae undergo several molts to reach the infective third stage
larvae and remain viable for a long time. When rats or humans eat this
infected mollusk, the larvae migrate to the brain or spinal cord. In the
normal host for this parasite, the rat, the larvae leave the nervous
system to the lungs to complete their development. In infected human
host, the larvae probably remain in the brain for a longer period and do
not develop to the adult stage.
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Male and female adults in the

pulmonary arteries of rats
⇗ ⇘
in the brain, larvae unembryonated eggs in blood
molt twice (mature stream,becomes embryonated
in 4 weeks) after 6 days,1st stage larvae hatch
⇧ ⇩
ingestion by rat, break through respiratory tract,
absorbed into swallowed and passed out with
circulation the feces of the rat
⇧ ⇩
after 2 molts become ⇦ first stage larvae enter the body
third stage larvae of mollusk through ingestion
or active penetration

Pathology:
The incubation period for this infection is from 12 – 47 days. The
clinical picture of eosinophilic meningoencephalitis is one of acute
onset of severe headache, low grade fever, nausea and vomiting. Other
clinical manifestations include stiffness of the neck, weakness of the
hands and legs and abdominal pain. During the illness the patient may
exhibit increasing confusion or incoherence, disorientation and
impairment of memory or profound coma. Clinical and laboratory
results maybe negative. Autopsy of the brain may show
leptomeningitis, encephalomalacia and ventricular dilation. It also
shows the worm in vascular and perivascular tissues. Infection due to
Angiostrongylus is self-limiting and the prognosis is good. The disease
is occasionally fatal.

Diagnosis:
It is difficult to diagnose the infection because the adults lay
primarily in the brain. In areas where the disease is endemic, people
showing brain dyscrasia and has a moderate or high eosinophilic
counts in the CSF should be considered as potential victim. History of
the patient as to ingestion of possible intermediate hosts should be
considered.

No immunologic test has been developed yet for infection. Post-

mortem examination must be done on persons suspected of dying with
the infection to search for the worms.
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Treatment:
No anti-helminthic treatment can be recommended at present.
Surgery maybe needed when it is lodged in the anterior chamber of the
eye.

Epidemiology:
The final host of A. cantonensis is the rat, Rattus rattus and
Rattus norvegicus. The intermediate hosts commonly found in our
country are Achatina fulica (giant Japanese snails), Pila luzonica
(kuhol), Parathelpusa mistio (talangka), Brotia asperata (suso), garden
slugs and even fresh water prawns or water and vegetables
contaminated with third stage larva. Man usually gets the infection
through the following:

1. ingestion of raw mollusk containing the third stage larvae

2. ingestion of raw leafy vegetable contaminated with mucus
secretions of the mollusks containing the third stage larvae
3. drinking water contaminated with the infective larva
4. ingestion of paratenic hosts such as freshwater prawns and
crabs containing the infective larva

In the Philippines, A. cantonensis has been reported in rats with

a prevalence rate of 7%. It was reportedly present in the following
places:

1. Batangas 8. Bulacan
2. Cavite 9. Ilocos Norte
3. Laguna 10. Mountain Province
4. Nueva Ecija 11. Pampanga
5. Pangasinan 12. Quezon
6. Rizal 13. Sorsogon
7. Tarlac 14. Metro Manila

Prevention and control:

Preventive measures include careful washing and cooking of
vegetables, thorough cooking of prawns and crabs and avoidance of
ingestion of raw Achatina fulica snails and slugs. Elimination of the
snail and slug intermediate host. Rodent eradication may help prevent
human infection.
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ANGIOSTRONGYLUS CANTONENSIS
FEMALE

ANGIOSTRONGYLUS CANTONENSIS
MALE
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Dracunculus medinensis
Common name : Guinea worm, Medina worm, Dragon worm,
Fiery Serpent worm of the Israelites
Disease : Dracontiasis, Dracunculiasis

Morphology:
Dracunculus medinensis is a tissue invading nematode of
medical significance. The adult worms inhabit the cutaneous and
subcutaneous tissue. The females are elongated, cylindroidal, bluntly
rounded at the anterior end and measures 70 – 120 cm by 0.7 to 1.7
mm. The life span of the female is 12 to 18 months and the fate of the
male is still unknown. The gravid female has no vagina and present
only prior to being gravid.

Life cycle:
The worms have a very simple life cycle, depending on fresh
water and a microcrustaceans (copepods) of the Genus Cyclops. In
about a year of infection, the gravid female migrates to the
subcutaneous tissues of the leg, arms, shoulders and trunks and other
parts of the body most likely to come in contact with water. When ready
to discharge larvae, the cephalic end of the worm approaches the skin
and a papule is formed in the dermis; this changes into blister within 24
hours. These lesions usually appear on the distal portion of the limbs.
Eventually the blister ruptures and on contact with fresh water, a loop
of the worm’s uterus prolapsed through a ruptured anterior end of the
worm or through its mouth and discharges the 1st stage motile
rhabditiform larvae. The slender rhabditiform move about in water and
are ingested by species of cyclops in which they metamorphose in the
body cavity into infective third stage larvae. Infective copepod in
unfiltered water provides opportunity for human infection. On arrival in
the duodenum, the larvae migrate through the wall of the digestive tract
and reach the loose connective tissue where they develop into adults.
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Adults in cutaneous tissues

⇗ ⇘
ingestion of infected gravid female migrates
cyclops by man to superficial cutaneous tissue
⇧ ⇩
larvae develop into larvae escape from skin blister
infective filariform larvae (1st stage rhabditiform larvae)
⇧ ⇩
larvae penetrate the free swimming larvae in
body cavity water
⇖ ⇙
larvae ingested by cyclops

Pathology:
Symptoms of infection usually occur one year after the initial
exposure when the gravid female creates vesicular lesions and ulcer in
the skin for the liberation of the larval worms. At the site of the ulcer,
there is erythema and pain, as well as an allergic reaction to the worm.
There is also the possibility of abscess formation and secondary
bacterial infection leading to further tissue destruction and
inflammatory reaction, with intense pain and sloughing of skin. If the
worm is broken in attempt to remove it, there maybe toxic reactions
and if the worm dies and calcifies, there maybe nodule formation and
some allergic reaction.

Diagnosis:
Diagnosis is establish by observation of the typical ulcer and
flooding the ulcer with water to recover the discharge of larvae.
Occasionally X-ray examination reveals worms in various parts of the
body.

Treatment:
The ancient method of slowly wrapping the worm on the stick is
still used in many endemic areas. Surgical removal is also a practical
and reliable procedure for the patient. The drug of choice is Niridazole,
with alternative drugs being metronidazole and thiabendazole.
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Epidemiology:
D. medinensis occurs in many parts of Asia and equatorial
Africa. Human infection results from ingestion of water from so-called
“step-wells” where people stand and bathe in water at which time the
gravid female worm discharges larvae from lesions on the arms, legs,
feet and ankles to infect Cyclops in water. Ponds and standing water
are occasional sources of infection when human uses these for
drinking water.

Prevention and control:

Education regarding the life cycle of the worm and avoidance of
water contaminated with cyclops is critical. Protection of drinking water
by prohibiting bathing and washing of clothings in wells is essential.
Treatment of water with chemicals and the use of fish that consume
cyclops as food are also helpful.
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PHYLUM PLATYHELMINTHES
(FLATWORMS)
Members of the Phylum Platyhelminthes are multi-celled animals,
usually leaf-like or tape-like rarely cylindrical, bilaterally symmetrical,
with three body layers, lacking body cavity, circulatory and respiratory
structures. They possess an incomplete digestive tract and with a
bilateral symmetrical excretory system. The sexual organs are highly
elaborated and complicated. The life cycle may involve a single
obligatory host or may require two or more consecutive hosts. The
Phylum consists of three classes:

I. Class Tubelaria
II. Class Trematodea
III. Class Cestodea

CLASS CESTOIDEA

Exclusively parasitic organisms; adults are hermaphroditic,

covered with non-ciliated integument; ciliated epithelium, when
present, confined to embryos hatched from eggs; scolex provided with
suckers and frequently hooks for attachment to host tissue; no
digestive tract in most species; divided transversely into separate
sexually complete units, called proglottids. There are two orders of
medical importance:

A. Order Pseudophillidea

Scolex typically unarmed, with a dorsal and ventral

grooves (bothria)never with 4 suckers. All representatives in man
belong to the superfamily Bothriocephaloidea.

B. Order Cyclophyllidea

Scolex with 4 suckers and usually a centrally placed apical

rostellum, frequently armed with hooks; sex pores when present, open
laterally; vitellaria, a single mass, usually posterior to the ovary. All
species in this order found in man belong to Superfamily Taeniodea.
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CESTODES OR TAPEWORMS

Introduction and General Considerations:

The tapeworms are parasitic worms of Class Cestodea of the

Phylum Platyhelminthes. The adult tapeworm is typically located in the
middle portion of the small intestine and the larvae inhabit the tissues
of the vertebrates and invertebrates. This elongated, ribbon-like adult,
generally flattened dorsoventrally, has no circulatory system and is
usually divided into segments or proglottids. All tapeworms are
hermaphroditic (monoecious) wherein male and female reproductive
organs are present in each segments. They have no digestive system
wherein the food is absorbed from the host’s intestine through the soft
body wall of the worms. The nervous system is confined primarily to
the scolex or the anterior portion of the worm.

All tapeworms are hermaphroditic. The genital organs are

elaborately developed in each proglottid. The testes are usually
multiple and distributed throughout the mature proglottids. The ovary
is commonly a bilobed mass (Taenia), a single mass (Dipyllidium) or
multiple follicles (Diphyllobothrium). The uterus may open through a
pore on the median ventral aspect of the proglottids (Pseudophillidea)
or may end blindly (Cyclophillidea). The vas deferens of the male and
the vagina of the female have a common genital pore that opens on the
median ventral surface (Pseudophillidea) or in the lateral margin of the
proglottids (Cyclophillidea). The genital pore in Cyclophillidea maybe
on the same side of each proglottids (Hymenolepis), irregularly
alternate (Taenia) or bilateral (Double pored) when two sets of
reproductive organs are common.

Adult Tapeworms
The adult tapeworm consists of three recognized regions
namely: (1) scolex or holdfast organ, (2) neck, which is the region of
growth and (3) strobila, a chain of proglottids or segments. The length
of the different species varies from 3 mm to 10 meters or more and the
number of proglottids ranges from 3 to 4,000.

The scolex is strictly an organ for attachment and orientation of

the strobila. It is more or less distended muscular organ, which in the
case of Pseudophillidea is spindle shaped or spatulate with two
elongated suctorial grooves or bothria. In Cyclophillidea, the scolex is
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more or less quadrate or globular in shape and provided with 4 cup like
suckers and in many species has an anterior rostellum which maybe
armed with hooks or spines.

The neck is constricted and in few species is lacking. It is the

portion of the adult worm where proglottids are primarily proliferated.
Germinal cells are present in the neck, which is responsible for
production of new segments.

The scolex and the neck are important structures, since infection
persists as long as these two portions of the worm remain attached to
the host’s intestinal wall, even though greater portion of the strobila
may have become free and been evacuated.

From the posterior part of the neck originate the chain of

proglottids, each an essentially functioning individual, a member of a
colonial chain of proglottids. Proceeding distalwards, these proglottids
become progressively more mature and most distinctly differentiated
both internally and externally. The region of immature segments is one
wherein these units are just being differentiated and where the sexual
organs are still immature. Next to these segments are the mature
segments which are larger units, each of which contains complete set
of well, developed reproductive organs. The gravid or ripe proglottids
are those distal from the scolex wherein the primary genitalia have
been atrophied and consist essentially of a uterus distended with eggs.
The strobila maybe described as craspedote (proglottids overlap with
one another) or acraspedote (no overlapping takes place). Proglottids
may also be described as apolytic, when proglottids detach or rupture
with mature eggs still inside, or anapolytic, when proglottids detach
only after segments are exhausted of eggs.

Eggs:
Eggs are stirred in uterus and consist of a fertilized ovum and
yolk material enveloped in an embryonic membrane and shell. Eggs of
Pseudophillidea are discharged from the uterus via uterine pore and
are ovoid, operculated and immature when passed in the feces. These
eggs would require a period of incubation in water before they become
mature. In Cyclophillidea, eggs are released from the uterus by
apolysis, which is the normal detachment or disintegration of the
gravid segment from the main body or strobila. These eggs are
spherical, non-operculated and almost fully embryonated when they are
discharged from the proglottids.
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Life cycle:
The fully embryonated egg (almost mature when discharged from
the uterus of Cyclophillidea and contains an oncosphere (hooked ball)
with three pairs of hooklets (hexacanth); mature only following
incubation in water in Pseudophillidea wherein the embryo known as
coracidium is surrounded by cilia. Hatching of eggs of Pseudophillidea
occurs in water while in Cyclophillidea, it occurs only after ingestion by
the appropriate intermediate host. In Pseudophillidea, two intermediate
hosts are required while in Cyclophillidea only one intermediate host is
necessary. In some tapeworms, the definitive host serves additionally
as intermediate host, since larval development occurs in the intestinal
mucosa of the definitive host.

Larval stages:
The embryo directs or eventually develops into one of the
following types of larva:

A. Solid type
(1) plerocercus/procercoid/procercus
This larva is relatively globular with the scolex invaginated
into the body of the larva.
(2) plerocercoid/sparganum larva
This larva is elongated with head free or invaginated only
to the neck.
B. Cystic type
(1) cysticercoid
This larva is provided with a slightly developed bladder
anteriorly, into which the head is invaginated and with an
elongated solid posterior portion.

(2) cysticercus (true bladder worm)

In this type of larva, the head is invaginated into the
proximal portion of the bladder.
a. simple - only one scolex (Taenia)
b. coenurus - with multiple scolices developed from
the inner germinal wall
c.echinococcus/hydatid – germinal layer produces many
scolices and develop into many
daughter bladders(broad capsules), each
of which in turn produces many scolices
internally
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The medically important species of tapeworms are:

I. Order Pseudophillidea

1. Diphyllobothrium latum

II Order Cyclophillidea
A. Species which require vertebrate intermediate host

1. Taenia solium

2. Taenia saginata

B. Species which require invertebrate intermediate host

1. Dipyllidium caninum

2. Hymenolepis diminuta

3. Raillietina garrisoni

C. Species which may or may not require intermediate host

1. Hymenolepis nana

D. Species which may infect man in their larval stage

1. Echinococcus granulosus

2. Echinococcus multilocularis

3. Taenia solium

4. Spirometra mansoni
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LARVAL STAGES OF TAPEWORMS

PROCERCOID PLEROCERCOID CYSTICERCOID

CYSTICERCUS COENURUS ECHINOCOCCUS

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ACTIVITY SHEET NO. 9

NAME_____________________________SEC_____DATE________

1. Tabulate the differences between Pseudophillideans and

Cyclophillideans.

2. What is the mode of transmission of the infective stage?

What is the infective stage?

3. Explain the significance of production of multiple scolices

by single cysticercus larvae.
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Diphyllobothrium latum
Common name : Broad or Fish tapeworm
Disease : Diphyllobothriasis, bothriocephaliasis,
Dibothriocephalus anemia, fish tapeworm
Infection

Morphology:
A. Adult

This ivory colored tapeworm is the longest tapeworm of

human measuring 3 to 10 meters in length (sometimes more) with as
many as 3,000 to 4,000 proglottids. The usual habitat of the worm is the
ileum and sometimes the jejunum. The scolex is small measuring 2 to 4
mm in length by 10 to 12 mm in width, spatulate or almond-shaped with
2 dorsoventral sucking grooves. The typical mature proglottids are
somewhat broader than long (latum) and is practically filled with
reproductive organs. The male organs terminate in muscular cirrus in a
common genital pore. A symmetricallly bilobed ovary, a vagina that
extends from a common genital pore in the midventral line,
characterizes the female organs. The gravid rosette like or highly coiled
uterus in the middle of the gravid segment is a diagnostic
characteristic. A single worm may discharge as many as 1 Million eggs
daily.

B. Eggs
Eggs of D. latum are broadly ovoid, operculated (with
inconspicuous operculum), moderately thick-shelled, light golden-
yellow and with a knob on the shell at the bottom of the egg. It
measures 58 to 76 microns and contain an immature embryo when
discharge in the feces.

Life cycle:
The definitive hosts are humans. The life cycle involves two
intermediate hosts. The first intermediate hosts are freshwater
copepods of the Genera Cyclops and Diaptomus. The second
intermediate hosts are some of the finest freshwater fishes like pike,
salmon, whitefish and turbot.
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The adult worm may live attached to the intestinal mucosa most
commonly of the ileum and sometimes the jejunum. Eggs are released
through uterine pore. Upon reaching the body of water, the eggs
mature in 11 to 15 days and liberate the ciliated embryo (coracidium)
via the operculum. The free-swimming ciliated coracidium must be
ingested by an appropriate copepod host to continue its development.
In the midgut of the copepod, the embryo cast off its ciliated coat and
with the aid of the pairs of hooklets penetrate into homocoel, where in
the course of 2 to 3 weeks, it will transform into procercoid larva
measuring up to 550 microns in length. This larva is elongated,
glistening, chalky white, spindle shaped. On eating raw or insufficiently
cooked flesh of infected fishes, man, the optimal host becomes
infected. The larva attaches into the intestinal wall and grows to
maturity and in about 5 to 6 weeks, eggs begin to appear in the feces.

Adult in the small ⇨ immature eggs passed ⇨ maturation of eggs

intestine in the feces into in water 11-15days
⇧ freshwater ⇩
scolex of plero- coracidium hatches
cercoid attaches from eggs
to intestinal mucosa, ⇩
develops into adult coracidium ingested
worm by copepod
⇧ ⇩
raw or insufficiently coracidium penetrate
cooked infected fresh GUT of copepod into
water fish ingested by man body cavity
⇧ ⇩
plerocercoid ⇦ procercoid penetrates ⇦ infected copepod
develops in the intestinal wall into eaten by fresh water
muscle the muscle of fish fish

Pathology:
Infection is limited to a single worm, although instances of
intestinal obstruction by a large number of worms have been reported.
Usually no symptom is present and patients become aware of the
infection by finding proglottids in the feces. In individuals predisposed
to pernicious anemia, bothriocephalus anemia may occur. Infection at
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the jejunal level causes impairment of the interaction between the

extrinsic and intrinsic factor of castle; hence the pernicious type of
anemia. The scolex attaches to the jenunum and competes with the
host for the available supply of Vitamin B12. The blood picture is that of
macrocytic anemia.

Diagnosis:
Stool examination reveals bile-stained operculated eggs with a
knob at the abopercular end. Typical proglottids with rosette-like uterus
may also be observed in stool specimens.

Treatment:
The drug of choice is praziquantel, if not available, niclosamide
and quanacrine hydrochloride maybe used.

Epidemiology:
This parasite is prevalent in the regions of the temperate zones
where raw or pickled fish is popular. It is common in countries like
Northern Europe, Russia, North America, Manchuria and Japan.
Insufficient cooking over campfires and tasting seasoning of gefullite
fish account for many infections. A reservoir of infected wild animals
such as bears, minks, walrusses and members of the canine and feline
families that eat fish are also sources of human infections. The practice
of dropping raw sewage into freshwater lakes contributes to the
propagation of the tapeworm.

It has been reported in man once in the Philippines. However, a

genus Spirometra sp. is a common tapeworm infection in dogs and
cats in the Philippines. This genus is also capable of parasitizing
humans.

Prevention and control:

The prevalence of infection due to this parasite is reduced by
avoiding the consumption of insufficiently cooked fish or by freezing
the fish for 24 to 48 hours at -18ºC which will kill the plerocercoid;
controlling the disposal of human feces, especially the proper
treatment of sewage prior to disposal in lakes and promptly treating
infections.
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D. latum scolex D. latum gravid segment

D. latum egg Sparganum larvae

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Sparganun mansoni/Spirometra mansoni

This parasite is a member of the genus Spirometra causing
sparganosis.

Morphology:

This parasite has no scolex and definite proglottids. It is

elongated, ivory white, ribbon-like larva measuring from a few to
several centimeters. This parasite is characterized by piling of uterus
coils distinguished from the rosette arrangement of the uterus of D.
latum. The eggs resemble that of D. latum but are ellipsoidal and
possess a rounded, conical operculum.

Life cycle:
Same as D. latum except that the main habitat of the sparganum
in the human body is the skin and subcutaneous tissues, conjunctiva,
vagina and internal vital organs. It does not reach maturity in man.

The 1st intermediate hosts are species of cyclops and the 2nd
intermediate hosts include rodents, snakes and frogs. The definitive
hosts are dogs, cats and wild carnivores.

Pathology:
The tissue infected with sparganum become edematous, and
very painful to touch. In the eye (ocular sparganosis), there will be
intense pain, irritation and edematous swelling of the eyelids. The
presence of spargana in the lymph channels may result in
elephantiasis; in subcutaneous tissues, acniform pustules may develop
and pulmonary artery may become infected.

Diagnosis:
Diagnosis is made by finding the white larva in the lesion.
Species identification is done through experimental infection of
animals.
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Treatment:
Surgical removal is the customary approach. When surgery is
not feasible, praziquantel maybe used.

Epidemiology:
Sparganosis is a common tapeworm in dogs and cats in the
Philippines. Frogs, lizards, snakes, birds and even some mammals like
monkeys and man maybe infected. The infective stage may either be
the procercoid larvae in the cyclops or the plerocercoid larvae itself in
the tissues of cold-blooded vertebrates.

Human sparganosis may result from:

(1) ingestion of infected cyclops containing the procercoid stage

(2) ingestion of plerocercoid larvae in raw flesh of an amphibian

reptile, bird or mammal

(3) application of the flesh of an infected vertebrate to the skin,

conjunctiva, or vagina (cold poultice)

(4) by eating raw pork

Prevention and control:

Drinking boiled or filtered water, thorough cooking of possible

intermediate hosts, avoid using flesh as cold poultice.
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ACTIVITY SHEET NO. 10

NAME________________________________SEC_______DATE________

1. Can sparganum larva of D. latum cause sparganosis in man?

How?

2. Explain how bothriocephalus anemia is brought about by fish

tapeworm infection?

3. What is the main morphological differences of D. latum and

S. mansoni?
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Taenia solium
Common name : Pork tapeworm
Disease : Pork tapeworm infection, Taeniasis solium

Morphology:
A. Adult
The adult Taenia solium lives in the small intestine with its
scolex attached to the mucosa and its body folded back and forth in the
lumen. It measures 2 – 7 meters and when fully developed contains 800
to 1000 segments. The scolex measures 1-mm, globular in shape, has 4
cup-like suckers and a conspicuous rounded rostellum armed with
double rows of large and small hooklets approximately 20 – 25 in
number. The neck region is short and only about one half as thick as
the scolex. The mature proglottid is roughly square with irregularly
alternate genital pores opening from side to side in adjacent
proglottids. The testes consist of 150 to 200 follicles, distributed
throughout the dorsal plane. The ovary, situated in the posterior third
of the proglottids, consists of 2 large symmetrical lobes and an
accessory lobe on the side of the genital pore. The gravid segment
contains uterus, which has 5 – 14 lateral uterine branches. Each gravid
segment contains 30,000 – 50,000 eggs. The gravid proglottids become
detached from the strobila in-groups or five or six (in chain) and are
passed in the feces.

Eggs:
The mature egg is spherical, measures 31 to 43 microns, pale
buff to walnut brown in color. It has two radially striated eggs shell. The
outer shell is thin and rarely seen while the inner shell is brown, thick
and striated. Within the thickly striated shell is a fully developed
oncosphere that has three pairs of hooklets. The eggs of T. solium can
not be distinguished from the eggs of T. saginata.

Life cycle:
The habitat of the worm is the upper part of the jejunum. More
than one worm maybe harbored, although one is usually present. The
worm may live up to 25 years or more. The usual intermediate hosts
that harbor the cysts are the hogs/pigs, rarely other mammals. The
infected meat is often called “measly pork”.
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On escape from the ruptured uterus of the gravid proglottids and

after deposition in the soil, the eggs may remain viable for weeks. On
ingestion by a susceptible intermediate host, the hexacanth embryo
escapes from its shell and by means of its hooklets penetrates through
the intestinal wall into the lymphatics or blood vessels and is carried
throughout the body. They are typically filter-out between the muscles
where they metamorphose into cysticercus cellulosae. This cyst is an
ellipsoidal, transluscent, thin wall bladder worm measuring 5 mm long
by 8 to 10 mm in breadth, with an opaque, invaginated scolex equipped
with suckers and hooks. Man becomes infected with the adult
tapeworm when the cysticercus larva is ingested from raw or
inadequately cooked pork. In the stomach, the larva is digested out of
the pork flesh and the cyst wall dissolve by the actions of the digestive
juices in the upper small intestine, the evaginated scolex attached to
the jejunal wall and in 5 to 12 weeks develops into adult worm.

Adult in small intestine ⇨ Eggs discharged in the feces

⇧ ⇩ ⇩
evaginated scolex attaches eggs in soil ingested eggs in soil
in the intestinal mucosa by pigs ingested by man
⇧ ⇩ ⇩
larvae digested out oncosphere liberated oncosphere
from the pork flesh in the intestine of liberated in the
⇧ pig, penetrates the intestine,pene-
cysticercus cellulosae intestinal wall into trate the intesti-
eaten by man in raw blood circulation nal wall into
or insufficiently ⇩ bld. circulation
cooked pork oncosphere carried ⇩
⇧ in blood stream and oncosphere
develops into cysticercus ⇦ filter out between the carried in blood
cellulosae muscle fibers stream,filter out
bet. muscle fiber
⇩
develop into
cysticercus
cellulosae
⇩
DEAD END
CYCLE
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Pathology:
Infection with the adult T. solium in the small intestine seldom
causes appreciable symptoms. The intestine maybe irritated at the sites
of attachment and abdominal discomfort, chronic indigestion and
diarrhea may occur. Most patients become aware of the infection only
when they see proglottids or strobila in their feces.

Diagnosis:
Stool examination or Scotch tape and anal swab may reveal the
characteristic eggs of T. solium. The eggs are identical to those of T.
saginata, so eggs alone are not sufficient for species identification.
Critical examination of proglottids reveals their internal structure,
which is important for the differential diagnosis of T. solium and T.,
saginata. Slide compression technique for gravid segment of T. solium
and the number of uterine branches are counted.

Treatment:
The drug of choice is praziquantel while niclosamide and
quanacrine are effective alternative. Criteria for cure include the ff.:

1. recovery of the scolex

2. negative stool examination 3 months after treatment

Epidemiology:
T. solium is a cosmopolitan parasite and infection is directly
correlated with the eating habits of the people. It is prevalent in Africa,
India, Southeast Asia, China, Mexico, and Latin American countries.
Man is the optimal definitive host. Inadequately heated or frozen pork is
the exclusive source for human infection with the adult worm. Man may
also harbor the cysticercus larva caused by the ingestion of eggs from
the contaminated food and water or by internal autoinfection, when the
eggs are carried by peristalsis back to the small intestine or stomach.
Infection with the larval stage is called cysticercosis cellulosae, a
condition wherein man acts as the intermediate host of T. solium.
Prevention and control:
Pork to be consumed should be cooked until the interior of the
meat is gray or frozen at -20ºC for at least 10 days. Sanitation is critical
effort must be made to keep human feces containing eggs out of water
and vegetables ingested by pigs.
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Cysticercus cellulosae
Cysticercus cellulosae involves infection of the individual with
the larval stage of T. solium, the cysticercus cellulosae, which normally
infects pigs. Humans may acquire the cyst from the eggs in three ways:

(1) ingestion of food and water contaminated with human

feces

(2) oral transmission by unclean hands of carriers of the

adult worm

(3) internal autoinfection by the regurgitation of eggs into the

stomach by reverse peristalsis

Pathology:
The cysticerci may invade any tissue or organs of the body, most
commonly striated muscles and brain. A few cysticerci in non vital
organs may provoke no symptoms, but serious disease may follow as
cysticerci lodge in vital organs such as brain, eyes, spinal cord, heart
and liver giving rise to pressure symptoms. In the brain, it may produce
hydrocephalus, meningitis, cranial nerve damage, seizures, hydroactive
reflexes and visual defects. Convulsions are the most common
manifestations of cerebral cysticercosis. When the cysticerci eventually
die and begin to calcify, symptoms may exacerbate because of
cytotoxic effects.

Diagnosis:
Computed axial tomography (CAT) scans and nuclear magnetic
resonance imaging (MRI) are useful for localizing cysticerci and
evaluating the pathology before and after treatment.

There are three main CAT scan patterns:

(a) a round low-density area without surrounding
enhancement after administration of contrast dye
 this pattern shows a viable larvae with no
inflammation
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(b) ring-like enhancement after injection of contrast dye

 shows a dead larva

(c) a small calcified area within a cystic space

 shows a dead scolex

Treatment:

The drug of choice is praziquantel or albendazole. Steroids are

often given to control symptoms secondary to the inflammation around
the dead larvae. Surgery maybe necessary for certain lesions.

Prevention and control:

Treatment of human cases harboring the adult to reduce the

transmission and controlled disposal of human feces.
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Taenia solium scolex

Taenia egg Cysticercus larvae

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109

Taenia solium mature segment

Taenia solium gravid segment

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ACTIVITY SHEET NO. 11

NAME______________________________SEC________DATE_________

1. Differentiate Taeniasis solium from cysticercosis cellulosae.

2. What is measly pork?

3. Explain autoinfection in Taenia solium and its effects to the host.

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Taenia saginata
Common name : Beef tapeworm
Disease : Taeniasis saginata, Beef tapeworm infection

Morphology:
A. Adult
The adult worm living with its head embedded in the
mucosa of the small intestine, measures 5 – 10 meters on the average,
although under favorable conditions, may attain a length of 25 meters
or more. There are more segments than in T. solium, numbering from
1,000 – 2,000 segments. The scolex measures 2 mm, quadrate in shape
and bears 4 prominent suckers but differs from that of T. solium in the
absence of a well developed rostellum and hooks. The mature
segments are somewhat broad, have irregularly alternate genital pores
and differ from T. solium in having as many testes numbering 330 – 400
follicles and in lacking the accessory ovarian lobe. In gravid proglottid,
the testes and ovary have atrophied and the uterus has 15 – 20 or more
lateral uterine branches (average 18). Each proglottid may contain
97,000 to 124,000 eggs.

B. Eggs
The eggs can not be distinguished from those of T. solium
or from those of Multiceps and Echinococcus.

Life cycle:
The life cycle of T. saginata is similar to that of T. solium except
for the intermediate host. Cattle are the most important intermediate
host, but other herbivores such as camels, goats, carabaos, etc. can
also be infected. When cattle ingest mature egg and reached the level
of the duodenum, the oncosphere is liberated, penetrates through the
intestinal wall, reaches the lymphatics or mesenteric venules and is
carried through the circulation. It is filtered out in the striated muscles,
particularly the pterygoid muscles, those of the tenderloin region and
the myocardium, where in 60 – 75 days develops into cysticercus bovis.
This larval stage is similar to that of T. solium except for the unarmed
scolex. Cysticercus larvae may remain viable in the tissues of cattle for
about 8 months. On ingesting raw or inadequately cooked infected
beef, man, the sole definitive host, becomes infected, with a prepatent
period of 10 –12 weeks.
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112

adult in small ⇨ mature eggs in ⇨ passed into soil,

intestine feces eaten by cattle
⇧ ⇩
scolex attaches larvae hatches in
to mucosa of intestine,into
small intestine blood vessels
⇩ ⇩
ingestion of ⇦ develop into ⇦ oncosphere carried
cysticercus from cysticercus to muscle
raw or insufficiently bovis
cooked beef

Pathology:
T. saginata is ordinarily well tolerated, inspite of its large size. At
times, it is responsible for intestinal disturbances and may produce
acute intestinal obstruction. Toward the end of the prepatent period,
diarrhea and hunger pains frequently develop and loss of weight may
occur. The most common symptoms are discomfort and
embarrassment occasioned by the crawling of the proglottids from the
anus, with a strong tendency to crawl during the day when the host is
active.

Diagnosis:
The diagnosis of T. saginata infection is similar to that of T.
saginata, with recovery of eggs or proglottids from the feces. Study of
the uterine branches in the gravid proglottids provides a differential
and specific diagnosis.
Treatment:
The drug of choice is praziquantel.

Epidemiology:
T. saginata occurs worldwide and is most prevalent in beef-
eating countries. Humans acquire the infection from eating raw or
insufficiently cooked beef containing the cysticerci. Cattle become
infected from grazing on ground polluted by sewage of human feces
containing the eggs of the parasites. Cases of human infection with
cysticercus bovis do not occur.
Prevention and control:
Education regarding cooking of beef and control of the disposal
of human feces are critical measures.
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Taenia saginata scolex

Taenia saginata Taenia saginata

mature segment gravid segment
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ACTIVITY SHEET NO. 12

NAME___________________________SEC__________DATE_______

1. How are you going to differentiate T. solium adult from T?

saginata adult?

2. Which is a more serious infection, with T. solium or infection with

T. saginata? Why?
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Dipylidium caninum

Common name : Double-pored tapeworm, Dog tapeworm

Disease : Dypilidiasis or dog tapeworm infection

Morphology:
A. Adult
D. caninum is a common tapeworm of the dog and cat and
wild canines throughout the world. Humans are occasional host. The
adult worm inhabits the small intestine and consists of a chain of
elliptical proglottids. It measures 10 – 70 cm in length, with 60 – 175
proglottids. The scolex is small, rhomboidal, has 4 prominent deeply
cupped suckers and a refractile conical rostellum armed with 1 – 7
circlets of rose- thorn shaped spines. The neck of the worm is short
and slender. Immature proglottids are first broader than long and later
squarish in outline. Mature and gravid segments are typically
pumpkinseed shaped or vase shaped. Each is provided with a double
set of reproductive organs with the genital pore opening on each lateral
margin of the proglottid. The gravid proglottid is filled with
membranous egg capsules of mother pockets containing 8 to 15 eggs.

B. Eggs
The eggs are spherical, thin-shelled and hyaline except for
a brick red tinge and measures 25 to 40 microns in diameter and have a
delicate hooklets. Gravid segments separate singly or in-group from
the strobila and frequently wander down the bowel and creep out of the
anus. The eggs and egg capsules are expelled by contraction of the
proglottids or by its disintegration outside the intestine.

Life cycle:
Eggs in capsules or proglottids passed out with the feces are
ingested by the larval stages of dog flea (Ctenophalides canis), the cat
flea (Ctenophalides felis) or the human flea (Pulex irritans), all of which
are common ectoparasites of the dog and cat serving as intermediate
hosts. The dog louse, Trichodectes canis has also been incriminated as
a suitable intermediate host. Eggs on reaching the intestine of the
intermediate host, hatch and freed oncosphere migrate into homocoel,
where it develops into cysticercoid. When the infected flea is ingested
by a definitive host, the cysticercoid larva is liberated into the small
intestine and in about 3 – 4 weeks becomes an adult worm.
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Adult in small intestine

⇗ ⇘
cysticercoid larvae gravid proglottids detach
liberated in the from the strobila and pass
small intestine out of the anus
⇧ ⇩
infected I.H. ingested capsules with eggs released
by definitive host from the ruptured segments
⇧ ⇩
cysticercoid larvae eggs in capsule ingested by
develops in homocoel flea
⇖ ⇙
oncosphere is liberated and
penetrate the GUT into homocoel

Pathology:
The degree of pathogenicity is associated primarily with the
number of worms present. Light infection is asymptomatic while
heavier worm burden produce slight intestinal disturbance, loss of
appetite, pruritus ani and sometimes diarrhea.

Diagnosis:
Diagnosis is based on the recovery of the characteristic eggs in
capsule or the proglottids passed out in the feces.

Treatment:
The administration of praziquantel, niclosamide or quanacrine
maybe used for this parasite.

Epidemiology:
D. caninum occurs worldwide, especially in children and its
distribution and transmission are directly correlated with dogs and cats
infected with fleas. Man is occasionally infected by accidental ingestion
of infected flea.
Prevention and Control:
Dogs and cats should be dewormed and not be allowed to lick
the mouths of children. Pets should be treated to eradicate fleas.
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117

Dipylidium caninum scolex

Dipylidium caninum Egg capsule

Gravid segment
 118

118

ACTIVITY SHEET NO. 13

NAME_____________________________SEC________DATE_________

1. Explain why D. caninum was named double pored tapeworm and

Dog tapeworm?

2. How do man acquire dipylidiasis? What is their infective stage

of this parasite?

3. What are the main differences of the ova of D. caninum and

ova of Taenia?
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Hymenolepis nana
Common name : Dwarf tapeworm
Disease : Hymenolepiasis nana

Morphology:
A. Adult
The adult worm measures 2 to 4 cm in length with 96 to
840 segments. The small, rhomboidal scolex has 4 suckers and bears a
short, refractile rostellum armed with a single ring of 20 to 30 Y-shaped
spines. The broad mature segments have a single genital pore on the
side, 3 round testes and a bilobed ovary. The gravid segment becomes
completely filled with eggs, the testes disappears while the uterus
hollow out becomes sac like and filled with eggs.

B. Eggs

The eggs are spherical, measuring 30 – 47 microns. Inside

the egg shell is an oncosphere enclosed in an inner membrane with
bipolar thickenings from which 4 – 8 polar filaments arises. Within the
oncosphere are three pairs of lancet-shaped hooklets.

Life cycle:
The natural definitive hosts are humans, mice and rats. The life
cycle maybe direct or indirect.

In direct cycle, the gravid proglottids of H. nana ruptures in

intestine setting free the eggs, which are immediately infective when
passed in the feces. Upon ingestion of the fully embryonated eggs by
the new host, the oncosphere is liberated and penetrates into the villi of
the anterior part of the small intestine and metamorphose into
cysticercoid. Then it breaks out of the intestinal villi into the intestinal
lumen, where it attaches itself to the mucosa and becomes a mature
strobila worm in the course of 2 weeks.

In indirect cycle, there are some murine strains like H. nana var
fraterna, which uses fleas and beetles as intermediate hosts and
infection of the definitive host results from the ingestion of this
intermediate host.
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120

Internal autoinfection results in heavy infection. The eggs instead

of passing out in the feces, hatched in the intestinal tract, the freed
oncospehere penetrates the villus and repeat its cyclic development.

Adults in small intestine ⇨ Eggs are passed out in feces

of the definitive host ⇩ ⇩
⇧ ⇘ ingested by ingested by
scolex attaches eggs remain man flea,beetles
to the mucosa in intestine ⇩ ⇩
of small intestine (autoinfection)⇨oncosphere metamorphose
⇧ hatches and into cysticercoid
cysticercoid penetrate villi larvae in the
breaks out of ⇩ homocoel
intestinal villi ⇦ cysticercoid ⇩
to the intestinal develops ⇙
lumen ⇦ ⇦ ⇦ ⇦ ⇦

Pathology:
With few worms in the intestine, there are no symptoms. In heavy
infection, especially if autoinfection and hyperinfection occur, patients
experience diarrhea, abdominal pain, headache, anorexia, dizziness
and other vague complaints.

Diagnosis:
Stool examination reveals the characteristic eggs with its six
hooklets embryo and polar filaments.

Treatment:
The drug of choice is praziquantel, with niclosamide as
alternative.
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121

Epidemiology:
This is the only tapeworm, which may not require any
intermediate host; infection is direct from person to person. Infection is
more common in children than adults and is more often seen in family
and institutional groups than in population as a whole. Humanity is the
chief source of infection, although occasionally infection may arise
from rodents’ sources. The murine strain utilizes intermediate hosts
which include C. canis, P. irritans, X. cheopis, Tenebrio molitor and T.
confusum, the cysticercoid stage develops and can be ingested by
both humans and mice.

Prevention and control:

Treatment of cases, improved sanitation and proper personal
hygiene are essential, especially in the family and institutional
environment.
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122

H. nana scolex H. nana mature segment

H. nana gravid segment H. nana ova

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Hymenolepis diminuta
Common name : Rat tapeworm
Disease : Hymenolepiasis diminuta

Morphology:
A. Adult
The adult worm measures 10 – 60 cm in length and with
800 to 1300 proglottids. The small, club-shaped scolex has 4 cup-
shaped suckers and a rudimentary unarmed rostellum. Each mature
segment has 3 ovoidal testes and an ovary and it’s hard to distinguish
this segment from those of H. nana. The gravid segment contains a
saccular uterus filled with eggs.

B. Eggs

The eggs are sub-spherical, have a slightly yellowish

faintly radially striated transparent outer membrane, measuring 60 to 79
microns by 72 to 86 microns and have an inner membrane around the
oncosphere which has two polar thickenings without polar filaments
but with an intralaminar layer giving the egg a “fried egg appearance”.
The six lanceolate hooklets of the oncosphere when at rest are
arranged in a fan like pattern.

Life cycle:
The adult worm inhabits the small intestine of thee definitive
host. Then the gravid proglottids detached from the strobila,
disintegrate and discharge their eggs, which are passed out in the
feces. The principal intermediate hosts are the larval stages of fleas (C.
canis, P. irritans, X. cheopis) and the mealworms of flour beetles
(Tenebrio and Tribolium).

In the intestine of these arthropods, the egg hatches and the

freed oncosphere penetrates into homocoel where it metamorphoses
into cysticercoid larva resembling that of H. nana. When infected
arthropod is ingested by a natural definitive host, the larva is liberated
in the intestine and become a mature adult in about 18 to 20 days.
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Adult in small intestine of the ⇨ eggs passed out in

Definitive host the feces
⇧ ⇩
scolex attaches to the mucosa eggs ingested by the
of small intestine intermediate host
⇧ ⇩
cysticercoid breaks out of cysticercoid develop
intestinal villi to the lumen the homocoel
⇖ ⇙
infected intermediate host
ingested by man

Pathology:
As in the case of other adult tapeworms, H. diminuta infection is
ordinarily well tolerated by the human host. Infections are usually light
and there is no autoinfection.

Diagnosis:
Stool examination demonstrates the characteristic bile stained
eggs that lacks polar filaments.

Treatment:
Niclosamide is the drug of choice with praziquantel as
alternative.

Epidemiology:
H. diminuta is a cosmopolitan cestode of the small intestine of
rats and mice. Accidental ingestion of the infected intermediate host
causes infection in man, an occasional or accidental host. All age
groups appear to be susceptible.

Prevention and control:

Rodent control in areas where grain products are produced or
stored is essential. Thorough inspection of uncooked grain products to
detect mealworms is also important.
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Hymenolepis diminuta scolex

Hymenolepis diminuta ova

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ACTIVITY SHEET NO. 14

NAME__________________________________SEC_____DATE______

1. Tabulate the similarities and differences in the life cycle of

H. nana and H. diminuta.

2. How would you differentiate adult H. nana from adult

H. diminuta?

3. Is internal multiplication possible in Hymenolepiasis nana?

Justify your answer.
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Echinococcus granulosus
Common name : Hydatid worm
Disease : Unilocular echinococcosis or hydatid disease

Morphology:
A. Adult
E. granulosus adult is the smallest tapeworm measuring
.25 to .9 cm in length. The adult lives attached to the mucosa of the
small intestine of the definitive hosts, which include dogs and other
canines. The scolex is pyriform with 4 suckers and a rostellum armed
with 28 to 50 hooks. The worm has a short neck and three proglottids,
one immature, one mature and one gravid. The terminal segment is the
longest and the broadest while the mature segment usually the
narrowest. In the gravid segment, the uterus resembles a loosely
twisted coil. Adult E. granulosus lives 5 to 29 months in dogs, the usual
definitive host.

B. Eggs

The eggs are sub-spherical with radially striated eggshell

which quite similar to Taenia eggs.

Life cycle:
The definitive hosts are dogs, jackals, wolves and other canines.
The adult tapeworm lives attached to the villi of the small intestine of
definitive hosts. The uterus burst either before or after evacuation of
the gravid segments from the bowel discharging relatively few eggs in
the feces of the dogs.

When swallowed by a suitable intermediate hosts such as sheep,

goats, camels, hogs or man, the eggs hatch in the duodenum and the
liberated oncosphere migrate through the intestinal wall and enter the
circulation to be carried to various organs and tissue sites, primarily
the liver and the lungs but also the central nervous system and bone. In
these foci, the larvae begin to develop a cystic cavity and eventually
grow in size. This is called the hydatid cyst, the infective stage to the
definitive host. When infected viscera are fed to the canines, the
scolices freed from the hydatid cyst attach to the intestine and develop
to adult worm. Humans do not participate in the complete life since
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infected human organs are not eaten by dogs. Adult hydatid worms do
not develop in the intestine of either herbivores or humans.

Adult in small intestine

(dogs )
⇗ ⇘
scolices attach to small eggs in feces of dogs
intestine of dog (infective to man, sheep)
⇧ ⇩
hydatid cyst ingested by dog eggs ingested by man
⇧ ⇩
hydatid cyst in liver, lungs, oncosphere hatch, penetrate
etc. of intermediate host intestinal wall
⇧ ⇩
blood circulation ⇦ larvae enter the lymphatics

Hydatid cyst:
The unilocular hydatid cyst is a slow-growing, tumor like space
occupying structure enclosed by a laminated germinitative membrane.
This membrane produces structures on its wall called brood capsule,
where tapeworm scolices arise. Daughter cyst may develop within the
original mother cyst and these also produce brood capsules and
protoscolices. Fluid accumulates as the cyst grows. This fluid is
potentially toxic, if spills into body cavities, anaphylactic shock and
death may result. Spillage and the escape of protoscolices can lead to
the development of cysts in other sites, because the protoscolices have
the germinative potential to form new cysts. Eventually, the brood
capsules and the daughter cysts disintegrate within the mother cyst,
liberating the accumulated protoscolices. These are known as the
“hydatid sand”.

This type of echinococcus cyst is called unilocular cyst, which

measures 1 to 7 cm in diameter, but some may grow as large as 20 cm.
The cyst may contain as much as 2 liters of fluid. Over a long period of
time, the cyst may die and become calcified.
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Pathology:
Since the unilocular cyst grow slowly, the symptoms usually
appear 5 to 20 years after. Pathology caused by the cyst maybe
mechanical or toxic. The pressure of the expanding cyst may grow
within the bone canals and the bone and result to permanent injury.
This type of unilocular cyst found in the bone canal is known as the
casseous hydatid cyst. In the brain, severe damage may occur as a
result of the cysts tumor-like growth into the brain tissue. Spillage of
fluid from the cyst may cause serious allergic reactions.

Diagnosis:
Aspiration of cyst contents may demonstrate the protoscolices.
Radiological examination, scanning procedure and ultrasound
techniques are all valuable and may provide the first evidence of cyst
pressure. Serological procedures are also available such as CFT, ELISA
and Casoni intradermal test.

Treatment:
A surgical procedure on operable sites is the treatment of choice.
In inaccessible sites, the drug mebendazole or albendazole maybe
used.

Epidemilogy:
Human infection with the larval stages of E. granulosus is most
prevalent in sheep raising countries such as Europe, South America,
Africa, Australia, New Zealand and others. Human acquires the
infection by ingestion of contaminated water or vegetables, as well as
hand to mouth transmission of canine feces carrying the infective eggs.

Prevention and Control:

The most important factor in preventing and controlling
echinococcosis is education regarding the transmission of infection
and the role of canine in the life cycle.
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Echinococcus granulosus adult

Hydatid cyst
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ACTIVITY SHEET NO. 15

NAME________________________________SEC______DATE________

1. Differentiate an osseous cyst from a unilocular cyst and from

Alveolar cyst.

2. Is man the definitive host or an intermediate host for

Echinococcosis. Justify your answer.

3. Why is it dangerous to aspirate a hydatid cyst?

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Raillietina garrisoni

Morphology:
A. Adult
The adult measures 60 cm in length. The scolex is minute,
sub-globular, has 4 cup-like suckers surrounded by very minute,
comma-shaped spines. The rostellum is armed with alternating two
circular rows of 90 – 140 hammer-shaped hooks and also surrounded
by a collar of comma-shaped spines.

The mature segment contains a bilobed ovary and 36 to 50

ovoid testes. Genital pores open on the side near the anterior lateral
border of the segments.

Gravid segments are divided into numerous egg capsules,

each containing 1 – 4 eggs. The free gravid proglottids have the shape
of rice grain.

B. Eggs

The eggs inside the capsules are spindle-shaped and the

oncosphere is provided with 6 hooklets and surrounded by two thin
membrane, an outer elongated oval membrane and an inner spherical
membrane enclosing the oncosphere.

Life cycle:
The life cycle of this tapeworm is similar to the mode of
development of most tapeworms and in particular to other species of
tapeworm, which utilize insects as intermediate hosts. The adult worm
inhabits the small intestine of the definitive host. The gravid segments
appear like rice grain, glistening white, opaque and motile. When
ingested by invertebrate hosts especially flour beetles (Tribolium
confusum) the egg hatch and liberate the oncosphere, which migrate
into homocoel of the beetle to develop into cysticercoid larvae. Rats
and man serve as definitive hosts, may acquire the infection from
accidental ingestion of infected flour beetles. The cysticercoid larvae
breaks out of the homocoel and attach to the villi to develop to the
adult stage in about 2 months.
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Adults in small intestine

(rat or man)
⇗ ⇘
immature worm gravid segments pass
attach to villi out in the feces
⇧ ⇩
larvae break out in segments rupture and
lumen of small intestine release eggs
⇧ ⇩
infected flour beetle eggs ingested by flour
ingested by man beetles
⇖ ⇙
eggs hatch, releasing oncosphere
which develop into cysticercoid
Pathology:
The pathology of this parasite infection has not been worked out
yet. Most cases have a single infection, which are expelled
spontaneously even without treatment.

Diagnosis:
This is based on the recovery of the gravid segment, which are
passed out in the feces or crawl out of the anus. The segments have
the characteristic appearance like rice grains and when pressed
between two slides, egg capsules are seen inside, each capsule
containing 1 – 4 eggs, which are spindle-shaped.

Treatment:
Niclosamide and Praziquantel maybe used for treating the
infection.

Epidemiology:
R. garrisoni is a common intestinal tapeworm that infect rodents
in the Philippines. Transmission occurs when the infected I.H. present
In the stored grain product is ingested by man.

Prevention and control:

 134

Prophylactic measures include destruction of rats and mice,

proper disposal of human feces and protection of food especially pre-
cooked cereals from being contaminated with flour beetles.

134

R. garrisoni scolex

R. garrisoni gravid segment R. garrisoni ova

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CLASS TREMATODEA

Introduction:
This species parasitic in human beings belong to the Digenia and
have a complicated life cycle involving alteration of generations and
hosts. The sexual reproduction or multiplication in adult is followed by
asexual reproduction in the larval stages in snails. Most flukes, which
parasitized man also animal parasites and their non-human vertebrate
hosts, serve as reservoir hosts for human infection.

General features:

The adult flukes are usually flat, leaf-like, elongated and

unsegmented. They maybe ovoid, conical or cylindrical depending
upon the state of contraction. They vary in size from less than 1 mm to
several cm. The worm is covered by non-cellular integument, which
maybe covered with spines or tubercles. The integument plays an
important role in the absorption of carbohydrates and may also serve
for secretion of excess metabolites and mucus. The most
distinguishing characteristic of adult trematodes will be the presence of
suckers, which are used for attachment to the host. An oral sucker is
situated at the anterior end of the worm and in most species, a larger,
blind ventral sucker or acetabulum is located on the ventral surface
posterior to the oral sucker.

The digestive system is incomplete; it has a mouth but no anus.

A muscular, globular pharynx extends from the mouth in the oral
sucker to a short narrow esophagus. Below the esophagus, the
intestine bifurcates into two. The intestine maybe branched/dendritic or
simple.

The excretory system includes diffusely scattered flame cells or

solenocytes, capillaries, collecting tubules, bladder and excretory pore.
The terminal flame cell is a hollow cell with tuft of cilia.

The primitive nervous system includes two lateral ganglia in the

region of pharynx connected by dorsal commisures. From each ganglia
arise anterior and posterior longitudinal nerve trunks connected by
numerous commisures.
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136

The parasitic trematodes are hermaphroditic with the exception

of blood flukes (dioecious). The male reproductive organs includes a
conspicuous testes usually two except in blood flukes and Haplorchis
taichu, are located in the posterior half of the body and may vary in
shape (globular, lobate, tubular, dendritic/branched)depending on the
specie.

The female reproductive organs include a single ovary, which

may vary in shape (lobed, dendritic, and globular, round) and is usually
smaller than the testes. oviduct, seminal receptacle, vitelline glands
and ducts.

The eggs of trematodes maybe mature or immature and consists

of vitelline cells, vitelline membrane and a shell. Its shape, appearance
and size are reasonably constant and diagnostic for each species. The
eggs of most trematodes are operculated, except the eggs of blood
flukes.
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137

ADULT MONOECIOUS FLUKE

OVARY TESTES
Shape: Shape: Arrangement:
a. lobed/lobate a. round a. tandem

b. dendritic/branched b. lobed b. oblique

c. round c. dendritic c. opposite

d. globular
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138

Life cycle:
All trematodes are heteroxenous and require two intermediate
hosts to complete its life cycle except for blood flukes. The definitive
host is usually a vertebrate and the intermediate hosts maybe a
mollusk, fish, water plants (vegetation).

The life cycle of trematodes includes (1) egg stage, (2) the larval
stages (miracidium, sporocyst, redia, cercaria, metacercaria) and (3)
adult. The definitive host, generally man, harbors the adult worm and
the first intermediate host usually a fresh water snail or mollusk
harbors the larval stages. The second intermediate host which maybe a
fish, another snail, crab, or vegetables is required for encystment and
harbor the infective larval stage.

In the typical life cycle of trematodes, the eggs escape from the
definitive host via the intestinal genito-urinary or pulmonary tracts.
When discharged the eggs may contain fully developed larvae or may
require subsequent development outside the body before hatching. At
the time of hatching in fresh water, the operculum pops open and the
larvae (miracidium) escape, whereas in non-operculated eggs, it split
by the energetic movement of the larvae. After escaping from the shell,
the ciliated pyriform miracidium swims actively in water. The
miracidium is attracted to an appropriate species of snail by chemotatic
stimulus and penetrate the exposed portion of the snail and the cilia are
shed as the organism enters the snail. Within the tissues of the snail,
the miracidium undergo metamorphosis into an irregular sac-like
sporocyst, then development into rediae and finally cercaria. Cercaria
escapes into the tissues of the snail and pass through the integument
of the snail into the water.

The typical cercaria has an elliptical body, an elongated tail for

swimming, oral and ventral suckers, various spines or stylets, digestive
tracts, rudimentary reproductive system, excretory system and
cephalic glands. The lytic secretions of these glands enable the
cercaria to penetrate the skin of the definitive host or penetrate the
tissue of intermediate hosts. The life of cercaria in water is limited
unless it finds suitable plant or animal hosts on which to encyst or
penetrate the skin of the definitive host. Once inside the secondary
intermediate host, it transforms into metacercaria.
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139

In order to invade the definitive host, the metacercaria in

secondary intermediate host present in fish, crustaceans, and plants
must be ingested or the cercaria must penetrate the skin of man.

In summary, the basic pattern of the life cycle of digenetic

trematodes is as follows:

Egg⇨ miracidium⇨sporocyst⇨redia⇨cercaria⇨metacercaria⇨adult

Variations to this pattern include the following:

1.) more than one generation of sporocysts or rediae
2.) deletion of either sporocyst or redial generations
3.) absence of metacercarial stage

The eggs of trematodes maybe:

(1) fully embryonated or nearly so at the time they are discharged

from the body (Schistosomes, Clonorchis, Opistorchis and
Heterophyds)

(2) may hatch soon upon contact with water (Schistosomes)

(3) may hatch only upon ingestion by intermediate host

Opistorchis, Clonorchis, Heterophyds)

(4) may require a period of embryonation after deposition in water

(Fasciola, Fasciolopsis, Paragonimus, Echinostoma)
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140

Life cycle of monoecious flukes

Adult fluke in habitat ⇨ eggs released into environment

(liver, intestine, lungs) (mature or immature)
⇧ ⇩
excyst in duodenum miracidium
⇧ ⇩
ingested by final host enters snail (1st I. H.)
⇧ ⇩
encyst as metacercaria sporocyst
⇧ ⇩
enters the 2nd I. H. rediae
⇖ ⇙
cercaria

Life cycle of Blood flukes

Adult in habitat ⇨ mature eggs passed out with

Mesenteric vein feces/urine into the water
⇧ ⇩
blood circulation miracidium
⇧ ⇩
skin penetration enters I. H.
⇧ ⇩
cercaria sporocyst 1
⇖ ⇙
sporocyst 2
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141

Classification of Trematodes

I. According to habitat

1. Portal vein
a. Schistosoma japonicum - Oriental blood fluke
b. Schistosoma haematobium - Vesical blood fluke
c. Schistosoma mansoni – Manson’s blood fluke\

2. Lungs
Paragonimus westermani – Oriental lung fluke

3. Liver and bile passages

a. Fasciola hepatica – Giant or Sheep liver fluke
b. Clonorchis sinensis – Chinese or Oriental liver fluke
c. Opistorchis felineus – Cat liver fluke

4. Intestine
a. Fasciolopsis buski – Giant intestinal fluke
b. Echinostoma ilocanum – Garrison’s fluke
c. Heterophyds
c.1 Heterophyes heterophyes – Von Siebold fluke
c.2 Metagonimus yokogawai
c.3 Haplorchis taichu

II. According to the type of eggs

A. Mature
1. Schistosomes
2. Clonorchis
3. Opistorchis
4. Heterophyds

B. Immature
1. Paragonimus
2. Fasciola
3. Fasciolopsis
4. Echinostoma
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ACTIVITY SHEET NO. 16

NAME______________________________SEC______DATE_________

1. Tabulate the differences between Cestodes and Trematodes.

2. Tabulate the differences between monoecious blood flukes and

Blood flukes.
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Fasciola hepatica
Common name : Giant liver fluke/Sheep liver fluke
Disease : Sheep liver rot, Fascioliasis

Morphology:
A. Adult
This is the largest fluke infecting man. The adult worm is
large, flat, leaf-like measuring 20 – 50 mm in length and 6 – 12 mm in
width. At the anterior end, a conical projection is present known as
cephalic cone and a characteristic shouldered appearance is also
observed which serve as distinguishing features of this parasite. The
posterior end of this parasite is broadly pointed. It has two relatively
small suckers, which are of equal size. The intestinal ceca are highly
branched or dendritic. It has two deeply branched or dendritic testes in
tandem formation and a single dendritic ovary.

Related specie, Fasciola gigantica, which commonly

infects cattle, water buffaloes and carabaos, is larger, more lanceolate
than F. hepatica. It measures 30 – 70 mm in length and 3 – 11 mm in
width. Compared to F. hepatica, it has a shorter cephalic cone, less
developed shoulders, a larger ventral sucker and the intestinal ceca is
more branched.

B. Eggs

The egg is large, ovoid, operculated, yellowish brown, with

a well rounded posterior end and it is characteristically hen-egg
shaped. It measures 140 – 180 by 80 – 100 microns and is unsegmented
at oviposition.

Life cycle:
This parasite infects herbivorous mammals like sheep, cattle,
deer and rabbits while man serve as occasional host. The adult worm
inhabits the biliary passages in the liver. The eggs are passed out
together with the feces and mature in water. A viable miracidium is
formed within 9 – 15 days.
 144

The miracidium escapes through the operculum and invade the

first intermediate host. For F. hepatica, the first intermediate hosts are
Lymnae philippinensis, Lymnae swinhoe and Lymnae truncatula. On

144

the other hand the first intermediate host of f. gigantica is Lymnae

rubiginosa. Inside the snail intermediate host, the parasite
metamorphoses into sporocyst, one or two generations of rediae and
cercaria.

The cercaria which is gymnocephalous emerge from the snail

and attach by way of their oral sucker on the surface of aquatic
vegetation like watercress which serve as their second intermediate
host, where they develop into metacercaria. Ipomea obscura or
kangkong and Ipomea reptans or morning glory serves as second
intermediate host. The definitive host can become infected either by
ingesting raw or inadequately cooked plants or drinking water
contaminated with cercaria.

Upon ingestion, the metacercaria excyst in the duodenum,

liberating the juvenile fluke, which penetrate through the intestinal wall
into the peritoneal cavity where it wander over the viscera until it,
reaches the liver capsule. The parasite then burrows through the liver
parenchyma, until it finally enters the bile ducts where it matures in 3 –
4 months. The adult worm survives for as long as 11 years in definitive
host.

Adult in the biliary tract (liver) ⇨ immature eggs passed in

⇧ feces
metacercaria excyst in duodenum, ⇩
migrate through intestinal wall, eggs mature in water,
peritoneal cavity and liver capsule 9 – 15 days
⇧ ⇩
man ingest plants with metacercaria miracidium hatch in water
⇧ ⇩
cercaria excyst on the surface of enters first intermediate
of 2nd intermediate host host
⇧ ⇩
free swimming cercaria leaves snail sporocyst
⇧ ⇩
cercaria ⇦ rediae 2 ⇦ rediae 1
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Pathology:
The extent of the damage and symptomatology depend upon the
intensity of the infection and the duration of the disease.

Fascioliasis is classified into two phases:

1. Acute or invasive phase

This corresponds to the period during which the parasite

migrate from the intestine to the liver. The usual clinical
manifestations exhibited by the patient are dyspepsia, prostation,
anorexia, sweating, myalgias, joint and bone pains, violent
headache, nausea, vomiting and urticaria. There is sudden onset
of high fever, enlargement of the liver and marked eosinophilia
which are all of diagnostic importance. Serious traumatic and
necrotic lesion is caused by the juvenile parasite as it burrows in
the liver.

2. Latent or chronic phase

This corresponds to the period when the parasite has

already settled in the bile ducts. The adult causes obstruction of
bile ducts and provokes inflammation on the epithelium of the
bile duct stimulating pipestem fibrosis.

Pharyngeal Fascioliasis or Halzoun result from ingestion

of raw sheep liver or goat liver containing the adult parasite. The
attachment of the worm in the pharyngeal mucosa may result to
asphyxiation (suffocation).

Diagnosis:
The diagnosis is based on the recovery of the eggs in the
patient’s stool. Fasciola eggs maybe present in stool of individual who
has earlier consumed infected animal liver (False fascioliasis). This
could be ruled out by keeping the patient on a liver free diet for three to
7 days before another stool examination is done.
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Immunodiagnostic tests involving techniques such as CFT,

precipitin test, immunoelectrophoresis, counterimmunoelectrophoresis
may also be useful.

The FAST (Falcon Assay Screening Test)-EIA alone or in

combination with EITB can detect F. hepatica excretory-secretory
antigens in serum. EIA with somatic antigen or excretory-secretory4
antigens from F. gigantica or F. hepatica (especially excretory-
secretory products), yield high sensitivity, including detection of
reactive IgM in acute fascioliasis and confirmation by enzyme-linked
immunoelectrotransfer blot (EITB).

Treatment:
Bithionol is the drug of choice.

Epidemiology:
This parasite has a worldwide distribution. It is more common
among populations that consume raw vegetables. Human cases are
rare in the Philippines but animal cases are common. Infection among
local cattle, carabaos, sheep and goats occur although G. gigantica is
probably more prevalent specie in cattle and carabao.

Prevention and control:

Thorough washing and cooking of vegetables and boiling
drinking water in areas where infection is endemic. Elimination of snail
intermediate hosts and killing the parasites present in the reservoir
host by chemotherapy.
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147

Fasciola hepatica adult

Fasciola hepatica ova

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ACTIVITY SHEET NO. 17

NAME______________________________SEC________DATE________

1. Discuss false fascioliasis and its effect to the affected individual.

2. Why is human infection with Fasciola hepatica rare in the

Philippines?

3. What are the diagnostic features of adult Fasciola hepatica?

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Clonorchis sinensis
Common name : Chinese liver fluke/ Oriental liver fluke
Disease : Clonorchiasis

Morphology:
A. Adult
This fluke is a parasite of fish-eating mammals and
humans.The adult worm is flat, elongated, aspinous, and transparent
gray worm that is tapering anteriorly and somewhat rounded
posteriorly. The adult measures 8 – 25 mm in length and 1.5 – 5 mm in
width. The ventral sucker is smaller than the oral sucker. The long
intestinal ceca are simple extending to the posterior end. The two
deeply branched testes in tandem formation are situated in the
posterior part of the body. The single ovary is relatively small with three
lobes and located anterior to the testes.

B. Eggs

The light yellowish-brown eggs measures 26 – 30 by 15 –

17 microns. The convex operculum rests in a rim with distinct shoulder.
At the thicker posterior end or aboperculum is a small protuberance.
The egg is similar to an old-fashioned electric bulb.

Life cycle:
The natural definitive hosts other than humans are dog, cat, hog
and rarely ducks. The worm attaches itself to the mucosa of the bile
duct by the use of their suckers and embedding themselves in sticky
mucus. Occasionally in heavy infections, it maybe found in the larger
bile ducts, the gall bladder and the pancreatic duct. It is not found in
the duodenum, since it can only survive the action of digestive juices
for a few hours. It feeds on the secretion of the upper bile ducts, tissue
fluids, red cells and mucus. Eggs are released from the worms in its
mature state. The adult worm has been reported to release as many as
4,000 eggs per day.

The eggs are deposited in the biliary passages of the definitive

host, pass from the body in the feces. Although the eggs contain fully
developed miracidium, they do not hatch upon reaching the water.
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150

The most common first intermediate host is Parafossarulus

manchoricus and other hydrobiid snails that live in fish culture ponds,
lakes, swamps, and sluggish parts of the river or small streams. The
miracidium is release only after having been ingested by the first
intermediate host. In the tissue of the snail, it metamorphoses into a
sporocyst within 4 hours, rediae in about 17 days and in turn each
rediae produces 5 – 50 cercaria that are released into the surrounding
water.

The free-swimming cercaria perishes unless it encounters a fish

within 24 – 48 hours. Fish serve as the second intermediate host like
Ctenopharyngodon idellus, Caridina nilotica gracilipes. It penetrates
beneath the scales, attaches itself to the epithelium with it suckers and
transform into metacercaria. The metacercaria encyst chiefly in the
muscles and subcutaneous tissues, less often on the scales, fins and
gills of fish.

When infected fish is eaten by the mammalian definitive host, the

metacercaria excyst in the duodenum. In the human duodenum, the
outer wall is dissolved by trypsin, while the inner layer is ruptured by
the activity of the metacercaria. The freed larva migrates to the
common bile duct and to the distal biliary ducts, where it becomes a
mature worm within a month. The entire life cycle can be completed in
three months. The life span of the adult is 15 – 20 years.

Adult in biliary tract

⇗ ⇘
man ingest insufficiently mature eggs passed
cooked infected fish out with the feces
⇧ ⇩
metacercaria enters the 1st I.H.
⇧ ⇩
enters the 2nd I. H. miracidium hatch
⇧ ⇩
free-swimming cercaria sporocyst
⇧ ⇩
cercaria ⇦ rediae
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Pathology:
Eggs have been associated with formation of gallstones. Diet
affects chronic infections. Increased intake of dimethylnitrosamines (in
fermented fish) usually leads to cholangiocarcinoma, a neoplasia of the
liver.

Symptoms experienced by patients are fatigue, weakness, weight

loss, abdominal distress and altered appetite. Fever, enlargement and
tenderness of the liver and eosinophilia are symptoms of acute
infection.

In heavy infections, anemia, liver enlargement, slight jaundice,

edema and diarrhea develop.

Diagnosis:
Diagnosis is based on finding the characteristic eggs in the
feces. The eggs require differentiation from those of other eggs like
Opistorchis and Heterophyds. Immunodiagnostic test and liver scan is
useful.

Treatment:
Praziquantel has been found effective in the treatment of
infection.

Epidemiology:
Humans are usually infected by eating uncooked fish containing
metacercaria and less often by the ingestion of the cyst in drinking
water. Metacercaria can withstand the effects of different food
processing so this can be present in frozen, pickled, dried or smoked
fish.

The parasite is prevalent in China, Taiwan, Hongkong, Korea,

Japan and Vietnam.

Prevention and control:

Thorough cooking of fish would practically eliminate the disease
in humans. Control measures include education of the population
regarding food habits and stopping the seeding of fish culture ponds
with human feces.
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Clonorchis sinensis adult

Clonorchis sinensis ova

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Opistorchis felineus
Common name : Cat liver fluke
Disease : Opistorchiasis felineus

Morphology:
A. Adult
This parasite lives in the biliary passage and infects
several species of fish-eating mammals. The reddish yellow adult worm
measures 7 –12 mm in length and 1.5 – 3 mm in width and is lancet-
shaped. The intestinal ceca is simple, the two testes are lobate and
arranged obliquely in tandem. The oral sucker is smaller than the
ventral sucker. The single ovary is lobed.

Another closely related species that infect man is

Opistorchis viverrini. This specie is differentiated from O. felineus in
that the ovary and testes are nearer to each other, both of which are
more deeply lobulated. The testes are obliquely arranged.

B. Eggs

The egg is yellowish-brown, ovoid and is smaller than C.

sinensis. It has an operculum that sits on the thickened rim and a
minute aboperculum is also present.

Life cycle:

When the egg is released from the adult worm, a fully

embryonated miracidium is present within the eggshell. The egg
containing the viable miracidium is released from the definitive host
and passed out with the feces. The egg is ingested by the first
intermediate host, which is Bithynia leachi for O. felineus and Bithynia
funiculata for O. viverrini. Upon ingestion of eggs, it hatches and
releases the miracidium. Inside the snail, the parasite undergoes
through the sporocyst and rediae stages of development.

Cercaria emerges from the rediae two months after infection. The
cercaria attaches itself and penetrates the skin of cyprinoid fishes like
Idus melanotus, Tinca tinca, and Cyprinus carpio, Barbus barbus that
serve as second intermediate hosts.
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The metacercaria present in the second intermediate host is

ingested by the definitive host where it excyst in the duodenum and
young flukes migrate into the bile passage, where they mature in 3 – 4
weeks. The entire life cycle can be completed in a minimum of 4
months.

Pathology:
The degree of clinical involvement depends largely on the worm
burden and the duration of the infection. Moderate infections harboring
several hundred to 1000 worms causes enlargement of the liver,
passive congestion of the spleen, with icterus and local eosinophilia in
the wall of the bile ducts. In heavier infections, worms can be found in
the pancreas and the gall bladder and the patient suffers from digestive
disturbances. Bile stones maybe formed around the parasite eggs.
Opistorchis has been linked to carcinoma of the bile ducts and the
liver.

Diagnosis:
The detection of eggs in stool.

Treatment:
Praziquantel is the drug of choice.

Epidemiology:
O. felineus is common in many countries in Europe, Turkey,
USSR, Japan, Vietnam and India. In the Philippines, only one case has
been reported. O. viverrini is found in Thailand, Laos and Malaysia.

Transmission is mainly by consumption of infected raw fish and

drinking water contaminated with metacercaria. Reservoir host
includes the dogs, cats, foxes, lions and rabbits.

Prevention and control:

Thorough cooking of fish would eliminate the disease in humans.
Control measures include education of the population regarding food
habits.
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Opistorchis felineus adult

Opistorchis felineus ova

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ACTIVITY SHEET NO. 18

NAME_______________________________SEC______DATE_________

1. What are the morphological features distinguishing C. sinensis

adult from O. felineus adult?

2. What are the possible ways man can acquire Opistorchis and
Clonorchis?

3. Discuss Opistochiasis and Clonorchiasis.

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Paragonimus westermani
Common name : Oriental lung fluke
Disease : Paragonimiasis, Pulmonary distomiasis,
Endemic hemoptysis

Morphology:
A. Adult
The adult worm is reddish-brown and measures 7 – 12 mm
in length, 4 –6 mm in width and 3.5 – 5 mm in thickness. The cuticle is
spinous; the oral and ventral suckers are of equal size. The intestinal
ceca are simple. The two testes are deeply lobed and situated opposite
each other. The ovary has 6 unbranched lobes and is anterior to the
testes. The shape of adult, when active resemble a spoon with one end
contracted and the other elongated and when preserved an oval,
flattened coffee bean shaped.

B. Eggs

The immature egg is golden brown, oval in shape, thick-

shelled measures 80 – 118 by 48 – 60 microns. The operculum is wide
and flattened with a thickened aboperculum.

Life cycle:
The adult worm inhabits the lungs and eggs escape with lung
exudates into the respiratory tract where they are moved up and out by
the ciliary epithelium. Arriving at the pharynx, they are either coughed
up or swallowed back into the alimentary tract to be passed out with
the feces.

The unembryonated egg leaves the body of the definitive host via
respiratory tract or intestinal tract. The egg embryonate in water and a
miracidium is formed within 2 – 7 weeks. The free-living miracidium
penetrate the body of snail, which serve as the first intermediate host.
In the Philippines, Antemelania asperata (formerly Brotia asperata) and
Antemelania dactylus serve as 1st interemediate hosts. Inside the snail,
the miracidium develop into sporocyst and to two redial stages of
development and then cercaria.

The cercaria will emerge from the snail in about 13 weeks and
penetrate a freshwater crab or crayfish, which will serve as secondary
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intermediate host. The second intermediate host is the mountain crab,

Sundathelphusa philippina (formerly Parathelphusa grapsoides). The
cercaria penetrates through the soft parts of the body of the crab and
encysts as metacercaria in the gills, legs, body muscles or the viscera.
The definitive host acquires the infection by ingestion of raw or
insufficiently cooked infected crabs.

After ingestion by the mammalian host, the excysted

metacercaria pass through the duodenal wall into the abdominal cavity.
The adolescent worms burrows through the diaphragm, enter the
pleural cavity and in about 20 days reach the lungs, where in cystic
cavities near the bronchi they become adult in 5 – 6 weeks. During the
prolonged migration, the adolescent worms may remain for long period
in the peritoneum and may enter and leave the liver and may become
lodged in organs other the lungs, the so-called ectopic lesion. The
worms are known to persist in humans for as long as 20 years or more.
Animal reservoir hosts of this parasite include dogs, cats, field rats and
other rodents.

Adult in the lungs ⇨ eggs passed in feces/sputum

⇧ ⇩
excyst in S.I.,migrate eggs mature in water in
through abdominal cavity 2 – 7 weeks, miracidium hatched
⇧ ⇩
man ingest insufficiently miracidium penetrate the first
cooked infected crab intermediate host
⇧ ⇩
cercaria penetrate 2nd I.H. Sporocyst
⇧ ⇩
free swimming cercaria Redia 1
⇧ ⇩
cercaria leave 1st I.H. ⇦ cercaria ⇦ Redia 2

Pathology:
In the lungs, the parasite provokes the development of a fibrous
tissue capsule. Within this cyst is a blood tinged, purulent material
containing eggs. At first, there will be dry cough and later production of
bloodstained, rusty brown sputum that is most pronounced on rising in
the morning. Pulmonary pain and hemoptysis occurs. Along with these
symptoms, the patient may experience fever, sweating, chest and
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pains, cough which are all symptoms of pulmonary tuberculosis. The

clinicians find it difficult to separate this infection from pulmonary
tuberculosis, pneumonia and bronchitis.

Abberant worms with cyst formation may localize in the

abdominal wall, abdominal cavity, mesenteric lymph nodes, omentum,
pericardium, and myocardium and in intestinal wall. They may produce
abdominal pain, rigidity and tenderness. In the brain, the worms may
cause Jacksonian epilepsy and visual disturbances. Worms situated in
the subcutaneous tissue cause creeping tumor.

Diagnosis:
Definitive diagnosis is established by finding the eggs in the
sputum, feces or bronchial washing. For sputum, treatment with 3 %
NaOH followed by sedimentation and washing is the method of choice.
Repetition maybe necessary to finally detect P. westermani ova.

Treatment:
Praziquantel, Emetine hydrochloride and bithionol are the drugs
used for the treatment of paragonimiasis.

Epidemiology:
P. westermani has a cosmopolitan distribution among mammals,
but its presence in humans is chiefly confined to the Far East. The
principal endemic regions are Japan, South Korea, Thailand, Taiwan,
China and Philippines, although in the Philippines it is not considered a
public health problem. The known endemic areas are Camarines,
Sorsogon, Mindoro, Samar, Leyte, Davao, Cotabato and Basilan.

Transmission is by ingestion or eating infected crabs and eating

most of the paratenic host that harbors the parasite.

Prevention and control:

Eating sufficiently cooked crabmeat can prevent Paragonimiasis.
Care should be taken when preparing crabs for cooking as
contamination of kitchen utensils and other food with viably
metacercaria can also result in infection. Health education can help in
controlling the parasitic infection.
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Paragonimus westermani adult

Paragonimus westermani ova

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ACTIVITY SHEET NO. 19

NAME_____________________________SEC_______DATE__________

1. How would you give a specific or definite diagnosis if the patient

will have the classical symptoms of pulmonary tuberculosis but
the patient is actually infected with P. westermani?

2. Discuss the different modes of transmission of Paragonimiasis.

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Fasciolopsis buski
Common name : Giant intestinal fluke
Disease : Fasciolopsiasis

Morphology:
A. Adult
Fasciolopsis buski is also a large trematode parasitizing
man, measuring 20 – 70 mm in length, 8 – 20 mm in width. It is
elongated and oval in shape. The oral sucker is about one- fourth the
size of the nearby ventral sucker. This fluke resembles F. hepatica,
however, it does not have any cephalic cone, and shoulder and the
intestinal ceca are simple but wavy and unbranched. The testes are
highly dendritic in tandem formation and the single ovary is branched.

B. Eggs

The yellowish ellipsoidal egg measures 80 – 85 microns,

thin-shelled, rounded at both ends and operculated.

Life cycle:
The adult inhabits the small intestine particularly the duodenum
and the jejunum. It is either attached to the intestinal mucosa by the
ventral sucker or lies buried in the mucous secretions. Each adult
produces an average of 16,000 eggs per day.

The egg is undeveloped when passed in the feces. In water it

undergoes further development and in 3 – 7 weeks, miracidium will be
released. The miracidium will penetrate the 1st intermediate host, which
maybe Segmentina trochoideus or Hippeutis umbilicalis.

In the snail intermediate host, the miracidium transform into

sporocyst, rediae 1, rediae 2 and cercaria. Cercaria will leave the body
of the 1st intermediate host in 4 – 7 weeks, actively swim in water and
attach themselves and encyst on the surfaces of the 2nd intermediate
hosts like Trapa bicornis (water caltrop), Eliocharis tuberosa (water
chestnut), Ipomea aquatica (water morning glory) and Nymphae lotus
(lotus) and encyst as metacercaria. Metacercaria are ingested when
these infected 2nd intermediate hosts are swallowed. The metacercaria
excyst in the duodenum and attach themselves to the intestinal wall
and becomes an adult worm in about three months.
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Pathology:
Pathology maybe due to the following:

a. Traumatic
There maybe inflammation and ulceration at the site of
attachment resulting to increase mucus secretion and minimal
bleeding. Epigastric pain, nausea and diarrhea may occur
especially in the morning.

b. Obstructive
In heavy infections, there maybe edema and partial
intestinal obstruction due to the large size of the worm.

c. Toxic
Intoxication is possible due to the absorption of the
metabolites of the worms and other excretory by-products which
become systematic upon absorption and patient may experience
generalized toxic and allergic symptoms. Profound intoxication
may result in death.

Diagnosis:
Diagnosis is by demonstration of eggs in stool.

Treatment:
Praziquantel, Niclosamide, Tetrachloroethylene, Hexylresorcinol
and Dichlorophen have been used to treat fasciolopiasis.

Epidemilogy:
This parasite is found in the countries in Southeast Asia. In the
Philippines, pigs have been reported to be infected with F. buski.

Prevention and control:

Pollution of swamps or ponds where aquatic plants are cultivated
should be stopped. Wash and boiling of plants is necessary.
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Fasciolopsis buski adult

Fasciolopsis buski ova

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ACTIVITY SHEET NO. 20

NAME______________________________SEC_______DATE_______

1. Differentiate morphologically adult F. hepatica from adult F.

buski.

2. Aside from humans, give other definitive host for F. buski.

3. Differentiated Fascioliasis from Fasciolopsiasis.

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Echinostoma species
Echinostoma are medium sized flukes, the adult worms are
unique due to the presence of collar of spines around the oral sucker.
Many species have been reported in man and are differentiated on the
basis of number of spines and number of lobes in testes. In the
Philippines, two species have been documented to infect man,
Echinostoma ilocanum and Echinostoma malayanum.
A. Adult
The adult Echinostoma ilocanum (Garrison’s fluke) is
reddish gray, measuring 2.5 – 6.5 mm in length, 1 – 1.5 mm in width.
The anterior end is provided with a horseshoe-shaped collar of spines
(Collarette of spines) or a circumoral disk surrounded with 49 – 51
spines in two rows. The oral sucker lies in the center of this disk. The
testes are bilobed in tandem formation while the ovary is globular and
is located anterior to the testes.
Adult Artyfechinostomum malayanum (Echinostoma
malayanum) measures 5 – 12 mm in length and 2 – 3 mm in width and is
provided with 43 – 45 collar of spines and with a multilobulated testes
(6 – 9 lobes) in tandem formation. The ovary is small, rounded or oval.
B. Eggs
The egg of E. ilocanum measures 86 – 116 microns by 58 –
69 micron, straw-colored, operculated, ovoidal and with characteristic
germ ball. A. malayanum egg is larger,measuring 120 – 130 micron by
80 – 90 micron, operculated with characteristic germ ball.

Life cycle:
The adult worm inhabits the small intestine and immature eggs
are passed out with the feces. The ova mature within 6 – 15 days and
the miracidium enters the first intermediate host. For. E. ilocanum, in
the Philippines, the first intermediate hosts maybe Gyraulus
convexiusculus or Hippeutis umbilicalis. The first intermediate host of
E. malayanum in the Philippines is still unknown. Inside the snail
intermediate host, they will metamorphoses from miracidium to
rediae 1, rediae 2 and then cercaria. Development into sporocyst was
abortive. Cercaria escape from the snail 42 – 50 days to infect the
second intermediate host which is also a snail, Pila luzonica or kuhol
and Vivipara angularis or susong pampang for E. ilocanum and Lymnae
cumingiana or birabid (formerly Bullastra cumingiana), Radix quadrasi
and Physastra hungerfordiana for E. malayanum. The cercaria
transform into metacercaria and man acquire the metacercaria by
eating infected snail. The metacercaria excyst in the duodenum and the
adult fluke attaches itself to the intestinal wall.
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Adult in small intestine

⇗ ⇘
man ingest insufficiently immature eggs passed in feces
cooked infected 2nd I.H. ⇩
⇧ eggs mature in water, 6 – 15 days
cercaria penetrate the ⇩
second intermediate host miracidium hatch
⇧ ⇩
free-swimming cercaria penetrate 1st Intermediate host
⇧ ⇩
cercaria rediae 1
⇖ ⇙
rediae 2

Pathology:
This parasite causes a little damage to the intestinal mucosa.
There will be inflammation at the site of attachment. In heavy infections,
the patient will manifest diarrhea and sometimes-bloody stool and
abdominal pain. The absorption of the metabolites of the worms may
result in general intoxication.

Diagnosis:
Diagnosis is by the recovery of eggs in the stool.

Treatment:
Praziquantel and Hexylresorcinol are the drugs of choice.

Epidemiology:
This parasite is found in Indonesia, India, China, Thailand and the
Philippines. In the Philippines, this parasite is prevalent in Northern
Luzon, Leyte, Samar and Mindanao. Pigs and rats serve as an important
reservoir hosts of this parasite.

Prevention and control:

Infection can be prevented by thorough cooking of snails.
Drinking water should be boiled.
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Echinostoma ilocanum Echinostoma malayanum

Adult Adult

Echinostoma ova
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ACTIVITY SHEET NO. 21

NAME_________________________________SEC_______DATE_____

1. Tabulate the differences of adult E. ilocanum and adult E.

malayanum.

2. How are you going to differentiate the egg of Echinostoma from

the eggs of Fasciola?

3. Discuss the mode of transmission of Echinostoma ilocanum.

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Family Heterophydiae

a. Heterophyes heterophyes - Von Siebold’s fluke

b. Metagonimus yokogawai
c. Haplorchis taichu

Introduction and morphology:

A. Adult
The adult Heterophyds are elongated, oval or pyriform in
shape and the smallest yet the deadliest measuring less than 2 mm in
length.

Heterophyes heterophyes adult is grayish and the smallest

fluke of man, measuring 1.3 by 0.5 mm. The oral sucker is very small
while the ventral sucker is large, situated in the anterior middle-third of
the body. A conspicuous genital sucker (gonotyle) lies in the lateral
posterior border of the ventral sucker. The two testes are ovoid side by
side in the posterior fifth of the body. The subglobuse ovary is anterior
to the testes.

Metagonimus yokogawai adult measures 1.4 by 0.6 mm.

The large ventral sucker is situated to the right of the midline. The two
oval testes are unequal in size, arranged obliquely side by side and
situated in the posterior third of the body. The globuse ovary is situated
at the junction of the middle and lower third of the body.

Haplorchis taichu adult is provided with a large ventral

sucker, a globuse ovary and only one testis.

C. Eggs

The egg is light yellow brown in color, ovoidal, operculated

and minute measuring 20 – 30 by 15 – 17 micron and is the smallest
trematode egg. The shell has a slight shoulder at the rim of the
operculum and sometimes a knob at the posterior pole maybe
observed. A fully developed miracidium is already present within the
egg when it is deposited by the adult worm.
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Life cycle:
The adult worm inhabits the small intestine of the definitive host.
Definitive host maybe man or domesticated or wild fish-eating
mammals. Large numbers of eggs are produced and passed out into
the environment with the feces. Eggs are ingested by fresh water snail
that serves as the first intermediate host. The first intermediate host of
the species of Heterophyds is:

a. H. heteophyes = Pironella conica (Egypt) and

Cerithidia cingula
b. M. yokogawai = Semisulcospira, Thiara and Hua
c. H. taichu = Melania juncea, Thiara riquetti

Inside the snail, the parasite transforms into sporocyst, one or

two generations of rediae and cercaria. Cercaria, that emerge from the
snails and penetrate a suitable fish species that serve as the second
intermediate host. The second intermediate hosts are:

a. H. heterophyes = Mugil, Salmo, Acanthogobius

b. M. yokogawai = Plecoglossus, Salmo, Richarsonium,
Odontobutis
c. H. taichu = Ambassis burensis (langaray),
Amphacathus jacus (samaral), Anabas
testidineus (martiniko). Arius
manilensis (kanduli), Claris batrachus
(hito), Gerris kapas (malakapas),
Glossogonius giurus (bia),
Hemiramphus georgii (cansusuit or
bugning), Ophiocephalus striatus
(dalag), Pelates quarilineatus (babansi)
and Therapon plumbeus (ayungin)

Metacercaria encyst on or under the scales, in muscles, fins tails

or gills of the second intermediate host. When raw or insufficiently
cooked infected fish is ingested by the definitive host, the metacercaria
escapes from the cyst and develops into an adult worm in about a week
and attaches itself to the intestinal wall.
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Pathology:
There is inflammation at the site of attachment causing damage
to the intestinal mucosa. The patient may experience colicky pain and
mucus diarrhea.

The adult worm may burrow deep into the intestinal wall where
they become trapped and eventually die. The eggs of the degenerating
worms are then spilled into the blood stream and lymphatics and are
carried to the different parts of the body. Eggs filtered in the heart
muscles may lead to cardiac failure resembling that of cardiac beri-beri.
Eggs deposited in the brain may result in fatal cerebral hemorrhage and
when the eggs are deposited in the spinal cord may result in loss of
motor and sensory functions at the levels where the lesions are
located.

Diagnosis:
Diagnosis is by recovery of eggs in stool.

Treatment:
Praziquantel and Tetrachloroethylene are the drugs of choice.

Epidemiology:
Heterophydiasis is prevalent worldwide. Reservoir hosts are
cats, dogs and birds. The snail intermediate host can be found in fresh,
brakish and salt waters in temperate, subtropical and tropical regions.

Prevention and control:

Ingestion of raw or inadequately cooked fish should be
prevented. Domestic animals should be not be given infected fish.
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Heterophyes heterophyes Heterophyes heterophyes

Adult egg

Metagonimus yokogawai Metagonimus yokogawai

Adult ova
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ACTIVITY SHEET NO. 22

NAME________________________________SEC_______DATE______

1. What are the diagnostic characteristics of each specie of

Heterophyds?

2. Why is Heterophyds considered as the deadliest fluke?

3. How are you going to differentiate the egg of Heterophyds

from the eggs of Clonorchis?
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Schistosoma species (Blood fluke)

Introduction:
Schistosomes or blood flukes are digenetic trematodes
inhabiting the veins of their vertebrate hosts and which require snail
intermediate host. Five Schistosome species, Schistosoma mansoni, S.
haematobium, S. japonicum, S. mekongi and S. intercalatum commonly
infect humans.

A. Schistosoma japonicum
Common name : Oriental blood fluke
Habitat : superior mesenteric vein of the
Small intestine
Disease : intestinal and hepatic schistosomiasis,
Oriental schistosomiasis,
Schistosomiasis japonica or Katayama
disease

B.Schistosoma mansoni
Common name : Manson’s blood fluke
Habitat : mesenteric vein of the large intestine
Disease : Schistosomiasis mansoni

C. Schistosoma haematobium
Common name : Vesical blood fluke
Habitat : portal vein of the urinary bladder
Disease : vesical schistosomiasis, bilharziasis,
Urinary schistosomiasis

Morphology:
A. Adult
Schistosomiasis adult is narrow, elongated and dioecious.
It has both oral and ventral suckers. The intestine bifurcates into two
ceca, unite to form a single blind stem. The female is longer and more
slender while the male is shorter but more robust. The male body is
folded to form a long ventral gynecophoral canal, a groove behind the
ventral sucker, which serve as attachment site of the female to the male
during copulation. It is where the female is held by the male during
copulation. The number of testes in male and number of eggs in uterus
are distinctive to the species.
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Schistosoma japonicum adult is provided with smooth

tuberculations. The male have 6 – 9 testes arranged in rows. The ovary
of the female lies somewhat behind the mid plane of the body and the
uterus can have 50 eggs at one time.

Schistosoma mansoni is provided with coarse tuberculations.

Male has 6 – 8 testes while the ovary of the female is situated in the
anterior half of the body. The uterus is short with 20 – 40 eggs.

Schistosoma haematobium is provided with fine tuberculations,

wherein the ventral sucker is larger than the oral sucker. The number of
testes in male is 4 – 5 and the ovary of the female is posteriorly located.
The number of eggs in the uterus is 20 – 100.

B. Eggs

Schistosoma japonicum eggs are ovoidal, non operculated,

measuring 70 – 90 microns by 50 – 65 microns. A rudimentary or
minute lateral spine is present.

Schistosoma mansoni eggs are elongated, non operculated,

measuring 114 – 175 microns with transparent shell and a prominent
lateral spine.

Schistosoma haematobium eggs are elongated, non-operculated,

light yellowish brown and possess a distinct terminal spine.

Life cycle:
The eggs are deposited by the female worm in the terminal
venules in the walls of their habitat. The female Schistosomes empties
its uterus 10 – 12 times a day and depending upon the specie of flukes,
from 300 to 3,500 eggs are passed out daily into the venules.
Maturation of the eggs with formation of a miracidium require 10 – 12
days and its lytic enzymes and the contraction of the venule liberating
eggs into the tissues of the intestine or urinary bladder. The eggs effect
a passage into the lumen of these organs and are evacuated in the
feces or the urine and may reach waters where the intermediate hosts
are present. On contact with water, the miracidium hatch from the eggs
and swim until it reach a suitable intermediate host which maybe
Oncomelania hupensis quadrasi for S. japonicum; Biomphalaria and
Tropicorbis for S. mansoni and for S. haematobium, Bulinus,
Biomphalaria and Physopsis.
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Inside the snail intermediate host, the miracidium develops into two
generations of sporocyst (sporocyst 1, sporocyst 2) and finally
cercaria. Cercaria leaves the body of the intermediate host and lives in
water until it penetrate the skin of the definitive host. Inside the
definitive host, cercaria transform into schistosomula, after skin
penetration, migrate via circulation to reach the portal circulation of
mesenteric veins where it will become adult worms.

Pathology:
Symptoms associated with schistosomiasis include weakness,
diarrhea, hepatosplenomegaly, and carcinoma of the intestine, liver,
uterus and urinary bladder

A. S. japonicun and S. mansoni

Pruritus and rashes maybe manifested by the infected

individual at the site of entry. Migration of the adolescent in the lungs
maybe the cause of pneumonitis (Pulmonary schistosomiasis.)
Deposition of eggs in the tissues may cause irritation and formation of
ulcers in the mucosa leading to the escape of the eggs into the
intestinal lumen. Ulceration is responsible for diarrhea or dysentery
seen in acute schistosomiasis. Granuloma of affected tissue and organ
is also evident. In the brain, granuloma may give rise to a number of
obstructions to the pulmonary circulation. Formation of pseudotubercle
in affected organs/tissues maybe observed. Schistosomiasis japonica
depending on the major sites of eggs deposition maybe hepato-
intestinal, hepato-splenic or pulmonary.The clinical course of infection
is divided into three progressive stages:
a. incubation - corresponding to the period from the
cercarial penetration and schistosomular
migration to the time the flukes mature,
b. period of early egg deposition and extrusion
c. period of tissue proliferation

B. S. haematobium
Since S. haematobium lives primarily in the pelvic veins,
its eggs are primarily deposited in the vessical plexus and produce
lesions in the urinary bladder, genitalia (seminal vesicle, vulva, cervix
and vaginal walls). Uric acid and oxalate crystals, phospate deposits,
eggs, blood clots, mucus and pus maybe present in urine. The most
characteristic symptom is hematuria. As the mucosal surfaces become
inflamed, there will be painful micturation and a constant urinary
residual. Pain in the suprapubic region and weakness may occur.
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Diagnosis:
A. S. japonicum and S. mansoni
Demonstration of eggs from stool by performing DFS,
Kato-Katz or concentration technique. Serological tests like COPT,
ELISA and Indirect hemeagglutination maybe performed to
demonstrate antibodies. COPT (Circum oval precipitin test)
demonstrates the formation of bleb or septate precipitates attached to
one or more points on the egg surface after incubation of schistosome
eggs in patient’s serum.

B. S. haematobium
Recovery of eggs in urine, direct examination of the last
few drops of urine passed at noon, or urine taken after exercise or
prostatic massage. A simple concentration test for diagnosis is
sedimentation in a conical urinary glass of a day’s output of urine. The
addition of water previously heated at 60ºC, permits the hatched free-
swimming miracidium to be detected by indirect lightning against a
black background.

Both EIA and IHA with adult worm antigen or soluble egg antigen
(SEA) are sensitive (~90%) for the diagnosis of S. mansoni and S.
haematobium

Treatment:
Praziquantel and niridazole are the drugs of choice.

Epimediology:
The endemic areas in the Philippines for S. japonicum are
Sorsogon, Samar, Leyte, Bohol and all provinces of Mindanao except
Oriental Misamis. Reservoir hosts include dogs, cats, mice and cattle.
Transmission and infection require contact of man with water serving
as breeding sites of the snail host. The reservoir hosts for S. mansoni
are rodents, monkeys and baboons while S. haematobium, monkeys
and baboons.

Prevention and control:

Health education, provision of satisfactory sanitary facilities and
water supply are essential for control and prevention of
Schistosomiasis. Infected individual should be treated immediately
and contact of bare skin with infested water should be prevented. Snail
intermediate host must be eradicated.
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Male and Female Schistosoma in copula

Schistosoma cercaria
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Schistosoma japonicum ova

Schistosoma mansoni ova

Schistosoma haematobium ova

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ACTIVITY SHEET NO. 23

NAME______________________________SEC_______DATE_______

1. Tabulate the morphological differences of adult stage of the

different species of Schistosomes.

2. Discuss COPT.

3. How do the eggs of Schistosomes reach the feces?

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PROTOZOA
Protozoa are unicellular or single-celled organism that occur
singly or in colony formation. Protozoa varies in size, shape, locomotor
apparatus/organelles and methods of reproduction. Each protozoa is
capable of performing the physiologic functions that in higher
organisms are carried by specific cells. For the most part, they are free-
living although some are parasitic.

Morphology:
The unit that performs the vital functions of protozoa is the
protoplasm consisting essentially of nucleus and cytoplasm. The
cytoplasm often consists of a thin outer ectoplasm and an inner
endoplasm. The different parts/structures present in protozoa and their
functions are:

A. Cytoplasm
a. Ectoplasm
This is the outer portion of the cell, enveloping the
endoplasm, less granular and more homogenous. The
structures present in the ectoplasm and their functions
are:
1. locomotor apparatus – for the movement of
protozoa
a. pseudopodia – Ameoba
b. flagella – Flagellates
c. cilia – Ciliates
d. undulating membrane – Flagellates

2. Structures for procurement and ingestion of food

Food maybe taken in any place in the
cytoplasm or ingested at a particular point. In
some species, there is a definite area, the
periostome, through which food passes directly
into the cytostome and then through a tubelike
cytopharynx to the endoplasm.

3. Structures for discharge of metabolic waste or

Excretion
Waste materials of the protozoa are
discharged through the excretory vacuole or cell
anus known as cytopyge.
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b. Endoplasm
This is the inner portion of the cell which
immediately surrounds the nucleus, granular and
concerned mainly with nutrition, food synthesis, storage of
food and reproduction.

1. contractile vacuole – for regulation of osmotic

pressure
2. organelles - mitochondria, golgi bodies, microsome
and endoplasmic reticulum
2. nucleus – contain the chromosomes which are
essential for life, reproduction and
transmission of the genetic constitution
of the organism. A nuclear membrane
envelops the nucleus. A single or several
masses of chromatin located around its
center is referred to as the karyosomes
or endosome or nucleolus. Karyosome
plays an important part in promitosis. In
many protozoa, a centrosome is also
present. The structure of the nucleus,
particularly the arrangement of the
chromatin and karyosome helps to
differentiate species. In Ciliates, a
macronucleus, which is concerned with
the vegetative activities of the cell and a
micronucleus, involved in reproduction
maybe present.

Common stages of development encountered in the life cycle and

specimen:
A. Trophozoite
This stage of protozoa varies in size and shape and
possess the locomotor apparatus. This is considered as the vegetative
and motile stage of the protozoa, although in some species without the
cystic stage, this is considered as the infective stage. This is usually
less resistant to unfavorable conditions. This stage of the protozoa is
chiefly found in fluid or watery and soft or semi-formed stool sample.
Certain protozoa at times enter the inactive cystic stage, in
which they secrete a resistant membranous wall and usually undergo
nuclear division. The development of cystic stage from trophozoite in
unfavorable conditions is known as ENCYSTATION.
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The factors responsible for encystation are:

1. deficiency or abundance of food supply
2. excess catabolic products of the organism or of associated
bacteria
3. marked change in pH
4. desiccation of the medium
5. depletion of excess supply of oxygen
6. overpopulation

There are two types of encystment namely:

1. protective
The cyst wall protects the organism outside the body of its
host and the protection against the digestive juices of the upper
gastrointestinal tract.

2. reproduction
The nuclei divides one or more times during the cystic
stage, with a corresponding increase in the number of
trophozoites following excystation.

The factors involve in excystation are:

1. osmotic changes in the medium

2. enzymatic action of the enclosed organism on the inner surface
of the cyst wall
3. among the parasitic protozoa, favorable pH and enzymatic action
of the host tissue

B. Cyst
This stage is considered as the transfer of infective stage
of some protozoa. It is also the non-motile and resistant stage.

Reproduction:
The survival of protozoa is largely due to their highly developed
reproductive powers. Reproduction maybe:
a. Asexual or simple fission
The division of the nucleus maybe amitotic, mitotic or
modified. Certain species may also reproduce in the encysted state, the
nucleus dividing so that upon excystation each cyst may give rise to
several new trophozoites.
b. Sexual union of two cells (syngamy)
This is temporary union or conjugation.
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CLASSIFICATION OF MEDICALLY IMPORTANT GROUP AND

SPECIES OF PROTOZOA

PHYLUM SARCOMASTIGOPHORA
Subphylum Mastigophora

Class Zoomastigophora

Order Trichomonadida: Trichomonas spp.

Order Retortamonadida : Chilomastic spp.
Order Diplomonadida : Giardia lamblia
Order Kinetoplastida : Leishmania spp.,
Trypanosoma spp.

Subphylum Sarcodina

Superclass Rhizopoda

Class Lobosea

Order Amoebida : Entameoba, Iodameba,

Endolimax, Acanthamoeba
Order Schizopyrenida : Naegleria

PHYLUM CILIOPHORA

Order Trichostomatida : Balantidium coli

PHYLUM APICOMPLEXA

Class Sporozoa

Subclass Coccidia

Suborder Eimeriina : Isospora, Sarcocystis,

Toxoplasma, Cryptosporidium,
Cyclospora
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ACTIVITY SHEET NO. 24

NAME_____________________________SEC______DATE_________

1. Describe the organ for locomotion of the different Protozoa.

2. Differentiate encystation and excystation

3. What are the different modes of transmission of Protozoa?

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AMOEBA

There are four genera of Ameoba established as parasites of man

and maybe differentiated based on their nuclear structure:

1. Entamoeba
This genus has a delicate nuclear membrane and small
karyosome, with chromatin granules lining the nuclear
membrane. Species under this genus are E. histolytica, E. coli, E.
hartmani, E. gingivalis

2. Endolimax
The nucleus is with irregular and large karyosome with
fibrils (achromatic threads) anchored to the nuclear membrane.
Specie under this genus is Endolimax nana.

3. Iodameoba
The nucleus has a fairly large karyosome with
periendosomal granules and radiating achromatic fibrils. The
specie under this genus is Iodameoba butschlii.

4. Dientameoba
The karyosome splits into four or more fragments and with
a fine achromatic fibrils and provided with two nuclei. Specie
under this genus is Dientamoeba fragilis.

General rules:
1. All Ameoba inhabit the large intestine except Entamoeba
gingivalis.

2. All Ameoba develop into cystic stage except E. gingivalis and D.

fragilis.

3. All Ameoba are commensals except Entamoeba histolytica.

4. Amoebiasis is applied only to E. histolytica since they elaborate

hyaluronidase, a lytic enzyme that can act on tissues.
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NUCLEI OF THE DIFFERENT GENUS AND SPECIES OF
AMOEBA

Entamoeba histolytica Entamoeba coli

Entamoeba gingivalis Endolimax nana

Iodamoeba butschlii Dientamoeba fragilis

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Entamoeba histolytica

Morphology:
There are two forms of Entamoeba histolytica:

a. E. histolytica ( magma form) – large race, pathogenic,

hematophagous and tissue invading

b. E. hartmanni (minuta form) – small race and non pathogenic

A. Trophozoite
The size and shape of the trophic stage of E. histolytica
varies. It measures 12 – 35 microns and when moving, it is elongated
and changing but in stationary condition, it is round. The cytoplasm is
clean looking with ingested RBC indicated blood eating activity. The
nucleus when stained has a distinct membrane lined by irregularly
arranged and uniformly sized chromatin granules. The karyosome is
small and centrally located.

The trophozoite using its finger-like pseudopodia moves in

one direction (directional) wherein the pseudopodia pushes forward
and the endoplasm flows quietly rapidly into it.

B. Cyst
The cyst measures 10 –16 micron and characteristically
rounded in shape. The cytoplasm possess a sausage-shaped or cigar-
shaped chromatoidal barr wherein the ends of this chromatoidal barr
are rounded. There maybe 1 – 4 nuclei with regular membrane and
small karyosome.

Life cycle:
Human beings are the principal hosts and source of infection.
The resistant infective stage, which is the mature or quadrinucleated
cyst (cyst with 4 nuclei) are formed in the lumen of the large intestine
and pass out in the feces and are immediately infective. On ingestion of
contaminated food or water, only the mature cyst which is resistant to
the acidic digestive juices of the stomach, pass to the lower part of the
small intestine. Here under the influence of the neutral or alkaline
digestive juices and the activity of the amoeba, the cyst will
disintegrates, liberating a four nucleated metacystic amoeba that
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ultimately divides into eight small trophozoite. Encystation occurs in

the infected individuals whose rate of bowel evacuation is not
increased so that there is adequate time for dehydration of colonic
contents. In the process of encystation, the nucleus undergoes two
divisions so that mature cyst has 4 nuclei. Cyst is seen in watery or
semi-formed stool while trophozoites are seen in watery or diarrheic
stool.

Mature cyst passed

out in the feces
⇗ ⇘
encystation in the ingestion of food/water
lumen of l. i. contaminated with mature cyst
⇧ ⇩
trophozoites in ulcers cyst pass through gastro-
in large intestine intestinal tract
⇧ ⇩
invade and colonize excystation in the ileum,
intestinal wall small intestine
⇖ ⇙
trophozoite reach colon

Pathology:
The lesions produced by E. histolytica are primarily intestinal
and secondary extra-intestinal. The pathogenic activities of E.
histolytica depend upon:
a. the resistance of the host
b. the virulence and invasiveness of the amoebic strain
c. the conditions in the intestinal tract

The early lesion is a tiny area of necrosis in the superficial

mucosa or a small nodular elevation with a minute opening that leads
to a flask-shaped cavity or ulcer containing cytolyzed cells, mucus and
amoeba. The pathology of amoebiasis maybe classified into:

A. Asymptomatic amoebiasis
The patient serves as a carrier. There will a mixed amebic
and bacterial attacks repeatedly and the lesion is localized in the cecal
area. The cystic stage is recovered in the stool.
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B. Acute symptomatic amoebiasis

1. Amoebic diarrhea
There are numerous extensive ulcers, stools are soft,
diarrheic, passing of stool is 3 – 6 times a day.

2. Acute amoebic dysentery

There are marked ulcerations in the cecal-sigmoidal rectal
regions. The symptoms are severe diarrhea (6 – 8 X/day), stool
with blood and mucus, painful defecation (tenesmus), fever,
vomiting, nausea, chilly sensation, pale skin, electrolyte
imbalance and loss of weight.

C. Chronic amoebic dysentery

There is thickening of the colonic mucosa of the sigmoid
and cecal area forming a tumor-like mass called “amoebomas”.
These are formed by the excess production of granular tissues.
The patient may experience pain.

D. Extra-intestinal amoebiasis

1. Hepatic amoebiasis
The amoeba reaches the liver via the portal circulation. The
early liver abscess is a small mass measuring only a few
millimeters in diameter. It increases in size and the central
portion is liquefied, containing chocolate-colored, “anchovy –
sauce” fluid and debris. The clinical manifestations include pain,
tenderness of the liver, hepatomegaly, low grade fever,
leukocytosis (10,000 – 16,000 WBC/ mm 3), loss of weight, chills,
intermittent diarrhea, nausea, vomiting and jaundice.

2. Pulmonary amoebiasis
There is invasion of the lungs; consolidation of the lower
lobe of the right lung is observed. The symptoms are slight fever,
tender liver, hemoptysis, and pain in the lower right chest and
unproductive cough.

3. Cerebral amoebiasis
The brain invasion is very rare, death usually occurs in one
or two weeks.
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4. Amoebic pericarditis
This is the involvement of the heart, very rare but fatal.

5. Cutaneous amoebiasis
There will be spreading ulcerations at the site of infection.
Symptoms are localized pain, fever, leukocytosis, pruritus,
urticaria (rashes) and dermatitis.

6. Genital amoebiasis
Men become infected with penile amoebiasis after
experiencing unprotected sex with a woman with vaginal
amoebiasis. Ulcerations may occur in the penis. The cervix and
vagina produces a purulent discharge, which will reveal amoebic
trophozoite. The disease may also be transferred during anal
intercourse.

Diagnosis:
A. Intestinal amoebiasis
1. Stool
DFS can be performed for watery and formed stool
sample and the following solutions maybe added to DFS:
a. Quensel's solution – best for trophozoite
b. Methylene blue
c. Lugol’s iodine – for cyst
d. Di Antonis – for cyst
Concentration techniques like FECT, MIFC and ZSFT
may also be performed on formed stool only.

The stool sample may also be cultured and the

following culture media can be used for cultivation of
amoeba:
a. LES – Locke’s Egg Serum
b. Boeck’s and Drbohlav’s
c. RES – Rice Egg Saline
d. Nutrient Agar Saline
e. Diamond
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2. Serum
Serological procedures maybe utilized for diagnosis
of Amoebiasis like ELISA, indirect hemeagglutination test
(IHA), gel-diffusion precipitin (GDP) and indirect
immunofluorescence (IIF).

3. Examination of rectal biopsy for parasites

4. For extra-intestinal amoebiasis
a. liver aspirate – examined for the presence of parasite
b. liver scan
c. serological tests

Treatment:
The drugs that maybe used for treatment of amoebiasis are
metronidazole (flagyl), tinidazole and diloxanide furoate.

Epidemilogy:
This parasite is cosmopolitan in distribution and the main source
of infection is cyst passed by the patient. Man gets the infection by
ingestion of contaminated food and water containing cyst.

Prevention and control:

Prevention and control includes the following: sanitary disposal

of human feces, provision for safe water supply, regulation of food
handlers and avoid using human excreta as fertilizer.
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Entamoeba histolytica trophozoite

Entamoeba histolytica cyst

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ACTIVITY SHEET NO. 25

NAME______________________________SEC________DATE______

1. Explain why RBC can be observed in the cytoplasm of the

trophic stage of E. histolytica?

2. How is amoebic dysentery differs from bacillary dysentery?

3. Why is it that watery stool must be examined immediately in the

laboratory for the presence of amoeba?
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Non pathogenic Amoeba of man

A. Entamoeba coli

The trophic stage measures 6 – 15 micron and oval or

elongated in shape. The pseudopodia are broad and short and
the movement is sluggish and moves in several directions. The
cytoplasm is dirty looking due to the presence of ingested
bacteria and food particles. The nucleus is visible in fresh state,
the membrane is irregular and karyosome is large and eccentric.

The cyst measures 10 – 30 microns round with 1 – 8 nuclei.

The chromatoidal barr is with splinter-like ends or broomstick in
appearance.

B. Endolimax nana
This is the smallest intestinal protozoa. The trophic stage
measures 6 – 15 micron and elongated in shape. It is provided
with plenty of small rounded pseudopodia and the movement is
sluggish. The cytoplasm is granular and vacuolated. The round
nucleus contains large karyosome which maybe centrally located
or eccentrically placed.

The cystic stage measures 5 – 15 micron and oval in

shape. There are 1 – 4 nuclei with large karyosome. The mature
cyst possesses 4 nuclei concentrated at one end of the cyst,
which is spherical in shape (cross-eyed cyst).

C. Iodamoeba butschlii

The trophozoite measures 6 – 20 micron and leaf like in

shape. The movement is slow and is provided with round
pseudopodia. The nucleus is with large oval karyosome which
maybe centrally or eccentrically located. The cytoplasm is with
glycogen vacuole.

The cyst varies in shape, which maybe oval or rounded

measures 5 – 20 microns, and with a single nucleus. A large
glycogen vacuole, which maybe stained brownish red by Iodine
solution (Iodine cyst), is present in the cytoplasm.
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D. Dientamoeba fragilis
The small, round trophozoite measures 5 – 12 micron and
is provided with two nuclei. The pseudopodia are blunt and leaf-
like and the movement is sluggish.

E. Entamoeba gingivalis
This is an oral parasite, wherein the trophozoite measures
5 – 35 microns. The cytoplasm contains phagocytosed and
partially digested host leukocytes and an epithelial cell at times
bacteria. The movement is vigorous and fast due to multiple
pseudopodia.

Life cycle:
The habitat of this amoeba is the large intestine except for E.
gingivalis, which inhabit the gingival tissues around the teeth. All
specie passes through the trophozoite, pre-cyst and metacystic
trophozoite except E. gingivalis and D. fragilis. Infection is usually
acquired by ingestion of contaminated food and water containing viable
cyst.

Diagnosis:
The specimen of choice for diagnosis is stool except for E.
gingivalis, wherein the specimen is taken from gums and between
teeth.

Treatment:
No treatment is necessary because these amoebas do not cause
disease.
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Entamoeba coli trophozoite Entamoeba coli cyst

Endolimax nana trophozoite Endolimax nana cyst

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Iodamoeba butschlii Iodamoeba butschlii

trophozoite cyst

Dientamoeba fragilis Entamoeba gingivalis

trophozoite trophozoite
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ACTIVITY SHEET NO. 26

NAME______________________________SEC_______DATE_______

1. Differentiate morphologically E. histolytica from E. coli.

2. What is the mode of transmission of E. gingivalis?

What is the infective stage?
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Free-living Pathogenic Amoeba

A. Naegleria
Naegleria is a free-living amoeba, the pathogenic specie is
Naegleria fowleri. The trophic stage measures 10 – 35 microns and
there are two morphologic forms:
a. amoeboid = provided with blunt pseudopodia and a
vesicular nucleus with large karyosome
and granules of peripheral chromatin
b. flagellated = elongated and with two long, equal and
anteriorly located flagella
The cystic stage measures 7 – 10 microns round with
double, smooth cyst wall wherein the outer wall is perforated by 3 – 8
pores (ostioles). It has a single nucleus and spherical chromatoidal
barr.

Life cycle:
Naegleria may enter the nose of the human host while swimming
in contaminated water. From the nasal passages, the trophozoites
migrate along the olfactory nerves through the cribiform plate and into
the meninges and brain.

Pathology:
The pathogenic Naegleria is the causative agent of Primary
Amoebic Meningoencephalitis (PAM) in man, which is an acute,
fulminant and most often fatal purulent type of meningitis that is
usually unresponsive to the usual anti-meningitic regimen. This
disease usually runs an acute fulminant course and usually fatal within
a week of onset. There will be several frontal headache, fever, vomiting,
blocked nose followed by signs of CNS involvement. There are signs of
meningeal irritation and encephalitis, with rapid progression to coma
and death. Patients with PAM also exhibit CSF findings of pleocytosis
with a high percentage of PMN cells and elevated protein levels.

Diagnosis:
The diagnosis of PAM is based on actual presence of the
trophozoites in the brain and CSF. However due to the rapid course of
the, diagnosis is usually done on autopsy. Naegleria trophozoites can
be identified by the presence of blunt, lobose pseudopodia and
directional motility
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Treatment:
Amphotericin B is the drug of choice for treating PAM.

Epidemiology:
Naegleria spp. have been isolated from samples obtained from
chlorinated swimming pools, freshwater lakes, thermal springs,
domestic water supplies, thermally polluted water, sewage, soil, air,
humidifier systems. Cases have been reported in U.S., Africa, New
Zealand and Australia. In the Philippines, the amoeba can be isolated
from moist soil and freshwater habitats as well as from thermally
polluted rivers, whether natural or industrial.

Prevention and control:

The only preventive measure is to avoid swimming in stagnant or
thermal waters. Chlorination of water for swimming pools will not kill
the parasite. Salination of water with .7% NaCl for swimming polls
maybe a useful measure.

B. Acanthamoeba
Acanthamoeba is a small free-living amoeba characterized
by an active trophozoite stage and a dormant cystic stage. The
trophozoite measures 10 –45 microns with a single vesicular nucleus
and large karyosome. The pseudopodia are broad, anterior from which
slender, hyaline projections (acanthopods) singly or in two or threes
are produced which taper to finely rounded ends. The movement is
sluggish.
The cyst is 8 - 25 micron, uninucleated and double-walled. The
outer ectocyst is wrinkled and closely adherent to the inner endocyst
which is usually polyhedral or stellate.

Life cycle:
The life cycle of Acantamoeba is not well defined. It is presumed
that most infections invade CNS from the lower respiratory tract or skin
or some inhaled the infective cyst from contaminated dust. A rapid
transformation from cyst to trophozoites occurs in the nasal mucosa.
Direct invasions of the eyes also occur.

Pathology:
Acanthamoeba is the causative agent of Granulomatous amebic
encephalitis (GAE). Symptoms of this condition include headaches,
seizures, stiff neck, nausea and vomiting. Granulomatous lesions of the
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brain are characteristic and may contain both Acanthamoeba

trophozoite and cyst. On occasion, this parasite may also invade other
organs of the body, including kidneys, pancreas, prostate and uterus
and form similar granulomatous lesions. Invasion of the cornea of the
interior of the eye has been reported and this is known as Amebic or
Acanthamoeba keratitis. Common symptoms include severe ocular
pain; vision problems, corneal ulcerations, clouding iritis and
perforation of the cornea may result, as well as subsequent loss of
vision.

Diagnosis:
Specific diagnosis depends on demonstration of the trophozoites
or cyst in tissues. The organisms can be isolated from the CSF and
cultured in PYGC medium (proteose-peptone, yeast extract, glucose
and cysteine). However due to initial lack of suspicion, inaccurately
early clinical diagnosis and rapid progression of the disease, diagnosis
of Acanthamoeba encephalitis is made only after death in the majority
of cases. Acanthamoeba keratitis is diagnosed by the presence of
trophozoites and cyst in the cornea and lens of contact lens wearers.

Treatment:
Some patients have responded to treatment with 5-
fluorocystosine, ketoconazole, itricanozole, pentamidine or
amphotericin B. Cases of Acanthamoeba keratitis have successfully
been treated with a combination of neomycin drops, dibromopropamide
ointment and Brolene.

Epidemilogy:
This parasite have been isolated from freshwater, seawater,
ocean sediment, frozen swimming water, bottled mineral water,
industrial cooling water, air conditioners, air, sewage, soil, compost,
chlorinated swimming pools, medicinal pools, dental treatment units,
gastric-lavage tubing, dialysis units and contact lenses. In the
Philippines, this parasite has been isolated in several canals in Metro
Manila and has been found to be pathogenic in mice.

Prevention and control:

Prevention of CNS infection by Acanthamoeba is difficult
because the life cycle is poorly understood. Since this parasite has
been isolated even from drinking water, boiling of water is the best
possible way of killing the parasite. Acanthamoeba keratitis maybe
prevented by proper cleaning of contact lenses.
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Naegleria amoeboid trophozoite Naegleria cyst

Acanthamoeba trophozoite Acanthamoeba cyst

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Flagellates
Flagellates possess whiplike locomotor apparatus known as
flagella. Special organs such as sucking disk, axostyle and undulating
membrane have been developed to withstand the peristaltic action of
the intestine. Most species have a rudimentary mouth known as
cytostome.

A. Atrial or lumen flagellates

These flagellates inhabit the visceral organ and non –
tissue invader.

Giardia lamblia
Giardia lamblia is the only pathogenic intestinal flagellates that
inhabit the small intestine. The trophozoite is pear-shaped or teardrop
shaped, the anterior portion is rounded and the posterior portion is
pointed. It measures 9 – 20 microns and a very prominent, ovoid,
concave-sucking disk is present. This disk serves as nourishment point
of entry by attaching to the intestinal villi of the host (holdfast organ).
There are four pairs of flagella (8 flagella), two flagella arise from the
anterior end of the sucking disk, two ventral and four lateral wherein
the flagella cross each other. There are two nuclei with a large
karyosome. The trophozoite is supported by an axostyle made up of
two axonemes. Posterior to the nuclei is the parabasal body or median
body, which is sausage-shaped. The characteristic movement is jerky,
falling leaf.

The cystic stage is ovoidal measuring 8 – 12 microns with a

smooth, well-defined wall and contains two to four nuclei. The axostyle
and other fibrillar remnants of the trophozoite organelles are found
inside the cyst.

Life cycle:
Man is the natural host of G. lamblia and transmission is through
ingestion of cyst from contaminated food and water. The cyst
undergoes excystation in the duodenum and become trophozoites.
They reproduce by binary fission. Encystation occurs in the large
intestine and cyst is passed out in the feces. Cyst is the infective stage
and they are transmitted through fecal-oral route.
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Pathology:
Attachment of the parasites to the intestinal mucosa provokes
intense inflammation that result to secretions of abundant mucus. This
would also lead to general malabsorption of fats and carbohydrates.
Patient with Giardial diarrhea may exhibit steatorrhea or passage of
greasy, and frothy stools, weight loss, generalized weakness, chills,
low grade fever, impaired absorption of carotone, folate and Vitamin
B12, nausea, anorexia, diarrhea, dehydration, flatulence (odor of
hydrogen sulfide or rotten eggs) and passage of foul smelling and
bulky stools.

Diagnosis:
Demonstration of trophozoites or cyst in the stool. Examination
of duodenal contents for trophozoites and Entero-string test can be
performed to obtain the specimen. Demonstration of this parasite in
small bowel biopsies can be done in some patients with negative
stools. ELISA using Giardial antigen in the stool maybe used.

Treatment:
The drug of choice is metronidazole. Furazolidone maybe used
especially for children under 5 years old.

Epidemiology:
Giardiasis is most common in warm, moist climates particularly
in children. The prevalence of Giardiasis is associated with poor
environmental sanitation. Important risk factors include poor hygiene,
poor sanitation, and overcrowding, bacterial and fungal overgrowth in
the small intestine and homosexual practices. Giardiasis has been
shown to be related to “gay bowel syndrome”.

Prevention and control:

Prevention includes proper disposal of human excreta to prevent
contamination of water supplies; avoid using human excreta as
fertilizer for vegetables and prevent food contamination from flies and
infected food handlers.
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Chilomastix mesnili
This organism inhabits the cecal region of the large intestine.
The trophic stage is pear-shaped as a result of a spiral groove
extending through the middle half of the body. It measures 6 – 10
microns and the nucleus is spherical situated medially near the anterior
pole with a distinct karyosome and few achromatic fibrils. There are
three free anterior flagella (two short, one long) and a delicate flagellum
lying within the cystostome. There are numerous food vacuoles. The
characteristic movement is stiff-rotary fashion (corkscrew motion).

The cystic stage is lemon-shaped, rounded at one end and

conical at the other end with a knob-like protuberance at the anterior
portion (nipple-shaped cyst). The cytoplasm is densely granular with a
single large nucleus. It measures 7 – 16 microns. Cytostome may also
be observed.

Transmission occurs through ingestion of cyst in food and

drinks. This is a harmless commensal so no treatment is necessary.
Preventive measures include proper sanitation and personal hygiene.
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Giardia lamblia trophozoite Giardia lamblia cyst

Chilomastix mesnili trophozoite Chilomastix mesnili

cyst
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ACTIVITY SHEET NO. 27

NAME_______________________________SEC______DATE________

1. Discuss malabsorption in Giardiasis.

2. Discuss the mode of attachment of G. lamblia to the host and its

effects to the host.

3. Why is C. mesnili cyst described as nipple-shaped cyst?

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Trichomonas species

General features:
1. No cystic stage, only the trophic stage is known.
2. They have rounded anterior end and somewhat pointed posterior
end.
3. A curved, rigid axostyle arise near the median anterior pole
extending through the entire body.
4. A small cytostome on one side of the anterior end is observed.
5. The nucleus is spherical.
6. A blepharoplast is present between the nucleus and the anterior
margin from which arises 3 – 5 flagella and a marginal flagellum
on an undulating membrane, the base attachment being a heavy
costa.

A. Trichomonas vaginalis

Morphology:
The trophic stage is pyriform in shape with cytostome, prominent
axostyle, four sub-equal anterior flagella, single nucleus at the anterior
portion and an undulating membrane with a marginal flagellum. This is
the largest Trichomonas measuring 15 – 20 microns in length. The
movement is fast, jerky (tumbling movement). Siderophil granules
maybe observed in the cytoplasm.

Life cycle:

The trophic stage inhabits the surface of vaginal epithelium of

female host and the epithelium of the urethra and prostate gland of the
male host. They reproduce by binary fission and transmitted through
sexual intercourse.

Pathology:

This is the only pathogenic Trichomonas. The vaginal walls are

inflammed with petechial hemorrhage and the surface of the vaginal
epithelium is covered with coagulated material containing leukocytes,
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RBC and Trichomonas. There will be disquamation of the epithelial

cells. Vaginal secretion is greenish yellow in color. There will be
intense itching of the vagina and burning sensation. It may cause non-
specific urethritis, vaginitis and prostatis.

Diagnosis:
The specimens collected for female patients are urine, urethral
secretion, vaginal and cervical secretions. In male semen and prostatic
secretions are the specimens for examination. Unstained wet
preparation can be done on these specimens to observe the
trophozoite and stain the smear with Giemsa, Pap’s, Romanowsky and
Acridine Orange. Specimen may also be cultured using Diamond’s
modified medium or Feinberg and Whittington culture media.

Treatment:
The most effective drug for treatment of Trichomonas in both
sexes is oral metronidazole. Acid douche maybe useful.

Epidemilogy:
The incidence of infection is 10 – 25 % in women and higher in-
groups in which feminine hygiene is deficient. The manner of infection
is by sexual intercourse. However, contaminated toilet seat and towel
may cause infection. The male hosts maybe asymptomatic carriers
whom maybe responsible for the spread of infection. Infection acquires
while passing through birth cabal probably account from some
infection in babies.

Prevention and control:

Proper personal hygiene is important to prevent infection with
this parasite. Promiscuous sexual intercourse should be avoided or
protective devices such as condoms should be used.
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B. Trichomonas tenax
This flagellate inhabits the oral cavity of the host. It
measures 5 – 12 microns, has four flagella and undulating membrane
which does not reach the posterior end of the body and lacks a free
posterior extension. It has a single nucleus and cytostome.

Transmission is usually by droplet spray from the mouth,

kissing or common use of contaminated dishes and drinking glasses.
Diagnosis is made by swabbing the tartar between gingival margin of
the gums or the tonsillar crypts.

C. Trichomonas hominis
The common habitat of this Trichomonas is the caecum.
The trophic stage has five anterior flagella, posterior flagellum
projecting from an undulating membrane measuring 7 – 13 microns.
Axostyle extends from the anterior end to the posterior end along the
mid-axis. A cytostome and a single nucleus are situated at the anterior
end.

Transmission occur though ingestion of contaminated

food and water. The trophozoites are presumed to pass out with
diarrheic stools.
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Trichomonas vaginalis Trichomonas hominis

trophozoite trophozoite

Trichomonas tenax trophozoite

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ACITIVTY SHEET NO. 27

NAME________________________________SEC_________DATE_____

1. Tabulate the differences of the three species of Trichomonas.

2. Discuss the clinical manifestations of Trichomoniasis

vaginalis?
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BLOOD AND TISSUE FLAGELLATES

A. Trypanosomes
1. Trypanosoma brucei gambiense
Disease : West African Sleeping sickness
Geographical Distribution : Central and West Africa
Vector : Glossina specie (Tsetse fly)

2. Trypanosoma brucei rhodesiense

Disease : East African Sleeping sickness
Geographical Distribution : East Africa
Vector : Glossina specie (Tsetse fly)

3. Trypanosoma cruzi
Disease : Chaga’s disease or American trypanomiasis
Geographical Distribution : Central and South America
Vector : Triatoma or Reduviid bugs (kissing bug or
Assassin bug)

B. Leishmania
1. Leishmania tropica
Disease : Oriental sore or Old World cutaneous
Leishmaniasis (OWCL)
Geographical Distribution : Asia Minor, Middle and South
West Asia, North Africa,
Mediterranean, Europe and
Central America
Vector : Phlebotomous specie (sandfly)

2. Leishmania braziliense
Disease : a. Espundia or muctaneous leishmaniasis (MCL)
b. Chiclero’s ulcer or New World Cutaneous
leishmaniasis (NWCL)
Geographical Distribution : Central and South America

3. Leishmania donovani
Disease : Kala azar or visceral leishmaniasis
Geographic distribution : India, China, Soviet Union,
Mediterranean, East and North
Africa, Caspian Littoral,
Arabian Peninsula, Persian Gulf
Vector : Phlebotomous specie (sandfly)
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Stages of Development of Hemoflagellates

1. Amastigote or leishmania form – ovoidal without free flagellum

2. Promastigote or Leptomonas form – elongated and spindle-

shaped with pointed end and a free flagellum that arise
from the kinetoplast at the anterior end

3. Epimastigote or Crithidia – elongated and spindle-shaped with

free flagellum continous from the anterior end
backward along the margin of the undulating membrane
and the ends of the kinetoplast which is situated
anterior to the nucleus

4. Trypomastigote or Trypanosoma – morphologically similar to the

epimastigote except that the flagellum on the margin of
the undulating membrane ends at the kinetoplast which
is situated anterior to the nucleus.

In Genus Leishmania, only the amastigote and promastigote

forms are present. In Trypanosoma brucei group, only the epimastigote
and Trypomastigote forms are present, while in Trypanosoma cruzi, all
stages of development are present.

Amastigote Promastigote of Leptomonas form

Epimastigote or Crithidia form Trypomastigote or Trypanosomes

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Trypanosomes
Trypanosoma have species pathogenic to man and other
animals. For Trypanosoma brucei group, the transitional forms in
invertebrates are epimastigote while in the blood of mammalian host
trypomastiogotes are produced. In case of T. cruzi, it has
trypomastigotes in the gut of the invertebrate host and in the blood of
mammalian host, amastigotes intracellularly in the mammalian host
and epimastigote in the midgut of the invertebrate host.

Morphology:
Trypanosomes are minute, actively motile, fusiform, flattened
from side to side measuring 14 – 33 microns in length and 1.5 – 3.5
microns in breadth. A large oval nucleus with a central karyosome is
centrally located. The flagellum along the margin of the undulating
membrane arises from the posteriorly located kinetoplast and
continues anteriorly as the free flagellum. Trypanosomes travel with a
wavy spiral motion produced by the contractile flagellum and
undulating membrane.

Amastigotes are intracellular forms, which have lost the

undulating membrane and flagellum. They are round or ovoid,
measuring 1.5 – 3 microns and found inside reticuloendothelial cells.
The nucleus is large and the kinetoplast is spherical or rod-like.

Life cycle:
A. T. brucei group
The main vertebrate host is man. The principal invertebrate
hosts for T. brucei gambiense are Glossina palpalis, Glossina fuscipes
and Glossina tachinoides . For T. brucei rhodesiense the invertebrate
hosts are Glossina morsitans, Glossina palipedes and Glossina
swynnertoni.

The infected Glossina (Tsetse fly) bites man, wherein these

infected flies, metacyclic trypomastigotes passed through the salivary
ducts after cyclic development in gut. After inoculation, the
trypomastigotes enter the circulation and the lymphatics and they
multiply by binary fission. Terminally they invade the CNS.
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B. T. cruzi
The infective metacylic trypanosomes escape through the
mucus membrane or puncture made in the skin. They multiply rapidly
at the site of inoculation, enter the circulation and mesenchymal tissue
(cardiac and skeletal muscles and reticulo-endothelial cells). They
transform into amastigotes (leishmania form) and multiply by binary
fission, forming pseudocyst. Amastigotes released during rupture of
pseudocyst invade new host cells. Terminally they invade the muscle
fibers of the heart, smooth muscle of the digestive tract and the
autonomic nerve ganglia.

In the host’s circulation, T. cruzi is in the form of

trypomastigotes (diagnostic form). Reduviid bugs of the genera
Panstrongylus, Rhodnius, Eutratoma and Triatoma get infected by
ingestion of trypomastigotes during a blood meal. Cyclic development
occurs in the gut of bugs and the metacyclic trypanosomes (infective
stage) are passed out in the feces of the bugs.

Pathology:
A. T. brucei group
In humans the disease varies in severity from a mild type,
with few trypanosomes in the blood to a severe fulminant type. In the
typical case the disease progresses from the acute stage, with
trypanosomes multiplying in the blood and lymphatics during the first
year or the beginning of the second year and terminates during the
second or third year. The acute disease lasts a year and is
characterized by irregular fever, headache, joint and muscle pains, rash
and the patient become hyperactive. Gradually the chronic phase of the
disease ensues with the development of characteristic central nervous
system changes. The fever and headache are more pronounced,
evidence of nervous impairment includes lack of interest and
disinclination to work, avoidance of acquaintances, morose and
melanchonic attitude, mental retardation, low and tremolous speech
and altered reflexes. The terminal sleeping stage now develops and
gradually patient becomes more and more difficult to rouse. Death
result either from the disease or from intercurrent infection, such as
malaria, dysentery and pneumonia. Prognosis is favorable if treatment
is instituted before involvement of the nervous system occurs.
Untreated infections may progress to a fatal termination or develop into
a chronic or latent disease.
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B. T. cruzi
The disease manifest primarily as chagoma, a slightly
painful nodule at the site of inoculation and later by metastatic lesions
throughout the body notably in the heart, esophagus and lower
intestine. Signs and symptoms of heart failure, megaesophagus and
megacolon eventually are observed when these organs are involved.
Chronic disease has no characteristic symptoms and may last for 20
years or more. Many asymptomatic cases are unrecognized. Chagas
disease is serious and often fatal in older children and adult.

Diagnosis:
Diagnosis of T. brucei group is based on the presence of
trypanosomes in stained blood preparation and lymph aspirates. For T.
cruzi, a thick blood smear maybe examined for the presence of
trypanosomes. Xenodiagnosis maybe employed using laboratory
reared bugs. These bugs are allowed to feed on patient’s suspected of
being infected and later examined for the presence of T. cruzi. Useful
serologic tests include immunofluorescent antibody test and indirect
hemeagglutination assay.

Treatment:
For African sleeping sickness, Pentamidine and Suramin have
been used although both drugs do not enter the CSF. Melarsoprol has
been used for late stage of the disease with CNS involvement. For
Chagas disease, Nifurtimox and Bezuidazole are only partially effective
in acute disease.

Epidemiology:
African trypanosomiasis is endemic in area known as “tsetse
belt”, extending over a third of Africa. Chagas disease is prevalent
throughout Central and South America.

Prevention and Control:

Infection with T. brucei group can be prevented by reduction of
the pool of contact with Tsetse fly through control measures (traps,
screens, insecticides) and by reduction of the pool of human infection
by diagnosis and treatment. Prevention of Chagas disease is based on
vector control, screening and sterilization of transfusion blood and
health education.
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Leishmania
Leishmania are flagellates that occur as intracellular amastigotes
in vertebrate hosts and as flagellate promastigote in invertebrate hosts.

Morphology:
Amastigotes are small, ovoid measuring 2 – 3 microns and living
intracellularly in monocytes, PMN or endothelial cells. The nucleus is
large while axoneme arises from the kinetoplast and extends to the
anterior tips. Promastigotes have a single free flagellum arising from
the kinetoplast at the anterior end measuring 15 – 20 microns.

Life cycle:
The life cycle of Leishmania involves an alternate existence in a
vertebrate and an insect host. Aside from man, natural reservoir hosts
include domestic dog and a wide variety of wild animals. The
invertebrate hosts are sandflies of the Genus Phlebotomus.
The infective promastigotes in the proboscis of the sandfly are
injected into the host’s skin during feeding. They invade the
reticuloendothelial cells, transform into amastigotes and multiply by
binary fission. When the parasitized cells ruptures, the amastigotes that
are released invade new cells. In L. tropica, it invade the lymphoid
tissue of the skin while for L. braziliensis, the skin and mucous
membrane and for L. donovani, the visceral organs.
The invertebrate vector takes up the amastigotes during feeding.
They transform into promastigotes in the gut, multiply by binary fission
and migrate into the pharynx.

Pathology:
1. Cutaneous leishmaniasis
There is ulceration in the skin, which upon healing leaves
an ugly scar. Diffuse cutaneous leishmaniasis causes widespread
thickening of the skin wherein the lesion resembles those of
lepromatous leprosy and these lesions does not heel spontaneously.

2. Mucocutaneous leishmaniasis
The initial lesion at the bite site is papule that later develop
into an ulcer. Metastatic spread may occur on the oronasal and
pharyngeal mucosa, causing highly disfiguring leprosy like tissue
destruction and swelling (Tapir nose).
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3. Visceral leishmaniasis
The usual clinical manifestations are fever, malaise, and
weight
loss, loss of appetite, cough, diarrhea, anemia, wasting, skin darkening,
splenomegaly, hepatomegaly and lymphadenopathy. The
phagocytosed parasites are present only in small numbers in the blood
but they are numerous in the reticuloendothelial cells of the spleen,
liver, lymph nodes, bone marrow, intestinal mucosa and other organs.

Diagnosis:
Smear of lesion can be stained with Wright or Giemsa. Specimen
can be cultured also NNN (Nicole, Novy, Mc Neal). Serological tests
have been used for supportive diagnosis, which include CFT, FAT and
counter-current electrophoresis. Montenegro skin test may also be
used for diagnosis. Another test is the formol-gel test making use of
0.1-ml serum and one drop of formalin and the positive result is gel
formation. This will serve as screening test.

Treatment:
Primary drug treatment is based on antimony compounds,
Pentavalent antimonials, Sodium atiboglucolate and N-methyl-
glucamine antimonate. Second line drugs include the antimicrobial
Amphotericin B, Pentamidine (for Kalaazar), Metronidazole and
Nifurtimox.

Epidemiology:
Leishmaniasis occur in the Southern regions of America, the
Mediterranean, East and North Africa, Arabian Peninsula, Persian Gulf,
Indian subcontinent, China and Southern Soviet Union.

Prevention and control:

Control measures include vaccination, control of sandfly vectors,
protective measures from sandflies, mechanical destruction of animal
reservoir habitats and poisoning of animals themselves.
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ACTIVITY SHEET NO. 29

NAME_____________________________SEC______DATE__________

1. How does leishmaniasis differ from trypanomiasis?

2. Differentiate the methods used in the diagnosis of Leishmaniasis

and Trypanomiasis.
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Balantidium coli
Balantidium coli is the largest intestinal protozoa, the only
pathogenic ciliates inhabiting the large intestine. It exhibits both
trophic and cystic stages.

Morphology:
The trophozoite measures 60 – 150 microns, ovoid or shape like
a sac and covered with spiral longitudinal rows of cilia, which are short,
threadlike extension of the ectoplasmic membrane. An indentation at
the anterior end forms the cytostome or primitive mouth and a similar
indentation at the posterior end is the cytopyge and excretory pore.
Within the granular cytoplasm are two contractile vacuoles and two
nuclei, a large bean-shaped or kidney-shaped macronucleus and a
small spherical micronucleus located in the concavity of macronucleus.
Numerous food vacuoles maybe observed. The movement is directional
in rolling motion.

The sub-spherical or oval cyst measures 40 – 70 microns and

covered with a thick cell wall. Macronucleus and contractile vacuoles
are found in the cytoplasm.

Life cycle:
Man gets infection through ingestion of food and water
contaminated with B. coli cyst. The ingested cyst undergoes
excystation in the small intestine and they become trophozoites.
Trophozoites inhabit the large intestine and multiply by binary fission
and cause pathologic changes in the colonic wall and mucosa.

Pathology:
The mucosa and submucosa of the large intestine are invaded
and destroyed by the multiplying organism. B. coli is a tissue invader.
Invasion is due to the cytolytic enzyme hyaluronidase and mechanical
penetration. The ulcer formed is very characteristic since the base is
rounded and the neck is wide. Trophozoites are abundant in the
exudates on the mucosal surfaces while the inflammatory cells and
trophozoites are numerous in the base of ulcers. Secondary bacterial
infection of these ulcers result in the formation of abscesses.
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Balantidiasis dysentery is similar to amoebic dysentery and the

symptoms are diarrhea with bloody and mucoid stool, abdominal pain,
nausea, vomiting and tenesmus. Most cases are asymptomatic.

Diagnosis:
Stool examination will reveal the cyst or trophozoites.

Treatment:
The drugs of choice are Tetracyclene or metronidazole.

Epidemiology:
The prevalence is associated with poor environmental sanitation.
25% of human cases show some association with exposure to swine
(pigs).

Prevention and control:

The method of prevention and control are essentially the same as
that of amoebiasis. An additional measure is to prevent contaminating
the food and water with fecal material.
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Balantidium coli trophozoite

Balantidium coli cyst

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ACTIVITY SHEET NO. 30

NAME______________________________SEC_______DATE________

1. Give the morphological differences of the ulcers observed in

amoebiasis and balantidiasis.

2. Who are at higher risk of acquiring balantidiasis?

3. Give the reservoir host of B. coli.

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Toxoplasma gondii

Morphology:
The actively multiplying asexual form in man is an obligate,
intracellular parasite, pyriform in shape and measures 3 – 6 microns.
This parasite is known as tachyzoites, has a cell membrane, nucleus
and various organelles. Tachyzoites maybe found singly in body fluids
but more commonly as intracellular parasites. Inside the host cells are
formed from the parent cell. An accumulation of tachyzoites in a host
cell with formation of a membrane around the parasites leads to
formation of cyst. Within the intestinal epithelium of the definitive host,
a variety of morphological forms have been described ultimately
leading to male and female gametocytes. The fertilized macrogametes
develop into oocyst, which measures-10 – 13, microns in diameter with
a two-layered wall. A mature cyst has two sporocyst.

Life cycle:
The only known definitive host is the cat where all stages of
development of the parasite are present. Tachyzoites multiply within
the host cells by a specialized form of division called endogeny, in
which two daughter cells are formed within a mother cell. As the
distended host cells are filled up with the parasites, they rupture,
releasing parasites that enter new cells. The infected host cell may
swell up, develop a membrane and become cyst. The cyst wall is
digested, releasing organisms that penetrate epithelial cells of the
small intestine. Several generations of intracellular multiplication
occur, finally culminating in the development of oocyst that are
discharged into the intestinal lumen by ruptured infected intestinal
epithelial cells. These oocysts are passed out in the feces of the cat
and upon reaching the soil, maturation takes place in several days with
formation of two sporocyst inside. Each sporocyst contains four
sporozoites. Mature oocyst is infective to other animals (including man)
when ingested.
Ingestion of the oocyst initiates infection in the liberated
sporozoites in the intermediate host. Sporozoites enter the epithelial
cells of the intestine and develop into tachyzoites and this may invade
other organs.
In chronic infection, the zoites affecting the brain, heart and
skeletal muscle multiply much more slowly and accumulate in large
numbers within a host cell. They are now called bradyzoites. Later on
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these groups of zoites become surrounded by a tough cyst wall and are
now called zoitocyst.
In other animals, including man, after the ingestion of the oocyst,
the sporozoites enter the epithelial cells of the intestine and develop
into tachyzoites and after multiplication by endodyogeny these
trophozoites invade other tissues and may continue producing
trophozoites or some developed into cyst. Sexual forms are never
produced thus these animals serve only as intermediate host.
Trophozoites in the blood may also be transmitted to the fetus by
intra-uterine or congenital transmission. It is generally assumed that
Toxoplasma crosses the placental barrier from the mother’s blood.

Pathology:
T. gondii has the ability to invade monocytes, reticulo-endothelial
cells and parenchyma or tissue cells which are destroyed. Most of the
infections are asymptomatic. In post-natally acquired infections, the
clinical manifestations include lymph adenopathy which maybe febrile
or afebrile, meningo-encephalitis and chorioretinitis due to localization
in the eyes. In the intra-uterine or congenitally acquired infections
manifestations of the newborn include hydrocephalus, epileptic
seizures, chorioretinitis and cerebral calcifications.

Diagnosis:
Biopsy can be performed to demonstrate the organism.
Serological tests maybe useful like indirect hemeagglutination test for
the circulating antibodies, ELISA and Sabin-Feldman dye.

Treatment:
The drugs of choice are Pyrimethamine or Sulfadiazine.

Epidemiology:
This parasite is widely distributed and with a wide range of hosts.
It has been isolated from rodents, most mammals and fowls. T. gondii
has not been isolated in the Philippines but there are immunologic and
clinical evidence of toxoplasmosis locally. Infection is acquired by
ingestion of food and water contaminated with cat’s feces containing
oocyst or eating raw or insufficiently cooked beef or pork containing
toxoplasma cyst.

Prevention and control:

Thorough cooking of all meats and careful attention to cat’s
feces. Pregnant women should be protected from exposure to infection
to prevent congenital infection in the fetus.
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ACTIVITY SHEET NO. 31

NAME_____________________________SEC_____DATE_________

1. Discuss the different mode of transmission of T. gondii.

2. Discuss the different stages of development of T. gondii and

the host that harbor these stages.
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Isospora belli

Morphology:
The oocysts, which are the forms found in the stool, are
elongated or ovoid measuring 25 – 33 microns. The granular cytoplasm
is contained within a smooth, colorless, two-layered wall is usually
unsegmented of unsporulated. Division takes place into two sporoblast
that secrete a cystic wall to become sporocyst. Within each sporocyst
further division produces four elongated nucleated sporozoites.

Life cycle:
Humans are probably infected by accidental hand-to-mouth
ingestion of the sporulated oocyst or in contaminated food and water.
Asexual and sexual stages of the parasites are observed in the mucosal
epithelium of the upper small intestine.

Pathology:
Infection with I. belli is usually asymptomatic. In symptomatic
infections, diarrhea usually occurs and there maybe fever, malaise and
abdominal pain, malabsorption syndrome, weight loss.

Diagnosis:
Demonstration of the oocyst in the feces or sporocyst in the
duodenal contents and intracellular stages of the parasites in intestinal
biopsies.

Treatment:
Patients without symptoms maybe managed by bedrest and a
balance diet. For symptomatic patients maybe treated with
Trimethoprimsulfamethoxazole.

Epidemiology:
High prevalence of these parasites in Tropical countries and
Haiti. Transmission is usually via food and water.

Prevention and control:

Proper personal hygiene, improved sanitation, thorough washing
and cooking of food are some of the preventive measures.
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Cryptosporidium

Morphology:
The oocyst in the stool is ovoid or spherical measuring 3 – 4
micra and contains four naked sporozoites, which is the infective stage.

Life cycle:
Man gets the infection through ingestion of the oocyst from
contaminated food and water. In the intestine, the four sporozoites
inside the oocyst are released and invade the gastrointestinal
microvilli. They develop into trophozoites and later into schizonts. Each
mature schizont contains 8 merozoites. Schizont will rupture, releasing
merozoites, which will invade other microvilli and start another
schizogonic cycle or some will develop into gametocytes and start the
sexual cycle. Fertilization by male and female gametocytes will result in
the formation of zygote, which develops into oocyst.

Pathology:
Cryptosporidiosis usually is an acute, self-limiting diarrhea for 12
weeks and associated with intense abdominal cramps, anorexia and
weakness.

Diagnosis:
The most reliable is microscopic examination of the trophozoites,
schizonts and merozoites in the microvilli in intestinal biopsies.
Demonstration of the oocyst in the stool may also be useful.

Treatment:
This disease is usually self-limiting but pyrimethamine is used in
chronic infections.

Epidemiology:
Cryptosporidial diarrhea is prevalent in children during their first
years of life. This parasite is one of the opportunistic agents in AIDS
patients. Reservoir animal hosts include chicken, turkeys, mice, guinea
pigs, sheeps and monkeys.

Prevention and control:

Prevention includes knowledge about the means of transmission
and limiting animal exposure.
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Plasmodium
The malarial parasites of man are species of the Genus
Plasmodium, a name which means a multinucleated mass and in which
the asexual cycle (schizogony) takes place in the red blood cells of
vertebrates and the sexual cycle (sporogony) in mosquitoes. There are
four species of Plasmodium:

1. Plasmodium malariae (Laveran) 1881

2. Plasmodium vivax (Grassi and Feletti) 1890

3. Plasmodium falciparum (Welch) 1922

4. Plasmodium ovale (Stephens) 1922

Morphology:
Some general characteristics are common to all malarial
parasites, but differential features make it possible to identify species.
The earliest form after invasion of red blood cells is a ring of bluish
cytoplasm with a dot like nucleus of red chromatin and this is the
trophic stage. When growing, the parasites divides, it is called a
schizont, showing multiple masses of nuclear chromatin. Merozoites
are observed in mature schizont. Some of the trophozoites develop into
gametocytes or sexual stages, which are differentiated by compact
cytoplasm and the absence of nuclear division.

Stages of development:
1. Trophozoite

This is the earliest stage with one nucleus

living inside the red cell. The early trophozoite is
ring-shaped with a red chromatin dot and a small
amount of blue cytoplasm when stained with
Giemsa or Wright’s stain.
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2. Schizont

This stage is provided with nucleus divided

into 8 – 24 nuclei. Each nucleus enclosed by some
cytoplasm forming a merozoites.

3. Gametocytes

Sexual forms with one large compact and round

or elongated nucleus.

Male gametocytes Female gametocytes

Pigment : Some parasites have granules of pigment in their

cytoplasm; others do not have any.

with pigment without pigments

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Plasmodium falciparum
Malignant Tertian Malaria

Young trophozoite
Cytoplasm:
Small, fine, pale blue ring
Chromatin:
1 to 2 small red dots, some
found in the margin of RBC
(Applique or Acole forms)
Size:
1/5 to 1/3 diameter of RBC

Mature trophozoite
Cytoplasm:
Thin, blue ring or comma-shaped
Chromatin:
1 or 2 medium sized red dots

Schizont
Merozoites:
8 – 24
Pigment:
Dark brownish-black

Gametocytes
Shape:
Banana/sickle/sausage/crescent
Color:
Blue (male) or dense blue (female)
Nucleus:
Reddish pink
Pigment:
Few blue-black granules in the
center of the cytoplasm or scattered

RBC: Normal in size

Pigments: Maurer’s dots

Stages in peripheral blood: ring forms and gametocytes

Length of asexual cycle: 48 hours

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Plasmodium vivax
Benign Tertian Malaria

Young trophozoite
Cytoplasm:
Irregular blue, thick ring
Chromatin:
Large red dots
Size:
¼ to 2/3 of diameter of RBC

Mature trophozoite
Cytoplasm:
Large, blue, irregular, small
particles of brownish orange pigment

Schizont
Merozoites:
12 – 24
large, compact red granules
against the pale blue cytoplasm

Gametocytes:
Female:
Oval or rounded, dense blue with
dense red triangular nucleus; many
particles of orange pigment in cytoplasm

Male:
Rounded, pale blue with a round
central pale red nucleus; some particles
of orange pigment in cytoplasm

RBC: enlarged, pale

Pigments: Shuffner’s dots

Stages in peripheral blood: All

Length of asexual cycle: 48 hours

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Plasmodium ovale
Benign tertian malaria

Young trophozoite
Cytoplasm:
Regular, dense blue ring
Chromatin:
Medium-sized red dot
Size:
¼ to 2/3 of diameter of RBC

Mature trophozoite
Cytoplasm:
Round, compact very blue with
a few particles of brown pigment
Chromatin:
Large red dot

Schizont
Merozoites:
8 – 14
large red granules in a rosette, round
and central mass of particles of
brown pigment

Gametocyte
Shape:
Large, oval or round
Nucleus:
1 round red spot
Pigment:
Few brown particles in the
cytoplasm

RBC: enlarged often with torn/jagged end or fringes or irregular edges

Pigments: James dots

Stages in peripheral blood : all

Length of asexual cycle: 48 hours

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Plasmodium malariae
Quartan malaria

Young trophozoite
Cytoplasm:
Thick, dense blue ring
with some granules of black
pigments
Chromatin:
1 large red dot
Size:
¼ to 2/3 of diameter of RBC

Mature trophozoite
Cytoplasm: either
1. round, compact, dark blue with
many black particles of pigment
2. in band form
Chromatin:
A round dot or a red band

Schizont
Merozoites:
8 – 10 each one a large red
spot enclosed by pale cytoplasm

Gametocytes
Shape:
Large, oval or rounded
Color:
Female-Dense blue; male-pale blue
Nucleus:
1 round spot of red chromatin
Pigment:
Large black granules in the cytoplasm

RBC : normal

Pigments : Ziemman’s dots

Stages in peripheral blood : all

Length of asexual cycle : 72 hours

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Life cycle:
The life cycle of Plasmodium is passed in two hosts, a vertebrate
host and a mosquito. The asexual cycle in the vertebrate host like
humans consists of schizogony, which leads to formation of
merozoites and gametony, which leads to the formation of
gametocytes. The sexual cycle in mosquito is sporogony, which leads
to the formation of sporozoites.

A. Asexual phase in man (Schizogony)

1. Pre-erythrocytic schizogony

The infectious sporozoites from the salivary glands of an

infected female Anopheles mosquito is injected during biting into
the human blood stream. Within 30 minutes this slender motile
organism enters a liver parenchymal cell where they undergo
nuclear division and cytoplasmic division and give rise to
merozoites. The duration of the pre-erythrocytic phase, which
corresponds to the incubation period, depends on the parasite
species. Thus,

a. Plasmodium falciparum = 5 – 7 days

b. Plasmodium vivax = 6 – 8 days
c. Plasmodium ovale = 5 days
d. Plasmodium malariae = 13 – 16 days

The parasitized liver cell then rupture, releasing

merozoites to initiate the erythrocytic cycle.

2. Exo-erythrocytic schizogony

In P. vivax and P. ovale, not all liberated merozoites from

the liver parenchymal cells infect the red blood cells. Some infect
other liver cells and continue the process of schizogony as the
exo-erythrocytic cycle. The merozoites formed are responsible
for the relapse in cases of infection with these species of
Plasmodium. Some schizonts called hypnozoites even become
dormant and when activated by still unknown factors cause
relapse even after a long period of time.
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3. Erythrocytic schizogony

The merozoites formed in the pre-erythrocytic cycle invade

red blood cells through the erythrocytic surface receptors. These
released merozoites and other metabolites cause the typical
intermittent chills, fever and sweating. Inside the red blood cells,
there is development into trophozoites, then schizont, the
rupturing of the cell and the re-invasion of new cells.

4. Gametony

Some of the merozoites released from the red blood cells

do not undergo schizogony nor infect more red blood cells, but
they develop into male and female gametocytes which are
infective to the mosquito.

B. Sexual phase in mosquito (Sporogony)

The male and female gametocytes sucked in by the

mosquito during blood meal undergo maturation and
differentiate into microgametes (male) and macrogametes
(female). The microgamete exflagellates and produce 8 sperm
like microgametes, fertilizes the macrogametes, producing
zygote. The zygote becomes motile and penetrates the
mosquito’s gut as an ookinete, which develops into oocyst. The
oocyst undergoes division (sporogony), giving rise to many
sporozoites, which is the infective stage, to man. When an
infected mosquito bites man, the sporozoites from its salivary
glands are inoculated through the skin into the circulation. The
entire developmental cycle in mosquito takes 8 – 35 days.
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merozoites ⇨ invade rbc ⇨ young trophozoites(ring)

⇧ ⇘ ⇗ ⇩
pre-erythro- Exo-erythrocytic phase ⇧ merozoites mature
cytic phase re-invade liver cells, ⇧ (re-invade trophozoites
Develop in develop into secondary ⇧ RBC) ⇩
Liver cells to exo-erythrocytic ⇧ ⇧ early
Pre-erythro- schizonts ⇩ ⇧ mature ⇦ schizont
Schizont ⇩ ⇩ ⇗ schizont
⇧ hypnozoites ⇩ ⇗
sporozoites ⇩ ⇙ ⇗ Macrogametocytes
invades liver merozoites Microgametocytes
parenchymal ⇩
cells ⇩
⇧ ⇩
⇧ Sexual cycle in Anopheles mosquito ⇩
mosquito infects macrogametes mature
man microgametes ex-
⇧ flagellates
sporozoites ⇩
(in salivary glands) zygote formed by union of gametes
⇧ ⇩
oocyst ⇦ ⇦ ⇦ ⇦ ⇦ ookinete

Pathology:

The appearance of clinical manifestations in cases of malaria is 8

– 40 days depending of the species involved. The clinical incubation for
the different species is as follows:

P. falciparum = 8 – 15 days
P. vivax = 12 – 20 days
P. ovale = 11 – 16 days
P. malariae = 18 – 40 days
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There are prodromal symptoms which may include a feeling of

weakness and exhaustion; aching toes, limbs and back; a desire to
stretch and yawn; loss of appetite; headache; nausea and vomiting.

Malaria is characterized by malarial paroxysm, which occur at the

end of the schizogonic cycle, when the merozoites of the mature
schizonts are released from infected RBC into the blood circulation.
There are three stages of malarial paroxysm:

1. Cold stage (chill)

The cold stage starts with a sudden feeling of cold, mild
shivering that quickly turns into violent teeth chattering and
shaking of the whole body. The peripheral blood vessels are
constricted and these stage usually last for 15 minutes to 1 hour.

2. Hot stage (fever)

The patient becomes hot wherein the body temperature
increases up to 103ºC to 106ºC F ( 39 to 41ºC). Other
manifestations include nausea, vomiting, headache, rapid pulse,
hot skin, flushed face and the patient may become confused or
delirious. This phase last for 2 to 6 hours.

3. Wet stage (sweating)

Patient perspires profusely.

The total duration of the typical attack is 8 to 12 hours. The

classic periodicity of attacks develops only if the patient is untreated
until the time when the life phases become synchronized and sufficient
number of red blood cells containing schizonts rupture at about the
same time. The interval between attacks is determined by the length of
the erythrocytic cycle. For P. malariae, 72 hours, causing paroxysms on
days 1 and 4, hence the term quartan malaria; for P. falciparum, it is 48
hours and for P. vivax and P. ovale, paroxysms occur on alternate days,
hence the term tertian malaria.

Plasmodium falciparum is the cause of virtually all fatalities due

to vascular obstruction. The infected RBC has the tendency to stick to
the endothelium of blood vessels and to each other and the ability of P.
falciparum to infect red blood cells of all ages and thus produce a high
parasitemia. P. falciparum may enter the kidney, brain and liver. Kidney
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involvement, known as black water fever, usually results in marked

hemoglobinuria, caused by P. falciparum-induced red cell destruction.
Acute renal failure, tubular necrosis, nephrotic syndrome and death
may result.

P. vivax and P. ovale invade only the young or immature RBC

while P. malariae can infect mature or older RBC.

The multiple organ pathology in malaria is essentially due to

tissue anoxia and immunopathological mechanism. If the malarial
infection continues, anemia develops and often the anemia is of greater
degree than can be explained by direct destruction of red blood cells by
the parasites.

Diagnosis:
The interval of time from sporozoite inoculation to detection of
parasites in the blood is dependent on the prepatent period, which
usually varies depending on the species of Plasmodium. For P.
falciparum it is 11 – 14 days; P. malariae, 3 – 4 weeks; P. ovale, 14 – 26
days and P. vivax, 11 t0 15 days.

Blood is the specimen examined for the presence of

Plasmodium. Thick and thin blood smears stained with Giemsa or
Wright’s stain is examined microscopically foe Plasmodium. Blood
maybe collected any time.

Serological tests maybe used for diagnosis like IHA and ELISA.
The Quantitative Buffy Coat (QBC) method uses a specially prepared
capillary tube coated with acridine orange. Malaria parasites take up
this stain and appear bright green and yellow when viewed under a
fluorescent microscope. The ParaSight F test is a dipstick test for the
simple and rapid diagnosis of P. falciparum infection.

Treatment:
The drug of choice for the treatment of malaria is Chloroquine.
Pyrimethamine/sulfadoxine combination or quinine maybe used in
areas where there maybe higher levels of resistance to chloroquine.
Treatment also includes general and supportive measures. If fluid
replacement or blood transfusion is necessary, it must be administered
with care to avoid pulmonary edema.
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Epidemiology:
In the Philippines, all provinces with slow, flowing, partly shaded,
clean mountain streams are endemic because this is the breeding
habitat of major vector, Anopheles minismus flavirostris. The minor
vectors are Anopheles mangyanus, a clean stream breeder; Anopheles
balabacensis, a forest rain pool breeder; Anopheles litoralis, thrives in
brakish water and Anopheles maculatus, a stream breeder.

Prevention and control:

For prevention, screening of houses, use of mosquito nets,
protective clothing and insect repellants. Early diagnosis and prompt
treatment are essential for control. Chemical insecticides and larvicides
are useful for vector control.
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ACTIVITY SHEET NO. 32

NAME___________________________SEC________DATE_________

1. Discuss relapse in case of invasion of P. vivax and P. ovale.

2. Discuss malaria caused by P. falciparum.

3. Describe the clinical manifestations in malarial infection; the time

interval between paroxysm for each specie.
 245

BIBLIOGRAPHY

Beaver, Paul C., Jung, Rodney C. & Wayne, Eddie C. Clinical

Parasitology 10th Edition, Lea and Febiger, Philadelphia 1990.

Beck and Davies Medical Parasitology 8th Edition St. Louis,

Mosby 1992

Belisario, Vicente Philippine Textbook of Medical Parasitology

Publication Program, University of the Philippines, Manila 1998.

Brown, Harold & Neva, Franklin Basic Clinical Parasitology 6th Edition
Appleton-Century-Crofts, Connecticut 1994

Buerden, L.I. et. Al. A New Short Textbook of Microbial and Parasitic
Infections. London 1987.

Goldsmith, Robert; Heyneman, Donald. Tropical Medicine and

Parasitology. Appleton and Lange, Connecticut 1989

Jueco, Nanette et. Al. A Study Guide in Medical Parasitology UP

Public Health , 1996.

Merkell,Edward & Voge, Marietta Medical Parasitology 7th Edition

W.B. Saunders Company, Philadelphia 1995

Noble & Noble Parasitology: The Biology of Animal Parasites 7th

Edition, Lea & Febiger, Philadelphia 1993

Zeibig,Elizabeth Clinical Parasitology. A Practical Approach. W.B.

Saunders Company, Philadelphia 1997
 246

COMPILED NOTES

IN

PARASITOLOGY

Prepared by:

FERDINAND MORTEL PhD

Manila Central University

Caloocan
(Revised)
2010
 247

PREFACE

This Compiled Notes in Parasitology has been revised to include

recent important additional knowledge in Parasitology. Likewise, more

illustrations of the different stages of parasites were included. Life

cycle is presented in a diagram form for better understanding of the

students.

I would like to express my deepest appreciation to all the authors

and publishers of references used in the preparation of this notes.

Sincerest gratitude is also extended to those who in one way or another

helped in the preparation of this Compiled Notes.

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TABLE OF CONTENTS

Page

Preface

I. Introduction to Parasitology 1
Types of Host 1
Host-Parasites Relationship 1
Parasitic Infection and Disease 2
Life cycle 4
Diagnosis 5
Treatment 5
Epidemiology 5
Prevention and control 6

II. Phylum Nematode

Introduction 9
Ascaris lumbricoides 18
Toxocara canis and Toxocara cati 25
Trichuris trichiura 28
Hookworms 33
Strongyloides stercoralis 41
Enterobius vermicularis 47
Capillaria philippinensis 53
Trichinella spiralis 58
Filarial worms 64
Angiostrongylus cantonensis 82
Dracunculus medinensis 86

III. Phylum Platyhelminthes

Class Cestodea
Introduction 90
Diphyllobothrium latum 96
Taenia solium 103
Taenia saginata 111
Dipylidium caninum 115
 249

Hymenolepis nana 119

Hymenolepis diminuta 123
Echinococcus granulosus 127
Railietina garrisoni 132

Page

Class Trematoda
Introduction 135
Fasciola hepatica 143
Clonorchis sinensis 149
Opistorchis felineus 153
Paragonimus westermani 157
Fasciolopsis buski 162
Echinostoma 166
Heterophyds 170
Schistosoma 175

IV. Phylum Protozoa

Introduction 182
Amoeba 187
Flagellates 205
Balantidium coli 223
Toxoplasma gondii 227
Isospora 230
Cryptosporidium 231
Plasmodium 232

Bibliography
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