CILIATE AND
FLAGELLATES
Phylum Ciliophora
Balantidium coli
Balantidium coli
Initially identified as Paramecium coli in 1857.
B. coli is the causative agent of the zoonotic disease
called balantidiasis or balantidial dysentery.
Considered the largest protozoan parasite affecting
humans, and is the only ciliate known to cause
human disease.
It is capable of attacking the intestinal epithelium,
resulting in ulcer formation which in turn, causes
bloody diarrhea similar to that of amebic dysentery.
This organism is primarily associated with pigs, its
normal host (reservoir host).
Parasite Biology
Trophozoite measures 30 to 150 mm long and 25 to 120 mm
wide.
For locomotion, trophozoites are covered with cilia arranged
in a longitudinal pattern extending from the oral to the caudal
region – rotary-type motion
It has a cytostome, an oral apparatus at the tapered anterior
end, through which it acquires food, and a cytophage (anus) at
the rounded posterior end through which it excretes wastes.
It has two dissimilar nuclei; the macronucleus is usually bean-
shaped and can easily be identified in stained specimens,
while the micronucleus is round and lies in the concavity of
the macronucleus.
The small micronucleus governs sexual reproduction
The large macronucleus governs metabolism and
growth
Both nuclei divide during asexual mitosis
B. coli has two contractile vacuoles that act as osmoregulatory
organelles; also contains extrusive organelles called
mucocysts which are located beneath the cell membrane.
The cysts are spherical to slightly ovoid in shape and
measure 40 to 60 mm in diameter; covered with thick cell
wall.
Unlike amebae, encystation does not result in an increase in
number of nuclei.
B. coli troph.
B. coli cyst
Life cycle
Human infection results from ingestion of food and water
contaminated w/ B. coli cysts.
Incubation period is normally 4 to 5 days.
Ingested cysts excyst in the small intestines and becomes
trophozoite, w/c then inhabit the lumen, mucosa, and
submucosa of the large intestine, primarily the cecal region
causing pathologic changes in the colonic wall & mucosa.
Reproduction occurs asexually through asymmetric binary
fission, although sexual reproduction through conjugation
has been reported.
Cysts are formed principally as protection for
survival outside the host.
The parasite encyst during intestinal transport or
after evacuation of semi-formed stools.
Cysts are the infective stage, and may remain viable
for several weeks.
Pathogenesis
B. coli troph are capable of attacking the intestinal epithelium
creating a characteristic ulcer w/ a rounded base and wide
neck, in contrast to the flask-shaped, narrow-necked ulcer of
amebiasis.
Ulceration is caused by the lytic enzyme hyaluronidase that
is secreted by the troph.
The troph are abundant in exudates on mucosal surfaces,
while inflammatory cells and trophozoites are numerous in
the base of the ulcers.
Troph also invade the submucosa and the muscular coat,
including blood vessels and lymphatics.
Intrinsic host factors including nutritional status, intestinal
bacterial flora, achlorhydria, alcoholism, and the presence of
chronic disease contribute to host susceptibility to and
severity of B. coli infection.
Balantidiasis has three forms of clinical manifestations:
1. Asymptomatic carriers – do not present w/ diarrhea but may
serve as parasite reservoir.
2. Fulminant balantidiasis or balantidial dysentery – involves
diarrhea w/ blood and mucoid stools.
3. Chronic form – the diarrhea may alternate w/ constipation, &
may be accompanied w/ abdominal pain, anemia & cachexia.
Acute cases may have 6 to 15 episodes of diarrhea
per day accompanied by abdominal pain, nausea
and vomiting; often associated w/
immunocompromised and malnourished states.
B. coli can spread to extraintestinal sites including the
mesenteric nodes, appendix, liver, genitourinary
sites, pleura and lungs.
Complications of balantidiasis include intestinal
perforation and acute appendicitis.
Diagnosis
Dx is made by microscopic demonstration of
trophozoites and cysts in feces using DFS or
concentration tech. (sedimentation or floatation)
Repeated stool exam may be done to increase
sensitivity.
Demonstrating the presence of trophozoites in
biopsy specimens from lesions obtained
sigmoidoscopy is likewise diagnostic.
Bronchoalveolar washings may also contain B. coli
Trophozoites in the case of pulmonary infection.
Treatment
Tetracycline or metronidazole are the drugs of choice.
Tetracycline, however, is contraindicated in children less
than 8 years of age and in pregnant women.
Iodoquinol may also be given; doxycycline and
nitazoxanide.
Currently, there are no reports of B. coli exhibiting drug
resistance.
Prevention & Control
Proper sanitation, safe water supply, good personal
hygiene, and protection of food from contamination.
Measure to limit of contact of pigs w/ water sources
and food crops may also contribute to reducing
transmission and infection.
Use of pig feces as fertilizer should also be avoided.
Boiling of water, since cysts are easily deactivated by
heat, and by use of 1% sodium hypochlorite.
Ordinary chlorination of water is not effective
against cysts of B. coli.
Subphylum
Mastigophora
DIGESTIVE TRACT AND GENITAL FLAGELLATES
Giardia
Trichomonas
Dientamoeba
Chilomastix
Embadomonas intestinalis (Retortamonas intestinalis)
Enteromonas
HEMOFLAGELLATES
Leishmania
Trypanosoma
Giardia duodenalis/
Giardia lamblia or intestinalis
Intestinal parasitic flagellate of worldwide distribution.
Known to cause epidemic and endemic diarrhea.
It was first discovered by Anton van Leeuwenhoek (1681) in
his own stools and was first described by Lambl who called
it Cercomonas intestinalis.
It was later renamed Giardia lamblia by Stiles.
The disease is called giardiasis, and this manifests as a
significant but not life-threatening gastrointestinal disease.
Parasite Biology
The parasite lives in the duodenum, jejunum, and upper
ileum of humans.
Has simple asexual life cycle that includes trophozoites and
quadrinucleated infective cyst stages.
A. trophozoites
Shape: pyriform or teardrop shaped, pointed posteriorly, w/ a
pair of ovoidal nuclei, one on each side of the midline.
Size: 9 – 12 mm long by 5 – 15 mm wide.
Structure:
- the dorsal side of the organism is convex, while the ventral
side is concave w/ a large adhesive disc used for attachment.
It is bilaterally symmetrical, w/ a distinct medial line
called the axostyle.
The parasite is propelled into an erratic tumbling
motion by four pairs of flagella arising from
superficial organelles in the ventral side of the body.
Trophozoites divide by longitudinal binary fission
and are found in diarrheic stools
B. Cysts
Shape: ovoid
Size: 8 – 12 mm long by 7 – 10 mm wide.
Structure:
- The young cysts have two nuclei, while mature cysts
have four.
- characterized by flagella retracted into axonemes,
the median or parabasal body, and deeply stained curved
fibrils surrounded by a rough hyaline cyst wall secreted
from condensed cytoplasm.
Life Cycle
Cysts from animals or human feces are transferred to the
mouth via contaminated hands, food, or water.
Once mature cysts (infective stage) are ingested, they pass
safely though the stomach and excyst in the duodenum (in
about 30 min) developing into troph that rapidly multiply and
attach to the intestinal villi causing pathologic changes.
The troph may then be found in the jejunum.
As the feces enters the colon and dehydrates, the parasite then
encysts.
After encystment, mature cysts are passed out in the feces and
are infectious.
Pathogenesis
Infection can occur w/ one ingesting as few as 10 cysts.
As the parasite attaches to the intestinal cells via adhesive
sucking disc, it causes mechanical irritation in the affected
tissues.
This attachment causes alterations in the villi, and lead to
decreased electrolyte, glucose, and fluid absorption, and cause
deficiencies in disaccharidases.
The physiologic disturbances subsequently result in
malabsorption and maldigestion, which in turn cause the
signs and symptoms experienced by the patient.
Bacterial colonization worsen the damage already caused by
the parasite.
From ingestion of the cysts, it takes about 1 to 4 weeks for the
disease to manifest.
Half of the infected patients maybe asymptomatic.
For acute cases, patients experience abdominal pain, described
as cramping, associated w/ diarrhea.
There is also excessive flatus w/ an odor of “rotten egg” due
to hydrogen sulfide.
Other clinical features include abdominal bloating, nausea,
and anorexia.
Diarrhea is the most common symptom, followed by malaise
and flatulence.
Chronic infection is characterized by steatorrhea, or
passage of greasy, frothy stools..
In some cases, periods of diarrhea have been
observed to alternate w/ normal or even constipated
bowel periods.
There may be loss weight, profound malaise, and
low-grade fever.
In developing countries, it has been described as a
cause of the failure-to-thrive syndrome.
Diagnosis
Dx is made by demonstration of G. duodenalis troph and/or
cysts in stool specimens.
Troph in DFS may be characterized by having a floating leaf-
like motility.
To detect cysts in stool, conc. techs. are recommended.
At least 3 stool exam on alternate days are recommended
because of spotty shedding of cysts.
If the parasite is not found in feces, duodeno-jejunal aspiration
may be done (give a higher % of positive findings than s/e).
Entero test also may demonstrate Giardia trophozoites.
Entero Test: Procedure:
Patient swallows a gelatin capsule attach to a nylon string, w/
one end of the string attached to the patient’s cheek.
After about 4 to 6 hours, the string is removed, and any adherent
fluid is placed on the slide for microscopic examination.
Serologic tests are presently available:
1. Antigen detection tests
2. Immunofluorescent tests
3. Immunochromatographic assays
Treatment
Metronidazole
Tinidazole
Furazolidone
Albendazole
Prompt treatment of asymptomatic individuals
reduce cyst passage and possible transmission
especially among high-risk groups such as food
handlers, institutionalized patients, children
attending day care, and day care workers.
Mode of Transmission
Direct oral-anal sexual contact among men who have
sex w/ men may increase the risk of giardiasis and
infection w/ other intestinal protozoans.
Most of the outbreaks of giardiasis are water-borne
(recreational water or drinking water).
Foodborne outbreaks have also been reported.
The low infective dose, prolonged communicability,
and relative resistance to chlorine facilitate the
transmission of Giardia through drinking and
recreational water, food, and person-to-person
contact.
Prevention and Control
Proper or sanitary excreta disposal of human excreta
to prevent contamination of food and water supply.
Food can be contaminated by the use of night soil as
fertilizer, by flies, or by infected food handlers.
Normal water chlorination will not affect cysts, but
usual water treatment modalities should be
adequate.
Trichomonas vaginalis
Causes sexually transmitted disease called trichomoniasis
w/ multiple sexual partners.
Now often described as the most prevalent nonviral sexually
transmitted infection.
This parasite exist only in the trophozoite form.
Trophozoite
Shape: pyriform shape
Size: 7 – 23 mm
Structure:
- w/ four free anterior flagella that appear to arise from a
simple stalk, and a fifth flagellum embedded in the undulating
membrane.
This membrane extends to about half of the
organism’s length.
The parasite has a median axostyle and a single
nucleus.
Life Cycle
The parasite is found in the urogenital tract.
In women, it is found in the vagina but may ascend
as far as the renal pelvis; can also be isolated from
the urethra, prostate, and less frequently in the
epididymis in men.
The troph multiply by binary fission in the host and
are transferred passively from person to person.
The usual mode of transmission is by sexual
intercourse.
Pathogenesis
Inflammation of the vaginal mucosa occurs several days after
inoculation of T. vaginalis troph.
4 to 28 days after inoculation into the vagina, proliferating
colonies cause degeneration and desquamation of the vaginal
epithelium followed by leukocytic inflammation of the tissue
layer.
The acute inflammation caused by the parasite results in the
characteristic liquid vaginal secretions, greenish or yellow in
color, that cover the mucosa down to the urethral orifice,
vestibular glands, and clitoris.
The vaginal secretions are very irritating and may cause
intense itchiness and burning sensation.
Aside from the common symptoms of vaginal discharge,
vulvitis, and dysuria, trichomonads appear to be associated
w/an increased incidence of postpartum endometritis;
complications in women include secondary bacterial infection
of the urogenital tract.
Speculum examination reveals punctate hemorrhages of the
cervix, the so called strawberry cervix.
Trichomonas infection in males may be latent and essentially
asymptomatic.
In some cases, it is responsible for an irritating persistent and
recurring urethritis; prostatitis is the most common
complication.
Diagnosis
Saline preparation of vaginal fluid is the quickest and most
inexpensive way to diagnose trichomoniasis.
The accepted gold standard is culture, w/c take 2 – 5 days.
The unstained wet drop preparation may be fixed and stained
w/ Giemsa, Papanicolau, Romanowsky, and Acridine orange
stain for easy identification of troph.
Trichomonas can also be cultured using Diamond’s modified
medium, and Feinberg and Whittington medium.
Other tests include Pap smear, antigen detection tests, and
PCR assays.
Among males, dx is more difficult.
For culture, the best results are seen with a
combination of cultures of urethral swabs and urine
sediment.
PCR appears to detect more cases than culture
among males.
InPouchTMTV test is another culture test that has a
comparable sensitivity to Diamond’s medium
culture.
Treatment
Metronidazole
Tinidazole
Sexual partners must be treated concomitantly to prevent
reinfection.
Prevention and Control
Limiting the number of sexual partners, and proper
use of protective devices such as condoms and
spermicidal foams may help prevent infection.
To prevent “ping-pong” or recurrent infections, there
should be simultaneous treatment of sexual partners.
Prompt follow-up of patients and their contacts, as
well as health and sex education about venereal
disease are also important.
Nonpathogenic
Flagellates
Trichomonas hominis
As with other Trichomonas spp. T. hominis occurs only in
trophozoite form.
Shape: pyriform shape
Size: 7 – 13 mm
Structure:
- It has five anterior flagella and a posterior flagellum
projecting from an undulating membrane.
- The cytostome and the nucleus are situated at the anterior
end.
- An axostyle extends from anterior to posterior along the mid-
axis.
Transmission occurs rapidly through fecal
contamination of food and drinks.
Its habitat is the cecal area of the large intestine of
human and other primates.
It is noninvasive.
Trophozoites pass out w/ diarrheic stools.
The prevalence in the Philippines is less than 1%.
Trichomonas tenax
Shape:pyriform
Size: 5 -12 mm
Structure:
Smaller and more slender than T. vaginalis
It has four free equal flagella and a fifth one on the margin of an
undulating membrane that does not reach the posterior end of
the body, and lacks a free posterior extension.
It has a single nucleus and a cytostome.
Multiplies by binary fission and thrives on the microorganisms
found in its environment.
Exposure results from droplet spray from the mouth, kissing,
or common use of contaminated dishes and drinking glasses.
T. tenax is a harmless commensal of the human mouth, living
in the tartar around the teeth, in cavities of carious teeth, and
in necrotic mucosal cells in the gingival margins.
It is quite resistant to changes in temperature and will survive
for several hours in drinking water.
Dx is made by swabbing the tartar between teeth, the gingival
margin, or tonsillar crypts.
Pulmonary trichomoniasis develop among those w/
underlying chronic pulmonary disease
Chilomastix mesnili
This inhabits the cecal region of the large intestine
It has a well defined trophic and cystic stages.
A. Trophozoite
Shape: pear-shaped as a result of spiral groove extending
through the middle half of the body.
Size: 6 – 10 mm
Structure”
- the characteristic boring and spiral forward movement is
made possible by the three anterior free flagella and a more
delicate one within the prominent cytostome.
B. Cyst
Shape:pear-shaped or lemon shape, broadly rounded at
one end and somewhat bluntly conical at the other end,
w/c has a knob-like protruberance that is visible
occasionally.
- In H & E stain, a single large vestibular nucleus
and the cytostome is clearly visible.
- good preparations reveal a fibril on either side
of the cytostome.
Mode of transmission is through ingestion of cysts in
food and drinks.
This is a harmless commensal diagnosed by
microscopic s/e and demonstration of either troph or
cyst.
No treatment is indicated.
Preventive and control measures include improved
sanitation and personal hygiene.
Causal Agents:
Enteromonas hominis
Retortamonas intestinalis
Pentatrichomonas hominis
They are less frequently encountered than
Chilomastix mesnili.
Presence of cysts and/or trophozoites in stool
indicates exposure to fecal contamination.
Both cysts and trophozoites of Enteromonas hominis
and Retortamonas intestinalis are shed in feces; only
trophozoites of Pentatrichomonas hominis (no
known cyst stage) are shed in feces.
Life cycle
Infection occurs after the ingestion of cysts (E.
hominis, R. intestinalis), or trophozoites (P. hominis) in
fecally contaminated food or water, or on fomites.
Excystation of E. hominis and R. intestinalis releases
trophozoites into the large intestine; P. hominis is
found as a trophozoite throughout its life cycle.
These three species colonize and replicate in the
large intestine, where they are regarded as
commensal organisms and are not known to cause
disease.
Humans are the primary host for all three of the
discussed flagellates.
Occasionally these species are found in apes and
monkeys.
Pathogenesis
Enteromonas hominis, R. intestinalis, and P. hominis are
considered non-pathogenic.
The presence of cysts and/or trophozoites in stool
specimens can however be an indicator of fecal
contamination of a food or water source, and thus
does not rule out other parasitic infections.
Non-pathogenic flagellates occur worldwide, and are
more prevalent in areas with inadequate sanitation
leading to fecal contamination.
Retortamonas intestinalis is the least frequently
encountered among the three species
Enteromonas hominis cyst
Cysts of Enteromonas hominis are ellipsoidal,
measuring 4-8 µm long by 3-5 µm wide.
Cysts may contain one, two or four nuclei, with
binucleate forms being the most common.
In binucleate forms, the nuclei are often at opposite
polar ends of the cyst; in forms with four nuclei, they
are often paired at opposite ends.
Nuclei possess a large, central karyosome, often
surrounded by a clear area, and do not contain
peripheral chromatin.
Troph of Retortamonas
intestinalis
Trophozoites of Retortamonas intestinalis are ovoid or
pyriform and measure 4—10 µm long by 3—8 µm
wide.
They possess two flagella, one directed anteriorly
and one extending posteriorly.
A cytostome is present at the anterior half of the
trophozoite and is bordered by a fibril.
The single, spherical nucleus is located at the anterior
end and contains a small karyosome and a fine layer
of peripheral chromatin.
Cyst of R. intestinalis
Cysts of Retortamonas intestinalis are ovoid or
pyriform and measure 4—7 µm long by 3—5 µm
wide.
Mature cysts contain a single nucleus, with a
compact central karyosome and varying amounts of
peripheral chromatin.
The fibril associated with the cytostome may be been
seen in close proximity to the nucleus.
Troph of P. hominis
There is no known cyst stage for P. hominis.
Trophozoites are pyriform in shape, measuring 6—
20 µm long.
They possess five flagella: four directed anteriorly
and a fifth directed posteriorly, that forms the outer
edge of the undulating membrane and projects
beyond the posterior as a free flagellum.
The axostyle is slender and projects from the
posterior end.
The single nucleus is located at the anterior end and
contains a small karyosome.
Lab dx of the three
Enteromonas hominis, R. intestinalis, and P. hominis are
identified through the detection of cysts and/or
trophozoites in stool specimens.
Identification is best accomplished by direct wet
mounts of freshly produced stool that reveal the
characteristic motility of the organisms.
Enteromonas hominis trophozoites present with a
distinctive “jerky” slowly directional motility in
fresh stool specimens.
R. intestinalis trophozoites exhibit rapidly directional
corkscrew motility, while P. hominis trophozoites
generally do not have directional motility, rather
being stationary but exhibiting marked rapid
undulations of the cytoplasmic membrane (compare
these to the stiff, rotary movement of Chilomastix
mesnili or the “falling leaf” motility of Giardia
duodenalis).
These protozoa may also be identified in permanent
stained smears, although their affinities for stain are
inconsistent and individual flagella may not be
readily visible.
Pentatrichomonas hominis trophozoites degrade
rapidly and timely fixation after passage is required
to detect trophozoites in permanently stained slides.
Other Intestinal
Protozoans
Blastocystis hominis
The taxonomic classification of Blastocystis hominis is mired in
controversy.
It has been previously considered as yeasts, fungi, or ameboid,
flagellated, or sporozoan protozoa.
Recently, however, based on molecular studies, especially
dealing with the sequence information on the complete
SSUrRNA gene, B. hominis has been placed within an informal
group, the stramenopiles (Silberman et al. 1996).
Cavalier-Smith (1998) considers stramenopiles to be identical
to his infrakingdom Heterokonta under the kingdom
Chromista.
Therefore, according to Cavalier-Smith, B. hominis is a
heterokontid chromista.
Stramenopiles are defined, based on molecular phylogenies,
as a heterogeneous evolutionary assemblage of unicellular
and multicellular protists including brown algae, diatoms,
chrysophytes, water molds, slime nets, etc. (Patterson, 1994).
B. hominis is known to occur in four morphological forms:
1. Vacuolated
2. Ameba-like
3. Granular
4. Multiple fission
More recently, additional cysts and avacuolar forms have
been recognized.
Vacuolated forms are the most predominant forms in fecal
specimens.
Ameba-like forms are occasionally observed in stool samples.
Life Cycle
Knowledge of the life cycle and transmission is still under
investigation, therefore this is a proposed life cycle for B.
hominis.
The classic form found in human stools is the cyst, which
varies tremendously in size from 6 to 40 µm
1. The thick-walled cyst present in the stools; it is believed to be
responsible for external transmission, possibly by the fecal-
oral route through ingestion of contaminated water or food
2. The cysts infect epithelial cells of the digestive tract and
multiply asexually
3. Vacuolar forms of the parasite give origin to multi vacuolar
and ameboid forms.
4. The multi-vacuolar develops into a pre-cyst that gives origin
to a thin-walled cyst thought to be responsible for
autoinfection.
5. The ameboid form gives origin to a pre-cyst which develops
into thick-walled cyst by schizogony
6. The thick-walled cyst is excreted in feces.
Pathogenesis
Whether Blastocystis hominis can cause symptomatic
infection in humans is a point of active debate.
This is because of the common occurrence of the
organism in both asymptomatic and symptomatic
persons.
Those who believe symptoms could be related to
infection with this parasite have described a
spectrum of illness including watery diarrhea,
abdominal pain, perianal pruritus, and excessive
flatulence.
Diagnosis
Stool examination using DFS is needed to confirm the dx w/
multiple stool samples collected.
Sensitivity is increased w/ the use of concentration
techniques.
Hematoxylin or trichrome staining offers a very convenient
and easy method to differentiate the various stages of
Blastocystis.
Leukocytes are usually seen in fecal smears and stool
eosinophilia may also be observed.
The organism can be cultured using the Boeck and
Drbohlav’s or the Nelson and Jones media.
Treatment
Metronidazole – drug of choice; however, there have
been reported cases of resistance.
Trimethoprim-sulfamethoxazole has also been found
to be highly effective.
Nitazoxanide has been clinically tested on patients
w/ blastocystosis and found to resolve the symptom
Prevention and Control
Consuming safe drinking water
Provisions for sanitary preparation may be of value
in efforts to prevent and control this infection.
Chlorination is ineffective at the standard
concentration.
Dientamoeba fragilis
Originally described as an ameba, but is actually a flagellate
w/ only the trophozoite stage known.
Size: 7 to 12 mm
Structure:
W/ one or two rosette-shaped nuclei; the nuclear membrane
does not have peripheral chromatin, and the karyosome
consists of four to six discrete granules.
The cytoplasm may contain vacuoles w/ingested debris.
Except for the absence of a flagellum, this protozoan is closely
related to and resembles Trichomonas.
D. fragilis lives in the mucosal crypts of the appendix,
cecum, and the upper colon.
Direct human-to-human transmission is probably via
the fecal-oral route or via transmission of helminth
eggs particularly that of E. vermicularis.
Dientamoeba like mononucleated and binucleated
forms have been observed in the lumen of Enterobius
adults and eggs present in the intestines.
Pathogenesis
D. fragilis does not invade tissues, but its presence in the
intestines produces irritation of the mucosa w/ secretion of
excess mucus and hypermotility of the bowel.
Infection is usually asymptomatic.
In symptomatic individuals, it is usually accompanied by
loss of appetite, colicky abdominal pain, and intermittent
diarrhea w/ excess mucus, abdominal tenderness, a bloating
sensation, and flatulence.
There is anal pruritus due to coinfection w/ E. vermicularis
Chronic infection can mimic the symptoms of diarrhea-
predominant irritable bowel syndrome (IBS).
Diagnosis
Stool examination by finding the binucleate troph.
Fresh stool samples are necessary since the troph degenerate
after a few hours of stool passage.
Purged stool specimens provide more suitable material for
examination than the average formed stool.
Even when formed, D. fragilis may be misdiagnosed as other
amebae.
The organism is not detected by stool concentration methods.
Prompt fixation of the fresh specimen w/ PVA fixative or
Schaudinn’s fixative has been found to be helpful.
Treatment, Prevention
and Control
Antimicrobial therapy resolves symptoms and
eradicates D. fragilis.
Iodoquinol, tetracycline, and metronidazole are
found to be effective.
Proper sanitation and disposal of human waste are
essential.
