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Neglected tropical diseases - Schistosomiasis (bilharzia)

Schistosomiasis, caused by blood flukes, primarily affects populations in tropical and subtropical regions, with over 200 million people infected globally. It presents various clinical manifestations including katayama syndrome and chronic complications such as urinary and intestinal pathologies. Accurate diagnosis involves both laboratory techniques for detecting eggs in urine and stool, with significant public health implications due to its morbidity and mortality rates.

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SCHISTOSOMIASIS DR OGECHUKWU MBANU FAMILY MEDICINE DEPARTMENT AKTH, KANO 17TH MAY 2018
OUTLINE • INTRODUCTION • HISTORY • EPIDEMIOLOGY • ETIOLOGY • LIFE CYCLE • PATHOGENESIS • CLINICAL MANIFESTATION • CLINICAL EVALUATION • TREATMENT • PROGNOSIS • PREVENTION • CONCLUSION
Intorduction • Caused by schistosomes( blood flukes) • A Platyhelminthes • In class trematode • Snail fever or bilharzia • Occurs mainly in rural agricultural and periurban areas • Infection occurs after contact with water that contains the infective stage (cercaria) of schistosomes • The disease is most commonly found in Africa, Asia and south America • Ranks second behind malaria in public health importance in tropical and subtropical areas of the world
History • Once known as bilharzia. • Named after Theodore Maximillian Bilharz • 1st to describe urinary schistosomiasis in man in 1851 at kasr-el- aini in Cairo, Egypt • S. Haematobium, first species to be discovered. • S. Mansoni, discovered in 1907 • 1st doctor to describe the entire disease cycle was Pirajá da Silva in 1908
HISTORY CONT’D • S. Japonicum, named by fijiro katsurada, professor of medicine at Okayama medical school. • Schistosome eggs were found in ancient Chinese and Egyptian mummies by Sir Armand Ruffer in 1910 • S. Intercalatum, officially named in 1934 • S. Mekongi, officially named in 1978. • Katayama fever named after the province of Katayama in Hiroshima Japan
EPIDEMIOLOGY • Widely distributed in tropical and sub tropical regions • > 200 million people infected world wide • > 600 million at risk of infection • About 280,000 deaths annually • On a global scale 1 in every 30 individual has schistosomiasis • Amongst parasite infections second only to malaria in its global impact
ETIOLOGY SPECIE REGION S. mansoni Sub-Saharan Africa , middle east, Turkey , India S.Japonicum China , Japan , Philippines , Thailand , Indonesia S. Intercalatum Central Africa , West Africa S . haematobium Africa and Middle east S. mekongi Laos , Cambodia , S. guineensis West Africa S. malayensis Peninsula Malaysia
Etiologic agent:the pathogen • Separate sexes. • The large male (0.6 to 2.2 cm × 2 to 4 mm) • Female (1.2 to 2.6 cm × 1 to 2 mm) • Has more than 2 Testes • The male has a ventral gynecophoric canal in which the female is held • Definitive host- humans • Intermediate host- fresh water snail • Reservoir hosts – cows ,pigs ,(S.Japonicum) ,rodents, monkeys, and baboons • Forked cercaria is the infective stage.
S .HEAMATOBIUM FEMALE S.Heamatobium male S. haematobium couple EGG
EGG OF S.MANSONI WITH LATERAL SPINE S. MANSONI IN COPULA S.MANSONI IN COPULA AND MALE FORM
MALE OF S.JAPONICUM OVA OF S.JAPONICUM SPINELESS
Etiologic agent : The intermediate Host BULINUS TRUNCATUS(S. heamatobium) BIOMPHALARIA ALEXZANDRINA(mansoni) S Japonicum
Forms of schistosomiasis Intestinal schistosomiasis • Intestinal and liver pathology • S.mansoni,S. japonicum ,(S. intercalatum , S. guineensis ,S. mekongi ) Urinary schistosomiasis • urogenital system pathology • S. heamatobium
Schistosomiasis :lifecycle
PATHOGENESIS 1
PATHOGENESIS 2
PATHOGENESIS 3
IMMUNOPATHOGENESIS • Immune response to the presence of the ova causes almost all the pathology and chronic complications in schistosomiasis • Acute schistosomiasis can cause severe febrile illness in humans • Substances released from the ova are toxic to human tissue e.g. can cause hepatotoxic ity
IMMUNOPATHOGENESIS cont’d  Soluble carbohydrate antigens from the ova are presented by Antigen presenting cell to naïve T cells (To)  This leads to proliferation of both Th1 and Th2 CD4+ T cells  Th1 produces IFN gamma, IL 2, TNF alpha  IFN gamma recruit and help in activation of the macrophages Activated Macrophage produces PDGF , TGF beta , TNF , IL 1 , IL 6
IMMUNOPATHOGENESIS cont’d  Th2 response is dominant at the chronic stage although Th1 response persist.  Th2 response may also be due to ova proteins t hat cause mast cell to produce IL 4 which induces fu rther Th2 differentiation and amplifies the respo nse.  Th2 produces IL 3, 4 , 5 ,13  IL 13 increases fibrosis by increase in synthesis of proline an important amino acid in collagen
CLINICAL PRESENTATION 2 Worm maturation : - katayama sydrome • 2 – 8 weeks after skin penetration. • Systemic allergic reaction to eggs antigens : fever , chills , rigors , myalgia ,arthralgia , lymphadenopathy ,hepatomegaly , • Usually lasts days or weeks , then resolves , • Severe cases: shock , coma , death • In S .japonicum , cerebral schistosomiasis can occure 1.7 to 4.3% , Usually as early as 6 weeks after infection
Clinical presentation 3 – chronic schisto S.Heamatobium :painless terminal heamaturia is a classic symptom • Urinary urgency ,incontinence , • There could be obstruction Granulomas at the lower end of the ureters obstruction  hydroureter and hydronephrosis • Female genital tract lesions  infertility ,increased risk of HIV acquisition • Urethral ulcerations ,Bladder polyposis • Fistulae between urinary tract and skin watering can scrotum • Bladder fibrosis , calcification , Squamous cell CA of the bladder • In the lungsfocal pulmonary arteritis and pulmonary HTN
Clinical presentation 4 - chronic scisto S.mansoni/S.japonicum : asymptomatic for a long time until late complications • abdominal pains , irregular bowel movements , hematochezia , • Firm hepatomegaly ,liver fibrosis (SYMMERS PIPE STEM fibrosis involving the portal vessels and periportal spaces), liver failure • Splenomegaly with left upper quadrant pain • Ascites , jaundice , Portal hypertension • Esophageal varices  heamatemesis  anemia • Colonic polyposis • Pulmonary hypertension
CLINICAL EVALUATION Clinical evaluation History physical examination General physical Systemic physical Laboratory tests
HISTORY • Biodata of patient • Presenting complaints • History of presenting complaints • Developmental history • Past medical and surgical history • Obstetrics and gynecological history • Drug history • Family and social history • Immunization history • Travel history
PHYSICAL EXAMINATION • General physical examination • Systemic physical examination
LABORATORY INVESTIGAIONS • Diagnosis in high and low endemic areas • Direct and indirect methods • low endemic : tests used have high sensitivity and specifity in order to find even light infections • Direct methods  detection of eggs, • Indirect methods  detection of specific antibodies and antigens • Stool sample – S.mansoni and S.japonicum • urine sample – S.heamatobium • Acute cases may be negative for eggs
Detection of Schistosoma haematobium • urine dipstick heamaturia and/ or proteinuria, • Gross heamaturia indicates heavy infection • Two methods are used for detection of eggs Sedimentation method and Filtration Method • Sedimentation method is less sensitive cheaper and simpler to perform. • Filtration method is used for quantitative analysis for epidemiological surveillance purposes
Materials needed • Microscope slides and coverslips • Centrifuge (sedimentation method) • Conical centrifuge tubes, 15 ml (sedimentation method) • Filter holder, 13 or 25mm diameter (filtration method) • Membrane filter, 12–20mm pore size (nylon or polycarbonate) • Conical flask for urine collection • Pipettes (sedimentation method) • Plastic syringe, 10 ml (filtration method) • Lugol iodine, 0.5% solution (filtration method) • Formaldehyde, 37% solution
Collection of urine specimens • Collected between 10am – 2pm • Consists of a single terminal urine specimen of at least 10 ml • Alternatively, a 24-hour collection of terminal urine • Containers should be wide-mouthed, clean and dry.
Collection of urine specimens cont’d • Examine the specimen at once • If the urine cannot be examined for an hour or longer, add 1 ml of undiluted formalin (37% formaldehyde solution) to each 100 ml of urine. • This will preserve any eggs that might be present. • If formalin is not available, 2 ml of ordinary household bleach can be added to each 100 ml of urine.
Sedimentation method • Shake the well and pour into the conical flask. • Allow the urine to sediment for 1 hour. • Remove the supernatant and transfer the sediment into a centrifuge tube. • Centrifuge at 2000rpm for 2 minutes. • Examine deposit with microscope for the presence of ova
SEDIMENTATION METHOD CONT’D • IMPORTANT: • Do not increase the centrifugation time and do not exceed 2000rpm • This may disrupt the ova and release miracidia • process the specimen as soon as possible; • shake container before pouring the urine specimen into the conical flask; • label slides and tubes carefully
Filtration method • Place a filter in the filter holder. • Agitate sample gently and draw 10ml into the syringe • Attach the syringe to the filter holder. • Expel the urine from the syringe through the filter over a container • Disconnect the syringe from the filter holder • Draw air into the syringe • reattach the syringe to the filter holder • expel the air through the filter
FILTRATION METHOD CONT’D
Filtration method cont’d • Disconnect the syringe from the filter holder. Using forceps, • Remove the membrane filter or filter-paper and place it on a microscope slide. • The nylon membrane and filter-paper should be placed face-up • while the polycarbonate membrane should be placed face-down. • Add one drop of Lugol iodine solution to improve the visibility of the eggs.
FILTRATION METHOD CONT’D • Examine the entire filter under the microscope at x10 or x 40. • Record the results as the number of eggs per 10 ml of urine. • Reporting the result • Light infection: 1–49 eggs per 10 ml of urine. • Heavy infection: > 50 eggs per 10 ml of urine.
STOOL EXAMINATION • Stool examination is done Macroscopically and Microscopically MACROSCOPICALLY • Colour: brown, pale • Consistency : formed ,semi-formed , watery • Odour: shigella ,amoebiasis may have offensive odour • Presence or absence of mucous or blood
STOOL EXAMINATION – PRECAUTIONS • Never leave stool specimens exposed to the air in containers without lids. • Never accept stool specimens mixed with urine (e.g. in a bedpan) • Always examine stool specimens within 1–4 hours after collection. • If several specimens are received at the same time, examine the liquid stools and those containing mucus or blood first, as they may contain motile amoebae (which die quickly).
MICROSCOPY (remains the gold standard) microscopy Concentration method Sedimentation method Floatation method Kato katz method Wet mount(direct ,quick) metho Unstained method Stained with iodine and eosin
WET MOUNT – UNSTAINED ITEMS NEEDED • Gloves • Labelled microscopic slide • Cover slip • Stool sample • Normal saline • Wooden stick/spatula • Pipette • microscope Procedure • Add one drop of normal saline with pipette to slide • Pick a tiny amount of stool sample with stick • Put the stool sample on the slide and mix thoroughly with the stick • Apply cover slip making sure no air bubbles • Examine under the microscope
Floatation method Permits separation of eggs by the use of liquid with high specific gravity Items needed: • Zinc sulphate • Iodine solution • 15ml conical centrifuge tube • Plastic pipettes • Tongue depressor • Funnel and plastic beaker • Slides and cover slips
Floatation method cont’d • With the tongue depressor take ½ to 1gram of stool, add to the plastic beaker and close the sample container • With the pipette add 7ml of zinc sulphate into the plastic beaker and mix well • Transfer into the centrifuge tube using the funnel and fill up with more zinc sulphate
Floatation method    
FLOATATION METHOD CONT’D • Close tube and centrifuge • With the pipette collect a little from the surface and drop on the slide • Add one drop of iodine,mix well with wooden stick • Cover with cover slip then view under the microscope
Floatation method cont’d      
Sedimentation method ITEMS NEEDED • Gloves • 10% formalin • Acetyl acetate solution • Iodine solution • 15ml conical centrifuge tube • Tongue depressor • Plastic pipette • Microscopic slides • Cover slide • Wooden spatula • Gauze and funnel • Plastic beakker PROCEDURE • with tongue depressor, collect stool sample,put inside the plastic beaker • With the pipette add 3ml of 10% formalin to the plastic beaker • Mix well and transfer into the centrifuge tube through funnel coated with gauze
PROCEDURE – SEDIMENTATION cont’d • Wash the gauze with 10% formalin then remove gauze • Add 3ml of acetyl acetate using pipette and put into the centrifuge tube • Cover centrifuge tube and mix well • Open the tube fast and close fast to allow some gas to escape • Centrifuge at 2000rpm. Add another tube to create balance
SEDIMENTATION cont’d • Remove the supernatant ,leaving few drops of sediment emulsion on ,close tube and shake well • Add drop of sediment on glass slide with the pipette • Add a drop of iodine and mix well with wooden spatula • Put a cover slip on the slide , avoiding air bubbles • View under the microscope
kato katz method ITEMS NEEDED Kato and Miura in 1954 cellophane thick-smear technique 1. Glass slides 2. Cellophane (25×30 mm) 3. 50% glycerol 4. a Piece of paper 5. Nylon screen (sieve) 6. Coverslips with hole in the middle 7. Pipettes 8. Stick 9. Gloves
KATO KATZ CONT’D • Transfer a small amount of faeces onto a piece of paper(scrap paper ) • Soak the cellophane strips (25×30 mm) in 50% glycerol malachite green Solution for at least 24 hrs before use. • Press the screen on top of faecal specimen • Using a plastic spatula, scrap across the upper surface of the screen to sieve the faecal sample • Transfer a small amount of the sieved faecal material into the hole of the template & carefully fill the hole. Level with the applicator stick
KATO KATZ CONT’D
KATO KATZ CONT’D • Remove the template carefully so that all the faecal material is left on the slide &none is left sticking to the template. • Cover the faecal sample on the slide with the glycerol-soaked cellophane strip, • wipe off excess glycerol with a small piece of toilet paper. • Invert the microscope slide & press faecal sample against cellophane on a smooth surface to spread sample evenly • Examine under microscope
KATO KATZ CONT’D
KATO KATZ CONT’D • Used for determination of intensity of infection in endemic areas • Kato – Katz method may need to be repeated (3x – different days) • The cover slip template delivers 41.7mg of feaces • Number of eggs observed is multiplied by 24 to get the number of eggs per gram of feaces QUANTITATIVE ANALYSIS Light infection 1 – 100eggs/gram feaces Moderate infection 100 – 400 /gram feaces Heavy infection >400 eggs / gram feaces
Egg viability test • Used to assess the effectiveness of treatment • Persons with inactive infection may continue to shed eggs into stool and urine for months DONE BY : 1. Egg hatching test 2. Microscopic Examination of eggs for flame cells • Stool or urine is mixed with distilled water at room temperature • It is the observed for hatching of the miracidium or movement of the flame cells • There are four flame cells, one at each corner of the embryo. • Use a x100 objective (slightly reduced illumination) • look for the rapid movement of cilia (short hairs) in the flame cells.
Test for viability wih the hatching test Living egg Dead egg • Opaque • Dead miracidium non motile silent • No RBCs • Does not hatch in fresh water(negative hatching test) • Transluscent • Intact moving miracidium contracting and relaxing • Surounded by RBCs • Hatches in fresh water (positive hatching test)
OTHER INVESTIGATIONS • FBC– eosinophilia , anemia , Thrombocytopenia(due to splenic sequestration) • Blood cultures – for salmonella bacteremia (a Salmonella urinary tract infection should always lead to suspicion of schistosomiasis • S /E/U/Cr • Lumbar puncture – eosinophilia , antischistosomal antibodies • LFT – Mild  alkaline phosphatase and gammaglutamyl transferase levels usually are within the reference range until the end stage of disease
OTHER INVESTIGATIONS CONT’D • SEROLOGY – Falcon assay screening test (FAST), enzyme-linked immunoassay (ELISA), and immunoblot assays  Detection of antibodies to ADULT WORM MICROSOMAL ANTIGENS(MAMA ,HAMA ,JAMA) • Antigen Tests – they reflect active infection circulating anodic antigen (CAA) and  circulating cathodic antigen (CCA). These antigens can be found in urine or serum. Still investigational • Urine deepstick detection of parasite antigens
OTHER INVESTIGATIONS CONT’D IMAGING STUDIES • Plain abdominal radiography – bladder , ureteral calcifications("fetal head" calcification) • Ultrasonography – Hydronephrosis , hydroureters, bladder wall irregularities periportal fibrosis , hepatosplenomegaly and ascites • Urography – abnormalities in ureter bladder wall • Intravenous pyelography (IVP) - Ureteric stricture • Barium swallow or Endoscopy - Esophageal varices
OTHER INVESTIGATIONS CONT’D • CT or MRI scan -interstitial fibrosis. Calcified liver capsules and septal , lesions in CNS schistosomiasis. • Echocardiography – pulmonary hypertension due to egg emboli to pulmonary vasculature BIOPSY AND OTHER PRROCEEDURES • Biopsy is helpful when stool sample findings are negative or in light infection e.g. – liver biopsy (unclear diagnoses or suspected co- infections) , – mucosal biopsy • Cystoscopy , Bronchoscopic washings , transbronchial biopsies ,upper GI endoscopy
TREATMENT • Praziquantel • Derivative of pyrazinoisoquinoline • High efficacy, affordable • Lack of serious short –term and long – term side effects • Usually given as single dose • Effective against adult worms >6wks post infection • 40 mg /kg - S.mansoni ,S.heamatobium • 60mg/kg in 2 or3 divided doses in a single day – S.japonicum • Side effects includes : fever , nausea & vomiting , headaches, dizziness, drowsiness, pruritus, fatigue
Prognosis • Almost all patients improve with treatment. • Most patients with early disease or without severe end-organ complications recover completely. • Resolution of pulmonary disease is less well documented. • Co-infection with malaria, HIV, or hepatitis worsens the prognosis • Patients with heavier worm burdens are less likely to improve and are more likely to require re-treatment
CONCLUSION • Schistosomiasis can be associated with serious morbidity and mortality. • Chronic complications are generally seen in those with a high parasite load, which usually occurs in individuals who live in endemic areas and have recurrent exposure • There is every need to capture patients early so to give better quality of life.
REFERENCE • Manual of basic techniques for a health laboratory.(2003) — 2nd ed.Geneva: WHO • Karin Leder . Peter Weller .(2011) Epidemiology ; pathogenesis ; and clinical features of schistosomiasis ACCESSED 15 JAN 2018 AVAILABLE AT https://www.uptodate.com/.../epidemiology- pathogenesis-and-clinical-manifestations • Monica Cheesbroug. (2009) District Laboratory Practice in Tropical Countries Part 1 Second Edition Cambridge University Press : United States of America • KATO THICK SMEAR TECHNIQUE (online) fac.ksu.edu.sa/sites/default/files/KATO_THICK__SMEAR__TECHNI QUE_0.pptx • NSENGIYUMVA Emmanuel . NSENGIMANA Bernard. NSENGIYUMVA Prosper. Diagnostic procedures of Schistosomiasis in high and low endemic areas/immigrants:
REFERENCE • Mccarthy J, Lustigman S, Yang GJ, Barakat R, Garcia HH, Sripa B, Willingham AL, Prichard RK, Basáñez MG. A Research Agenda For Helminth Diseases Of Humans: Diagnostics For Control And Elimination Programmes • Nurse Jennifer Brown . Vcfishhawk.The Intestinal Parasite Exam .Accessed Feb 09 2018 • Sedimentation Method . Medical Students Al –Quraa University College Of Applied Medical Sciences Department Of Parasitology .Ray Bin Ahmed May 02 2014 Accessed Jan12 2018 • Floatation method . Medical Students Al –Quraa University College Of Applied Medical Sciences Department Of Parasitology .Ray Bin Ahmed May 02 2014 Accessed Jan12 2018
REFERENCE • Mccarthy J, Lustigman S, Yang GJ, Barakat R, Garcia HH, Sripa B, Willingham AL, Prichard RK, Basáñez MG. A Research Agenda For Helminth Diseases Of Humans: Diagnostics For Control And Elimination Programmes • Ahmed S H .Schistosomiasis (Bilharzia) Workshop .Medscape Journal . Jul. 2017.Pages 1-6 .Accessed Mar 02 2018 https://www.emedicine.Medscape.com • The Trematodes By Dr Alkhalifi . Accessed Jan . 2018 • Schistosomiasis By Li Qian .Accessed Jan 11 2018 • Paul Poltinger .Helminths .Schistosomiasis .Robert Wood Johnson Foundation ,RWJF Microbiology Immunology And Infections .Accessed Jan.11 2018 • Schistosomiasis By Dr Mohammed Sannusi Pathology Department AKTH Kano • Schistosomiasis By Gordana And Goldis Jan . 2008 • Davies J.S . Schistosomiasis In The World .Jul .14 2017 Accessed Jul 14 2017 • WHO Media Center .Schistosomiasis .Fact Sheet Oct .2017 .Accessed Jan 12 2018 • Schistosomiasis By Dacosta Shaquice • Ranil Appuhamy .James Clark Schistosomiasis (Bilharzia) An Overview .Lets Learn About Bugs Feb07 2917

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In this document
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Introduction to schistosomiasis, its importance in public health, and presentation outline.

Schistosomiasis is a disease caused by blood flukes (schistosomes), mainly found in tropical regions. It ranks second to malaria in public health significance.

History of schistosomiasis and key discoveries through the years, including named species and significant findings in ancient mummies.

Schistosomiasis affects over 200 million worldwide, primarily in tropical regions, with 280,000 annual deaths.

Different species of schistosomes by region, along with characteristics of the male and female schistosomes.

Explanation of the disease’s life cycle, immune responses, and pathology associated with schistosomiasis.

Symptoms for both acute and chronic schistosomiasis, including specific complications for different species.

Methods for evaluating schistosomiasis, including history-taking, physical exams, and laboratory tests for diagnosis. Different laboratory techniques for confirming schistosomiasis diagnosis, focusing on urine and stool specimen analysis.

Detailed laboratory techniques for schistosomiasis including microscopy, serology, imaging studies, and biopsies.

Treatment using Praziquantel, including dosage guidelines, possible side effects, and efficacy.

Outcomes and prognosis after treatment, highlighting recovery factors influenced by co-infections and worm burden.

The need for early detection of schistosomiasis to improve patient quality of life and reduce morbidity.

Neglected tropical diseases - Schistosomiasis (bilharzia)

  • 1.
  • 2.
    OUTLINE • INTRODUCTION • HISTORY •EPIDEMIOLOGY • ETIOLOGY • LIFE CYCLE • PATHOGENESIS • CLINICAL MANIFESTATION • CLINICAL EVALUATION • TREATMENT • PROGNOSIS • PREVENTION • CONCLUSION
  • 3.
    Intorduction • Caused byschistosomes( blood flukes) • A Platyhelminthes • In class trematode • Snail fever or bilharzia • Occurs mainly in rural agricultural and periurban areas • Infection occurs after contact with water that contains the infective stage (cercaria) of schistosomes • The disease is most commonly found in Africa, Asia and south America • Ranks second behind malaria in public health importance in tropical and subtropical areas of the world
  • 4.
    History • Once knownas bilharzia. • Named after Theodore Maximillian Bilharz • 1st to describe urinary schistosomiasis in man in 1851 at kasr-el- aini in Cairo, Egypt • S. Haematobium, first species to be discovered. • S. Mansoni, discovered in 1907 • 1st doctor to describe the entire disease cycle was Pirajá da Silva in 1908
  • 5.
    HISTORY CONT’D • S.Japonicum, named by fijiro katsurada, professor of medicine at Okayama medical school. • Schistosome eggs were found in ancient Chinese and Egyptian mummies by Sir Armand Ruffer in 1910 • S. Intercalatum, officially named in 1934 • S. Mekongi, officially named in 1978. • Katayama fever named after the province of Katayama in Hiroshima Japan
  • 6.
    EPIDEMIOLOGY • Widely distributedin tropical and sub tropical regions • > 200 million people infected world wide • > 600 million at risk of infection • About 280,000 deaths annually • On a global scale 1 in every 30 individual has schistosomiasis • Amongst parasite infections second only to malaria in its global impact
  • 8.
    ETIOLOGY SPECIE REGION S. mansoniSub-Saharan Africa , middle east, Turkey , India S.Japonicum China , Japan , Philippines , Thailand , Indonesia S. Intercalatum Central Africa , West Africa S . haematobium Africa and Middle east S. mekongi Laos , Cambodia , S. guineensis West Africa S. malayensis Peninsula Malaysia
  • 9.
    Etiologic agent:the pathogen •Separate sexes. • The large male (0.6 to 2.2 cm × 2 to 4 mm) • Female (1.2 to 2.6 cm × 1 to 2 mm) • Has more than 2 Testes • The male has a ventral gynecophoric canal in which the female is held • Definitive host- humans • Intermediate host- fresh water snail • Reservoir hosts – cows ,pigs ,(S.Japonicum) ,rodents, monkeys, and baboons • Forked cercaria is the infective stage.
  • 10.
    S .HEAMATOBIUM FEMALE S.Heamatobiummale S. haematobium couple EGG
  • 11.
    EGG OF S.MANSONIWITH LATERAL SPINE S. MANSONI IN COPULA S.MANSONI IN COPULA AND MALE FORM
  • 12.
    MALE OF S.JAPONICUM OVAOF S.JAPONICUM SPINELESS
  • 13.
    Etiologic agent :The intermediate Host BULINUS TRUNCATUS(S. heamatobium) BIOMPHALARIA ALEXZANDRINA(mansoni) S Japonicum
  • 14.
    Forms of schistosomiasis Intestinalschistosomiasis • Intestinal and liver pathology • S.mansoni,S. japonicum ,(S. intercalatum , S. guineensis ,S. mekongi ) Urinary schistosomiasis • urogenital system pathology • S. heamatobium
  • 16.
  • 17.
  • 18.
  • 19.
  • 20.
    IMMUNOPATHOGENESIS • Immune responseto the presence of the ova causes almost all the pathology and chronic complications in schistosomiasis • Acute schistosomiasis can cause severe febrile illness in humans • Substances released from the ova are toxic to human tissue e.g. can cause hepatotoxic ity
  • 21.
    IMMUNOPATHOGENESIS cont’d  Solublecarbohydrate antigens from the ova are presented by Antigen presenting cell to naïve T cells (To)  This leads to proliferation of both Th1 and Th2 CD4+ T cells  Th1 produces IFN gamma, IL 2, TNF alpha  IFN gamma recruit and help in activation of the macrophages Activated Macrophage produces PDGF , TGF beta , TNF , IL 1 , IL 6
  • 22.
    IMMUNOPATHOGENESIS cont’d  Th2response is dominant at the chronic stage although Th1 response persist.  Th2 response may also be due to ova proteins t hat cause mast cell to produce IL 4 which induces fu rther Th2 differentiation and amplifies the respo nse.  Th2 produces IL 3, 4 , 5 ,13  IL 13 increases fibrosis by increase in synthesis of proline an important amino acid in collagen
  • 24.
    CLINICAL PRESENTATION 2 Wormmaturation : - katayama sydrome • 2 – 8 weeks after skin penetration. • Systemic allergic reaction to eggs antigens : fever , chills , rigors , myalgia ,arthralgia , lymphadenopathy ,hepatomegaly , • Usually lasts days or weeks , then resolves , • Severe cases: shock , coma , death • In S .japonicum , cerebral schistosomiasis can occure 1.7 to 4.3% , Usually as early as 6 weeks after infection
  • 25.
    Clinical presentation 3– chronic schisto S.Heamatobium :painless terminal heamaturia is a classic symptom • Urinary urgency ,incontinence , • There could be obstruction Granulomas at the lower end of the ureters obstruction  hydroureter and hydronephrosis • Female genital tract lesions  infertility ,increased risk of HIV acquisition • Urethral ulcerations ,Bladder polyposis • Fistulae between urinary tract and skin watering can scrotum • Bladder fibrosis , calcification , Squamous cell CA of the bladder • In the lungsfocal pulmonary arteritis and pulmonary HTN
  • 26.
    Clinical presentation 4- chronic scisto S.mansoni/S.japonicum : asymptomatic for a long time until late complications • abdominal pains , irregular bowel movements , hematochezia , • Firm hepatomegaly ,liver fibrosis (SYMMERS PIPE STEM fibrosis involving the portal vessels and periportal spaces), liver failure • Splenomegaly with left upper quadrant pain • Ascites , jaundice , Portal hypertension • Esophageal varices  heamatemesis  anemia • Colonic polyposis • Pulmonary hypertension
  • 27.
  • 28.
    HISTORY • Biodata ofpatient • Presenting complaints • History of presenting complaints • Developmental history • Past medical and surgical history • Obstetrics and gynecological history • Drug history • Family and social history • Immunization history • Travel history
  • 29.
    PHYSICAL EXAMINATION • Generalphysical examination • Systemic physical examination
  • 30.
    LABORATORY INVESTIGAIONS • Diagnosisin high and low endemic areas • Direct and indirect methods • low endemic : tests used have high sensitivity and specifity in order to find even light infections • Direct methods  detection of eggs, • Indirect methods  detection of specific antibodies and antigens • Stool sample – S.mansoni and S.japonicum • urine sample – S.heamatobium • Acute cases may be negative for eggs
  • 31.
    Detection of Schistosomahaematobium • urine dipstick heamaturia and/ or proteinuria, • Gross heamaturia indicates heavy infection • Two methods are used for detection of eggs Sedimentation method and Filtration Method • Sedimentation method is less sensitive cheaper and simpler to perform. • Filtration method is used for quantitative analysis for epidemiological surveillance purposes
  • 32.
    Materials needed • Microscopeslides and coverslips • Centrifuge (sedimentation method) • Conical centrifuge tubes, 15 ml (sedimentation method) • Filter holder, 13 or 25mm diameter (filtration method) • Membrane filter, 12–20mm pore size (nylon or polycarbonate) • Conical flask for urine collection • Pipettes (sedimentation method) • Plastic syringe, 10 ml (filtration method) • Lugol iodine, 0.5% solution (filtration method) • Formaldehyde, 37% solution
  • 33.
    Collection of urinespecimens • Collected between 10am – 2pm • Consists of a single terminal urine specimen of at least 10 ml • Alternatively, a 24-hour collection of terminal urine • Containers should be wide-mouthed, clean and dry.
  • 34.
    Collection of urinespecimens cont’d • Examine the specimen at once • If the urine cannot be examined for an hour or longer, add 1 ml of undiluted formalin (37% formaldehyde solution) to each 100 ml of urine. • This will preserve any eggs that might be present. • If formalin is not available, 2 ml of ordinary household bleach can be added to each 100 ml of urine.
  • 35.
    Sedimentation method • Shakethe well and pour into the conical flask. • Allow the urine to sediment for 1 hour. • Remove the supernatant and transfer the sediment into a centrifuge tube. • Centrifuge at 2000rpm for 2 minutes. • Examine deposit with microscope for the presence of ova
  • 36.
    SEDIMENTATION METHOD CONT’D •IMPORTANT: • Do not increase the centrifugation time and do not exceed 2000rpm • This may disrupt the ova and release miracidia • process the specimen as soon as possible; • shake container before pouring the urine specimen into the conical flask; • label slides and tubes carefully
  • 37.
    Filtration method • Placea filter in the filter holder. • Agitate sample gently and draw 10ml into the syringe • Attach the syringe to the filter holder. • Expel the urine from the syringe through the filter over a container • Disconnect the syringe from the filter holder • Draw air into the syringe • reattach the syringe to the filter holder • expel the air through the filter
  • 38.
  • 39.
    Filtration method cont’d •Disconnect the syringe from the filter holder. Using forceps, • Remove the membrane filter or filter-paper and place it on a microscope slide. • The nylon membrane and filter-paper should be placed face-up • while the polycarbonate membrane should be placed face-down. • Add one drop of Lugol iodine solution to improve the visibility of the eggs.
  • 40.
    FILTRATION METHOD CONT’D •Examine the entire filter under the microscope at x10 or x 40. • Record the results as the number of eggs per 10 ml of urine. • Reporting the result • Light infection: 1–49 eggs per 10 ml of urine. • Heavy infection: > 50 eggs per 10 ml of urine.
  • 41.
    STOOL EXAMINATION • Stoolexamination is done Macroscopically and Microscopically MACROSCOPICALLY • Colour: brown, pale • Consistency : formed ,semi-formed , watery • Odour: shigella ,amoebiasis may have offensive odour • Presence or absence of mucous or blood
  • 42.
    STOOL EXAMINATION –PRECAUTIONS • Never leave stool specimens exposed to the air in containers without lids. • Never accept stool specimens mixed with urine (e.g. in a bedpan) • Always examine stool specimens within 1–4 hours after collection. • If several specimens are received at the same time, examine the liquid stools and those containing mucus or blood first, as they may contain motile amoebae (which die quickly).
  • 43.
    MICROSCOPY (remains thegold standard) microscopy Concentration method Sedimentation method Floatation method Kato katz method Wet mount(direct ,quick) metho Unstained method Stained with iodine and eosin
  • 44.
    WET MOUNT –UNSTAINED ITEMS NEEDED • Gloves • Labelled microscopic slide • Cover slip • Stool sample • Normal saline • Wooden stick/spatula • Pipette • microscope Procedure • Add one drop of normal saline with pipette to slide • Pick a tiny amount of stool sample with stick • Put the stool sample on the slide and mix thoroughly with the stick • Apply cover slip making sure no air bubbles • Examine under the microscope
  • 45.
    Floatation method Permits separationof eggs by the use of liquid with high specific gravity Items needed: • Zinc sulphate • Iodine solution • 15ml conical centrifuge tube • Plastic pipettes • Tongue depressor • Funnel and plastic beaker • Slides and cover slips
  • 46.
    Floatation method cont’d •With the tongue depressor take ½ to 1gram of stool, add to the plastic beaker and close the sample container • With the pipette add 7ml of zinc sulphate into the plastic beaker and mix well • Transfer into the centrifuge tube using the funnel and fill up with more zinc sulphate
  • 47.
  • 48.
    FLOATATION METHOD CONT’D •Close tube and centrifuge • With the pipette collect a little from the surface and drop on the slide • Add one drop of iodine,mix well with wooden stick • Cover with cover slip then view under the microscope
  • 49.
  • 50.
    Sedimentation method ITEMS NEEDED •Gloves • 10% formalin • Acetyl acetate solution • Iodine solution • 15ml conical centrifuge tube • Tongue depressor • Plastic pipette • Microscopic slides • Cover slide • Wooden spatula • Gauze and funnel • Plastic beakker PROCEDURE • with tongue depressor, collect stool sample,put inside the plastic beaker • With the pipette add 3ml of 10% formalin to the plastic beaker • Mix well and transfer into the centrifuge tube through funnel coated with gauze
  • 51.
    PROCEDURE – SEDIMENTATIONcont’d • Wash the gauze with 10% formalin then remove gauze • Add 3ml of acetyl acetate using pipette and put into the centrifuge tube • Cover centrifuge tube and mix well • Open the tube fast and close fast to allow some gas to escape • Centrifuge at 2000rpm. Add another tube to create balance
  • 52.
    SEDIMENTATION cont’d • Removethe supernatant ,leaving few drops of sediment emulsion on ,close tube and shake well • Add drop of sediment on glass slide with the pipette • Add a drop of iodine and mix well with wooden spatula • Put a cover slip on the slide , avoiding air bubbles • View under the microscope
  • 53.
    kato katz method ITEMSNEEDED Kato and Miura in 1954 cellophane thick-smear technique 1. Glass slides 2. Cellophane (25×30 mm) 3. 50% glycerol 4. a Piece of paper 5. Nylon screen (sieve) 6. Coverslips with hole in the middle 7. Pipettes 8. Stick 9. Gloves
  • 54.
    KATO KATZ CONT’D •Transfer a small amount of faeces onto a piece of paper(scrap paper ) • Soak the cellophane strips (25×30 mm) in 50% glycerol malachite green Solution for at least 24 hrs before use. • Press the screen on top of faecal specimen • Using a plastic spatula, scrap across the upper surface of the screen to sieve the faecal sample • Transfer a small amount of the sieved faecal material into the hole of the template & carefully fill the hole. Level with the applicator stick
  • 55.
  • 56.
    KATO KATZ CONT’D •Remove the template carefully so that all the faecal material is left on the slide &none is left sticking to the template. • Cover the faecal sample on the slide with the glycerol-soaked cellophane strip, • wipe off excess glycerol with a small piece of toilet paper. • Invert the microscope slide & press faecal sample against cellophane on a smooth surface to spread sample evenly • Examine under microscope
  • 57.
  • 58.
    KATO KATZ CONT’D •Used for determination of intensity of infection in endemic areas • Kato – Katz method may need to be repeated (3x – different days) • The cover slip template delivers 41.7mg of feaces • Number of eggs observed is multiplied by 24 to get the number of eggs per gram of feaces QUANTITATIVE ANALYSIS Light infection 1 – 100eggs/gram feaces Moderate infection 100 – 400 /gram feaces Heavy infection >400 eggs / gram feaces
  • 59.
    Egg viability test •Used to assess the effectiveness of treatment • Persons with inactive infection may continue to shed eggs into stool and urine for months DONE BY : 1. Egg hatching test 2. Microscopic Examination of eggs for flame cells • Stool or urine is mixed with distilled water at room temperature • It is the observed for hatching of the miracidium or movement of the flame cells • There are four flame cells, one at each corner of the embryo. • Use a x100 objective (slightly reduced illumination) • look for the rapid movement of cilia (short hairs) in the flame cells.
  • 60.
    Test for viabilitywih the hatching test Living egg Dead egg • Opaque • Dead miracidium non motile silent • No RBCs • Does not hatch in fresh water(negative hatching test) • Transluscent • Intact moving miracidium contracting and relaxing • Surounded by RBCs • Hatches in fresh water (positive hatching test)
  • 61.
    OTHER INVESTIGATIONS • FBC–eosinophilia , anemia , Thrombocytopenia(due to splenic sequestration) • Blood cultures – for salmonella bacteremia (a Salmonella urinary tract infection should always lead to suspicion of schistosomiasis • S /E/U/Cr • Lumbar puncture – eosinophilia , antischistosomal antibodies • LFT – Mild  alkaline phosphatase and gammaglutamyl transferase levels usually are within the reference range until the end stage of disease
  • 62.
    OTHER INVESTIGATIONS CONT’D •SEROLOGY – Falcon assay screening test (FAST), enzyme-linked immunoassay (ELISA), and immunoblot assays  Detection of antibodies to ADULT WORM MICROSOMAL ANTIGENS(MAMA ,HAMA ,JAMA) • Antigen Tests – they reflect active infection circulating anodic antigen (CAA) and  circulating cathodic antigen (CCA). These antigens can be found in urine or serum. Still investigational • Urine deepstick detection of parasite antigens
  • 63.
    OTHER INVESTIGATIONS CONT’D IMAGINGSTUDIES • Plain abdominal radiography – bladder , ureteral calcifications("fetal head" calcification) • Ultrasonography – Hydronephrosis , hydroureters, bladder wall irregularities periportal fibrosis , hepatosplenomegaly and ascites • Urography – abnormalities in ureter bladder wall • Intravenous pyelography (IVP) - Ureteric stricture • Barium swallow or Endoscopy - Esophageal varices
  • 64.
    OTHER INVESTIGATIONS CONT’D •CT or MRI scan -interstitial fibrosis. Calcified liver capsules and septal , lesions in CNS schistosomiasis. • Echocardiography – pulmonary hypertension due to egg emboli to pulmonary vasculature BIOPSY AND OTHER PRROCEEDURES • Biopsy is helpful when stool sample findings are negative or in light infection e.g. – liver biopsy (unclear diagnoses or suspected co- infections) , – mucosal biopsy • Cystoscopy , Bronchoscopic washings , transbronchial biopsies ,upper GI endoscopy
  • 65.
    TREATMENT • Praziquantel • Derivativeof pyrazinoisoquinoline • High efficacy, affordable • Lack of serious short –term and long – term side effects • Usually given as single dose • Effective against adult worms >6wks post infection • 40 mg /kg - S.mansoni ,S.heamatobium • 60mg/kg in 2 or3 divided doses in a single day – S.japonicum • Side effects includes : fever , nausea & vomiting , headaches, dizziness, drowsiness, pruritus, fatigue
  • 66.
    Prognosis • Almost allpatients improve with treatment. • Most patients with early disease or without severe end-organ complications recover completely. • Resolution of pulmonary disease is less well documented. • Co-infection with malaria, HIV, or hepatitis worsens the prognosis • Patients with heavier worm burdens are less likely to improve and are more likely to require re-treatment
  • 68.
    CONCLUSION • Schistosomiasis canbe associated with serious morbidity and mortality. • Chronic complications are generally seen in those with a high parasite load, which usually occurs in individuals who live in endemic areas and have recurrent exposure • There is every need to capture patients early so to give better quality of life.
  • 69.
    REFERENCE • Manual ofbasic techniques for a health laboratory.(2003) — 2nd ed.Geneva: WHO • Karin Leder . Peter Weller .(2011) Epidemiology ; pathogenesis ; and clinical features of schistosomiasis ACCESSED 15 JAN 2018 AVAILABLE AT https://www.uptodate.com/.../epidemiology- pathogenesis-and-clinical-manifestations • Monica Cheesbroug. (2009) District Laboratory Practice in Tropical Countries Part 1 Second Edition Cambridge University Press : United States of America • KATO THICK SMEAR TECHNIQUE (online) fac.ksu.edu.sa/sites/default/files/KATO_THICK__SMEAR__TECHNI QUE_0.pptx • NSENGIYUMVA Emmanuel . NSENGIMANA Bernard. NSENGIYUMVA Prosper. Diagnostic procedures of Schistosomiasis in high and low endemic areas/immigrants:
  • 70.
    REFERENCE • Mccarthy J,Lustigman S, Yang GJ, Barakat R, Garcia HH, Sripa B, Willingham AL, Prichard RK, Basáñez MG. A Research Agenda For Helminth Diseases Of Humans: Diagnostics For Control And Elimination Programmes • Nurse Jennifer Brown . Vcfishhawk.The Intestinal Parasite Exam .Accessed Feb 09 2018 • Sedimentation Method . Medical Students Al –Quraa University College Of Applied Medical Sciences Department Of Parasitology .Ray Bin Ahmed May 02 2014 Accessed Jan12 2018 • Floatation method . Medical Students Al –Quraa University College Of Applied Medical Sciences Department Of Parasitology .Ray Bin Ahmed May 02 2014 Accessed Jan12 2018
  • 71.
    REFERENCE • Mccarthy J,Lustigman S, Yang GJ, Barakat R, Garcia HH, Sripa B, Willingham AL, Prichard RK, Basáñez MG. A Research Agenda For Helminth Diseases Of Humans: Diagnostics For Control And Elimination Programmes • Ahmed S H .Schistosomiasis (Bilharzia) Workshop .Medscape Journal . Jul. 2017.Pages 1-6 .Accessed Mar 02 2018 https://www.emedicine.Medscape.com • The Trematodes By Dr Alkhalifi . Accessed Jan . 2018 • Schistosomiasis By Li Qian .Accessed Jan 11 2018 • Paul Poltinger .Helminths .Schistosomiasis .Robert Wood Johnson Foundation ,RWJF Microbiology Immunology And Infections .Accessed Jan.11 2018 • Schistosomiasis By Dr Mohammed Sannusi Pathology Department AKTH Kano • Schistosomiasis By Gordana And Goldis Jan . 2008 • Davies J.S . Schistosomiasis In The World .Jul .14 2017 Accessed Jul 14 2017 • WHO Media Center .Schistosomiasis .Fact Sheet Oct .2017 .Accessed Jan 12 2018 • Schistosomiasis By Dacosta Shaquice • Ranil Appuhamy .James Clark Schistosomiasis (Bilharzia) An Overview .Lets Learn About Bugs Feb07 2917

Editor's Notes

  • #10 DEFINITIVE HOST IS THE HOST IN WHICH THE PARASITE RECHES ITS MATURE FORM ,IT IS HE HOST IN WHICH THE PARASITE REACHES ITS FINAL STAGE OF DEVELIOPMENT ,THE HOST HARBOURS THE SEXUALLY REPRODUCTIVE STAGE OF THE A PARASITE THE INTERMEDIATE HOST HABOURS LARVAL OR ASEXUAL REPRODUCTIVE STAGE OF THE PARASITE RESERVOIR HOSTS ARE THE VERTEBRATE HOSTS WHICH HARBOUR THE SAME SPECIES OF PARASITE AT THE SAME STAGE AS A HUMAN HOST
  • #20 UNLESS ADULT WORMS MIGRATE TO AN UNUSUAL LOCATION EG SPINAL CORD OR THE BRAIN ,THEY DO LITTLE DAMAGE TO THE HOST MOST OF THE IMMUNOLOGICAL RESPONSE ARE DUE TO THE EGGS . EGGS RELEASE TOXINS AND ENZYMES AND PROVOKE TH2 IE TYPE 2 HELPER T CELL RESPONSE INFLAMMATION AND GRANULOMA FORMATION OCCURS AROUND DEPOSITED EGGS, WHICH CAN LEAD TO FIBROSIS AND SCARRING OF AFFECTED TISSUES . S. MANSONI , S.,JAPONICUM ,S.MEKONGKI S.INTERCALATUM EGGS EITHER PENETRATE THE BOWEL (ADJACENT TO THE MESENTERIC VESSELS IN WHICH THE ADULT WORMS ARE RESIDING )OR TRAVEL VIA THE PORTAL VENOUS SYTEM TO THE LIVER. IN THE BOWEL GRANULOMATOUS INFLAMMATION AROUND THE EGGS CAN RESULT IN INTESTINAL SHISTOSOMIASIS CHARACTERISED BY ULCERATION AND SCARRING IN THE LIVER EGGS LODGE IN THE PORTAL NIENS ELICITING OUS FIBROSING REACTIONS THAT CAN EVENTUALY LEAD TO BLOCKAGE OF VENOUS FLOW SECONDARY PORTAL VENOUS HYPERTENSION RESULTS WITH COMPENSATORY PORTO SYSTEMIC BLOOD FLOW AND TISSUE DAMAGE THE CHARACTERISTIC PATHOLOGY SEEN WITHIN THE LIVER IS KNOWN AS SYMMERS PIPE STEM FIBROSIS . IT IS DISTINCT FROM CIRRHOSIS AS THERE IS NO HEPATOCYTE DYSFUNCTION ,INSTEAD THE PORTAL HYPERTENSION RESULTS FROM FIBROSIS WITHIN THE BLOOD VESSELS. S.HEAMATOBIUM CAUSES GRANULOMATOUS INFLAMMATION AND ULCERATION OF THE VESICAL AND URETRAL WALLS  FIBROSIS .THIS LEADS TO FUNCTIONAL BLADDER NECK OBSTRUCTION HYDROURETER AND HYDRONEPHROSIS CAN ENSUE ALSO CALCIFICATION OF THE URINARY TRACT AND BLADDER AND THUS RENAL FAILURE. S.HEAMATOBIUM IS ALSO ASSOCIATED WITH LIVER FAILURE.
  • #22 PLATELET DERIVED GROWTH FACTOR == PDGF TRANSFORMING GROWTH FACTOR == TGFS
  • #26 IN ADDITION TO THE DIRECT INVASION OF THE URINARY SYSTEM, INFECTION WITH ANY SCHISTOSOMAL SPECIES CAN BE ASSOCIATED WITH IMMUNE COMPLEX DEPOSITION IN THE KIDNEYS, LEADING TO PROTEINURIA AND THE NEPHROTIC SYNDROME SYMPTOMS IN FEMALE PATIENTS INCLUDE HYPERTROPHIC AND ULCERATIVE LESIONS OF THE VULVA, VAGINA, AND CERVIX [6]. INVOLVEMENT ON THE OVARIES OR FALLOPIAN TUBES CAN LEAD TO INFERTILITY. IN MEN, THE EPIDIDYMIS, TESTICLES, SPERMATIC CHORD OR PROSTATE CAN BE INVOLVED
  • #27  SYMMERS PIPE STEM FIBROSIS WITH NO FINDINGS OF HEPATOCELLULAR DYSFUNCTION UNLIKE LIVER CIRRHOSIS DIFFUSE COLLAGE DEPOSITS IN THE PERIPORTAL SPACES LEADS TO PATHOGNOMONIC PERIPORTAL OR "SYMMER'S PIPESTEM FIBROSIS“ WITH ACCOMPANYING SPLENOMEGALY AND PORTAL HYPERTENSION. HOWEVER, HEPATOCELLULAR FUNCTION REMAINS NORMAL.
  • #29 FOR PREGNANT WOMEN THERE IS INCREASED RISK OF ANEMIA ,LOW BIRTH WEIGHT, SINCE MATERNAL HEALTH IS LINKED TO GESTATIONAL OUTCOMES, SCHISTOSOMIASIS MAY POTENTIALLY IMPACT FETAL HEALTH THROUGH ITS DETRIMENTAL EFFECTS ON THE HEMATOLOGIC AND NUTRITIONAL STATUS OF THE MOTHER
  • #37 Rpm ==REVOLUTIONS PER MINUTE
  • #43 Dispatch of stools for detection of parasites Stools may be sent to a specialized laboratory for the identification of rare parasites that are difficult to recognize. In such cases a preservative should be added to the specimens before they are dispatched for examination. The following preservatives are used: — formaldehyde, 10% solution (reagent no. 28), for wet mounting; — Lugol iodine, 0.5% solution (reagent no. 37); — polyvinyl alcohol (PVA) fixative (reagent no. 44); — thiomersal–iodine–formaldehyde (TIF) fixative (reagent no. 58), for wet mounting
  • #62 IF LIVER FUNCTION TEST RESULTS ARE ABNORMAL, LOOK FOR OTHER CO-INFECTIONS OR DISEASES ANTIBODY TESTING IS EPIDEMIOLOGICALLY USEFUL BUT CANNOT BE USED TO DIFFERENTIATE ACTIVE AND PAST ILLNESS. IT ALSO DOES NOT ALLOW QUANTIFICATION OF EGG BURDEN. SEROLOGIC FINDINGS CAN BE USED TO REACH A DIAGNOSIS IN A PATIENT FROM A NONENDEMIC AREA, BECAUSE A NEGATIVE ANTIBODY TEST RESULT WOULD BE EXPECTED. WESTERN BLOT TESTS ARE OFTEN USED TO CONFIRM ELISA RESULTS ANTIBODY TESTS ARE GENERALLY NEGATIVE DURING THE ACUTE PRESENTATION OF KATAYAMA SYNDROME, ALTHOUGH SEROLOGY OFTEN BECOMES POSITIVE BEFORE EGGS BECOME DETECTABLE. SEROCONVERSION GENERALLY OCCURS 4-8 WEEKS AFTER INFECTION
  • #63 IF LIVER FUNCTION TEST RESULTS ARE ABNORMAL, LOOK FOR OTHER CO-INFECTIONS OR DISEASES ANTIBODY TESTING IS EPIDEMIOLOGICALLY USEFUL BUT CANNOT BE USED TO DIFFERENTIATE ACTIVE AND PAST ILLNESS. IT ALSO DOES NOT ALLOW QUANTIFICATION OF EGG BURDEN. SEROLOGIC FINDINGS CAN BE USED TO REACH A DIAGNOSIS IN A PATIENT FROM A NONENDEMIC AREA, BECAUSE A NEGATIVE ANTIBODY TEST RESULT WOULD BE EXPECTED. WESTERN BLOT TESTS ARE OFTEN USED TO CONFIRM ELISA RESULTS ANTIBODY TESTS ARE GENERALLY NEGATIVE DURING THE ACUTE PRESENTATION OF KATAYAMA SYNDROME, ALTHOUGH SEROLOGY OFTEN BECOMES POSITIVE BEFORE EGGS BECOME DETECTABLE. SEROCONVERSION GENERALLY OCCURS 4-8 WEEKS AFTER INFECTION ANTIGEN TESTS ==BECAUSE THESE TESTS MEASURE PARASITE ANTIGEN AS OPPOSED TO HOST ANTIBODY RESPONSE, THEY REFLECT ACTIVE INFECTION. THE TESTS ARE STILL INVESTIGATIONAL. WITH EFFECTIVE TREATMENT A REDUCTION IN ANTIGENEMIA IS EXPECTED. ANTIGEN TITERS ALSO CORRELATE WELL WITH THE DETERMINATION OF INFECTION INTENSITY BY EGG COUNTS AND WITH CLINICAL SEVERITY OF DISEASEANTIGEN TITERS CAN BE USED TO ASSESS TREATMENT EFFICACY POSTTHERAPY, SINCE LOSS OF CIRCULATING ANTIGENS INDICATES CURE. ANTIGEN TESTS MAY BECOME NEGATIVE AS EARLY AS 5 TO 10 DAYS POSTTREATMENT
  • #64 A CT OR MRI SCAN OF THE BRAIN AND SPINAL CORD MAY SHOW LESIONS IN CNS SCHISTOSOMIASIS. NODULAR AND RING-ENHANCING LESIONS WITH SURROUNDING EDEMA ARE SEEM ON CT AND MRI BRAIN SCANS. EGGS REACH THE LOWER SPINAL CORD THROUGH THE BATSON PLEXUS WITH S HAEMATOBIUM AND S MANSONI INFECTION. THESE PRODUCE GRANULOMATOUS LESIONS OF THE CAUDA EQUINE AND CONUS MEDULLARIS.
  • #66 CANNOT BE USED PROPHYLACTICALLY. HIGH RE INFECTION RATES REGARDING PREGNANCY NO ADEQUATE WELL CONTROLLED STUDIES PEADIATRICS PATIENTS SAFETY IS NOT ESTABLISHED FOR CHILDREN UNDER 4YEARS ,HOWEVER WHO SUGGESTS TREATMENT IS EFFECTIVE AS YOUNG AS 1YEAR NOTE – OXAMNIQIUNE, METRIRONATE LUCANTHONE,NIRIDAZOLE,HYCANTHONE ARE NO MORE RECOMMENDED
  • #67 Surprisingly, patients with hepatic and urinary disease, even with fibrosis, may improve significantly over months or years following treatment.
  • #68 4-SNAIL CONTROL: A. PHYSICAL METHODS: – DRYNESS OF CANALS OR USE ALTERNATE CANALS (WINTER CLOSURE PERIOD). – PERIODIC CLEARANCE OF CANALS FROM M VEGETATIONS AND WEEDS. – PITCHING CANAL BANKS WITH CONCRETE TO PREVENT GROWTH OF AQUATIC PLANTS. –WIRE SCREENS AT INLETS OF CANALS TO PREVENT & COLLECT SNAILS. B.BIOLOGICAL METHODS: – NATURAL ENEMIES OF SNAILS E.G BIRDS (DUCKS, GEESE) OR SNAILS (MARISA). – CERTAIN TOXIC PLANTS E.G BALANITES AEGYPTIACA AND AMBROSA MARITIMA (DAMSISA). – PATHOGENS: INFECTION OF SNAILS BY MIRACIDIA OF AVIAN SCHISTOSOMIASIS TO DECREASE ITS VITALITY. C. CHEMICAL METHODS (MOLLUSCICIDES): – COPPER SULPHATE: 10-20 PPM. – SODIUM PENTACHLONOPHENATE : 5- 10 PPM. – BAYLUCIDE: 2 PPM. • THE FIRST ONE IS WIDELY USED IN EGYPT. IT IS NOT EFFECTIVE AGAINST EGGS OF SNAILS, SO IT SHOULD BE REAPPLIED EVERY 3 MS TO KILL NEWLY HATCHED SNAILS OR APPLIED AS A CHEMICAL BARRIER AT INLET OF CANAL TO GIVE A CONCENTRATION OF 0.5 PPM