Schistosomiasis infection and clinical presentation.pptx

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1. Case discussion on schistosomiasis Presenter Alemnew T(R3) Moderator Dr Segenet (consultant Internist and Endoscopist)

2. Outline Case presentation History physical exam and investigation Schistosomiasis Epidemiology and life cycle Pathogenesis Clinical feature and diagnosis management

3. Identification MRN 1218585 Age 30 years Sex male Occupation farmer Address Adrkay

4. History This is a 30 years old male patient LRH 8 months back at which time he develops abdominal swelling and bloody vomiting for this he visit debark general hospital where he was give IV fluid and PO medication likely diuretics from his explanation and he was referred to our hospital but he denies referral and went home, then the abdominal swelling improved. 2months back he was having similar complaints and he visit again same hospital then transfused blood and sent home. Currently referred from Debark general hospital with Dx of UGIB 2 nd to? For better IVx & Mx after he presented with 3 episode bloody vomiting with coffee ground appearance of 1 day duration. each episode estimated to be around 700ml. He had also Hx of initially black tarry stool then bloody diarrhea(frank blood) of same duration. Associated to this he was having light headedness and easy fatigability.

5. CONT. Had also Hx of HGIF of same duration He usually swims at local river and had Hx of generalized body itching around 10 years ago that resolve by it self. Had also Hx of burning type of epigastric pain and repeatedly treated for gastritis. Had also Hx of repeated malarial attack Drinks alcohol occasionally Otherwise no Hx of LOC or ABM No hx of jaundice No hx of urinary complaint No hx of cough or chest pain No hx of DM, HTN, renal or cardiac illness

6. Physical examination GA .. ASL VS.. BP =90/60, PR =120 ,RR =20 ,T 37.7 SPO2 96%ATM HEENT, pale conjunctiva NIS Abdomen flat moves with respiration spleen is palpable 6cm along its line of growth IGS, has some palmar pallor

7. Investigations Investigations 09/ 11 / 202 4 9 /14/ 202 4 9 /16/ 202 4 CBC WBC = 3960 N=67.2% L=19% Mon=12.3% Hg = 6.2 MCV= 64.3 Plt = 85K WBC = 250 N=55.8% L=26.2% Mon=14.7% Hg = 1.2 Mcv 66.1 Plt = 11k WBC = 3200 N=61.4% L=20% Mon= 12.4 Hg=7.7 Mcv =68.9 Plt = 91k RBS=120mg/dl BG=B+ HBSAg…Neg HCVAb…Neg BF…Trophozoit of p,vivax AST=33 ALT=18 PT=20.5 INR=1.75 Cr=0.98 Urea=17 Stool no O/P seen Stool h,pylori ..neg Na=127 K=3.9 7

8. Cont. PM RBC = anisopoikilocytosis ,normochromic WBC :- count decreased Neutrophil=57% no hypersegmentation Lymphocyte=43% No blast PLT =decreased

9. Cont. UGI endoscopy Esophagus large dilated high risk esophageal veins seen. Stomach mosaic vascular lesions and dilated submucosal veins at the fundus. Conclusion F3 GOV1, mild portal HTN gastropathy

10. Cont. Abdominal ultrasound Liver has normal size(13.8cm) and surface There is pericholecystic and periportal fibrosis Portal vein is dilated 17mm but normal velocity. Spleen enlarged measuring length of 18cm There are randomly distributed small echogenic nodules( gamna gandy bodies) otherwise normal surface There is anechoic intraperitoneal fluid collection largest measuring 3cm depth on Lt paracolic space. There is long segment symmetric circumferential bowel wall thickening involving splenic flexure, descending colon and proximal sigmoid colon, maximum thickness measuring 4mm. Index Splenomegaly+Ascites 2 nd to likely HSS+ long segment bowel wall thickening 2 nd to likely infectious colitis

11. Diagnosis P1 =HSS with Cxn(portal HTN ,variceal bleeding ,splenomegaly with hypersplenism) +infectious colitis R/o intestinal schistosomiasis P2 =malaria

12. Management 2 unit of blood transfused Omeprazole 80 loading then 40mg IV BID Spironolactone 50mg PO daily Propranolol 40mg PO BID ceftriaxone Artesunate Primaquine Praziquantel EVL appointed

13. Schistosomiasis epidemiology Human schistosomiasis is an acute and chronic parasitic disease caused by infection with blood flukes (trematode worms) of the genus Schistosoma . reported from 78 countries. About 230 million persons worldwide are infected. 236.6 million people required preventive treatment worldwide in 2019.

14. Cont. Seven species of Schistosoma are responsible for the two major forms of the disease (intestinal and urogenital schistosomiasis). S. mansoni , S. japonicum , S. mekongi , S. guineensis and S. intercalatum S.malayensis S. haematobium causes urogenital schistosomiasis. cause intestinal schistosomiasis

15. pathogenesis clinical disease is caused by the host immune response to migrating eggs . Migration of eggs through tissues can be associated with entrapment, inflammation, and subsequent fibrosis. Adult worms absorb host proteins and coat themselves with host antigens, allowing prolonged residence in the bloodstream with evasion of immune attack.

16. Cont. The course of infection divided to three phases: Migratory Acute and Chronic

17. migratory phase-phase 1 Swimmer's itch   (cercariae dermatitis). Is a pruritic papular or urticarial rash at the site of larval entry. The rash is a hypersensitivity reaction that occurs with repeat exposure (never with initial exposure) Usually to non-human schistosome species Rash clears with few days and Mx is supportive care for pruritus

18. Acute phase( Katayama syndrome) Due to host immunologic response to eggs & mature worms Occurs approximately 4-6 weeks after exposure. Occurs almost exclusively among non-immune hosts such as travelers and may be observed in more than half of infected individuals. Should be considered in a patient with; A history of exposure √ Abdominal pain Diarrhea √ Fever Manifestations include headache, fever, chills, cough, diarrhea, myalgias, arthralgias, tender hepatomegaly, and eosinophilia.

19. Diagnosis Nonspecific tests – population screening Fecal occult Urine dipstick for heme Serum eosinophil count Specific tests Ova detection – urine , stool , rectal snips 6-12 week after infection Infection intensity - Mild, moderate, severe for stool sample - Light-moderate, severe for urine sample Serology Negative antibody test is useful for ruling out infection in endemic settings PCR: serum, feces, and urine More sensitive than serology in early infection (<3Mos) Antigen tests (CCA, CAA): from urine/serum

20. Management Prednisolone 1mg/kg/day, until symptoms subside & for 48 hrs thereafter (typically 3-10 days). Subsequently Praziquantel after 8-12 wks. of exposure together with 1mg/kg/day of prednisolone for 3 days Retreatment after 2-3 mnths is often necessary after Katayama fever

21. Chronic schistosomiasis Occurs in subsequent months in response to the deposition of schistosome eggs in tissues and the host reactions against them. Common among individuals in endemic areas The severity of disease is related to The number of eggs trapped in tissues Anatomic distribution The duration The host immune response The nature of clinical manifestations depends on the organ tropism of the infecting species

22. Eggs are deposited in the large intestine, especially in the; Rectum Sigmoid Descending colon most common symptoms are abdominal pain, poor appetite, and diarrhea Colonic ulceration lead to intestinal bleeding Intestinal polyps and dysplasia Bowel strictures , Obstruction , acute appendicitis Intestinal schistosomiasis  

23. Case report colonic schistosomiasis A 19-year-old male in Addis Ababa (Ethiopia) with an 8-month history of recurrent abdominal pain, loss of appetite, and occasional blood in the stool . Physical and basic laboratory examinations, including liver enzymes, were unremarkable. The stool examination was negative for ova and parasites. The abdominal ultrasonography results were normal. A colonoscopy was performed with a working diagnosis of inflammatory bowel disease . The examination revealed a patchy mucosal erythema with scattered nodularity and multiple vascular lesions in the ascending colon, sigmoid, and rectum Colon biopsies revealed multiple  Schistosoma  eggs with surrounding eosinophilic inflammation and granuloma . It was noted that the patient resides in Bahir Dar, On inquiry, the patient reported a history of swimming in the lake and washing clothes in the river.

24. Cont. The patient was treated with one dose of oral praziquantel 40 mg/kg. He reported complete resolution of symptoms during a clinic visit 2 weeks later

25. Case report from morocco a 21-year-old male who suffered from chronic diarrhea and abdominal pain. Physical examination found no abnormalities, blood tests were normal, and stool examination was negative. A colonoscopy revealed a nodular terminal ileal mucosa, two cecal polypoid lesions with no particular surface pattern, and millimetric erosions in the rectum . on histopathological examination Schistosoma  eggs with thick peripheral capsules and viable embryos inside and numerous eosinophils surrounding the egg capsule were observed .

26. Cont. Final Dx Colonic schistosomiasis The patient received praziquantel, and his symptoms were resolved.

27. hepatosplenic schistosomiasis Early inflammatory hepatosplenic schistosomiasis Mainly seen in children and adolescents. Reversible with treatment Late hepatosplenic schistosomiasis with periportal or Symmers pipestem fibrosis Develop in adults with long-standing, high-level exposure to infection. Patients with periportal fibrosis may excrete very few or no eggs in feces. Partially reversible Variceal bleeding is the most severe complication Hepatic encephalopathy, ascites, and liver failure are uncommon

28. Liver Parenchyma patterns and IP scores

29. Treatment Reduction of parasitic load Praziquantel 40mg/kg stat; S. Mansoni, S. haematobium 60mg/kg with divided dose for S. japonicum In endemic areas, a single dose of praziquantel is curative in 20 to 100% of cases Among individuals who are not cured, praziquantel reduces the parasite burden by more than 90% Presence of viable eggs 6 to 12 weeks after initial therapy warrants repeat treatment with praziquantel Antimalarial drugs: Oxamniquine & dihydroartemisinin-piperaquine Effective against the juvenile stages of schistosome species Prevention of variceal hemorrhage: non-selective BB

30. Those who are likely reversal are children and adolescents and early disease

31. Surgery For recurrent bleeding despite NSBB and EVL To avoid re bleeding keeping liver function preserved Avoiding encephalopathy Treating hypersplenism Surgical options Distal splenorenal shunt (Warren operation) EGDS (Esophagogastric devascularization with splenectomy) TIPS- Transjugular intrahepatic portosystemic shunt placement At risk for hepatic encephalopathy

32. There is no difference in overall mortality Variceal rebleeding following devascularisation is statistically significant higher than after DSRS DSRS is associated with a statistically significant higher post procedure encephalopathy Portal vein thrombosis, hemolysis, ascites and shunt dysfunction are serious complications of the procedures

33. Occur most frequently among patients with hepatosplenic disease Embolization of schistosome eggs into the pulmonary circulation via portosystemic collaterals Eggs can cause granulomatous pulmonary endarteritis CXR = fine milliary nodules Cause pulmonary hypertension and cor pulmonale These manifestations represent end-stage disease and are generally irreversible Pulmonary complications  

34. Due to S. haematobium or hybrids The eggs provoke granulomatous inflammation, ulcerations, and development of pseudopolyps , fibrosis and calcification Hematuria ,dysuria Can result in infertility , increased risk for HIV transmission , hydronephrosis , bladder Ca Female genital schistosomiasis Vulva ,vagina , cervix , fallopian tubes and ovary can be affected Genitourinary schistosomiasis 

35. Cont. Male genital schistosomiasis involve the epididymis , testicles , spermatic cord , prostate Painful ejaculation , hemospermia ,perineal pain Biopsy - visualization of schistosome eggs Ultrasonography IVP = strictures , hydronephrosis Urinary tract lesions are reversible with treatment prior to onset of fibrosis and calcification

36. Glomerular schistosomiasis asymptomatic and self-limited glomerular disease may be relatively common patients with MPGN (class III), the most common histologic form , frequently present with features of both nephrotic and nephritic syndrome . Such patients generally have hematuria (82 %), HTN(71%), and low C3 levels (65%). Nephrotic syndrome (without nephritic syndrome) can be the presentation in patients with a histologic pattern of FSGS; class IV), Unlike other causes of nephrotic syndrome, despite severe hypoproteinemia, serum lipid concentrations are usually low due to associated nutritional deficiency and hepatic dysfunction

37. Cont. Diagnosis clinical suspicion in a patient presenting with kidney disease who has known  S. mansoni  infection, exposure to an endemic area, or clinical evidence of chronic HSS. Stool exam/Urine analysis Renal biopsy A definitive diagnosis requires identification of parasitic antigens in the glomeruli Treatment Praziquantile +/- antibiotics Immunosuppressive therapy for class VI coinfection with HCV Class I&II reversible Other classes are progressive to end stage renal disease

38. Neuro-schistosomiasis Is a medical emergency Occurs when adult worms embolize/migrate to CNS or spinal cord The granulomatous reaction to ova is major factor for pathogenesis

39. Cont. Patient may present with Focal and generalized seizure Headache Increased ICP in cerebellar schistosomiasis Eosinophilic meningitis Myeloradiculopathy with lower limb and back pain Bladder dysfunction, paresthesia and weakness Transverse myelitis

40. Stool Brain/spinal MRI: nonspecific contrast-enhancing infiltrates : characteristic arborization pattern PCR from CSF Abnormal CSF High protein, pleocytosis, eosinophil Rarely from brain/spinal cord biopsy Diagnosis

41. (A) Sagittal T2-weighted MRI shows diffuse signal prolongation and expansion of distal spinal cord and conus (arrow). (B) Sagittal contrast-enhanced T1-weighted MRI shows central linear enhancement surrounded by multiple punctate enhancing nodules (arrows) that form masslike structure 32-year-old man with cerebral schistosomiasis: (A) Axial contrast-enhanced T1-weighted MRI shows punctate multinodular enhancement pattern surrounding central linear enhancement. (B) Sagittal contrast-enhanced T1-weighted MRI confirms linear (arrow) and nodular enhancement pattern in different imaging plane. (C) Axial T2-weighted MR image shows hyperintense mass (arrow) with surrounding vasogenic edema involving right parietal lobe

42. Corticosteroid Prednisone 1 to 2 mg/kg for 2-6 months Praziquantel (40 mg/kg single dose) A few days after initiation of corticosteroid treatment Treatment

43. Prevention Comprehensive integrated control program Preventive chemotherapy Snail control Applications molluscicides (Niclosamide, copper sulfate ) to eliminate snails Promotion of health education, access to safe water, and sanitation Vaccines development

44. Summary of recommendations

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48. Reference Up-to-date 2024 Harrison 21 edition WHO US practice guideline WHO schistosomiasis prevention and control guideline Google scholar

49. THANK YOU