Se ha denunciado esta presentación.
Se está descargando tu SlideShare. ×


Próximo SlideShare
Cargando en…3

Eche un vistazo a continuación

1 de 75
1 de 75

Más Contenido Relacionado

Audiolibros relacionados

Gratis con una prueba de 30 días de Scribd

Ver todo


  1. 1. Presentation contents  Introduction.  History & epidemiology.  Types & Morphology.  Life cycle.  Pathogenesis.  Immunology.  Clinical features.  Investigations.  Treatment.  Complications.  Management of complications.  Prevention & Control.
  2. 2. Schistosomiasis or ( Snail Fever ) is an important cause of disease in many parts of the world, most commonly in places with poor sanitation. School-age children who live in these areas are often most at risk because they tend to swim or bath in water containing infectious cercariae. If you live in, or travel to, areas where Schistosomiasis is found & are exposed to contaminated freshwater, you are at risk.
  3. 3. Areas where human Schistosomiasis is found include: S.Mansoni & S.Haematobium distributed throughout Africa. There is risk of infection in freshwater in southern & sub- Saharan Africa–including the great lakes & rivers as well as smaller bodies of water.
  4. 4. In Sudan specially, due to agriculture & irrigation of cannels creating a favorable environment for snails. The highest Schistosoma prevalence is in: - Al-Jazeera state. - White Nile state. - River Nile state specially after Marawi dam.
  5. 5. Transmission also occurs in the Nile River valley in Sudan, Egypt & the Maghreb region of North Africa. South America: including Brazil, Suriname, Venezuela Caribbean. In areas of East of Asia: S. japonicum found in Indonesia, parts of China & Southeast Asia. S.Mekongi found in Cambodia & Laoss. Intercalatum found in parts of Central & West Africa.
  6. 6. .. Main types that affect humans ..
  7. 7. Schistosoma Haematobium: - Causes urogenital Schistosomiasis. - It is scattered throughout Africa, parts of Arabia, the Near East, Madagascar and Mauritius. Schistosoma Mansoni: - Is mainly found in Africa & Madagascar. - It was exported by the slave trade to parts of South America, the Caribbean & Arabia, where permissive snail intermediate hosts were present.
  8. 8. First discovered in JAPAN, Nowadays is found in China, the Philippines & Sulawesi. There’s also a small focus in the Mekong river on the east border of Thailand caused by Schistosoma Mekongi. Schistosoma Mansoni & S. japonicum cause disease of the bowel & liver. Schistosoma Intercalatum.
  9. 9. Adult worms in humans reside in the mesenteric venules in various locations, which are specific for each species: S. Japonicum is more often in small intestine. S. Mansoni occurs more often in the superior mesenteric veins draining the large intestine. S.Haematobium most often occurs in the venous plexus of bladder & uterus, but it can also be found in the rectal venules.
  10. 10. S.Intercalatum: which found in urine & it’s related to S.Haematobium. S.Bovis: which infects cattle. S.Makongi: similar to S.japonicum.
  11. 11. Adult schistosomes are white greyish worms. ( 6 – 28 ) mm long & in breadth of ( 0.25 – 1 ) mm. Schistosomes have separate sexes ( male & female ). Both have an oral sucker opening into the alimentary tract, & a posteriorly situated sucker.
  12. 12. Flat in shape. It has a large ventral groove ( gynaecophoric canal ), encloses the female during pairing. The digestive system consists of short esophagus opening into an intestine. The male reproductive system comprises 4 or 5 pairs of testes.
  13. 13. Cylindrical in shape. More longer, slender & much darker color than male. The digestive system is similar to that of male. The reproductive system consist of a pear shaped ovary in the mid body line.
  14. 14. The different schistosomes spices use different spices of snails as intermediate host:
  15. 15. Stages of life cycle & their time frames: (1) Cercarial invasion & Schistosomular migration. (2) Maturation of schistosomes, pairing & commencement of egg-laying. (3) Established infection with continuous egg-laying. (4) Late stages & complications.
  16. 16. The clinical complement of cercarial dermal invasion is a schistosome ( cercarial or allergic ) dermatitis lasting for 24 - 48 hours. The pathophysiological response is the initiation of the 1st mechanisms of the immune response with marked eosinophilia & an antibody-dependent cell mediated cytotoxic response involving IgG.
  17. 17. After 2 to 16 weeks after cercarial invasion, during the migration of schistosomulae, their maturation, pairing & initiation of egg-laying, the clinical manifestations of acute toxemic Schistosomiasis ( katayama syndrome ) may arise. Worm or egg antigens produce a marked antigenic stimulus with rapidly rising antibody levels & an increase in serum IgG, IgA & IgM levels.
  18. 18. Then circulating antigen antibody complexes are found & may be deposited in glomeruli, producing immune complex glomerulopathy. The whole clinical picture is one resembling the acute serum sickness syndrome. From 2 months onwards the stage of established infection occurs, with continuous egg-laying associated with the classical symptoms & signs of established Schistosomiasis.
  19. 19. SEAs from miracidia in the eggs provoke a T lymphocyte-mediated host response which in time result in the characteristic granuloma with eosinophils prominent in the destruction of the eggs. After some years, change in clinical symptoms & physical sign appear, & there is superimposi- tion of late stage complication such as: Obstructive Uropathy, Hydronephrosis & Pyelonephritic renal failure.
  20. 20. Overtime T suppressor lymphocyte & antibody blockade diminish the host immune response fibroblasts stimulate collagen production and fibrotic complications involving a variety of anatomical sites will developed ( e.g. periportal hepatic fibrosis and obstructive Uropathy ).
  21. 21. Acute Schistosomiasis It is a systemic hypersensitivity reaction against the migrating schistosomulae and/or the onset of egg production, occurring within a few weeks to months after a primary infection. The onset is sudden, with: - Fever & Myalgia. - Fatigue & Malaise. - Nonproductive cough. - Elevated IgE. - Patchy infiltrates on chest X-Ray.
  22. 22. Most patients recover spontaneously after 2-10 weeks but some develop a persistent & serious illness with: Weight loss. Dyspnea. Diarrhea. Diffuse abdominal pain. Toxemia. Hepatosplenomegaly. Generalized rash. Intense infections are occasionally fatal.
  23. 23. Katayama fever caused by S.japonicum infections can present as serious & sometimes fatal, serum sickness- like disease which possibly results from the early release of large quantities of egg antigens that cross- reacts with antibodies to schistosomulae, resulting in immune complexes that cause hypertrophy of lymph reticular tissue characterized by: Fever. Hepatosplenomegaly. Cachexia. Which may evolve directly to severe hepatosplenic fibrosis & portal hypertension.
  24. 24. Chronic Schistosomiasis: It is largely associated with the granulomatous & fibrotic responses to Schistosoma ova during mature infections and mainly include: A- Urinary Schistosomiasis. B- Intestinal Schistosomiasis.
  25. 25. Urinary Schistosomiasis: The eggs of S. haematobium provoke granulomatous inflammation, ulceration and pseudopolyposis of the mucosa & sub mucosa of the bladder and the ureters Common early symptoms include Dysuria, Urinary frequency & urgency, Terminal hematuria. In endemic areas ( Terminal hematuria ) is the “red flag of Schistosomiasis” in children between the age of 5 and 10 years old.
  26. 26. Chronic infection may lead to: - Obstructive Uropathy. - Renal failure. - Bladder cancer ( SCC ). Intestinal Schistosomiasis: The eggs of S. Mansoni, S. japonicum & other species migrate through the intestinal wall where they provoke mucosal granulomatous inflammation, pseudopolyposis, micro-ulcerations & superficial bleeding. Most lesions are situated in the large bowel & the rectum.. small bowel pathology is rare.
  27. 27. The human immune response in Schistosomiasis is primarily due to antibody-dependent cell- mediated cytotoxicity. So based on the mixture of preformed circulating antibodies, cytokines & the responsiveness of lymphoid cells in the peripheral blood.
  28. 28. 4 to 6 weeks after a primary infection, schistosome- specific immunoglobulin is produced that, together with complement, eosinophils, macrophages, platelets & mast cells is able to form complexes & attack schistosomules. Acute Schistosomiasis: It occurs in individuals who have no previous history of exposure & become infected after travelling into an endemic area.
  29. 29. There is a remarkable level of peripheral- blood mononuclear cells (PBMCs) produce large quantities of tumor-necrosis factor (TNF), interleukin-1 (IL-1) and IL-6, reflects a dominant T helper 1 (TH1), rather than TH2 response.
  30. 30. There was a correlation between elevated levels of nitric oxide ( NO ) & disease severity, which indicates that a combination of reactive oxygen & nitrogen intermediates might have a role in acute disease.
  31. 31. TH2 responses seem to have a crucial role in modulating potentially fibrosis life- threatening chronic disease. The main TH2 cytokine that is responsible for fibrosis is IL-13. Chronic Schistosomiasis:
  32. 32. It has been recognized that the egg stage of the schistosome is responsible for inducing the TH2 response. TH2 induces CD4+ T-cell response that initiates the development of granulomatous lesions, which are composed of collagen fibers & cells, including macrophages, eosinophils & CD4+ T cells around the individual eggs.
  33. 33. Physical Examination: Physical findings vary with the stage of illness, worm burden, worm location, and end organ involvement.
  34. 34. Clinical Features: swimmer’s itch Acute manifestations: Generalized lymphadenopathy. Pruritic rach ( swimmer’s itch ). Mild Fever & Headache. Hepatosplenomegaly. Katayama syndrome ( ). Diarrhea. Urticaria. Cough.
  35. 35. Continue Acute manifestations: - Right upper quadrant tenderness. - Decreased physical performance. - Growth retardation. - Anorexia. - Malaise. - Myalgia. Chronic manifestations: - Pedal Edema. - Portal HTN. - Anemia. - HTN. - Renal Failure. - Easy fatigability. Pedal Edema
  36. 36. Abdominal pain. Abdominal distention. Signs of malnutrition. Hepatosplenomegaly. Distended abdominal veins. Ascites, Pallor, & Dysentery. Intestinal Schistosomiasis:
  37. 37. Cardiopulmonary Schistosomiasis: Cor pulmonale with signs of right HF. Larval pneumonitis with cough. Mild wheezing. Low grade fever. Palpitations. Dyspnea on exertion. Hemoptysis.
  38. 38. Focal & generalized seizures. Headache. Spinal cord lesions. Symptoms of increased intracranial pressure ( ICP ). CNS Schistosomiasis: Focal Seizure Generalized Seizures
  39. 39. Dysuria. Urinary frequency. Terminal Hematuria. Burning in micturition. Urinary frequencyHematuria
  40. 40. Genital Schistosomiasis: - Postcoital bleeding. - Genital ulcerations. - Nodular lesions of the cervix & vagina. - Hypertrophic lesions. - Pelvic pain.
  41. 41. Laboratory Diagnosis & Imaging Samples: - Stool. - Urine. - Serum. Macroscopic: - Stool speciment ( may be dysenteric ). - Urine speciment ( may be terminal hematuria ).
  42. 42. Microscopically: 1- Demonstration of parasite eggs in stool or urine is gold standard test for diagnosing Schistosomiasis. 2- The sensitivity my be low especially with light infection & take 6 weeks for eggs to be detect after the initial infection. 3- S.Haematobium eggs are usually found in urine but my also be present in stool. 4- S.Mansoni & the other intestinal schistosomes, S.japonicum, S.Merangi & S.Intercalatum are found in stool.
  43. 43. laterally
  44. 44. URINE DIPSTICK: S.Haematobium infections are usually associated with hematuria on dipstick testing.
  45. 45. Full blood count: 1- May show an eosinophilia which is frequently marked during the acute stage of infection. 2- Anemia patient may also be seen due to chronic blood loss from the urinary or intestinal tract. 3- Pation with hepatosplenic Schistosomiasis my have thrombocytopenia secondary to splenic sequestration. Diagnosis can also be made by demonstrating eggs in tissue biopsy specimens from the rectum, liver, bladder or cervix depending on the site of infection.
  46. 46. Antigen detection:  Schistosoma the antigen weaks are present in the serum & urine.  To antigen referred to as circulating anodic antigens (CCA) & circulating cathodic antigens ( CCA ) can be detected in laboratory sensitivity of these test depend on largely & intensity of infection. Antibody test:  Schistosoma antibodies can be detected by enzyme linked lmmunosorbent assay ( ELISA ).  it is application is limited as these antibodies will only appear after 4-6 weeks.  present of IgE antibody is marked of chronic active disease.
  47. 47. Polymerase chain reaction PCR: Specific & highly sensitive detection of Schistosoma. DNA in urine, stool & serum. Advantage able to diagnosis Schistosomiasis in all stage of infection.
  48. 48. ( For S.Haematobium ) look for signs of hematuria, Dysuria, & Eosinophilia. These should be enough to suggest a diagnosis for those living in endemic regions. A plain X-ray for the abdomen may show the calcification of the urinary bladder. An I.V.P should be done to determine the extent of the disease in the kidneys & ureters. The changes in the urinary system are usually reversible on treatment.
  49. 49. Fatigue. Abdominal pain even without dysenteric symptoms in endemic regions should suggest a diagnosis. Dysenteric symptoms. A chest x-ray is indicated in a patient who comes in with signs of pulmonary hypertension ( mottling of the lungs is seen ). ( For S.Mansoni )
  50. 50. A Barium meal or endoscopy is used to detect any varices. A liver biopsy is indicated to show periportal fibrosis. splenic-venoprtography may be done to outline the portal system.
  51. 51.  Praziquantel affective against all adult schistosome species & it has no side effects.  In the treatment of a patient of S. Haematobium or S. Mansoni or S. Intercalatum a single oral dose ( 40 mg/kg ).  But the S.japonicum total dose is ( 60 mg/kg ), Best given after food.  Cure rate is 80% !! With acute infection corticosteroids may given
  52. 52. Oxamniquine Only against S.Mansoni. - High cure rates ( 60 - 90% ). Side effects: dizziness, drowsiness, headache. - Should not be given during the first 4 months of pregnancy. Metrifonate against S.Haematobium. - Artemisinin. - Hycanthone ( Etrenol ). - Niridazole ( Ambilhar ). - Lucanthone ( Mirasil D ). OtherDrugs
  53. 53. Complications: 1- pulmonary Schistosomiasis: Chronic S.Mansoni causing obliterative arteries which lead to : - Pulmonary hypertension. - Increase right heart pressure. - Right arterial dilatation. - Right ventricular hypertrophy. 2- Glomerularnephritis: Due to deposition of immune complex in the renal glomeruli. May be asymptomatic or manifested as nephrotic syndrome.
  54. 54. 3- Genital: - In female lead to infertility. - In male causing hemospermia. 4- Neuroschistosomisis: S.Haematobium & S.Mansoni caused spinal cord & transverse myelitis. Others: - Paraplegia. - Pain or loss of sensation. - Skin rash. - Personality change. - Confusion.
  55. 55. Complication of Schistosomiasis in GIT : Gastrointestinal bleeding this case in patient with nonvariseal upper gastrointestinal bleeding induced by gastric & duodenal involvement of Schistosoma Mansoni which unique case sever & recurrent upper gastrointestinal bleeding was induced by central ulceration of gastric pseudopolypoid & duodenal polypoid lesions.
  56. 56. • portal hypertension as complication are due to mechanical obstructive pathology resulting from periportal fibrosis where eggs are still found. • Hepatitis due to chronic S.Mansoni infected patient co infected with hepatitis B or C are prone to have clinically more sever infection prior parenteral treatment for Schistosomiasis my also have substantially increased risk for hepatitis.
  57. 57. Complication of Schistosomiasis in pregnancy: 1- Associate with anemia and low birth weight. 2- High risk of ectopic pregnancy. 3- Pregnancy complication from uvular or fallopian granuloma. Schistosomiasis-associated Bladder Cancer: Bladder cancer diagnosis & mortality are elevated in affected area. Risk of bladder cancer appear to be high in smokers due to chronic irritation of bladder lining allowing it to be exposed to carcinogens from smoking.
  58. 58. Bleeding form esophageal varices may be treated systematically with β-blockers, endoscopy, Splenectomy, or porta caval shaunts. In advanced urinary Schistosomiasis destructed & Non-functional kidneys may have be removed.
  59. 59. Topical steroid & oral antihistamines can provide symptomatic relief for adversarial dermatitis. katayama fever is primarily treated with corticosteroids, for example: Prednisolone 40 mg daily, for 5-14 days, to suppress the hypersensitivity reaction. The treatment should be followed be Praziquantel to eliminate the adult worms.
  60. 60. Neuro anastomosis requires specialized care, again with corticosteroids and if necessary anticonvulsants prior to Praziquantel treatment.
  61. 61. Prevention & Control
  62. 62. Mass Drug Administration aims to: 1- Reducing morbidity & mortality rate due to the infection. 2- Prevent new infection by limiting transmission through reduction of the overall prevalence in the population. 3- Reduction in excretion of schistosome eggs. The administration of drugs to whole populations irrespective of disease status is referred to as Mass Drug Administration ( ).
  63. 63. Prevention: 1- Early diagnosis &Treatment. 2- Snails Control. 3- Health Education & Community Participation. 4- Water Supply & Environmental Sanitation. 5- Capacity building. Control: Is dominated by chemotherapy & molluscicides.