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Multisystem infection
- 1. Bilal Sami Al-Moshaigah Multisystem Infection
- 2. Schistosoma Mansoni Leishmania donovani Main properties Pathogenic mechanism Clinical significance Multisystem infection Laboratory diagnosis Learning Objectives
- 3. Schistosomes It causes water-borne disease constituting an important public health problem Dioecious, (sexes are separate) trematodes, Which lead to schistosomiasis (bilharziasis) Gynecophoric canal It is estimated that over 100 milion people are infected with S. haematobium, S. mansoni, and S. japonicum The female resides in a groove in the male
- 4. Schistosoma Mansoni Eggs have a prominent lateral spine Morphology Helminths
- 5. Life cycle Adult worm lives in the inferior mesenteric vein. Habitat Biomphalaria Sexual cycle Asexual cycle
- 6. Schistosoma Mansoni Pathogenesis Most of the pathologic findings are caused by the presence of eggs in the liver, spleen, or wall of the gut or bladder. Induce granulomas in liver Hepatomegaly Portal hypertension Splenomegaly S. Mansoni eggs damage the wall of the distal colon Evolved a remarkable process for evading the host defenses Their surface becomes coated with host antigens Stage of Invasion Stage of Migration Stage of Deposition Dermatitis Pass into the portal circulation Larva Adult Granulomas
- 7. Schistosoma Mansoni Clinical Findings Most patients are asymptomatic, but chronic infections may become symptomatic. The acute stage The chronic stage Begins shortly after cercarial penetration Consists of itching and dermatitis followed 2 to 3 weeks later by fever, chills, diarrhea, lymphadenopathy, and hepatosplenomegaly Usually resolves spontaneously Can cause significant morbidity and mortality Gastrointestinal hemorrhage, hepatomegaly, and massive splenomegaly can develop The most common cause of death is exsanguination from ruptured esophageal varices
- 8. Schistosoma Mansoni Laboratory Diagnosis Stool Microscopy Serological Diagnosis Rectal Biopsy Imaging Blood Examination Detect hepatosplenomegaly and periportal fibrosis May reveal eosionophilia, and increased levels of alkaline phosphatase ?
- 9. Leishmania donovani Morphology Amastigote Promastigote The parasite exists in 2 forms Amastigote form: in humans and other mammals Promastigote form: in the sandfly and in artificial culture. Protozoa belonging to the order kinetoplastida
- 10. ? Amastigote form Promastigote form
- 11. bite Other? vector Prevent fusion of the vacuole with lysosomes Life Cycle
- 12. Leishmania donovani Pathogenicity L. donovani causes visceral leishmaniasis or kala-azar and Post Kala-azar Dermal Leishmaniasis Reticuloendotheliosis resulting from the invasion of reticuloendothelial system The parasitized macrophages disseminate the infection to all ? parts of the body Spleen, liver, and bone marrow particularly The amastigotes multiply enormously in the fixed macrophages to produce a ‘blockade’ of the reticuloendothelial system Incubation period of 2 weeks - 6 months
- 13. Leishmania donovani Pathogenicity Spleen: The spleen is the most affected organ Enlarged and the capsule is thickened Soft and friable and cuts easily due to absence of fibrosis. Cut section is red or chocolate in color Liver: The Kupffer cells and vascular endothelial cells are heavily parasitized, but hepatocytes are not affected Liver function ? The liver is enlarged The sinusoidal capillaries are dilated and engorged ‘nutmeg’ appearance
- 14. Leishmania donovani Pathogenicity Bone marrow: Heavily infiltrated with parasitized macrophages, which may crowd the hematopoietic tissues Severe anemia with hemoglobin levels of 5–10 g/dL may occur in Kala-azar WBCs ? Secondary infections Reduced activity
- 15. Leishmania donovani Clinical Features of Kala-Azar The onset is typically insidious. The clinical illness begins with fever Splenomegaly Hepatomegaly and lymphadenopathy Skin becomes dry, rough, and darkly pigmented Kala-azar Cachexia with marked anemia Epistaxis and bleeding from gums are common Untreated patients die in about 2 years ?
- 16. Leishmania donovani Post Kala-azar Dermal Leishmaniasis About 3–10% cases of patients of visceral leishmaniasis in endemic areas develop PKD PKDL is a nonulcerative lesion of skin. The lesions are of 3 types Depigmented macules Erythematous patches Nodular lesion
- 17. Leishmania donovani Laboratory Diagnosis Diagnosis is usually made by detecting ? in a bone marrow, spleen, or lymph node biopsy The organisms can also be cultured Skin test Serologic (indirect immunofluorescence) tests are positive in mostpatients.
- 18. Laboratory diagnosis Clinical significance Main properties Organism Stool Microscopy Rectal Biopsy Serological Diagnosis Imaging Schistosomiasis disease (bilharziasis) Trematodes Sexes are separate Schistosoma Mansoni Examination of bone marrow, lymph node or splenic aspirates, peripheral blood for amastigotes PCR Kala-azar (visceral leishmaniasis) Post Kala-azar Dermal Leishmaniasis 2 forms (amastigotes, promastigotes) Definitive host: Human Vector: Female sandfly (Phlebotomus species). Leishmania donovani Summary
- 19. Any Question
- 20. Reference Warren E. Levinson (2014) Review of Medical Microbiology and Immunology, 13th edn., New York, United States: McGraw-Hill Education - Europe. Neal R. Chamberlain ( 2009) Medical Microbiology: The Big Picture, New York, United States: McGraw-Hill Education - Europe. Sougata Ghosh, C. K. Jayaram Paniker (2013) Paniker's Textbook of Medical Parasitology, 7th edn., Philadelphia, PA 19106, USA: Jaypee Brothers Medical Publishers (P) Ltd., 2013..
Editor's Notes
- The male worm is broader than the female The male has 6 to 9 testes, and the male genital pore opens ventrally, immediately posterior to the ventral sucker. Female has a single ovary located in the anterior portion of the body. The skin is covered with many tubercles. Have 2 suckers oral and ventral
- In the gravid female, the uterus contains very few eggs, usually 1–3 only. The prepatent period (the interval between cercarial penetration and beginning of egg laying) is 4–5 weeks. The egg has a characteristic lateral spine, more near to the rounded posterior end. The eggs are non operculated and yellowish brown.
- The epidemiology of schistosomiasis depends on the presence of the specific freshwater snails that serve as intermediate hosts. Mesenteric veins of the connections of the small intestine to the posterior abdominal membranes lining the cavity provide an anatomic site for these organisms to colonize Eggs may be emitted through either the bladder or through the intestine Sexual cycle Definitive host Asexual cycle Intermediate hosts
- due both to digestion of tissue by proteolytic enzymes produced by the egg and to the host inflammatory response that forms granulomas in the venules Schistosomes have evolved a remarkable process for evading the host defenses. There is evidence that their surface becomes coated with host antigens, thereby limiting the ability of the immune system to recognize them as foreign.
- Eosinophilia is seen in response to the migrating larvae
- A mastigote form: Rounded form multiplies in macrophages and other phagocytic cells in internal organs, skin or mucocutaneous tissues. Promastigote form: flagellated highly motile form of the parasite, found in sand fly vectors and in vitro cultures. It multiplies in the gut of the sand fly characterised by the presence of an organelle with a large massed DNA called kinetoplast (hence the name).
- Definitive host: Man, dog, and other mammals. reservoir of infection Vector: Female sandfly (Phlebotomus species). Infective form: Promastigote form present in midgut of female sandfly
- . This leads to a marked proliferation and destruction of reticuloendothelial tissue in these organs. the organs of the reticuloendothelial system (liver, spleen, and bone marrow)
- The striking enlargement of the spleen is due to a combination of proliferating macrophages and sequestered blood cells. The marked increase in IgG is neither specific nor protective.
- Blood cell production in the bone marrow is greatly depressed. the patient becomes anemic, leucopenic and thrombocytopenic with many a mastigotes in macrophages.
- Most untreated patients die in about 2 years, due to some intercurrent disease such as dysentery, diarrhea, and tuberculosis Patients who recovered from visceral Leishmaniasis are immune to reinfection.