ANNA ROZALIYANI

Department of Parasitology- Faculty of Medicine, Universitas
Indonesia

Deficiencies of the immune system often
develop because of abnormalities that are not
genetic

Two main types of pathogenic mechanisms:
 Immunosuppression may occur as a biologic
complication of another disease process.
 Iatrogenic immunodeficiencies may develop
as complications of therapy for other
diseases.

& dendritic cells • • • Dysfunction of the immune system Inducing opportunistic infection . CD4 was a viral receptor destruction of CD4 T cells in HIV infected inviduals. macrophages. • HIV Infection Infecting CD4 T lymphocyte.

g. cyclosporine  The drugs cause cytotoxic both mature and developing lymphocyte as well as tp granulocyte and monocyte precursors. Due to some drugs either for the treatment of inflammatory diseases or to prevent rejection of tissues allografts e. corticosteroids. .

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 Exposure to contaminated faeces can result in transmission of this disease.  The worm has an autoinfective cycle that allows infection to persist in the host indefinitely without the need for an external enviroment Transformation of rhabditiform larvae into invasive filariform larvae in the gut of human host .

.Increase number of larvae completing the autoinfectious cycle large numbers of worms can enter the systemic circulation hyperinfection syndrome.

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HIV infection. organ transplantation High risk of hyper infection syndrome in patients with strongyloidiasis .Immunosuppression caused by:   Iatrogenic: use of systemic corticosteroids) Intercurrent illness HTLV-1/Human T cell Lymphotropic Virus-1.

 Corticosteroids (endogenous & exogenous) increase ecdysteroid like substances (naturally occurring non-hormonal anabolic effects) in the body mainly in the intestinal wall.  Molting signals for eggs and rabditiform larvae  Number of filariform larvae .

Corticosteroids (endogenous & exogenous) affect the immunity by  Increasing the apoptosis of Th2 cells  Reducing the eosinophil count  Inhibiting the mast cells response .

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Humoral and cell mediated immunity   Rodent models: Induction of goblet cells and intestinal mastocytosis by IL-13 secreted by Th2 cells expulsion of worm from GI tract Human: Lack of cell activation in the mucosa no change in jejunal morphology. mast cells. different T cell subset numbers. eosinophils and goblet cells. BUT a decrease of mature macrophages and dividing enterocytes in the crypts of intestinal walls may preserve the architecture of mucosa and absence of immune mediated diarrhea .

survival) and adaptive immunity (IgM production by plasma cells) B cells: important role in subsequent challenge infections (increased parasite-spesific IgM) Specific IgE against filariform larvae: Protective role not clear. differentiation. maturation. maybe useful for immunodiagnosis? ADCC (IgE activation of eosinophils & IgG activation of neutrophils) in strongyloidiasis: not effective against larvae? .     IL-4: important regulator of IgE production & mast cell activation Il-5: innate immunity (induce eosinophil production.

IgG. IgM specific for primary infective filariform larvae is not effective against autoinfective filariform larvae (have different surface antigens) Eosinophils can cause destruction of helminth larvae esp. IgM. in disseminated infections .    Compared to asymtomatic or mildly symptomatic: lower levels of IgA.host-adopted filariform larvae. BUT not sufficient for complete protection Lower eosinophil counts in severe strongyloidiasis: suppression of eosinophils esp.

    Stool culture for larvae Serology test (ELISA) Albendazole Ivermectin – not registered for human use in Indonesia .

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 Transmission occurs by the fecal-oral spread of oocysts.  Fecal contamination of drinking water sources can serve as a vehicle for transmission of oocysts and is a subtantial public health concern Outbreak .

.  Oocyts lose infectivity when undergoing heat treatment above 65 0C pasteurization. sterilization for food. and therefore infectivity. Oocyts retain viability. under moist and cool conditions for several months. ozone or exposure to UV for water (chlorination is not effective).

 The parasite resides at the apical surface of intestinal epithelial cells and does not invade deeper layers of the human gasrointestinal mucosa.  Moderate to severe infection with this intraepithelial parasite is characterized by mucosal inflammation with neutrophils and macrophages in the lamina propria underlying epithelial cell. .

increased epithelial Interleukin 8 (IL-8) and GROα production (potent neutrophil chemoattractants) could attract inflammatory cells into the mucosa. After infection.  The infection in the intestinal epithelial cells also rapidly upregulate the production of IFNγ (proinflammatory cytokine) important for host innate and reacuired immunity to clearance the infection but the mechanism has not defined yet .

 In addition. parvum infection in the absence of significant mucosal inflammation. . increased mucosal prostaglandine production (PGE2) following infection with enteroinvasive bacteria can inhibit neutral NaCL absorption and result in secretory diarrhea.  PGE2 can downregulate inflammatory cytokine production by macrophages explaining why diarrhea can develop during C.

Humoral immunity is not an absolute requirement for clearing infection.  The ability to clear acute and chronic parasite in human correlates with host CD4 T-cell levels. In mice model. CD4+ T cells play the dominant role in resistance to C. Parvum. .  In addtion to CD4+ T cells. Th1 cytokine (IFNγ as innate response) play a major role to prevent initiation as well as limit the extent of infection  .

parvum infection. with invasion of other organ systems including the lungs and the bile duct. . followed by abdominal pain and vomiting. the disease may be much more severe and persistent. Diarrhoea is the most common symptom of C. and it is life threatening.  In immunocompromised individuals.

 Finding oocysts in stool specimens by light microscopy.  PCR to detect the DNA of parasite Oocyst .

   Paromomycin Nitazoxanide Highly active antiretroviral therapy (HAART) aspartyl protease inhibitors of the human immunodeficiency virus which directly interfere with the life cycle of the parasite. .

. a relationship between disease severity and CD4+ count. Patients with AIDS may need higher doses and long-term maintenance treatment. AZT therapy should be started In these patients.   In AIDS patients without antiretroviral therapy.