1. Be concise and direct. Show me what you have learned in a lucid way.Discuss h

Question

1. Be concise and direct. Show me what you have learned in a lucid way.Discuss how your body develops specific immunity against an infectious disease (choose an infectious disease). However, the exam should have a title, and several subheadings to separate the different sections of your answers, e.g. (Title: My Development of Specific Immunity Against…. Include a short description of the infectious agent you chose, its mechanism of disease causation, the perils it goes through from the portal of entry to the point it succeeds in causing the disease, finally how you become immune against this disease, how you determine that you are immune by a laboratory method.

Explanation / Answer

I would like to write about visceral leishmaniasis (VL) which is caused by Leishmania donovani. It is an intracellular protozoan parasite usually invades the lymphoid tissues and establish a persistent infection in spleen and liver. The parasites transmitted via the bite of an infected female sand fly vector. The infective stage parasites subsequently invade into different cell types that have encountered. In fact, neutrophils rapidly recruit at the bite site followed by dendritic cells, fibroblasts and mainly the macrophages. Typically, parasites engulfed by different antigen presenting cells (i.e. dendritic cells and macrophages) by a process called phagocytosis. In the parasitophorous vacuole, the metacyclic promastigotes transform into amastigotes followed by the release of lysosomal content into vacuole that does not affect the amastigotes. During transformation, metacyclic promastigotes turned into ovoid and non-motile amastigotes (3-7 m in diameter) by losing their flagella. Notably, the amastigotes divide multiple times and attach to the walls of parasitophorous vacuole using its posterior end. The parasitophorous vacuole enlarges in size and occupies the entire cytoplasm that followed by the burst of the cell. Then, amastigotes reach the extracellular space and appear in monocytes and blood stream. From there, parasites metastasize to reticulo-endothelial system by disseminating through the lymphatic and vascular systems and infects other macrophages, thereby infiltrate into bone marrow and visceral organs eventually causes hepatosplenomegaly and lymphadenopathy

In which, majorly the cell-mediated immunity (CD4+ Th1-cell) offers the protection ( by the cytokines like IFN-g, IL-12 and IL-2) against disease. Typically, infection always neutralized by the host specific cell-mediated immunity and VL exacerbates due to the T-cell unresponsiveness to L. donovani antigens and abundant production of interleukin (IL)-10. The humoral response against this disease is not clearly understood, but IgG2a is found to be protective among all subclasses of immunoglobulins. In the case of innate immunity NK cells and dendritic cells would play a major role along with macrophages to kill the parasites.They produce IL-12 and IFN-g eventually nitric oxide NO a potent antimicrobial component. If the disease is exacerbated the CD4+-Th2 type cytokines (IL-10, IL-4 and TGF-b) will be upregulated along with humoral components like IgG1 and IgG3 etc.

Laboratory diagnosis can be done using ELISA, direct agglutination test (DAT) with Leishmania antigen and patient serum and PCR diagnosis by the k-DNA amplification. But the microscopic visualization of parasites in the splenic aspirates is highly preferable to confirm the disease.

Malnutrition, co-infections like HIV and poor hygienic conditions are highly endemic factors for this disease.

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