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Clinical Mycology 7 part 2.pdf

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PreciousField

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Ibn Sina National College for Medical Studies

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medicine fungal infections histoplasmosis

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Systemic Mycoses (2) DR.WIFAG RABIH Histoplasmosis (Darling ‘s disease, Reticuloendotheliosis, Reticulo-endothelial cytomycosis) (Dimorphic fungi) Histoplasmosis is the most common type of systemic fungal infection caused by Histoplasma capsulatum (classic or small form) and Histoplasma duboissi (Af...

Systemic Mycoses (2) DR.WIFAG RABIH Histoplasmosis (Darling ‘s disease, Reticuloendotheliosis, Reticulo-endothelial cytomycosis) (Dimorphic fungi) Histoplasmosis is the most common type of systemic fungal infection caused by Histoplasma capsulatum (classic or small form) and Histoplasma duboissi (African or large form). Histoplasmosis, caused by H. capsulatum, shared many characteristics with coccidioidomycosis. Both diseases extend over a spectrum from acute self-limited to chronic, granulomatous infection, and both are endemic in man. However, histoplasmosis occurs worldwide Epidemiology Geographic Distribution Histoplasma capsulatum infection occurs in many parts of the world. notably in the USA along the Mississippi river, and in many areas along the East cost. Histoplasma duboissi It occurs in tropical Africa. It is common in areas with optimal growth conditions like accumulation of bird or bat droppings to enrich the soil with nutrient (eg. Nitrogen) that encourages the growth of H. capsulatum. Pathogenesis and clinical picture Infection begins with the small primary focus of lung infection much like the early lesions of tuberculosis. The causative agents are ingested by alveolar macrophages in the lung. These macrophages carry the fungi to nearby lymph nodes, usually the hilar nodes. The fungi multiply within the node tissue and ultimately are released into circulating blood, from which they go on to seed other organs, the liver, spleen, lymph nodes, adrenal glands, and bone marrow, or are destroyed by the body’s defenses. The majority of the infections are either asymptomatic or mild, and the diagnosis is elusive cough, fever, malaise, and chest X-ray findings of hilar adenopathy with or without one or more areas of pneumonitis are typical features. Acute disseminated histoplasmosis may be mistaken for miliary tuberculosis. Common findings include fever, Flu, Cough, Chest pain hepatosplenomegaly, thrombocytopenia. lymphadenopathy, Jaundice, anemia leukocytopenia, and In such individuals the infection may occur either as an acute disease, as a chronic cavitary disease, or as a severe blood-born disseminated disease Acute pulmonary histoplasmosis ranges from asymptomatic to a severe self-limiting disease in which symptoms resemble a mild cold. ◦ Chronic pulmonary histoplasmosis is the outcome of the continued progression of the initial infection or the result of reactivation of an old quiescent lesion. shortness of breath, excessive sweating, liver infection, or spleen infection. ◦ Chronic pulmonary histoplasmosis is characterized by a gradual onset (over weeks or months) of increasing productive cough, weight loss, and sometimes night sweats. ◦ The disease resembles chronic pulmonary tuberculosis clinically. Disseminated Histoplasmosis is commonly a generalized disease of the reticuloendothelial system that presents lesions in almost every organ of the body. including the central nervous system ◦ ◦ ◦ ◦ Skin and mouth sores, including rashes Joint and muscle pain Headache Neck stiffness It is rare, occurring mostly in individuals with patients of depressed cellular immune response (e.g. Patients with AIDS, T-cell defects, or lymphoma) In children younger than age one year who appear to have a reticuloendothelial defect (fulminant disease of childhood) Diagnostic Testing LAB Findings: ◦ Leukopenia, anemia, and thrombocytopenia suggestive of marrow infiltration. Radiology. Antigen detection:Urine: most sensitive rapid assay-up to 95% Serum: -up to 85 % sens in AIDS. Serologic Testing: Ab develop at high levels within 4-6 weeks. Culture: Gold standard for diagnosis, but isolation takes up to 4 weeks. Thin walled oval yeast Dimorphic: ◦ Filamentous in environment. ◦ Yeast in tissue. Paracoccidioidomycosis(paracoccidi-oidl granuloma, Lutzsplendore-almeida’s disease) Paracoccidioidomycosis formerly called South American blastomycosis, which is a chronic granulomatous systemic mycosis caused by a saprophytic P. brasiliensis. A dimorphic fungus. P. brasiliensis grows as budding yeast in tissue but may grow as either yeast or a mold on culture medium. Geographic Distribution Para coccidioidomycosis is found in Brazil and also in other South American countries, Central America and Mexico. Source of infection: The exact mechanism by which paracoccidioidomycosis is acquired is unclear; however, it is speculated that is the origin is pulmonary which is acquired by inhalation of organisms from the environment The infection begins as primary pulmonary infection. It is often a symptomatic and then disseminates to produce ulcerative lesions of the mucous membrane. Ulcerative lesions are commonly present in the nasal and oral mucous, gingival, and less commonly in the conjunctiva. Lesion occurs most commonly on the face is associated with Oral membrane infection. The lesions are characteristically ulcerative, with serpinous active border and a crusted surface. Pulmonary infection is seen most often, and progressive chronic pulmonary infection is found in approximately 50% of the cases. Dissemination to other anatomic site, including the lymphatic system, spleen, intestine, liver, brain meninges, and adrenal glands occur in some patients Common signs include indurated ulcers of mouth, oropharynx, larynx, and nose; enlarged and draining lymph nodes;lesions of the skin and genitalia; and productive cough, weight loss, and some times fever.

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