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Term paper

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Treatment and also the exisitence of the disease in three forms which are:
Acute or Primary Pulmonary Histoplasmosis
Chronic Pulmonary Histoplasmosis
Extra pulmonary-Dissemination Histoplasmosis

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Term paper

  2. 2. PROF. MOSES ADETUMBI TABLE OF CONTENTS TOPIC PAGE Introduction 1 Etiology 2 Symptomatology 3-4 Pathogenecity 5 Epidemiology 6 Diagnosis 7-8 Treatment 9 Conclusion 10
  3. 3. HISTOPLASMOSIS INTRODUCTION Histoplasmosis (also known as cave disease, Darling's disease, and Ohio valley disease). Histoplasmosis is a primary pulmonary infections disease caused by inhaling dusts containing microconidia of the soil-dwelling mold Histoplasma capsulatum. The causative fungus occurs in soil mixed with bird droppings or bat guano and can persist in such sites for months or years. Accumulation of bird droppings or bat guano also occurs in attics and belfries of old buildings and can cause outbreaks during their renovation or demolition. Histoplasmosis has a well- defined endemic area in the United States and smaller foci worldwide. The U.S. endemic area for Histoplasmosis is in the eastern and Midwestern states, especially along the upper Mississippi, Ohio, and Missouri river valleys extending north along the St. Lawrence River valley and south the Rio Grande River in Texas When H. capsulatum microconidia are inhaled, they lodge in the lungs, germinate, convert to yeast forms, and cause lesions. Anyone can contract histoplasmosis, but especially persons whose occupation or recreational pursuits bring them in contact with dusts mixed with bird droppings of bat guano. Histoplasmoses, and all systemic mycoses caused by dimorphic fungal pathogens, are not contagions. The disease exists inthree major forms. • Acute or Primary Pulmonary Histoplasmosis. This form most often causes influenza-like symptoms. Most persons who are infected recover without medical
  4. 4. intervention. Residual pulmonary foci can persist, however, leaving open the possibility of later endogenous reactivation. • Chronic Pulmonary Histoplasmosis. This is most often seen in the setting Of COPD • Extra pulmonary-Dissemination Histoplasmosis. This form affects multiple organs and can be fatal, especially to immunosuppressed persons, including those living with AIDS. (Medical Mycology, 2012a) ETIOLOGY Histoplasma capsulatum, a soil-dwelling mold, grows in soil mixed with bird droppings or bat guano, for example, soil of chicken house, blackbird roosts, and pigeon- or bat-occupied buildings and caves. Birds are not infected because of their high body temperatures but bat have a lower body temperature and can be infected. Infected bats can excrete the organism in their droppings. Histoplasma capsulatum demonstrate temperature-sensitive dimorphism, growing as a mold in the soil, and in the laboratory on artificial medium at ambient temperature. It converts to a yeast form infection and at 370C on enriched laboratory medium. Histoplasma capsulatum var. duboisii has a colony and microscopic morphology similar to H. capsulatum. Yeast forms are larger, 8-15 micrometer in diameter, lemon-shaped with a narrow isthmus between mother and daughter cells. The mold form of H. capsulatum and var. duboisii are indistinguishable. Variety duboisii causes systemic mycoses endemic to sub-Saharan, western and central Africa. It
  5. 5. is classically associated with cutaneous nodules and ulcers and osteolytic bone lesions, especially affecting the skull, ribs, and vertebrae. Histoplasma capsulatum var. farciminosum is the cause of epizootic lymphangitis in horses and also is endemic to Africa. (Medical Mycology, 2012b) SYMTOMATOLOGY Most infection are asymptomatic fever, cough and chest pain are the most common symptoms, or with shortness of breath. Mouth sore may develop especially in children (Eugene W. Nester et al, 2009). Some people experience mild symptoms such as ashes, pains, and coughing, but a few develop more severe symptoms, including fever, night sweats, and weight loss. Primary cutaneous histoplasmosis, in which the agent enters via the skin, is very rare. Symptoms usually are mild and nonspecific, resembling a cold or influenza; fever, chills, dry cough, myalgia, headache, pleuritis chest pain, enlarged lymph glands, and fatigue. From 5% to 10% of patients with self-limited histoplasmosis may experience other sysmtoms: • Arthritis and arthralgias • Mediastinal lymphadenopathy • Cutaneous symptoms including erythema nodosum or maculopapular rash. PATHOGENICITY
  6. 6. Histoplasma present a formidable arrays of manifestations. It can show pulmonary, systemic or cutaneous lesions. Inhaling a small dose of microconidia into the deep recesses of the lung establishes a primary pulmonary infection that is usually asymptomatic. Its primary location of growth is in the cytoplasm of the phagocytes such as mycrophages. Within these cells, it flourishes and is carried to other sites. The most serious systemic forms of the Histoplasmosis occur in patients with defective cell- mediated immunity such as AIDS patients. In Children, this can lead to liver and Spleen enlargement, anemia, circulatory collapse, and death. Adults with systemic disease can acquire lesions in the brain, intestine, adrenal gland, heart, liver, spleen, lymph nodes, bone marrow, and skin. Persistent colonization of patient with emphysema and bronchitis cause Chronic pulmonary histoplasmosis, a complication that has sign and symptoms similar to those of tuberculosis. (Kathleen park Talaro and Barry Chess, 2012) CLINICAL MANIFESTATION Acute Pulmonary Histoplasmosis About 950%of persons infected with H. capsulatum experience inapparent, subclinical, or mild self-limited benign disease. When symptoms occur, they appear 3-17 days after exposure (average time is 10 days). Pediatric Histoplasmosis
  7. 7. Children having a high rate of asymptomatic or mild infections. Immune-normal children with symptomatic acute histoplasmosis present with fever, malaise, mild cough, and nonpleuritic chest pain. This sysmtoms usually subside in 2-3days. Central Nervous System Histoplasmosis$ It may present as chronic meningitis, intracranial mass lesions (Histoplasmonas). Symtoms may include headache, altered state of consciousness, and cranial nerve deficits. (Medical Microbiology, 2012c) EPIDEMIOLOGY Histoplasma capsulatum is endemically distributed in eastern and central regions of the United State (the Ohio Valley). This fungus appears to grow most abundantly in moist soils high in nitrogen content especially those supplementary by bird and bat guano. A useful tool for determining the distribution of H.capsulatum is to inject a fungal extract called histoplasmin into the skin and monitor for allergic reactions. An application of this test has verified the extremely widespread distribution of the fungus. In high prevalence areas such as Southern Ohio, Illinois, Missouri, Kentucky, Tennessee, Michigan, Georgia, and Arkansas, 80% to 90% of the population show signs of prior infection by the age of 20. Histoplasmosis incidence in the United State is estimated at about 500,000 cases per year, with several thousands of them requiring hospitalization and a small number resulting in death.
  8. 8. The Spore of the fungus is probably dispersed by the wind and, to a lesser extent, animals. The most sticking outbreaks of histoplasmosis occur when concentration of spores have been dislocated by humans working in parks, bird roosting areas, and olds buildings. People of both sexes and all ages incur infection but adult males experience the majority of cases. The oldest and youngest members of a population are most likely to develop serious disease. DIAGNOSIS Direct Examination In acute pulmonary histoplasmosis, H. capsulatum may be seen microscopically in sputum or bronchial washings as very small ovoid yeast forms with dimensions of 2-4 micrometer. When cells are buddings, buds have a narrow base. Direct smears of sputum are stained with Wright’s GMS, or PAS stains. Histopathology The yeast form of H.capsulatum usually can be found in tissue removed from the diseased site, often within macrophages in granulomas. GMS or PAS stains are best for fixed, embedded tissues. The yeast forms stains brown to black with GMS stain. Bone Marrow Aspirate Bone marrow aspirates or peripheral blood smears stained with Wright’s stain display intracellular yeast forms. Colony Morphology
  9. 9. On Saboroud Dexrouse Agar or other nonenriched medium, the colony usually is white and cottony, becoming tan with age. Microscopic Morphology The H. capsulatum mold form grows as hyaline and septate, with branching hyphae that produce two types of conidia. Tease mounts are examined first; then if there is insufficient sporulation, a slide culture is prepared. Viewed microscopically, tease mounts and slides cultures illustrate tuberculate macroconidia and microconidia. (Medical Mycology, 2012d) TREATMENTAND PREVENTION Mild forms of Histoplasmosis do not generally require treatment. Moderate severe forms of Histoplasmosis, such as acute pulmonary disease, or chronic pulmonary cavitary disease, and treated with oral ITC, 200-600mg/day. Severe forms of Histoplasmosis generally are treated initially with either AmB-deoxycholate at 1 mg/kg/day or a lipid preparation of AmB at 3.0-5.0 mg/kg/day. Other azole drugs including fluconazole (FLO), voriconazole (VRC), and posaconazole (PSC). Resistance to FLC may develop during therapy, and there are reports of VRC failing in patient who have previously failed FLC. Therefore, PSC may be a better alternative to ITC than either FLC or VRC. The echinocandin class of antifungal agents does not have activities against H. capsulatum. The following guideline reduce exposure to H. capsulatum • Avoid contaminated sites; bird roosts, caves, chicken coops. • Control aerosolized dusts by the use of water sprays. • Avoid activities such as cave exploring and the demolition of old building.
  10. 10. • Decontaminate with disinfectants (e.g formaldehyde solutions). CONCLUSION Histoplasmosis, like Coccidioidomycosis is usually, is usually benign but occasionally mimics tuberculosis. Rare, serious forms of the disease suggest that AIDS or another immune deficiency may also be present. The distribution is more widespread than that of Coccidioidomycosis and is associated with different soil and climate. It is similar to tuberculosis, in that it is intracellular pathogen that evokes a granulomatous host response. Inhaled conidia germinate undergoing a dimorphic shift to the yeast form, which initially resist lysis by alveolar macrophages, neutrophils, and natural killer lymphpcytes. Once phagocytosed, yeast forms divides into alveolar macrophages and are carried to lymph nodes draining the lings, and then via the blood to tissues of the monocytic-phagocyte system: the spleen, liver, and bone marrow REFRENCES Medical Microbiology,2012a Medical Microbiology,2012b Engene W.Nesteretal, 2009. Human perspective,6th edition,McGraw-Hill ,New York,NY10020, 526p. KathleenParkTalaroandBarry Chess,2012, FoundationinMicrobiology,8th edition,McGraw-Hill,New York, NY 10020, 666p. Joanne M. Willeyetal,2011, Prescott’sMicrobiology,8th edition,McGraw-Hill,New York,NY10020, 986p.