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Nocardia

الكلية كلية الطب     القسم  الاحياء المجهرية     المرحلة 3
أستاذ المادة حبيب صاحب نهر المزيداوي       4/16/2011 7:16:46 PM

 Nocardia: 
Clinical Manifestations: The most common manifestation of nocardial infection is pneumonia: fever, weight loss, cough, pleuritic chest pain, and dyspnea. In about 20 percent of patients there are granulomatous skin lesions and/or central nervous system abnormalities.

Structure: The bacteria are Gram-positive, partially acid-fast rods, which grow slowly in branching chains resembling fungal hyphae.

Classification and Antigenic Types: Three species cause nearly all human infections: N. asteroides, N. brasiliensis, and N. caviae. These are distinguished by proteolytic and fermentation patterns in culture.
Pathogenesis: Infection is by inhalation of airborne bacilli from an environmental source (soil or organic material); the disease is not contagious. Skin lesions caused by N brasiliensis often result from direct inoculation. Nocardia subverts antimicrobial mechanisms of phagocytes, causing abscess or rarely granuloma formation with hematogenous or lymphatic dissemination to the skin or central nervous system. Mortality is up to 45 percent even with therapy.
Host Defenses: The natural resistance to infection is high in normal individuals, and the disease is usually associated with cellular immune dysfunction, immunoglobulin deficiencies, or leukocyte defects. Acquired resistance is complex and involves activated macrophages, cytotoxic T cells, and neutrophil inhibition.

Epidemiology: Nocardiosis is rare in normal persons. It usually occurs in recipients of organ transplants; in patients with leukemia, lymphoma, humoral, or leukocyte defects; or after prolonged steroid therapy.

Diagnosis: Diagnosis is by Gram stain, modified acid-fast stain, and culturing of organisms from sputum, bronchoscopic specimens (washing, brushing), aspirates of abscesses, or by biopsy.

Treatment: Nocardiosis is treated by prolonged (up to 1 year) therapy with trimethoprim-sulfamethoxazole.

Clinical Manifestations: Nocardia rarely causes clinical disease except in immunocompromised individuals, especially organ transplant recipients. Ninety percent of such patients present with pulmonary involvement, including cough, pleuritic chest pain, dyspnea, and radiologic abnormalities such as nodules and nodular infiltrates. Other clinical findings include weight loss, malaise, fever, and night sweats. About 20 percent of patients with nocardiosis present with cutaneous lesions, either localized or disseminated, and/or central nervous system involvement. About 50 percent of patients have an associated disease process (another infection or a tumor). Cutaneous infection with N brasiliensis results in localized development of granulomata and abscesses with soft tissue and bone involvement .

Structure :Nocardia organisms are Gram-positive rods, which in old cultures or clinical specimens may appear as branching chains resembling fungal hyphae. The filamentous morphology is evident. Nocardia are weakly acid-fast following staining with the modified Ziehl-Neelsen or Kinyoun stain. Cultures may grow in a few days, but typically require 2 to 3 weeks of incubation.

Classification and Antigenic Types: Three species of Nocardia are responsible for most human infections. Nocardia asteroides causes most nocardial pulmonary infections in this country (80 to 90 percent), with N brasiliensis (5 to 6 percent) and N caviae (3 percent) being recovered from only a few patients with nocardiosis. In the southern United States and in the tropics, N brasiliensis is an important agent of cutaneous nocardiosis. The three species can be distinguished by their patterns of proteolytic hydrolysis or of acid fermentation of several substrates.

Pathogenesis: Nocardia cells have been isolated from soil and organic material throughout the world. Natural infections occur in domestic animals. Human infection usually results from the inhalation of airborne bacilli or the traumatic inoculation of organisms into the skin. The infection is not transmissible between individuals. Natural resistance, mediated by intact mucous membranes and alveolar and tissue phagocytes, is quite strong.
In immunocompromised hosts, pulmonary infection results in the formation of abscesses and, rarely, granulomas with hematogenous or lymphatic dissemination to the skin or central nervous system. Nocardia can subvert the antimicrobial mechanisms of phagocytes by inhibiting phagosome-lysosome fusion. Owing to the debilitated nature of the infected patients, mortality is high (up to 45 percent), even with appropriate therapy.

Host Defenses: Nocardiosis is usually associated with T-cell dysfunctions, immunoglobulin deficiencies, or leukocyte abnormalities. Acquired resistance to Nocardia is complex, involving antibody-dependent phagocytosis by neutrophils, macrophage activation by the products of immune T cells, and the development of cytotoxic T lymphocytes. Neutrophils ingest opsonized bacteria but may not kill them. Macrophage activation is associated with containment and clearance of Nocardia organisms from the lungs. In a murine model, resistance to nocardiosis can be transferred with whole spleen cells or splenic T cells from immune mice.

Epidemiology: Although nocardiosis has been diagnosed in individuals with no detectable deficiency of humoral or cell-mediated immunity, it usually occurs in patients whose immune status has been compromised by post-transplant immunosuppressive therapy, leukemia, lymphoma, dysgammaglobulinemia, pancytopenia, humoral defects, chronic granulomatous disease, or steroid therapy. The male/female ratio in nocardiosis is approximately 2:1, and infections occur from infancy to old age.

Diagnosis : Nocardia can be identified presumptively by Gram and acid-fast stains and definitively by culture from appropriate clinical specimens. Sputum culture is useful for patients with a productive cough. The presence of branching, weakly acid-fast organisms in histologic sections, pus, or sputum suggests the clinical diagnosis. In one series, nearly 40 percent of cases required more invasive procedures (e.g., thoracentesis, transtracheal aspiration, bronchial washing, or biopsy) to obtain useful material for stain and culture of Nocardia.

Treatment and Control : Antimicrobial therapy with sulfa drugs (e.g., trimethoprim-sulfamethoxazole) is the treatment of choice. The duration of therapy ranges from 2-3 months for minor infections to 1 year for major infections.


 


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