Nocardiosis occurs in two major forms. The pulmonary form is an acute bron- chopneumonia with dyspnea, cough and sputum production. A cutaneous form produces localized pustules in areas of traumatic inoculation usually the exposed areas of the skin.
Nocardia species are ubiquitous in the environment, particularly in soil. In fact, fully de-veloped colonies of Nocardia give off the aroma of wet dirt. The organisms have been isolated in small numbers from the respiratory tract of healthy persons, but are not considered members of the normal flora. The pulmonary form of disease follows inhala-tion of aerosolized bacteria, and the cutaneous form follows injection by a thorn prick or similar accident. The majority of pulmonary cases occur in patients with compromised immune systems due to underlying disease or the use of immunosuppressive therapy.
Transplant patients have been a prominent representative of the latter group. There is no case-to-case transmission.
Factors leading to disease following inhalation of Nocardia are poorly understood. Neu-trophils are prominent in nocardial lesions but appear to be relatively ineffective. The bacteria have the ability to resist the microbicidal actions of phagocytes and may be re-lated to disruption of phagosome acidification or resistance to the oxidative burst. No specific virulence factors are known. The primary lesions in the lung show acute inflam-mation, with suppuration and destruction of parenchyma. Multiple, confluent abscesses may occur. Unlike Actinomyces infections, there is little tendency toward fibrosis and lo-calization. Dissemination to distant organs, particularly the brain, may occur. In the cen-tral nervous system (CNS), multifocal abscesses are often produced. The great majority of Nocardia pulmonary and brain infections are produced by N. asteroides.
Skin infections follow direct inoculation of Nocardia. This mechanism is usually asso-ciated with some kind of outdoor activity and with relatively minor trauma. The species is usually N. brasiliensis, which produces a superficial pustule at the site of inoculation. If Nocardia gain access to the subcutaneous tissues, lesions resembling actinomycosis maybe produced, complete with draining sinuses and sulfur granules. This infection may occur with Nocardia species or related organisms such asActinomadura madurae (formerly No-cardia madurae), a cause of the mycetoma syndrome .
There is evidence that effective T cell – mediated immunity is dominant in host defense against Nocardia infection. Increased resistance to experimental Nocardia infection in an-imals has been mediated by cytokine-activated macrophages, and activated macrophages have enhanced capacity to kill Nocardia that they have engulfed. Patients with impaired cell-mediated immune responses are at greatest risk for nocardiosis. There is little evi-dence for effective humoral immune responses.
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