Immunology of Coccidioidomycosis

  • David A. Stevens
Part of the Current Topics in Infectious Disease book series (CTID)

Abstract

The arthroconidium is the optimum size (< 10 mm) to breach the first lines of pulmonary defense: filtration, mucociliary transport in the upper airways, and the chemical inhibitors in the mucoid blanket. The initial response of the host to the arthroconidia in the lower airways is an ingress of macrophages and polymorphonuclear leukocytes.1 The stimulus for this response may be a nonspecific irritation, but in vitro studies have suggested that C. immitis antigens activate the complement mech-anism, generating chemotactic factors.2 The function of this “ingress” response is presumed to be phagocytosis and intracellular killing. In vitro studies have shown killing of other fungi by polymorphonuclear leukocytes and macrophages.3,4 In several days mononuclear cells are more in evidence.1 This is coincident with the start of conversion of the fungus from the saprophytic to the parasitic phase. There is in vitro evidence that neutrophils may be important in this conversion.5 Included among these mononuclear cells are presumed to be lymphocytes that are beginning to recognize the fungal antigens as foreign, and monocytes that are undergoing transformation to macrophages. The immediate origin of these mononuclear cells is as yet undefined—peripheral blood, the network of paratracheal, carinal and hilar nodes, broncho-aveolar cells, and bronchial-associated lymphoid tissue are possible sources.6

Keywords

Skin Test Migration Inhibitory Factor Mucociliary Transport Skin Test Reactivity Autologous Plasma 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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© Springer Science+Business Media New York 1980

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  • David A. Stevens

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