microbiology, Vol 140, 237-244, Copyright © 1994 by Society for General Microbiology

ARTICLES

Phagocytosis by pig alveolar macrophages of Actinobacillus pleuropneumoniae serotype 2 mutant strains defective in haemolysin II (ApxII) and pleurotoxin (ApxIII)

JM Cullen and AN Rycroft
Department of Veterinary Pathology, University of Glasgow, UK.

The ability of pig alveolar macrophages to phagocytose Actinobacillus pleuropneumoniae HK 361, which produces both haemolysin II (ApxII) and pleurotoxin (ApxIII), has been studied. Macrophages incubated with HK 361 in the presence of normal pig serum were rapidly killed. Incubation of the macrophages with a haemolysin-deficient mutant (HK 361 e), which possesses only cytotoxic activity (ApxIII), also caused gross damage to the macrophages. A mutant (HK 361 h) which produces neither ApxII nor ApxIII in its culture supernatant allowed longer survival of the macrophages than did either the parent strain or mutant e when incubated with normal pig serum. Prolonged incubation with mutant h resulted in an increase in the number of damaged macrophages, but not to the same extent as with either HK 361 or mutant e. The number of mutant h cells phagocytosed in the presence of normal pig serum was low. The addition of either hyperimmune rabbit serum, raised against whole formalin-treated HK 361 cells, or convalescent pig serum from a pig recovering from a serotype 3 infection, which contained antibody against both ApxII and ApxIII, did not increase the survival of macrophages incubated with either HK 361 or mutant e. However, incubation of mutant h with convalescent pig serum did not result in damage-free macrophages. This serum, which possessed neutralizing capabilities against the toxic activities of ApxII and ApxIII, enhanced the number of mutant h cells phagocytosed compared to the numbers phagocytosed in normal pig serum. Killed bacteria were rapidly phagocytosed and did not damage macrophages.(ABSTRACT TRUNCATED AT 250 WORDS)

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