The Effect of Passage with Chloramphenicol Upon the Behavior of Penicillin-Resistant Feline Pneumonitis Virus During SubsequentPassage with Penicillin

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Abstract
Penicillin-resistant feline pneumonitis virus produced by serial chick embryo yolk sac passage in the presence of penicillin was distinguished from the parent virus by its high resistance to penicillin, by its failure to form hemagglutinin in the allantoic cavity, and by the failure of its neutralizing antiserum to reduce significantly the infectivity of parent virus. Penicillin-resistant virus was on two separate occasions transferred five times in the yolk sacs of chick embryos treated with chloramphenicol. Such passage had no apparent effect on the resistant virus. However, when this chloram-phenicol-passed virus was returned to serial transfer in the presence of penicillin, alterations in one or more virus properties occurred in 8 of 9 trials. In two series of penicillin passages, virus with increased susceptibility to penicillin was obtained. In 6 series, the original resistant type (normal resistant virus) was replaced by a new kind of virus. This type was designated as spread resistant virus because the deaths of embryos inoculated via the yolk sac with this virus were spread over a period of 5 to 10 days instead of being grouped within a period of 1 to 2 days, as with normal virus. Spread virus differed from normal in that it was completely resistant to penicillin, grew to a lower titer, was not neutralized by antiserum against either parent or normal resistant virus, and showed cross-resistance to chloramphenicol. All but one of the spread resistant strains were stable during drugless passage. The spread pattern of chick embryo death seems to reflect a heterogeneous response of the chick embryo population to infection with spread virus. When mixtures of normal and spread virus were inoculated into the yolk sac, normal progeny predominated in the absence of penicillin; in its presence, spread progeny were chiefly produced. The action of chloramphenicol in facilitating the emergence of the new variants was explained by assuming the selection during chloramphenicol passage of a resistant genotype with a higher frequency of mutation than that of the original resistant virus.