Fatal measles infection in marmosets pathogenesis and prophylaxis

Abstract

Moustached marmosets (Saguinus mystax) were infected intranasally with either of two low-passaged, wildlike strains of measles virus, strain Edmonston or strain JM. The infection resulted in 25 and 100% mortality, respectively, 12 to 14 days after infection. Clinical signs, gross pathological findings, and histology lacked the characteristic features of measles in other primates. A deficient immune response and widespread gastroenterocolitis appeared to be the main causes for the fatal outcome. Fluorescent-antibody staining detected large amounts of measles antigen in lymphatic tissues, the gastrointestinal and respiratory tracts, the salivary glands, pancreas, liver, kidney, and other visceral tissues. Live attenuated or inactivated measles vaccine proved equally effective in preventing fatal measles in marmosets. Challenge with live virus of animals which were primed 1 year previously with inactivated alum-absorbed vaccine resulted in a precipitous response, with a 100- to 1,000-fold increase in antibody titers. This vigorous booster response suggests the existence of a primary deficiency in lymphocyte cooperation in marmosets, which upon adequate priming is followed by extensive clonal expansion and antibody synthesis. Marmosets appear to be the most susceptible primate species to measles infection. They are capable of distinguishing differences in virulence of virus strains with a level of sensitivity not available in other animals.