Investigations into the role of reovirus in the malabsorption syndrome

Abstract

Malabsorption syndrome, defined by five criteria, could not be reproduced by oral inoculation of newly hatched chicks with six reoviruses isolated from six different cases. Passage in birds of four reoviruses with intestinal homogenates did not result in increased pathogenicity. In contrast, inoculation of complete infectious intestinal homogenate caused great weight loss, long lasting excretion of yellow‐orange mucoid and wet faeces, increased plasma alkaline phosphatase activity, decreased carotene concentration and bone abnormalities. Malabsorption syndrome could not be reproduced with infectious intestinal homogenate comprising only reovirus and possibly other non‐enveloped viruses after treatment with methanol or chloroform. Infectious homogenate made reovirus‐free by incubation with anti‐serum was as pathogenic as homogenate that had been treated the same way with broth and that still contained viable reovirus. While infectious homogenate was almost apathogenic for 3‐day‐old chicks, its pathogenicity for birds of this age was greatly enhanced by a pre‐infection with reovirus immediately after hatching. Reovirus therefore may act as a trigger in the malabsorption syndrome. This enhancing effect, however, was not specific for reovirus; it was also achieved with an adenovirus. Vaccination of two groups of breeders with two different inactivated reovirus vaccines, resulted in effective transfer of antibody to the offspring, but did not protect the offspring against malabsorption syndrome.