Ultrastructural Changes in the Chlamydia-Infected Ileal Mucosa of Newborn Calves

Abstmct. Ultrastructural changes induced by chlamydia1 infection of niucosal cells of the ileum of ncwborn calves after oral inoculation were investigated. Depending on the stage of chlamydia1 development, the organelles of all infected cells became damaged. The damage was degenerative and included vesiculation of microvilli and swelling of the terminal web of absorptive epithelial cells. The mitochondria were swollen and had fragmented cristae. The endoplasmic reticulum was dilated and vesiculated, and infected cells gradually lost their ribosomes. The lateral junctional complex between infected cells became occasionally dislocated and fragmented. The basal lamina was thrown into folds, became discontinuous and separated from the basal border of the epithelial cells. The nuclei of infected cells were affected last, lost their chromatin pattern, and ultimately became pyknotic. Enteric disease represents a serious problem for the newborn of many different animal species and man. The newborn encounters numerous infectious agents during the postnatal period when the intestinal microbial flora is being established. Intestinal infections with viruses and other obligate intracellular parasites such as chlamydiae are also known to occur during this period. Chlamydia1 agents have been isolated from feces of clinically normal young calves [ 151 and from specimens of newborn calves with diarrhea and polyarthritis [ 121. After oral inoculation with specific chlamydia1 strains, young calves developed diarrhea and died rapidly because of water and electrolyte losses, but only minor gross and histopathologic lesions were detected in the intestine [5]. Since chlamydiae replicate by going through a welldefined developmental cycle, infected cells can be identified ultrastructurally. The purpose of this investigation was to analyze ultrastructural changes induced by chlamydiae in the ileal mucosa of calves that developed diarrhea after oral inoculation.