Five malabsorption syndrome (MAS) homogenates from The Netherlands and Germany were used to reproduce MAS in broilers. We studied the histopathology after inoculation of 1-day-old broiler chicks and the agents that might be involved. Generally, the MAS homogenates induced signs that differed in severity and pathobiology. We could distinguish and classify the inoculated groups best by histopathology: proventriculitis, lesions in the small intestines in combination with proventriculitis, or lesions of the small intestines only. Lesions in the small intestine had more impact on weight gain depression than lesions in the proventriculus. In three out of five inoculated groups, microscopic lesions of the pancreas were found. Reovirus was detected in the inoculated groups by virus isolation and seroconversion, and reoviral antigen was detected by immunohistochemistry of the small intestine. Also, enteroviruslike particles were detected in three of the five inoculated groups, although not in the most affected group. Additionally, bacteriophages and bacteria (hemolytic Escherichia coli, Pasteurella hemolytica, and Enterococcus durans) were isolated from inoculated chicks. The role these agents play in pathogenesis of MAS is still unsolved.

Attempts to reproduce malabsorption syndrome (MAS) by oral inoculation with several different combinations including intestinal homogenate, reovirus, and hemolytic Escherichia coli obtained from MAS-affected chickens and intestinal homogenate from healthy chickens (healthy homogenate) were performed in 1-day-old specific-pathogen-free (SPF) broilers. The MAS homogenate, serving as a positive control, induced weight gain depression and intestinal lesions such as cystic crypts of Lieberkuhn, villus atrophy, and lymphoid and/or granulocytic infiltration. The healthy homogenate, the formalin-treated MAS homogenate, the formalin-treated healthy homogenate, and phosphate-buffered saline caused neither weight gain depression nor intestinal lesions. We were able to reproduce both weight gain depression and intestinal lesions by inoculation of reovirus either combined with the formalin-treated MAS homogenate or combined with healthy homogenate. Surprisingly, when hemolytic E. coli was added to the combination of reovirus with formalin-treated MAS homogenate, this did not cause weight gain depression although this combination caused the described intestinal lesions. Identical results were obtained with the combination of formalin-treated MAS homogenate with hemolytic E coli or the combination of reovirus with hemolytic E. coli. The intestinal lesions were more severe and developed faster by combinations including reovirus and formalin-treated MAS homogenate. This study indicates that a combination of enteropathogenic reovirus with other agents or substances that are present in an intestinal homogenate from MAS-affected and healthy chickens can induce MAS in SPF broilers. Escherichia coli is not essential for induction of weight gain depression but can play a role in development of intestinal lesions. Furthermore, intestinal lesions alone will not always result in weight gain depression.

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Growth retardation in young broiler chicks due to poor nutrient metabolism, commonly known as malabsorption syndrome (MAS), is a widespread problem caused by enteric infections with a combination of pathogens mainly viruses. Genetic lines of broiler chickens differ in susceptibility to the syndrome. A difference in growth retardation was observed among four broiler lines (BL) after oral inoculation at 1 d of age with intestinal homogenates obtained from MAS-affected birds. Two of the lines that are more susceptible to MAS had severe weight gain depression. To uncover the factors that play a role in the susceptibility to MAS, we analyzed the growth rate of the body and vital organs and the quantity of leukocytes in the peripheral blood and intestinal mucosa. The development of the intestine, liver, bursa of Fabricius, and spleen was similar among the BL. The resistant BL had higher numbers of peripheral blood leukocytes, especially lymphocytes, at 1 d of age. A significant difference was noted in the numbers of CD4+ T cells and CD8+ T cells in the intestinal villi. At the ages of 3 and 8 d, the susceptible BL had more CD8+ T cells in the villi, whereas the ratios of CD4+:CD8+ T cells were higher in the resistant BL. This difference in the number of T-cell subpopulations in the intestinal mucosa might be an important factor in the difference in susceptibility to the enteric infections associated with MAS.