RELATIONSHIP BETWEEN ILEAL SYMBIONT INTRACELLULARIS AND PORCINE PROLIFERATIVE ENTERITIS

Citation
Gf. Jones et al., RELATIONSHIP BETWEEN ILEAL SYMBIONT INTRACELLULARIS AND PORCINE PROLIFERATIVE ENTERITIS, Infection and immunity, 61(12), 1993, pp. 5237-5244
Citations number
50
Categorie Soggetti
Immunology,"Infectious Diseases
Journal title
ISSN journal
00199567
Volume
61
Issue
12
Year of publication
1993
Pages
5237 - 5244
Database
ISI
SICI code
0019-9567(1993)61:12<5237:RBISIA>2.0.ZU;2-X
Abstract
The relationship between Ileal symbiont (IS) intracellularis, formerly known as a Campylobacter-like organism, and porcine proliferative ent eritis (PE) was studied by use of pigs with experimentally transmitted PE. Twenty one pigs were experimentally inoculated with homogenized i leal mucosa from a pig that died with PE, and 7 were maintained as uni noculated controls. Real samples were collected, and pigs were necrops ied weekly postinoculation. Light microscopy and electron microscopy w ere used to examine tissues for lesions of PE and infectious agents. D NA was extracted from the fecal samples and assayed for the presence o f sequences specific for IS intracellularis by dot blot hybridization and polymerase chain reaction amplification. IS intracellularis was de tected by the polymerase chain reaction in the feces of 20 of 21 inocu lated pigs but not in the feces of uninoculated pigs. Seven inoculated pigs but no uninoculated pigs were detected shedding IS intracellular is by dot blot hybridization. Shedding was detected 1 to 5 weeks after inoculation, and clinical signs were seen in the second to fifth week s after inoculation. Few pigs without lesions of PE were found to shed IS intracellularis. There was a highly significant association betwee n the presence of IS intracellularis in feces or tissue and the presen ce of microscopic proliferative lesions and between the severity of th e lesions of PE and the percentage of IS intracellularis-infected inte stinal crypts. Pigs that ceased shedding TS intracellularis were signi ficantly less likely to have proliferative lesions. These and previous reports are consistent with the hypothesis that IS intracellularis is a necessary causative agent of PE.