CLINICAL AND PATHOLOGICAL DIFFERENCES IN ENTERIC INFECTIONS IN PIGS CAUSED BY <i>ESCHERICHIA COLI</i> AND BY TRANSMISSIBLE GASTROENTERITIS VIRUS

Bohl, E. H.; Cross, R F

doi:10.1111/j.1749-6632.1971.tb35001.x

Cited by 12 publications

(5 citation statements)

References 8 publications

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“…A comparison of the S gene sequences among 11 TGEV isolates showed that isolate C11 had the lowest computing distance (0.35) with isolate C8, while the computing distances with the Miller strain (MIL65) and the porcine respiratory coronaviruses (PRCoVs) were higher than 2.0 and 3.0, respectively (44). These data strongly suggest that isolate C8 is derived from C11 and not from other viruses circulating at the same time and in the same geographical area, such as the Miller strain, which was isolated in Fredericksburg, Ohio (8,67). The relationship between the two isolates is in agreement with the results obtained by generating an evolutionary tree of TGEV (53).…”

Section: Discussionmentioning

confidence: 78%

Targeted Recombination Demonstrates that the Spike Gene of Transmissible Gastroenteritis Coronavirus Is a Determinant of Its Enteric Tropism and Virulence

Sánchez

Izeta

Sánchez-Morgado

et al. 1999

J Virol

200

224

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Targeted recombination within the S (spike) gene of transmissible gastroenteritis coronavirus (TGEV) was promoted by passage of helper respiratory virus isolates in cells transfected with a TGEV-derived defective minigenome carrying the S gene from an enteric isolate. The minigenome was efficiently replicated in trans and packaged by the helper virus, leading to the formation of true recombinant and pseudorecombinant viruses containing the S proteins of both enteric and respiratory TGEV strains in their envelopes. The recombinants acquired an enteric tropism, and their analysis showed that they were generated by homologous recombination that implied a double crossover in the S gene resulting in replacement of most of the respiratory, attenuated strain S gene (nucleotides 96 to 3700) by the S gene of the enteric, virulent isolate. The recombinant virus was virulent and rapidly evolved in swine testis cells by the introduction of point mutations and in-phase codon deletions in a domain of the S gene (nucleotides 217 to 665) previously implicated in the tropism of TGEV. The helper virus, with an original respiratory tropism, was also found in the enteric tract, probably because pseudorecombinant viruses carrying the spike proteins from the respiratory strain and the enteric virus in their envelopes were formed. These results demonstrated that a change in the tropism and virulence of TGEV can be engineered by sequence changes in the S gene.

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Section: Discussionmentioning

confidence: 78%

Targeted Recombination Demonstrates that the Spike Gene of Transmissible Gastroenteritis Coronavirus Is a Determinant of Its Enteric Tropism and Virulence

Sánchez

Izeta

Sánchez-Morgado

et al. 1999

J Virol

200

224

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“…The use of conventional pigs makes it impossible to decide if E. coli caused this defect. In experiments with neonatal pigs, infection with enterotoxigenic E. coli did not impair lactase activity, whereas the enzyme was absent completely from small intestines of pigs infected with transmissible gastroenteritis [4].…”

Section: Resultsmentioning

confidence: 99%

Bacterial Colonization and Morphology of the Intestine in Porcine Escherichia Coli Enterotoxemia (Edema Disease)

Bertschinger

Pohlenz

1983

Vet Pathol

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Twenty-one pigs were divided into three groups. Pigs in one group were inoculated with the intestinal contents which included bacteria from a pig with edema disease. Pigs in another group were inoculated with a culture of Escherichia coli serogroup O 139:K12(B):H1 isolated from the aforementioned contents, and pigs in a third group served as uninoculated controls. The infection was similar following both inocula. Enterotoxemia developed in 11 of the 14 pigs allowed to survive for more than two days. The onset varied from two to seven days after inoculation. There were maximal viable counts of E. coli in the intestine from the second day post-inoculation and thereafter. In frozen and paraffin sections, as well as by scanning electron microscopy, the organisms were seen on the surface of the small intestinal epithelium where they formed either isolated colonies or continuous layers. They colonized the lower small intestine more intensely than the upper section. The intestinal epithelium and the villi of infected pigs were indistinguishable morphologically from the tissues of three uninoculated control pigs. The diarrhea which was observed in controls and inoculated pigs before inoculation and the villus atrophy in controls and inoculated pigs indicated a preexisting infection with at least one other agent.

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“…Experimental S. typhimurium infection in rats resulted in no change in stomach and upper small bowel in most (Maenza et al, 1970). However, pigs with transmissible gastroenteritis, a viral infection of the upper small bowel, showed severe villous atrophy and cellular infiltration (Bohl and Cross, 1971). …”

Section: Resultsmentioning

confidence: 99%

Duodenal mucosal damage in 31 infants with gastroenteritis

Barnes¹,

Townley²

1973

Archives of Disease in Childhood

137

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CLINICAL AND PATHOLOGICAL DIFFERENCES IN ENTERIC INFECTIONS IN PIGS CAUSED BY ESCHERICHIA COLI AND BY TRANSMISSIBLE GASTROENTERITIS VIRUS

Cited by 12 publications

References 8 publications

Targeted Recombination Demonstrates that the Spike Gene of Transmissible Gastroenteritis Coronavirus Is a Determinant of Its Enteric Tropism and Virulence

Targeted Recombination Demonstrates that the Spike Gene of Transmissible Gastroenteritis Coronavirus Is a Determinant of Its Enteric Tropism and Virulence

Bacterial Colonization and Morphology of the Intestine in Porcine Escherichia Coli Enterotoxemia (Edema Disease)

Duodenal mucosal damage in 31 infants with gastroenteritis

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