Proliferative Enterocolitis Associated with Dual Infection with Enteropathogenic
            <i>Escherichia coli</i>
            and
            <i>Lawsonia intracellularis</i>
            in Rabbits

Schauer, David B.; McCathey, Sonya N.; Daft, B. M.; Jha, Sharda; Tatterson, Lisa E.; Taylor, Nancy S.; Fox, James G.

doi:10.1128/jcm.36.6.1700-1703.1998

Cited by 19 publications

(6 citation statements)

References 22 publications

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“…Several studies have noted concurrent infections in animals suffering from PE: spirochetosis in rhesus macaques and Escherichia coli enteropathy in European hamsters and rabbits. Unfortunately, researchers were not able to determine the pathogenesis of these dual infections: if L intracellularis was at the root of the infection and allowed another disease to develop, if a synergism mechanism was at play or if those coinfections were incidental 4 8 18…”

Section: Discussionmentioning

confidence: 99%

Suspicion of epizootic Lawsonia intracellularis disease in a group of pileated gibbons (Hylobates pileatus)

Quintard

François-Brazier²,

Giorgiadis³

et al. 2020

Vet Record Case Reports

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Within a month, all five individuals of a pileated gibbon (Hylobates pileatus) family presented the same symptoms: diarrhoea, vomiting and severe apathy. During this first outbreak, three of them died acutely and a fourth died during another outbreak 7 months later. Extensive virology, bacteriology and parasitology undertaken on faeces did not reveal any pathogen. Haematology and extensive biochemistry did not demonstrate any obvious medical disorder. Necropsy revealed a severe proliferative enteropathy, and rare argyrophilic bacteria were noted within the lumen of hyperplastic colonic glands on histology with silver staining. Specific faecal PCR was positive for Lawsonia intracellularis infection. These combined elements led to a strong suspicion of L intracellularis epizooty, despite the absence of large numbers of argyrophilic bacteria, as usually expected in this disease process. L intracellularis has mostly been described in pigs even if reported in a broad range of mammalian species including primates. L intracellularis may be underdiagnosed in zoos as it requires a faecal PCR for identification and silver staining for histological visualisation.

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Section: Discussionmentioning

confidence: 99%

Suspicion of epizootic Lawsonia intracellularis disease in a group of pileated gibbons (Hylobates pileatus)

Quintard

François-Brazier²,

Giorgiadis³

et al. 2020

Vet Record Case Reports

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show abstract

“…Other examples of dual infections with EPEC and another pathogen have also been reported. For example, Schauer et al noted an outbreak of enterocolitis in rabbits due to the combination of rabbit EPEC and an intracellular pathogen, Lawsonia intracellularis (48). In a study of turkeys, Guy et al found that dual infection with an avian EPEC and turkey coronavirus produced a much higher mortality rate than with either microbe singly (30).…”

Section: Discussionmentioning

confidence: 99%

Mutual Enhancement of Virulence by Enterotoxigenic and Enteropathogenic Escherichia coli

et al. 2006

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Enterotoxigenic Escherichia coli (ETEC) and enteropathogenic E. coli (EPEC) are common causes of diarrhea in children in developing countries. Dual infections with both pathogens have been noted fairly frequently in studies of diarrhea around the world. In previous laboratory work, we noted that cholera toxin and forskolin markedly potentiated EPEC-induced ATP release from the host cell, and this potentiated release was found to be mediated by the cystic fibrosis transmembrane conductance regulator. In this study, we examined whether the ETEC heat-labile toxin (LT) or the heat-stable toxin (STa, also known as ST) potentiated EPEC-induced ATP release. We found that crude ETEC culture filtrates, as well as purified ETEC toxins, did potentiate EPEC-induced ATP release in cultured T84 cells. Coinfection of T84 cells with live ETEC plus EPEC bacteria also resulted in enhanced ATP release compared to EPEC alone. In Ussing chamber studies of chloride secretion, adenine nucleotides released from the host by EPEC also significantly enhanced the chloride secretory responses that were triggered by crude ETEC filtrates, purified STa, and the peptide hormone guanylin. In addition, adenosine and LT had additive or synergistic effects in inducing vacuole formation in T84 cells. Therefore, ETEC toxins and EPEC-induced damage to the host cell both enhance the virulence of the other type of E. coli. Our in vitro data demonstrate a molecular basis for a microbial interaction, which could result in increased severity of disease in vivo in individuals who are coinfected with ETEC and EPEC. Along with rotavirus, enterotoxigenic Escherichia coli (ETEC)and enteropathogenic E. coli (EPEC) are among the most common causes of diarrhea in children in developing countries (29). Dual infections with both pathogens have been noted fairly frequently in studies of diarrhea around the world for many years (41,42). More recent studies of diarrhea etiology have begun to describe multiple infections carefully, and evidence is emerging that patients with multiple pathogens are likely to experience more-severe diarrheal disease (2,8,24,35,40,59).One might expect dual infections with EPEC and ETEC to occur occasionally by chance alone, especially in povertystricken areas with poor hygiene. However, studies of diarrhea etiology in areas with good sanitation also noted dual infections with EPEC and ETEC. The tendency of EPEC and ETEC to occur in multiple infections has been noted in epidemiology surveys in developed countries such as northern Italy (8), Israel (24), and Yugoslavia prior to the Balkan war (13). EPEC and ETEC coinfection was also found in an investigation of a hospital outbreak in Durban, South Africa (1). Several of the children in the latter outbreak had a triple infection with EPEC, ETEC, and rotavirus.Recent work from our laboratory suggested a molecular mechanism by which EPEC and ETEC might interact. Specifically, we found that cholera toxin (CT) and forskolin enhance EPEC-induced ATP release from the host cell (15) without any enha...

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“…Rabbit EPEC is an attaching and effacing E coli strain, where bacterial adherence, via a fimbrial adhesin, results in destruction of the brush border and rearrangement of the enterocyte structure. High levels of Shiga toxin are not expressed by EPEC strains [62]. Transmission is by the fecal-oral route.…”

Section: Coliobacillosismentioning

confidence: 99%

“…Loperamide hydrochloride and fluid rehydration proved successful in the treatment of an E coli outbreak in 22 adult New Zealand white rabbits all fully recovered within 2 weeks [57]. Prognosis is guarded to poor, but is dependent on the strain of E coli, immunocompetence of the animal and presence of synergistic copathogens such as Lawsonia intracellularis (Campylobacter-like organism) or rotavirus [62].…”

Section: Coliobacillosismentioning

confidence: 99%

Rabbit Gastroenterology

Reusch

2005

Veterinary Clinics of North America: Exotic Animal Practice

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Proliferative Enterocolitis Associated with Dual Infection with Enteropathogenic Escherichia coli and Lawsonia intracellularis in Rabbits

Cited by 19 publications

References 22 publications

Suspicion of epizootic Lawsonia intracellularis disease in a group of pileated gibbons (Hylobates pileatus)

Suspicion of epizootic Lawsonia intracellularis disease in a group of pileated gibbons (Hylobates pileatus)

Mutual Enhancement of Virulence by Enterotoxigenic and Enteropathogenic Escherichia coli

Rabbit Gastroenterology

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