Introduction

• Cause: not yet determined, thought to be bacterial.
• Signs: anorexia, reduced growth, mild watery diarrhea, abdominal distension, mucus excretion and cecal impaction.
• Diagnosis: based on epidemiology of group outbreak and pathological findings.
• Treatment: antibiosis may reduce group mortality.
• Prognosis: poor.

Pathogenesis

Etiology

• Major changes in intestinal microbial communities - dysbiosis.
• Disease transmission by intestinal contents, ie ingestion of contaminated feed, feces and contact with affected rabbits:
  • Etiological agent not been identified, but most likely a bacterial infection: In one study, genus Clostridium and species Cloacibacillus porcorum and Akkermansia muciniphila associated with the disease.
  • In another study on infected rabbits, high concentrations of Clostridum sordelli and Bacillus firmus were isolated from intestinal contents.
  • Disease has been associated with presence of Clostridium perfringens alpha toxin but inoculation with these bacteria has not resulted in consistent clinical signs.
  • One study identified a single novel Clostridium spp (Clostridium cuniculi) on day or ERE onset.
• Diet may be a factor: high-insoluble fiber diets appear to increase development of ERE. In one study, ERE was reproduced by feeding a low-fiber diet.

Predisposing factors

General

• Feeding a low-fiber diet may predispose to ERE Nutrition: dietary requirements.

Specific

• Age: post-wearing.

Pathophysiology

• Difference in diversity and abundance of gastrointestinal microbiota compared to healthy rabbits.
• Frequent co-infection with other common rabbit pathogens.
• One study showed multiple changes in the digestive tract microbiota when feeding low-fiber diets:
  • Overgrowth of Bacteroides fragilis, Clostridium perfringen, Enterobacter sakazakii and Akkermansia muciniphila
  • Inhibition of Bifidobacterium spp and Butyrivibrio fibrisolvens in stomach/small intestine/cecum.
  • This in turn led to a decrease in butyrate yield and to ERE.
• A disease with similar clinical signs has been described in China, with epizootic outbreaks of mucoid enteropathy syndrome (MES) Enteritis/enteropathy and associated economic losses. Mortality rate in one study was 70%. Deemed a different disease as microbiota cecal changes differed from ERE.
• Changes in gene expression patterns have been shown – with high levels for mucins and inflammatory cytokines. This suggests inadequate immune defense mechanisms may be involved in the disease pathophysiology.

Timecourse

• Highly contagious, with 30-40% mortality in a few days.
• Incubation as low as 1-2 days.
• Disease peaks 4-6 days after experimental inoculation in a group.
• Reduced growth rates seen from 2 days until end of second week after experimental inoculation.

Diagnosis

Treatment

Prevention

Outcomes