Equine Infectious Gastrointestinal diseases

infectious causes of equine GI disease

• Salmonella spp.

• Clostridium perfringens & Clostridium difficile

• Equine Coronavirus

• Rotavirus (foals)

• Ehrlichia risticii –Potomac Horse Fever

Biosecurity hazard

admission policy - policy is not to admit any horse with a high suspicion of having infectious colitis in a hospital without an appropriate isolation facility

when referring veterinarian has established that a horse has any 2 of the following 3 clinical signs =

• acute diarrhoea

• fever

• low white blood cell count

case needs full isolation in a dedicated isolation facility 

equine isolation unit - entering

salmonella - enterocolitis and diarrhoea 

salmonella enterica

• 6 subspecies esp salmonella enterica aubsp enterica

• over 2000 serovars esp typhimurium

• other incl newport, anatum and agona

host specific cause more systemic disease 

salmonella - host-pathogen and environment interactions - pathogen

gram -ve motile bacillus

modified flagellae and pilli used for plasmid exchange

facultative anaerobe

facultatively intracellular esp pathological strains

wide range of antibiotic resistance 

1. adhesion molecule - 3 different types

2. invasion genes - encode proteins that cause ruffles in enterocyte membrane and salmonellae become interiorized

3. salmonella virulence plasmids - allow for intracellular growth, serum resistance and cellular invasion 

4. 3 exotoxins that all result in diarrhoea - cAMP, cytotoxin, phospholipase A activity 

salmonella risk factors - host

• Antibiotic treatment

• General anaesthesia

• Transport

• Competition

• Hospitalisation

• Surgery

• Feed withdrawal, change in feed

• Anthelmintic treatment

• Suppression of gastric acid?

• ANY STRESS

salmonella - host response

without invasion theres no response

lipopolysaccharide triggers massive neutrophil dominated inflammatory cascade 

LPS → macrophage → IL-1 and TNF → neutrophil activation 

persistence of facultative intracellular pathoggen in macrophages maintains inflammatory reaction 

inflammation and tissue necrosis lead to leakage of protein and fluid → diarrhoea 

exotoxins exacerbate inflammation and necrosis and promote more diarrhoea 

systemic inflammatory response syndrome(SIRS) aka endotoxaemia

low arterial blood pressure is major part of pathology due to =

• fluid loss - diarrhoea, oedema

• widespread/ dysregulated vasodilation - ABP = CO x SVR, reduced venous return to heart 

• multiorgan failure - incl. heart, CO = HR x SV

salmonella - hosr response

diarrhoea dilutes salmonella and toxins and removes them from body

diarrhoea and endotoxaemia leads to severe shock adn cardio-circulatory collapse

variable mortality - if hydration can be maintained diarrhoea and inflammation response eliminates infection and mucosa heals 

salmonella - host-pathogen and environment interactions - environment

survuve in damp soil up to 9 months

contagious - spread by direct contact and fomites

water and feed contaminated with faecal material 

recovered animals may be shed for wks or months 

host stress increases susceptibility and lowers required spore dose 

most frequently reported outbreaks are among hospitalised patients 

good for management and hygiene is effective control 

salmonella - control and prevention - personal

gloves, shoe covers and outer protective clothing must be put on before entering stable

gloves, show covers and outer protective clothing must be removed upon leaving stable and boots dipped before leaving isolation area 

washing hands after working with horses is essential - appropriate technique, antibacterial soap 

salmonella - control and prevention - stable

• Horses in isolation should be mucked out last to avoid spreading faecal contamination to neighbouring stables

• Soiled bedding and feed from isolated cases should be bagged and disposed of as clinical waste (do not compost)

• After the horse has been discharged the stable should be completely emptied, with all bedding, waste feed and disposable protective clothing being disposed of as clinical waste

• Other equipment from the stable should be rinsed to remove visible faecal contamination and then cleaned thoroughly with Bleach (hypochlorite) or Virkon and dried completely

• The stable should be steam cleaned or scrubbed with detergent to remove visible faecal contamination from the walls and then sprayed with bleach (0.5%) and left for 10 min then rinsed and the walls and floor sprayed with Virkon S (1%) and left 10 min, the stable rinsed and excess water removed.

• The stable should then be swabbed for bacterial culture and then left empty to dry completely

• If the culture results identify persistent contamination then the stable should be cleaned with Bleach (hypochlorite) or Virkon and then steam cleaned again, before repeating swabs.

• Once culture results suggest that the stable has been sufficiently disinfected, then it may be used for new admissions

how long does horse need to stay in isolation 

until 5 consecutive faecal cultures for salmonella(q12-24hrs) are negative 

salmonella - control and prevention

ensure safety of food and water sources

quarantine newly admitted horses for 10 days

avoid crowding

avoid rapid changes in diet

remove from pasture

barrier nurse at risk horses

zoonotic

other differential diagnosis for acute diarrhoea/ colitis

colostridium perfringens and clostridium difficile

acute necrotic colitis and dysentery 

equine coronavirus 

rotavirus - acute enterocolitis in foals 

ehrlichia resticii - potomac horse fever 

cyathastomiasis

right dorsal colitis 

clostridium perfringens and clostridium difficile colitis

saprophytic and part of normal intestinal flora

large gram +ve endospore forming bacilli

obligate anaerobes and haemolytic in culture

C. perfirnges - non-motile 

C.difficile - motile 

also C. septicum and sordellii

clostridium difficile - host-pathogen and enviroment interactions - pathogen

C. perfringens type A is most common in horses

• Enterotoxin –cytotoxic

• Alpha toxin –lecithinase (phospholipase activity)

• β2-toxin (toxigenic strain)

C. difficile –Toxin A & B

• proinflammatory (IL-1 & TNF)

• toxic to macrophages

clostridium difficile - host-pathogen and enviroment interactions - host

part of normal flora

requires host stress or intestinal flora change

high mortality rates 

good management and hygiene is usually effective control 

C. difficile is significant cause of diarrhoea in people - CDAD

stress factors 

• intercurrent infections

• extreme temp

• water deprivation 

• over crowding

• sudden change in diet

• antibiotic therapy 

• general anaesthesia 

clostridium difficile - host-pathogen and enviroment interactions - environment 

spore forming - survive indefinitely 

resistant to heat and cold

resistant to many disinfectants 

Clostridium perfringens & Clostridium difficile colitis - Diagnosis

culture is not reliable - part of normal flora and not all isolates are toxigenic

identification of C.perfringens enterotoxin or Beta2 toxin by ELISA or toxogenic genes by PCR

identification of C. difficile toxin A or B by ELISA or toxogenic genes by PCR

prevention and management a

void crowding and stress

avoid rapid changes in diet 

quarantine affected animals 

• barrier nurse

• dispose of soiled bedding carefully

• change outer clothing

• wash hands

equine coronavirus

can cause anorexia, fever, lethargy and colitis - often with lymphopaenia and neutropaenia

testing now comercially available - PCR faeces 

low mortality - incl in miniature breeds

varibale morbidity 

rotavirus - young(<2 months) foals

• Genus of the family Reoviridae (as is AHS & Blue Tongue)

• Multiple strains & serotypes (range of virulence)

• Strains appear to be predominantly host species specific

• Coat protein VP4 is the haemagglutinin that dictates species susceptibility

• VP4 protein - target antigen of neutralising antibody response

Rotavirus: Host-pathogen and environment interactions: pathogen

• Virus is ingested and infects the absorptive epithelium of the apices of the villi

• Mostly the small intestine is involved (occasionally colon)

• Damage and loss of cells in villi leads to villus atrophy, resulting in poor nutrient absorption and osmotic diarrhoea

• Virulent strains cause more necrosis and haemorrhage

• Humoral response by the host neutralizes virus

• Incubation period 18-24 hours

• Disease course is usually 5-7 days (self limiting)

• Recovered foals shed for 2 weeks

Rotavirus: Host-pathogen and environment interactions: host

most common infectious diarrhoea of horses

recovered animals may shed for weeks

host stress increases susceptibility

low mortality but can be high morbidity

age less than 2 months

intercurrent infections

extreme temperature

poor food and water sanitation

overcrowding

transportation

high levels of infection on property in previous yr

stressed adult horses may intermittently shed

Rotavirus: Host-pathogen and environment interactions: environment

contagious - spread by direct contact and fomites

water and feed contaminated with faecal material

survive in environment up to 9 months

resistant to bleach disinfectant - ethanol, phenols and formalin can inactive the virus

good management and hygiene is effective control

rotavirus diagnosis

clinical signs and identification of virus in faeces

PCR - rotavirus type A and B

electronmicroscopy - latec aggultination or ELISA field test

must rule out concurrent disease

rotavirus - control and prevention 

• Ensure clean food and water sources

• Avoid crowding foals together

• Clean foal bedding frequently

• Isolate severely affected foals

– Barrier nurse

– Wash hands

– Change outer garments

• Vaccination Equine Rotavirus vaccine (Zoetis)

– Mare in 8th , 9th & 10th months of EACH pregnancy

– Relies on good passive transfer and protects for approximately 60 days