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Year 2 Equine ID > Equine Infectious GI disease > Flashcards

Equine Infectious GI disease Flashcards

1
Q

Infectious causes of equine gastrointestinal disease

A
  1. Salmonella
  2. Clostridium perfringens and clostridium difficile
    Top 2 tend to be more severe
  3. Equine coronavirus - milder
  4. Rotavirus - foals only
  5. ## Ehrlichia risticii - Potomac Horse FEver (not UK yet)Acute necrotic colitis and dysentery
    All tend to cause diarrhoea
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2
Q

What rick does equine gastrointestinal disease pose?

A

Biosecurity hazard

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3
Q

Due to the biosecurity hazard of equine infectious gastrointestinal disease, what is the administration policy?

A

• Policy is not to admit any horse with a high suspicion of having infectious colitis in a hospital without an appropriate isolation facility.
• Therefore, when a referring veterinarian has established that a horse has any 2 of the following 3 clinical signs horse goes straight into isolation in a dedicated facility:
1. Acute diarrhoae
2. Fever
3. Low white blood cell count

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4
Q

What is classed as a fever and low WBC count in horse?

A 
o	Fever (temperature over 38.5oC)  
Normal = 37.5-38.5°C 
o	Low white blood cell count (less than 4.0x109cells/L)
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5
Q

Isolation facility

A

Own water and feed source. Mucked out directly into yellow bags

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6
Q

What bacteria causes salmonellosis in horses?

A
  1. Salmonella enterica (most common) or salmonella bongori

2. It causes Salmonella Enterocolitis - bacterial infection in small intestine lining

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7
Q

Talk about salmonelle enterica

A

the vast majority seen in equine hospital
o 6 subspecies esp Salmonella enterica subsp enterica
o Over 2000 serovars esp. Typhimurium
o Others include Newport, Anatum and Agona
• can be Host specific and non‐host specific
o Host specific cause more systemic disease

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8
Q

Morphology and Pathogenesis of salmonella enterica

A
  • Gram –ve motile bacillus
  • Modified flagellae & pilli used for plasmid exchange
  • Facultative anaerobe
  • Facultatively intracellular –the most pathologic strains are best at this – best at going into cells and causing damage
  • Wide range of antibiotic resistance

P:
Bacteria penetrates through SI epithelium, binds to epithelium with adhesions, release effectors which lead to bacterial mediated endocytosis, trigger cascade of celleular signals, release endotoxins lead to intestinal damage

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9
Q

What are the properties of salmonella enterica that aid virulence?

A
  • Adhesion molecules –3 different types (species selectivity)
  • Invasion genes –encode proteins that cause ruffles in enterocyte membrane and Salmonellae become interiorized.
  • Salmonella Virulence Plasmids –allow for intracellular growth, serum resistance and cellular invasion
  • 3 Exotoxins that all result in diarrhoea –cAMP, Cytotoxin, Phospholipase A activity
  • Leads to intestinal damage which results in endotoxemia
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10
Q

What factors inc host susceptibility to salmonella?

A 
o	Antibiotic treatment 
o	General Anaesthesia 
o	Transport 
o	Competition 
o	Hospitalisation 
o	Surgery 
o	Feed withdrawal, change in feed (hospital hay)
o	Anthelmintic treatment 
o	Suppress gastric acid?
o	ANY STRESS
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11
Q

What is the pathological response to invasion?

A

o Inc neutrophil recruitment
o GI inflammation
o Inc fluid secretion into GI lumen
o Then neutrophils release inflammatory mediators which cause massive epithelial damage, tissue necrosis - loss of protein, loss of SIRS, and endotoxin release
• Exotoxins exacerbate inflammation and necrosis and promote more diarrhoea
• Endotoxemia

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12
Q

What is endotoxemia known as?

related to whihc GI infection?

A

systemic inflammatory response syndrome (SIRS)

SALMONELLA

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13
Q

Broadly what is the host response to salmonella and so what is the main treatment?

A
  1. AIM - get rid of salmonella nad toxins

2. Treatment - SUPPORTIVE

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14
Q

What is the host response to salmonella?

A

• Diarrhoea dilutes Salmonella and toxins and removes them from body
• Diarrhoea and endotoxaemia leads to severe shock and cardio‐circulatory collapse
o If hydration can be maintained diarrhoea and inflammatory response eliminates infection

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15
Q

Treatment for salmonellosis

A
  1. Supportive
  2. fluid therapy to replace losses, colloids to replace loss of proteins and balance electrolytes
  3. Not all treatment will be successful, can lead to this level of necrosis, horses often lost to this disease
    • Antibiotics are controversial:
    o often haven’t proven salmonella for few days until positive culture
    o AB disrupts normal GI flora – risk factor in first place
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16
Q

SAlmonella in environment

A
  • Survive in damp soil up to 9 months
  • Does stay in hospital so physical cleaning essential and swab stable to ensure clean before another goes in
  • Got to be super care with hospital population as all will be vulnerable
  • Contagious spread by direct contact & fomites
  • Water and feed contaminated with faecal material
  • Recovered animals may shed for weeks or months
  • Host stress increases susceptibility and lowers required spore dose
  • Most frequently reported outbreaks are amongst hospitalised patients
  • Good management, biosecurity and hygiene is effective control
17
Q

Control and prevention of salmonella spreading human

A

• Washing your hands after working with horses and particularly before eating or drinking is essential
• Be careful when taking off PPE
• When washing your hands you must ensure to use an appropriate antibacterial soap and to thoroughly wash all parts of your hands
o pay particular attention to the area under nails
• Gloves, shoe covers and outer protective clothing (disposable overalls) must be put on before entering the stable
• Gloves, shoe covers and outer protective clothing must be removed upon leaving the stable and boots dipped before leaving the isolation area
• After leaving the stable your hands should be washed immediately and thoroughly with an antibacterial soap
**DO NOT SUCK or BLOW on tube of horse with suspected salmonella or clostridia

18
Q

Control and prevention of salmonella: stable (see notes week 9)

A
  • 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 on muck heap)
  • 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 Virkonand dried completely - keep equipment with horse till leaves
  • The stableshould 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 VirkonS (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 Virkonand 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
19
Q

How long does horse will salmonella need to stay in iso for?

A

• Once a horse is placed in isolation, the isolation protocol must remain in place until either all 5 faecal cultures for Salmonella ( taken 12 hours apart due to intermittent shedding) are reported back as negative, or the horse goes home

20
Q

Control and prevention salmonellosis

A

• Ensure safety of food and water sources
• Quarantine newly admitted horses for 10 days
• Quarantine affected and recently recovered animals
• Avoid crowding (sales, transport)
• Avoid rapid changes in diet
• Remove from pasture
• Barrier nurse at risk horses (???which are these)
o Hard to define as a lot of horses would be at risk
• Zoonotic

21
Q

If tested horse and NOT salmonella. What are the other things we need to consider?

A

• Clostridium perfringens & Clostridium difficile
• Acute necrotic colitis & dysentery (Colitis X)
o Sever colitis, neg for clostridum and salmonella. Organism for causing disease unknown
• Rotavirus –acute enterocolitis in foals (tends to be limited to foals)
• Ehrlichia risticii – Potomac Horse Fever (acute colitis) (tends to be problem only in US and Europe, currently not UK!)
• (Cyathastomiasisi)
• (Right dorsal colitis) – d following use of non steroidals in horse

22
Q

Clostridium perfringens& Clostridium difficile colitis

A
  • Saprophytic and part of normal intestinal flora
  • Large G +ve endospore forming bacilli
  • Obligate anaerobes and haemolytic in culture
  • C. perfringens‐non‐motile
  • C. difficile‐motile
  • (also C septicum and sordelli)
  • Fact that shedding doesn’t necessarily mean diseased
  • CLostrdium is spore forming so can be in environemtfor a long time
23
Q

Pathogens of Clostridium perfringens& Clostridium difficile colitis

A

• C. perfringens type A is most common in horses
o Enterotoxin–cytotoxic
o Alpha toxin –lecithinase (phosplipase activity)
o β2‐toxin (toxigenic strain)
• C. difficile–Toxin A pro inflammatory (IL‐1 & TNF)
o toxic to Macrophages

24
Q

Environemtn and host interaction of Clostridium perfringens& Clostridium difficile colitis

A

• Part of normal flora
• Requires host ‘stress’ or intestinal flora change (grain overload, rapid diet change)
• High mortality rates
• Good management and hygiene is usually effective control
• C. difficile is a significant cause of diarrhoea in people
• Stress Factors (similar to what we see in salmonella)
o Intercurrent infections
o Extreme temperature
o Water deprivation
o Overcrowding
o Sudden change in diet
o Transportation
o Antibiotic therapy
o General anaesthesia

25
Q

Clostridium perfringens& Clostridium difficile colitis in environment

A

• Spore forming bacteria (survive indefinitely)
o Can be huge issue for stud farms
o Problem one year – vulnerable population the next year
• Resistant to heat and cold
• Resistant to many disinfectants

26
Q

Diagnosis of clostridium perfringens and clostridium difficile colitis

A
  • LOT of false positives as normal horses shed
  • Culture is not reliable (part of normal flora and not all isolates are toxigenic)
  • Identification of C. perfringens enterotoxin by ELISA (enzyme linked immunoabsorbant) or β2‐toxin by ELISA or PCR
  • Identification of C. difficile toxin A by ELISA or PCR
27
Q

Prevention and management of clostridium perfringens and clostridium difficile colitis

A

• Prevention easier said than done
• Avoid crowding & stress (sales, transport)
• Avoid rapid changes in diet
• Good clinical reason for use of antibiotic
• Quarantine affected animals
o Barrier nurse o
o Dispose of soiled bedding carefully to ensure faeces from infected animal doesn’t come into close contact with any other
o Change outer clothing
o Wash hands

28
Q

What is the standard protocol of tests for a horse presenting with diarrhoea?

A

Salmonella, Clostridia and Corona virus

29
Q

Equine corona virus

A
  1. tends to be mild
  2. Presents with: anorexia, fever, lethargy, colitis often wiht lymphopaenia and neutropaenia - fits isolation criteria
  3. Lower mortality that S and C
  4. Variable morbidity
30
Q

Rotavirus

A

• Most common cause of foal enteritis (inflammation of SI)
• Genus of the family Reoviridae (as is AHS & Blue Tongue)
o Same genera are diseases that can cause blue tongue and African horse sickness
o Grouped A-G, differentatied due to innercapsin
• Multiple strains & serotypes (range of virulence)
• Strains appear to be predominantly host species specific
• Outer Coat protein VP4 is the haemagglutinin that dictates species susceptibility
• VP4 protein ‐target antigen of neutralising antibody response

31
Q

PAthogeneiss of rotavirus

A
  • 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
32
Q

Rotavirus - host

A
  • Good foal management, if had disease before increased risk the following year
  • 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 (ie naïve immune status)
  • Intercurrent infections
  • Extreme temperature
  • Poor food and water sanitation
  • Overcrowding
  • Transportation
  • High levels of infection on property in previous year
  • Stressed adult horses may intermittently shed
33
Q

Pathogeneis rotavirus

A

• Virus is ingested and invades rapidly dividing cells
• infects the absorptive epithelium of the villi tips of Duodenum and jejunum  villus blunting and atrophy
o causes reduce in lactase production (secondary lactose intolerance) and hyperosmotic GI lumen  osmotic diarrhoea
o crip cells not as affected
• 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

34
Q

Rotavirus environment

A

• Contagious organism – spread by direct contact & fomites
• Water and feed contaminated with faecal material
• Survive in environment up to 9 months
o Multiple foals, 11 months from 1 to next batch, likely to survive until the next year
• Resistant to bleach disinfectant
o Early detection is really important
o Ethanol, phenols and formalin can inactive the virus
• Good management and hygiene is effective control

35
Q

Diagnosis rotavirus

A

• clinical signs & identification of virus in faeces
o cow pat – watery faecces
o if watery might not see staining on the foal as learns to lift tail very quickly
o Reduced suckling, maybe fever
• Electron microscopy to diagnose (gold standard) latex agglutination or ELISA field tests
• Must rule out concurrent disease

36
Q

Control and Prevention rotavirus

A

• Ensure clean food and water sources
• Avoid crowding foals together
• Clean foal bedding frequently
• Isolate severely affected foals
o Barrier nurse
o Wash hands
o Change outer garments
• Vaccination Equine Rotavirus vaccine (Zoetis)
o Mare in 8th, 9th& 10thMonths of EACH pregnancy
o Relies on good passive transfer and protects for approximately 60 days
 Cholostrum
 Most foals not affected when over 2 months so this gives good protection

37
Q

Summary of equine gasterointestinal

A
  • Pathogen –host and environment interactions determine susceptibility and degree of disease
  • Diagnosis is pathogen specific and must be initiated immediately. It is KEY. Limits disease passing to both animals and humans
  • Similar protocols for isolation, biosecurity and management of affected horses
  • Disease specific prevention is available for some diseases, but in all cases excellent management and hygiene are key

Year 2 Equine ID (7 decks)

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