Equine 2 Flashcards
explain how equine grass sickness can lead to ileus
generalised dysautonomia –> decreased intestinal motility and GI secretions –> ileus +/- large colon impactions leading to ileus
what are the clinical signs of equine grass sickness
- death in 48 hours if acute
- colic
- gastric fluid reflux on NG intubation
- pseudoimpactions
- tucked up posture
- sweating
- muscle fasciculations
- ptosis
- tachycardia (beyond that expected for degree of pain/hypovolaemia)
- rhinitis sicca
what is the current thought on EGS aetiology?
toxicoinfection with Clostridium botulinum types C and D whereby the toxin is locally produced in the horse’s GIT
what are the horse related risk factors of EGS
- age 2-7yo (rare in foals and older horses)
- good/fat condition
- low antibody levels to C botulinum type C and BoNT/C
what are the seasonal risk factors of EGS
- spring and early summer (can be year round)
- cooler, dry weather with irregular frosts in 2 weeks before outbreak
what are the premises risk factors of EGS
- high numbers of horses
- young horses present
- stud/livery/riding school
- sand and loam soils > clay > chalk
- increased soil nitrogen
- previous occurrence at site
what are the management risk factors of EGS
- access to grass
- dietary change
- movement/stress
- pasture disturbance
- anthelmintic use (ivermectins)
- mechanical droppings removal
how is EGS definitively diagnosed
histopathology of autonomic or enteric ganglia at PM or following ileal biopsy (exlap will lead to diagnosis but worse for prognosis)
see chromatolysis, vacuolation of cells within autonomic ganglia
what is the result of topical administration of phenylephrine drops 0.5% to the eye
reversal of ptosis in ipsilateral eye
false positives can be seen e.g. if A2A used
what may be seen on oesophgeal endoscopy and barium swallow in EGS
linear oesophageal ulcers (due to GI reflux)
defective oesophageal motility
how is acute or subacute EGS treated
IV fluids analgesia regular gastric decompression feeding once definitive diagnosis made recommend euthanasia or some subacute cases may become chronic and survive
how is chronic EGS treated
- analgesia
- palatable, high energy food available
- hand feed
- box rest with regular walks and grass access
- warmth
- monitor weight
- bute or flunixiin and omeprazole for post-prandial colic
- mucolytics/steam for rhinitis
- prokinetics (cisapride no longer available)
- appetite simulation (diazepam uncommonly used)
when should you consider treating EGS
- horse attempting to swallow feed and drink and retains some ability to do so
- no continuous moderate/severe colic signs
what premises factors may help prevent EGS
- avoid previously affected sites
- soil exposure
what management factors may help to prevent EGS
minimise
- grazing
- movement
- change of feed
- pasture disturbance
- frequent ivermectin use
- mechanical droppings removal
what protective factors may help prevent EGS
- cograzing with ruminants
- regular grass cutting
- manual droppings removal
- supplementary forage feeding
What are the main features of enterobacteriaceae
- gram negative rods
- facultative anaerobes
- most are motile
- tolerate bile salts in selective media
- grow on non-enriched media
- oxidase negative
- catalase positive
- ferment glucose
- reduce nitrate
name the major enteric pathogenic enterobacteriaceae
E coli
salmonella serotypes
yersinia
name some opportunistic enterobacteriaceae
- proteus
- enterobacter
- klebiella
how are enterobacteriaceae differentiated
- lactose fermentations
- reactions on selective media
- eosin-methylene blue agar (E coli)
- colonial morphology
- PCR
which enterobacteriaceae have mucoid colonial mophology
- klebsiella
- enterobacter
which enterobacteriaceae swarms on rich media
proteus
which enterobacteriaceae has red pigmentation
serratia marcescens
which strains of E coli are important
- ETEC
- EPEC
- VTEC
What are the cultural properties of campylobacter
- flat, droplet-like, glistening colonies that spread along the direction of the streak on moist agar
- white to salmon coloured when older
- characteristic odour
- take two days to grow
what are the microscopic properties of campylobacter
- gram negative
- slender
- vibrio shaped
which species of campylobacter are important (GI and repro)
- jejuni subsp jejuni
- coli
- fetus subsp fetus
- fetus subsp venerealis
what occurs during initial colonisation of campylobacter in birds
inflammatory response
reduced weight gain and hock burn are correlated to colonisation with which organism in birds
campylobacter
when might campylobacter be associated with disease in dogs
- young or debilitated animals
- synergy with other pathogens
what are the microbiological properties of clostridia
- gram positive
- rod shaped
- tetani are thin
- perfringens are large and wide
- obligate anaerobes
- produce endospores
which species of Clostridia are important
- botulinum
- difficile
- perfringens
- tetani
what are the cultural properties of clostridia
small to medium sized, grey/yellow, translucent colonies
rough with lobate margin, or flat with irregular surface and filamentous margin
perfringens is non-proteolytic and has no distinct odour
how should sampling for clostridia be carried out
- anaerobic transport medium
- prompt culture on enriched blood agar
- anaerobic atmosphere with hydrogen and 5-10% CO2
where can clostridia be sampled from
- soil
- fresh water
- marine water
- part of normal GI flora
- fresh cadaver material (overgrowth if old)
how can clostridia species by differentiated
perfringens - double haemolysis
biochemical identification
ELSIA for toxins
antibody based techniques from lesion samples
how is lawsonia diagnosed
- clinical signs and gross pathological findings
- PCR or immunofluorescent tests
why is lawsonia hard to culture
obligate intracellular pathogen
intestinal spirochetes are important pathogens of which species
pigs
poultry
how are spirochetes and brachyspira diagnosed and differentiated
observation in stained faecal smears
grown anaerobically and confirmed by culture on selective blood agar
differentiate on haemolysis
which bacterium causes Johne’s disease in ruminants
Mycobacterium avium subspecies paratuberculosis
how is M avium subsp paratuberculosis sampled from animals
scrapings
punch biopsies from rectum
which diagnostic methods can be used for M avium subsp paratuberculosis
histopathology - affected tissue or lymph nodes
microscopy with ZN technique
culture is difficult and time consuming
what are the properties of actinobacillus lignieresii
- gram negative rod
- facultative anaerobe
- oxidase positive
- urease negative
- commensal of mucous membranes
which bactrium causes wooden tongue in cattle
actinobacillus lignieresii
how does actinobacillus lignieresii cause wooden tongue
invade through breaks in mucous membrane
spread limited to soft tissues of tongue and LNs of head
tongue becomes hard, swollen and painful
what are the properties of actinomyces bovis
gram positive anaerobic (some other species facultative) non-spore forming rod shaped branched networks of hyphae
which bacterium causes lumpy jaw in cattle
actinomyces bovis
describe lumpy jaw
tumour like swellings on the upper and lower jawbones of cattle that develop slowly over months consisting of honeycombed masses of bone filled with pus. can develop and discharge small amounts of pus containing yellow granules
how does actinomyces infect cattle
breaks in the mucous membrane lining of the mouth
what is the treatment of lumpy jaw
iodine therapy
tetracyclines
what are the features of fusobacterium necrophorum
- gram negative
- obligate anaerobe
- non-spore forming
- non-motile
where is fusobacterium necrophorum found in animals
alimentary tract
cattle - respiratory tract
what does fusobacterium necrophorum infection involve
injury to epidermal layer allows infection to be established. Affects the mucous membranes and underlying tissues of the oral cavity epithelium. self-limiting.
what are the potential pathogenic mechanisms of fusobacterium necrophorum
toxins:
- leucocidins
- haemolysin
- cytoplasmic
how is fusobacterium necrophorum treated
penicillins
generally self-limiting
describe the process of testing resistance profiles with disc diffusion
- 100ul bacteria on non-selective agar plate
- discs placed on agar label up
- incubation under specified conditions
- compare zone diameter to standard measurements
describe MIC testing using E strips
place strip on agar with bacteria. MIC is at the point where the edge of the zone of inhibition crosses the E strip.
define intrinsic resistance
organism naturally resistant to certain groups of antibiotics
describe acquired resistance
transferable or heritable modification of self
What is EGUS
Equine gastric ulcer syndrome
what has EGUS now been split into
ESGD (equine squamous gastric disease) and EGGD (equine glandular gastric disease)
list the disorders of the equine stomach
ESGD EGGD Gastric disease in foals gastric rupture gastric impaction habronemiasis gasterophilus gastric neoplasia
explain the pathogenesis of ESGD
- prolonged exposure to mucosal aggressive factors
- mucosal protective factors absent in squamous region (lack of mucosal-bicarbonarte film)
- reduced gastric pH
- Acid splashes up onto the surface of the squamous region
what factors are mucosal aggressive
- HCl
- pepsin
- bile acids
- other organic acids
what factors are mucosal protective
- mucous
- bicarbonate
only present in the glandular region
what factors reduce gastric pH
- no food buffer (especially fibre)
- ileus (increase in bile acids in stomach)
- high carbohydrate diet (more VFAs, dissociate at low pH)
- stress
ESGD is seen most commonly in which types of horses?
performance horses and broodmares
At what grade does ESGD cause clinical signs
generally grade 3 or more
list the clinical signs of ESGD
- often none
- poor performance
- attitude changes
- mild, acute or recurrent colic
- decreased appetite –> weight loss/reduction in BCS
how is ESGD diagnosed
gastroscopy - diagnose and grade level of ulceration
how is ESGD treated
Omeprazole (first choice)
- proton pump inhibitor
- licensed
- PO SID
- £350-500/month
Ranitidine
- H2 blocker
- more effective in rested horses
- unlicensed
- cheaper
- TID
- almost never used
describe grade 1 ulcers
yellow hyperkeratinisation on surface but mucosa still intact. not associated with clinical signs
describe grade 2 ulcers
multiple, small, multifocal lesions. reasonably extensive. may start seeing signs if there are a lot
describe grade 3 ulcers
larger, deeper, more extensive lesions. more likely to bleed. associated with clinical signs
describe grade 4 ulcers
deep craters. need to contract and granulate to heal so will take a long time. clinical signs seen
how is ESGD prevented
dietary management - small, regular feeds, high fibre, small-holed haynets, feed prior to exercise
low dose omeprazole licensed but not generally indicated
pectin-lethicin compounds - some efficacy
why are biopsies for EGGD problematic
transendoscopic not representative of full thickness
trucut likely lead to peritonitis (do not perform)
disease may only manifest at pyloric antrum but often whole glandular region is affected
what are the theories of the possible underlying cause of EGGD
- immune mediated (like IBD)
- infectious (less popular theory)
explain the pathogenesis of EGGD
anything that inhibits mucosal blood flow
- decreased PGE2: normally promotes secretion of mucous-bicarbonate layer, stimulates production of surface PLs, enhances mucosal repair and controls Na concentration in cells preventing swelling and death.
- increased gastric acid
- disruption of mucosal protective factors
what may disrupt mucosal protective factors (often relates to decreased gastric blood flow)
- stress
- NSAIDs (no evidence in horses currently)
- furosemide
- hypovolaemia - colic, diarrhoea, sepsis
- anorexia/intermittent feeding
- ileus
what are the clinical signs of EGGD
- temperament change (nervousness, aggression)
- cutaneous sensitivity (biting flanks, resentment of girth, rugging, leg aids etc)
- reluctance to go forward when ridden
- unexplained weight loss
- reduced appetite or altered eating patterns
- colic (mild, recurrent)
what are the risk factors of EGGD
- undertaking more exercise per days of the week
- increased number of carers (management, stress)
- intense exercise (although less common than ESGD) performance horses
how is EGGD diagnosed
gastroscopy - although lesions seen on the surface may not represent the true extent of the disease
how is EGGD treated
options
- oral omeprazole and sucralfate - increases mucosal blood flow
- misoprostol - suppresses acid, increases PGE2. currently most effective.
- injectable omeprazole - weekly IM. more effective than oral.
steroids if refractory - not understood why they work
unknown how to manage the 30-40% that don’t respond to drugs
how is EGGD prevented
- minimum 2 days rest from work per week
- turnout where possible (providing not stressful)
- minimise changes in companions and carers
- minimise management changes/stressors
- feed 30mins prior to exercise
- feed pectin-lethicin supplements or sugar beet BID
- add corn oil to diet
when is gastric disease in foals a concern
sick, septic, PAS, stressed and hospitalised foals. need a disruption of mucosal protective factors –> reduced gastric blood flow
describe the pathogenesis of gastric disease in foals
Ischaemic damage and reduction in mucosal blood flow rather than acid damage as in adults.
what are the clinical signs of gastric disease in foals
young - moderate to severe colic
older - bruxism and ptyalism. oesophageal reflux and pyloric/duodenal strictures and gastric rupture
life threatening
how is gastric disease in foals diagnosed
- gastroscopy
- faecal occult blood test
- contrast radiography
- abdominal ultrasound especially if looking for gastric rupture
- peritoneocentesis
how is gastric disease in foals treated
controversial
- sucralfate: especially if there is concurrent oesophageal ulceration
(do not give omeprazole -reduction in gastric acid can predispose to severe secondary bacterial infection due to C difficile. some vets still use)
how does the prognosis of gastric disease in foals compare to EGGD or ESGD in adults
much less favourable
what is the prevalence of gastric disease in pigs
up to 60% of growers at slaughter
5% in sows
what are the clinical signs of gastric disease in pigs
- anorexia
- vomiting
- anaemia
- teeth grinding
- black faeces
- weight loss in growers (chronic form)
- death due to haemorrhage
what factors are involved in causing gastric disease in pigs
- nutrition (low protein, fibre, vit E, selenium or zinc, high energy, wheatm iron, copper, calcium, unsaturated fats, whey and skimmed milk)
- ground up feed rather than pellets
- irregular feeding patterns
- shortage of feeder space
- increased stocking density
- transportation
- other stress
- aggression between animals
- poor stockmanship
- fluctuating environmental temperatures
- concurrent disease (pneumonia, sepsis)
- breed
how is gastric disease in pigs diagnosed
- clinical signs
- PME
- faecal occult blood test
what are the differentials for gastric disease in pigs
- eperythrozoonosis
- hyostrongylus rubidus (gastric worm)
- porcine enteropathy
when may gastric rupture occur in horses
- secondary to small intestinal strangulating lesions
what are the signs of gastric rupture in horses
painful --> pain free suddenly due to decreased pressure septic shock due to peritonitis - reluctant to move - tachycardic (>100) - purple mm - no borborygmi
how is gastric rupture diagnosed in horses
- peritoneal tap
when may gastric rupture occur in foals
rare, usually secondary to perforating gastric ulcers likely due to necrotising enterocolitis (bacterial infection)
when may gastric rupture occur in pigs
secondary to perforating gastric ulcers
what are the signs of gastric impaction
- acute: colic signs
- chronic: anorexia and weight loss
why may gastric impaction occur
- primary or secondary motility disorder
- secondary to dental disease, gorging or dehydration due to inadequate water intake (rare)
- rarely associated with poor quality forage, FBs or improper mastication
how is gastric impaction diagnosed
NG tube hitches/gets stuck on passage - no fluid
gastroscopy - full after 24 hours of food being withheld
abdominal ultrasound
surgery
(abdominal radiograph in ponies, donkeys, miniatures)
how is gastric impaction treated
- aggressive gastric lavage (water or caffeine free cola)
- promotility agents (erythromycin, metaclopramide)
- surgery to empty
need to act quickly, left longer then function may not return
how do habronema travel to the stomach
eggs laid in sores, larvae hatch and burrow into mucosa, penetrates and migrates to stomach
how is habronemiasis treated
avermectins every 4 weeks x3
what are the rare consequences of habronemiasis (usually of little consequence)
- granulomatous reaction around pyloric antrum
- pyloric outflow obstruction
- mild, recurrent colic
- intermittent tachycardia and NG reflux
how is clinical habronemiasis diagnosed and what are its differentials
ddx - SCC (or other tumour) - EGGD diagnosis - gastroscopy and biopsy
describe the importance of gastrophilus
- no importance in terms of clinical disease
- clients get upset when pupae are passed in faeces
- incidental finding during gastroscopy in winter
- respond to avermectins
describe the life cycle of gastrophilus
- adult flies lay white/yellow eggs on horses’ legs
- eggs hatch spontaneously or when stimulated by horse’s saliva when grooming
- L3 attaches to squamous gastric mucosa along with the margo plicatus (G intestinalis) or dorsoproximal duodenum (G nasalis)
- larvae survive here for 10-12 months
- pupae passed in faeces
what is the most common stomach tumour in horses (although rare overall)
squamous cell carcinoma. can metastasise to lungs and LNs
what are the signs of a gastric SCC in horses
weight loss
recurrent, chronic, mild colic
anorexia
depression
how are gastric SCC diagnosed in horses
gastroscopy - can’t always see
abdominal ultrasound
what is the prognosis of gastric SCCs in horses
no treatment - can’t resect. invariably PTS.
what is the prognosis for EGS
80% chronic cases survive. main problems seen in first 2 months post-discharge e.g. colic, inappetence, dysphagia, sweating. variable time to return to normal bodyweight
