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GI2 > Equine 2 > Flashcards

Equine 2 Flashcards

1
Q

explain how equine grass sickness can lead to ileus

A

generalised dysautonomia –> decreased intestinal motility and GI secretions –> ileus +/- large colon impactions leading to ileus

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2
Q

what are the clinical signs of equine grass sickness

A
  • 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
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3
Q

what is the current thought on EGS aetiology?

A

toxicoinfection with Clostridium botulinum types C and D whereby the toxin is locally produced in the horse’s GIT

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4
Q

what are the horse related risk factors of EGS

A
  • age 2-7yo (rare in foals and older horses)
  • good/fat condition
  • low antibody levels to C botulinum type C and BoNT/C
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5
Q

what are the seasonal risk factors of EGS

A
  • spring and early summer (can be year round)

- cooler, dry weather with irregular frosts in 2 weeks before outbreak

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6
Q

what are the premises risk factors of EGS

A
  • high numbers of horses
  • young horses present
  • stud/livery/riding school
  • sand and loam soils > clay > chalk
  • increased soil nitrogen
  • previous occurrence at site
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7
Q

what are the management risk factors of EGS

A
  • access to grass
  • dietary change
  • movement/stress
  • pasture disturbance
  • anthelmintic use (ivermectins)
  • mechanical droppings removal
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8
Q

how is EGS definitively diagnosed

A

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

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9
Q

what is the result of topical administration of phenylephrine drops 0.5% to the eye

A

reversal of ptosis in ipsilateral eye

false positives can be seen e.g. if A2A used

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10
Q

what may be seen on oesophgeal endoscopy and barium swallow in EGS

A

linear oesophageal ulcers (due to GI reflux)

defective oesophageal motility

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11
Q

how is acute or subacute EGS treated

A 
IV fluids
analgesia 
regular gastric decompression 
feeding 
once definitive diagnosis made recommend euthanasia or some subacute cases may become chronic and survive
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12
Q

how is chronic EGS treated

A
  • 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)
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13
Q

when should you consider treating EGS

A
  • horse attempting to swallow feed and drink and retains some ability to do so
  • no continuous moderate/severe colic signs
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14
Q

what premises factors may help prevent EGS

A
  • avoid previously affected sites

- soil exposure

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15
Q

what management factors may help to prevent EGS

A

minimise

  • grazing
  • movement
  • change of feed
  • pasture disturbance
  • frequent ivermectin use
  • mechanical droppings removal
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16
Q

what protective factors may help prevent EGS

A
  • cograzing with ruminants
  • regular grass cutting
  • manual droppings removal
  • supplementary forage feeding
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17
Q

What are the main features of enterobacteriaceae

A
  • 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
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18
Q

name the major enteric pathogenic enterobacteriaceae

A

E coli
salmonella serotypes
yersinia

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19
Q

name some opportunistic enterobacteriaceae

A
  • proteus
  • enterobacter
  • klebiella
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20
Q

how are enterobacteriaceae differentiated

A
  • lactose fermentations
  • reactions on selective media
  • eosin-methylene blue agar (E coli)
  • colonial morphology
  • PCR
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21
Q

which enterobacteriaceae have mucoid colonial mophology

A
  • klebsiella

- enterobacter

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22
Q

which enterobacteriaceae swarms on rich media

A

proteus

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23
Q

which enterobacteriaceae has red pigmentation

A

serratia marcescens

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24
Q

which strains of E coli are important

A
  • ETEC
  • EPEC
  • VTEC
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25
Q

What are the cultural properties of campylobacter

A
  • 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
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26
Q

what are the microscopic properties of campylobacter

A
  • gram negative
  • slender
  • vibrio shaped
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27
Q

which species of campylobacter are important (GI and repro)

A
  • jejuni subsp jejuni
  • coli
  • fetus subsp fetus
  • fetus subsp venerealis
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28
Q

what occurs during initial colonisation of campylobacter in birds

A

inflammatory response

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29
Q

reduced weight gain and hock burn are correlated to colonisation with which organism in birds

A

campylobacter

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30
Q

when might campylobacter be associated with disease in dogs

A
  • young or debilitated animals

- synergy with other pathogens

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31
Q

what are the microbiological properties of clostridia

A
  • gram positive
  • rod shaped
    • tetani are thin
    • perfringens are large and wide
  • obligate anaerobes
  • produce endospores
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32
Q

which species of Clostridia are important

A
  • botulinum
  • difficile
  • perfringens
  • tetani
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33
Q

what are the cultural properties of clostridia

A

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

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34
Q

how should sampling for clostridia be carried out

A
  • anaerobic transport medium
  • prompt culture on enriched blood agar
  • anaerobic atmosphere with hydrogen and 5-10% CO2
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35
Q

where can clostridia be sampled from

A
  • soil
  • fresh water
  • marine water
  • part of normal GI flora
  • fresh cadaver material (overgrowth if old)
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36
Q

how can clostridia species by differentiated

A

perfringens - double haemolysis
biochemical identification
ELSIA for toxins
antibody based techniques from lesion samples

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37
Q

how is lawsonia diagnosed

A
  • clinical signs and gross pathological findings

- PCR or immunofluorescent tests

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38
Q

why is lawsonia hard to culture

A

obligate intracellular pathogen

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39
Q

intestinal spirochetes are important pathogens of which species

A

pigs

poultry

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40
Q

how are spirochetes and brachyspira diagnosed and differentiated

A

observation in stained faecal smears
grown anaerobically and confirmed by culture on selective blood agar
differentiate on haemolysis

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41
Q

which bacterium causes Johne’s disease in ruminants

A

Mycobacterium avium subspecies paratuberculosis

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42
Q

how is M avium subsp paratuberculosis sampled from animals

A

scrapings

punch biopsies from rectum

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43
Q

which diagnostic methods can be used for M avium subsp paratuberculosis

A

histopathology - affected tissue or lymph nodes
microscopy with ZN technique
culture is difficult and time consuming

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44
Q

what are the properties of actinobacillus lignieresii

A
  • gram negative rod
  • facultative anaerobe
  • oxidase positive
  • urease negative
  • commensal of mucous membranes
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45
Q

which bactrium causes wooden tongue in cattle

A

actinobacillus lignieresii

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46
Q

how does actinobacillus lignieresii cause wooden tongue

A

invade through breaks in mucous membrane
spread limited to soft tissues of tongue and LNs of head
tongue becomes hard, swollen and painful

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47
Q

what are the properties of actinomyces bovis

A 
gram positive 
anaerobic (some other species facultative) 
non-spore forming 
rod shaped 
branched networks of hyphae
48
Q

which bacterium causes lumpy jaw in cattle

A

actinomyces bovis

49
Q

describe lumpy jaw

A

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

50
Q

how does actinomyces infect cattle

A

breaks in the mucous membrane lining of the mouth

51
Q

what is the treatment of lumpy jaw

A

iodine therapy

tetracyclines

52
Q

what are the features of fusobacterium necrophorum

A
  • gram negative
  • obligate anaerobe
  • non-spore forming
  • non-motile
53
Q

where is fusobacterium necrophorum found in animals

A

alimentary tract

cattle - respiratory tract

54
Q

what does fusobacterium necrophorum infection involve

A

injury to epidermal layer allows infection to be established. Affects the mucous membranes and underlying tissues of the oral cavity epithelium. self-limiting.

55
Q

what are the potential pathogenic mechanisms of fusobacterium necrophorum

A

toxins:
- leucocidins
- haemolysin
- cytoplasmic

56
Q

how is fusobacterium necrophorum treated

A

penicillins

generally self-limiting

57
Q

describe the process of testing resistance profiles with disc diffusion

A
  1. 100ul bacteria on non-selective agar plate
  2. discs placed on agar label up
  3. incubation under specified conditions
  4. compare zone diameter to standard measurements
58
Q

describe MIC testing using E strips

A

place strip on agar with bacteria. MIC is at the point where the edge of the zone of inhibition crosses the E strip.

59
Q

define intrinsic resistance

A

organism naturally resistant to certain groups of antibiotics

60
Q

describe acquired resistance

A

transferable or heritable modification of self

61
Q

What is EGUS

A

Equine gastric ulcer syndrome

62
Q

what has EGUS now been split into

A

ESGD (equine squamous gastric disease) and EGGD (equine glandular gastric disease)

63
Q

list the disorders of the equine stomach

A 
ESGD
EGGD
Gastric disease in foals 
gastric rupture 
gastric impaction 
habronemiasis 
gasterophilus 
gastric neoplasia
64
Q

explain the pathogenesis of ESGD

A
  • 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
65
Q

what factors are mucosal aggressive

A
  • HCl
  • pepsin
  • bile acids
  • other organic acids
66
Q

what factors are mucosal protective

A
  • mucous
  • bicarbonate
    only present in the glandular region
67
Q

what factors reduce gastric pH

A
  • no food buffer (especially fibre)
  • ileus (increase in bile acids in stomach)
  • high carbohydrate diet (more VFAs, dissociate at low pH)
  • stress
68
Q

ESGD is seen most commonly in which types of horses?

A

performance horses and broodmares

69
Q

At what grade does ESGD cause clinical signs

A

generally grade 3 or more

70
Q

list the clinical signs of ESGD

A
  • often none
  • poor performance
  • attitude changes
  • mild, acute or recurrent colic
  • decreased appetite –> weight loss/reduction in BCS
71
Q

how is ESGD diagnosed

A

gastroscopy - diagnose and grade level of ulceration

72
Q

how is ESGD treated

A

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
73
Q

describe grade 1 ulcers

A

yellow hyperkeratinisation on surface but mucosa still intact. not associated with clinical signs

74
Q

describe grade 2 ulcers

A

multiple, small, multifocal lesions. reasonably extensive. may start seeing signs if there are a lot

75
Q

describe grade 3 ulcers

A

larger, deeper, more extensive lesions. more likely to bleed. associated with clinical signs

76
Q

describe grade 4 ulcers

A

deep craters. need to contract and granulate to heal so will take a long time. clinical signs seen

77
Q

how is ESGD prevented

A

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

78
Q

why are biopsies for EGGD problematic

A

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

79
Q

what are the theories of the possible underlying cause of EGGD

A
  • immune mediated (like IBD)

- infectious (less popular theory)

80
Q

explain the pathogenesis of EGGD

A

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
81
Q

what may disrupt mucosal protective factors (often relates to decreased gastric blood flow)

A
  • stress
  • NSAIDs (no evidence in horses currently)
  • furosemide
  • hypovolaemia - colic, diarrhoea, sepsis
  • anorexia/intermittent feeding
  • ileus
82
Q

what are the clinical signs of EGGD

A
  • 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)
83
Q

what are the risk factors of EGGD

A
  • undertaking more exercise per days of the week
  • increased number of carers (management, stress)
  • intense exercise (although less common than ESGD) performance horses
84
Q

how is EGGD diagnosed

A

gastroscopy - although lesions seen on the surface may not represent the true extent of the disease

85
Q

how is EGGD treated

A

options

  1. oral omeprazole and sucralfate - increases mucosal blood flow
  2. misoprostol - suppresses acid, increases PGE2. currently most effective.
  3. 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

86
Q

how is EGGD prevented

A
  • 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
87
Q

when is gastric disease in foals a concern

A

sick, septic, PAS, stressed and hospitalised foals. need a disruption of mucosal protective factors –> reduced gastric blood flow

88
Q

describe the pathogenesis of gastric disease in foals

A

Ischaemic damage and reduction in mucosal blood flow rather than acid damage as in adults.

89
Q

what are the clinical signs of gastric disease in foals

A

young - moderate to severe colic
older - bruxism and ptyalism. oesophageal reflux and pyloric/duodenal strictures and gastric rupture
life threatening

90
Q

how is gastric disease in foals diagnosed

A
  • gastroscopy
  • faecal occult blood test
  • contrast radiography
  • abdominal ultrasound especially if looking for gastric rupture
  • peritoneocentesis
91
Q

how is gastric disease in foals treated

A

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)

92
Q

how does the prognosis of gastric disease in foals compare to EGGD or ESGD in adults

A

much less favourable

93
Q

what is the prevalence of gastric disease in pigs

A

up to 60% of growers at slaughter

5% in sows

94
Q

what are the clinical signs of gastric disease in pigs

A
  • anorexia
  • vomiting
  • anaemia
  • teeth grinding
  • black faeces
  • weight loss in growers (chronic form)
  • death due to haemorrhage
95
Q

what factors are involved in causing gastric disease in pigs

A
  • 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
96
Q

how is gastric disease in pigs diagnosed

A
  • clinical signs
  • PME
  • faecal occult blood test
97
Q

what are the differentials for gastric disease in pigs

A
  • eperythrozoonosis
  • hyostrongylus rubidus (gastric worm)
  • porcine enteropathy
98
Q

when may gastric rupture occur in horses

A
  • secondary to small intestinal strangulating lesions
99
Q

what are the signs of gastric rupture in horses

A 
painful --> pain free suddenly due to decreased pressure 
septic shock due to peritonitis
- reluctant to move 
- tachycardic (>100)
- purple mm 
- no borborygmi
100
Q

how is gastric rupture diagnosed in horses

A
  • peritoneal tap
101
Q

when may gastric rupture occur in foals

A

rare, usually secondary to perforating gastric ulcers likely due to necrotising enterocolitis (bacterial infection)

102
Q

when may gastric rupture occur in pigs

A

secondary to perforating gastric ulcers

103
Q

what are the signs of gastric impaction

A
  • acute: colic signs

- chronic: anorexia and weight loss

104
Q

why may gastric impaction occur

A
  • 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
105
Q

how is gastric impaction diagnosed

A

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)

106
Q

how is gastric impaction treated

A
  • 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
107
Q

how do habronema travel to the stomach

A

eggs laid in sores, larvae hatch and burrow into mucosa, penetrates and migrates to stomach

108
Q

how is habronemiasis treated

A

avermectins every 4 weeks x3

109
Q

what are the rare consequences of habronemiasis (usually of little consequence)

A
  • granulomatous reaction around pyloric antrum
  • pyloric outflow obstruction
  • mild, recurrent colic
  • intermittent tachycardia and NG reflux
110
Q

how is clinical habronemiasis diagnosed and what are its differentials

A 
ddx 
- SCC (or other tumour)
- EGGD
diagnosis 
- gastroscopy and biopsy
111
Q

describe the importance of gastrophilus

A
  • 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
112
Q

describe the life cycle of gastrophilus

A
  • 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
113
Q

what is the most common stomach tumour in horses (although rare overall)

A

squamous cell carcinoma. can metastasise to lungs and LNs

114
Q

what are the signs of a gastric SCC in horses

A

weight loss
recurrent, chronic, mild colic
anorexia
depression

115
Q

how are gastric SCC diagnosed in horses

A

gastroscopy - can’t always see

abdominal ultrasound

116
Q

what is the prognosis of gastric SCCs in horses

A

no treatment - can’t resect. invariably PTS.

117
Q

what is the prognosis for EGS

A

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

GI2 (27 decks)

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