Equine 6 Flashcards
what are the predisposing factors to hyperlipidaemia in the horse
- ponies/miniatures/donkeys
- decreased calorie intake/change in feed
- systemic infection
- obesity
- adult females with insulin resistance
- season: February to May
- pregnancy
- lactation
- stress
- pain
- chronic disease
- secondary to enterocolitis, dental disease, bacterial infection, colic impactions, parasitism
summarise the pathophysiology of hepatic lipidosis
- negative energy balance leads to more fat metabolism
- FFAs, NEFAs and glycerol formed in liver
- FFA oxidation
- either enter the tricarboxylic acid cycle, undergo gluconeogenesis or form triglycerides
- triglycerides stored or form VLDLs
- fat mobilisation exceeds liver capacity
- profound hepatocyte cytosolic expansion with triglyceride stores
what will blood from an animal with elevated triglyceride look like in a serum tube
serum will be turbid and cloudy in moderately-severely affected animals (>5.5mmol/L)
what is the treatment for hyperlipaemia if anorexic
- 5% dextrose/glucose at maintenance rate (short term)
- enteral nutrition if primary disease allows
- partial parenteral nutrition if enteral not possible
what is the treatment for hyperlipaemia if also hyperglycaemic
- introduce insulin therapy
- insulin zinc suspension 0.15 IU/kg
dubious efficacy with insulin resistance
what may be used to inhibit fat metabolism in hyperlipaemia
nicotinic acid - unproven efficacy
what may be used to increase triglyceride uptake by peripheral tissues in hyperlipaemia
heparin - stimulates lipoprotein lipase to remove triglycerides. however LPL already at maximum so benefit is questionable
list the parasites in the horse
Gasterophilus spp. or ‘bots’ Habronema spp. Parascaris equorum Strongyloides westeri Anoplocephala perfoliata Dictyocaulus arnfieldi Strongylus vulgaris Strongylus equinus Strongylus edentatus Small strongyles - Cyathostomosis Oxyuris equi
how is gasterophilus diagnosed
gastroscopy
not seen on faecal analysis
what is the significance of gasterophilus infestation
rarely causes disease even in large numbers - cause a mild gastritis by grazing on mucosa
poor performance
eat slower when in mouth
colic
inconclusive association with ulcers
more of an issue for owners seeing L3 in faeces
how is gasterophilus prevented and treated
can’t control flies
remove eggs in summer months using bot knife/topical insecticides
sensitive to ivermectin and moxidectin (not worth using)
describe habronemiasis infection
associated with skin sores (and conjunctivitis)
adult worms live and reproduce in stomach
uncommon
cause local disease in wounds
seen June-September
some horses prone to re-infection
occasional gastric disease due to immune response to worms causing nodules of granulation tissue (contain eosinophils)
how is habronemiasis diagnosed
faecal analysis difficult due to fragile eggs rupturing
gastroscopy - see lesions
how is habronemiasis prevented
good fly control and muck heap management
frequent bedding replacement
collection/removal of droppings in paddocks
cover wounds
treat ocular disease in which discharge is present
will be killed when worming for other parasites
describe parascaris equorum infection
disease usually affects horses under 2yo (immune response not yet developed)
prevalence 10-50%
adult horses act as reservoirs
briefly describe the life cycle of parascaris equorum
involves migration through the liver, vena cava, alveoli, bronchi and trachea.
adults 4cm long, cream and round
eggs coughed up and swallowed
what are the clinical signs of parascaris equorum infestation
coughing and nasal discharge when parasites are in lungs
poor coat
poor weight gain
dull
anorexic
occasional colic including bowel obstruction
severe - disorders of bone and tendons
often mini-outbreaks seen in young horses
describe the diagnosis of parascaris equorum
difficult due to long PPP (10-14 weeks)
repeated faecal analysis
endoscopy down to duodenum
eosinophils on tracheal wash/BAL but not often peripheral blood
TA ultrasound in future
insignificant bloodwork - slightly elevated liver parameters
how is parascaris equorum treated and prevented
multi-drug resistance (don’t use avermectins)
pyrantel first line - works on 50% of yards
undertake FECRT annually/every other year
pasture management - poo picking and pasture rotation
deworm mares just after foaling and keep in clean stall
de-worm foals regularly
what are the clinical signs of S westeri infection
very mild
dematitis - fenzy behaviour
enteritis - profuse, non-fetid diarrhoea in foals with no temperature
occasional cough due to migration
how is S westeri prevented
poo-picking
generally no treatment needed
anthelmintics
- BZ 2-3x normal dose (use as not effective against much else)
- ivermectin effective against larvae and adults
- worm dam on day of parturition and 12 hours later to prevent passage in milk
describe anoplocephala perfoliata infestation
usually around ileo-caeco-colic junction or in caecum (drug avoidance)
graze on mucosa
disease common in Oct/Nov
immune response stronger in adults so more likely to clear infection
describe the life cycle of anoplocephala
egg shedding irregular and released from segments in LI or excreted from horse
eggs infective to orbatid mites
mites overwinter in soil (overwintering in horses has less of a role)
horse ingests mites in spring
PPP 6-10 weeks
how is anoplocephala diagnosed
ELISA for exposure in populations not diagnosing individuals
- many false positives
- blood useful, saliva not great
faecal analysis difficult due to intermittent shedding
- flotation better
- use for individuals
what are the clinical signs of anoplocephala infection
ileal impaction intussusceptions caecal impaction and motility disorders spasmodic colic diarrhoea - less common
how is anoplocephala treated and prevented
double dose pyrantel
praziquantel in autumn/winter to prevent overwintering
stable for 48hrs after worming to prevent increased pasture contamination
can’t kill the mites
describe the importance and prevalence of strongylus vulgaris
most clinically important large strongyle - causes verminous arteritis
60% 20 years ago
dropped to 6% now due to ivermectin use
resistance likely will increase and prevalence rise again
describe the epidemiology of strongylus vulgaris
some immunity but never complete to stop re-infection disease often most severe in young/naive horses
seen in all ages - worse in weanlings and yearlings (not under 6-7months)
asymptomatic horses act as reservoirs and shed a large number of eggs
describe the diagnosis of strongylus vulgaris
difficult as PPP disease - caused by larval stage
may be able to feel thrombi when performing rectal
faecal analysis - not always useful, can’t tell from other strongyle eggs and increased count doesn’t mean larger burden
larval culture (high PPV, low NPV)
history of recurrent colic
ensure if worm burden correlates to disease
describe the disease process and clinical signs of strongylus vulgaris
high numbers on pasture in spring/summer
often in arteries in autumn/winter so disease seen at this point
- colic, diarrhoea, anorexia
- gut ischaemia –> death
lameness/poor performance if thrombi at aorto-iliac junction form
occasional aberrant migration up in the brain, kidneys, lungs, liver and can form granulomas
how is S vulgaris treated and prevented
avermectins kill larvae and adults pyrantel kills adults only (~50%, need FECRT) avoid overgrazing rotate fields poo-pick regularly
other than vulgaris, what are the other species of strongyle and briefly describe them
S. edentatus - hepatoperitoneal strongyle - PPP 11 months - colic due to liver disease or peritonitis S. equinus - hepatopancreatic strongyle - don't enter blood vessels - PPP 9 months - mild colic - some association with pancreatic disease and primary diabetes mellitus
both worse in young animals, signs in winter and with stress. asymptomatic horses can shed large numbers of eggs.
diagnosis, prevention and treatment same as S vulgaris
which equine parasite disease is the most important in terms of prevalence and severity of clinical signs
cyathostominosis
what are the key points of cyathostome life cycle
hypobiotic population makes up 50% of larval population (which is 90% total) - unaffected by any anthelmintic
larvae max in horse in autumn, emerge in spring often many at once
PPP 6-14 weeks if there is no hypobiosis
immunity may develop but never complete
Egg shedding highest in spring, re-infection in June-Oct if not too dry
how is cyathostominosis diagnosed
difficult as PPP disease
history - young animal, poor/change in worming
clinical signs - colic, diarrhoea
larvae in faeces or on glove after rectalling if acute
future - ELISA for larvae
describe spring syndrome in cyathostominosis
acute larval disease due to mucosal damage from emergence of LL3
- colic
- weight loss
- diarrhoea (acute and chronic)
- wasting
- death
describe autumn syndrome in cyathostominosis
occurs when larvae enter the intestinal wall
less common than spring syndrome
- colic
- diarrhoea due to inflammation
describe the epidemiology of oxyuris equi (pinworms)
common relatively benign affect any age parasite of stabled horses other infected horses and immediate environment act as reservoir prevalence ~25% PPP 5 months
describe the clinical signs of pinworm
anal pruritus
skin excoriation
myiasis
rarely colic if huge burden
how is pinworm diagnosed
eggs in perianal region on examination
sellotape test
how is pinworm treated and managed
all anthelmintics should be effective but some resistance apparent
topical/systemic anti-inflammatories to decrease pruritus
keep area clean
good stable hygiene
