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
describe the resistance of parasites to ivermectins
emerging in cyathastomes
large strongyles sensitive
widespread resistance in ascarids
describe the resistance of parasites to moxidectin
emerging in cyathostomes
large strongyles sensitive
widespread resistance in ascarids
describe the resistance of parasites to fenbendazole
widespread in cyathastomesand
probably ok in large strongyles
anecdotal in ascarids
describe the resistance of parasites to pyrantel
some resistance in cyathostomes
large strongyles sensitive
some cases of resistance in ascarids in USA
describe the SMART approach to managing anthelmintic resistance
S - stop anthelmintic overuse M - minimise pathogenic stages A - avoid increasing worm burdens in individuals R - rely on environmental control T - target for stage and shedding
describe surveillance and strategic treatment approach to worms in adults
pick up faeces perform FECs - Spring EPG> 200 - Pyrantel - June/Jul EPG>200 - Pyrantel - Sept/Oct EPG>200 – Ivermectin - Nov/Dec - Moxidectin/praziquantel – 1 post treatment FECR
describe the approach to worm control in foals in the first year of life
susceptible animals so no selective therapy is recommended
if worming mares prior to foaling then must be 2-3 months in advance
FECRT important on studs
<6 months - BZS/pyrantel based on FECRT for ascarids
6 months - faecal sample for ascarids and strongyles and dose accordingly. check in 2 weeks
5d fenbendazole at weaning
9mo - avermectins/pyrantel for strongyles
12mo - as above plus praziquantel for tapeworm
describe the GIT and diet of foals
Predominantly liquid diet
Hindgut underdeveloped compared to adults
Stomach and small intestine relatively larger
Diet is very rich in sugars (lactose)
Maternal passive transfer provides humoral immunity - colostrum vital
list potential oral congenital abnormalities in foals
cleft palate - milk will come out nostril when nursing
campylorhinus lateralis (wry nose) - will struggle to latch on and nurse
subepiglottic cysts
brachygnathisms (parrot mouth)
list potential oesophageal congenital abnormalities in foals
Stenosis Persistent right aortic branch Vascular abnormalities Duplication cysts Idiopathic megaoesophagus
all rare
list potential hindgut congenital abnormalities in foals, the clinical signs and diagnosis
atresia - coli - recti - ani 2-48hours old, no meconium passed, bloated and colicking diagnosis - digital palpation (ani) - contrast radiography - US/colonoscopy
list some causes of colic in foals
meconium impactions - most common
gastric ulceration
parascaris equorum infestation
intestinal obstruction
what are the clinical signs of colic in foals
more demonstrative of abdominal pain, harder to assess severity
- Tachycardia (>120 - likely need surgery)
- Tachypnoea
- Anorexia
- Tooth-grinding
- Abdominal distension
- Flank watching
- Rolling
- Dorsal recumbency
- Tail flagging - tenesmus
- signs of sepsis (pyrexia, depression, petechiae, synovitis, uveitis, diarrhoea)
what aspects of the history are important in a colic investigation in foals
parturition process
colostrum consumption
meconium production
faecal/urinary production
what may be felt on abdominal palpation in foals with colic
gas distension - obstruction
hard masses - intussusception, meconium if aboral
presence of free fluid on ballottment - bladder rupture
hernias
pain detected
should also percuss
hoe is nasogastric tubing carried out in foals
use stallion urinary catheter if very young or specific foal tube (large as possible)
hard to obtain reflux
muzzle if refluxing
what diagnostic methods are used in foal colic cases
- history
- clinical signs
- physical exam
- abdominal palpation
- digital rectal exam
- NGT
- abdominal ultrasonography
- abdominal radiography +/- contrast
- haematology
- biochemistry
- +/- abdominocentesis
what may be seen on haematology and biochemistry in colic cases in foals
hypovolaemia especially if not nursing
neutropenia - coping poorly with inflammatory response
acute phase proteins - serum amyloid A
biochem - check renal function
what may be seen on abdominocentesis in foal colic
normally have lower TNCC than adults and <25g/L total protein.
serosanguinous colour suggests need for surgery
peritoneal creatinine:serum creatinine ratio normally <2, higher if uroabdomen
what is meconium
a mixture of glandular secretions, mucous, bile and digested amniotic fluid.
yellow colour
expelled in first 12 hours of life
colostrum promotes expulsion due to laxative effect
what are the signs of meconium impaction
tenesmus without defaecation
sometimes see moderate pain signs
gas distension due to obstruction
how is meconium impaction diagnosed
digital palpation per rectum
manual abdominal palpation
abdominal ultrasound
abdominal radiography
how is meconium impaction treated
enemas with soapy water
retention enemas (acetylcysteine, baking soda and water infused and left for 30-45mins)
pain management - fluxinin, opioids
what is the prevalence of gastric ulceration in foals
22-57%
usually related to suppression of protective factors from concurrennt disease (PAS, other illness, NSAIDs)
what are the clinical signs of EGUS in foals
may be none colic diarrhoea excessive salivation teeth grinding (bruxism) perforation is a concern
how is EGUS/GDUS (gastroduodenal ulcer syndrome) diagnosed in foals
clinical signs
endoscopy
- EGUS, smaller scope than adults
- GDUS
what are the clinical signs and endoscopy findings of GDUS (gastroduodenal ulcer syndrome) in foals
foals 2-6mo pot-bellied and unthrifty
pyloric ulceration and stricture due to scar formation
delayed gastric emptying
how is EGUS treated
acid suppression - omeprazole? + sucralfate or misoprostol. other: ranitidine, Al/Mh hydroxide supportive care - IV FT - antibiotics - NSAIDs
how is GDUS treated
acid suppression
supportive care
gastrojujunostomy in selected cases (difficult to perform)
describe parascaris equorum infection in foals
ingested –> SI –> liver and lungs –> coughed up –> re-ingested
adults cause obstruction of SI post-anthelmintic administration
increasing resistance to ivermectins
what may cause intestinal obstruction in foals
volvulus hernias - scrotal, richter's, mesenteric rents, diaphragmatic intussusceptions adhesions faecaliths - typical of miniature breeds other, foals at least 3 weeks old, lodged in small colon, need enterotomy foreign body
briefly describe uroperitoneum and its clinical signs in foals
rupture of the bladder in colts during the first week of life
see abdominal distension with ballottment
absent or reduced urine production depending on site of rupture
how is uroperitoneum diagnosed and treated
electrolyes - increase K, decreased NA
ultrasonography - large volume of peritoneal fluids
peritoneal fluid creatinine: serum creatinine >2
treat by stabilising electrolyte abnormalities then surgical repair
what are the differentials for diarrhoea in foals
viral - rota - corona - adeno bacterial - clostridia - salmonella - E coli - Rhodococci - lawsonia parasitism - cryptosporidium - strongyloides westeri foal heat PAS
describe the predisposing factors to diarrhoea
failure of passive transfer other disease - sepsis - PAS - antimicrobials - omeprazole close contact with other foals poor hygiene coprophagia (foal eating mare's faeces if something is wrong with the mare or foal hasn't got enough enough Igs)
what metabolic disturbances occur due to foal diarrhoea
hypovolaemia hypoalbuminaemia metabolic acidosis sepsis, SIRS endotoxaemia lactose intolerance
how is diarrhoea in foals managed
consider referral IVFT +/- glucose TPN if anorexic hyperimmune plasma if IgG low fluxinin meglumine umbilicus disinfection barrier nursing alcohol fans/fans if pyrexic sudocreme/oil around perineum
describe foal heat diarrhoea
5-15 days old
related to changes in GI microflora
no pyrexia usually
may progress rapidly so monitor closely and intervene if looks systemically ill
describe perinatal asphyxia syndrome
decreased oxygen supply and ischaemia-reperfusion injury during birth
results in decreased GI function (ileus or diarrhoea)
what are the clinical signs and treatment of PAS
signs
- dullness
- inappetence
- colic
- hypothermia/pyrexia
- tachycardia
- tachypnoea
treatment
- supportive/nursing care
- antimicrobials
- hyperimmune plasma
describe necrotising enterocolitis in foals
bacterial mediated
pathophysiology is multifactorial - GI immaturity, hypovolaemia, inflammation, genetics, dysbiosis, diet
controverisl role of clostridia/salmonella
how is necrotising enterocolitis presented and diagnosed
present similar to PAS - dullness, inappetence, colic, hypo/hyperthermia, tachycardia, tachypnoea
diagnosis - intestinal wall intramural gas
GI necrosis on PM
what is the treatment and prognosis of necrotising enterocolitis in foals
supportive care
BS antimicrobials +/- metronidazole
poor prognosis
describe the presentation of rotavirus in foals
5-35 days old
pyrexia, anorexia, depression, profuse watery diarrhoea, hypovolaemia
how is rotavirus diagnosed, treated and prevented in foals
faecal analysis (ELISA, RT-PCR, immunochromatography) supportive treatment lactase supplementation prevent - isolate affected foals - good hygiene - vaccinate mares
how does coronavirus present in foals
usually adults, occasionally foals co-infection with rota or Cl perfingens hypovolaemia pyrexia, anorexia, lethargy neutropenia, hypoalbuminaemia
how is coronavirus diagnosed, treated and prevented
faecal PCR
supportive treatment
prevent with strict biosecurity
describe clostridia difficile related diarrhoea
occurs with and without Abx therapy
risk factors - hospitalisation, stress, surgery, starvation and diet change
watery or haemorrhagic diarrhoea, SIRS, hypovolaemia, abdominal distension, colic
describe Cl perfringens related diarrhoea
very severe high mortality birth on sand/gravel/dirt is a risk factor more pronounced SIRS and shock watery haemorrhagic diarrhoea
how is clostridial diarrhoea diagnosed
positive toxin ELISA or RT-PCT (difficile)
faecal gram stain - high count gram positive rods/spores (perfringens)
how is clostridial diarrhoea treated
supportive care
metronidazole
describe rhodococcus equi infection
primarily respiratory pathogen
foals 1-4 months old show signs but infection from birth
33% develop diarrhoea
how is rhodococcus equi diagnosed
uniquitous - hard to prove significance
VapA-PCR
thoracic US screening due to common subclinical infection
how is rhodococcus equi treated
supportive care
macrolide and rifampin
describe proliferative enteropathy in foals
due to lawsonia intracellularis
foals 2-8months old, occasionally adults
induces proliferation of crypt epithelial cells in the SI leading to PLE
what are the signs of proliferative enteropathy
oedema lethargy diarrhoea weight loss pyrexia colic hypoalbuminaemia severe SI thickening on US
how is proliferative enteropathy diagnosed
clinical signs
serology
faecal PCR
how is proliferative enteropathy treated
lipophilic antimicrobials for 3 weeks (oxytet, doxycycline, macrolides)
good prognosis
how is bacterial diarrhoea diagnosed and treated
blood culture with sepsis
faecal culture
haematology
treat with antibiotics and supportive care
describe cryptosporidium parvus infection in foals
1-4 weeks old diarrhoea weight loss may have concurrent disease zoonotic
how is C parvus diagnosed and treated in foals
faecal analysis (flotation/staining, ELISA, RT-PCR) self limiting so just supportive care
describe strongyloides westeri infection in foals
trans-mammary infection
diarrhoea only if in high numbers
responds to ivermectins
describe lactose intolerance in foals
secondary process following previous disease e.g. rota or clostridia
often seen in association with milk replacers
lactase activity decreases gradually with age (negligible by 4yrs old)
diagnose - oral lactose tolerance test
