Equine 5 Flashcards
What broad age groups are horses classed into
neonatal foals <1mo
older foals and weanlings 1-9mo
adults >9mo
list the differentials for diarrhoea in foals
- foal heat diarrhoea
- necrotising enterocolitis
- neonatal sepsis
- viral diarrhoea (rotavirus)
- bacterial diarrhoea (clostridia)
- parasitic diarrhoea (s. westeri)
- cryptosporidium
what is the presentation of foal heat diarrhoea
5-14 days old
mild, self limiting diarrhoea
foal remains bright and suckling
normothermic (mean 38.3 degrees)
what is the pathogenesis of foal heat diarrhoea
likely a change in GI function or diet
unlikely that it is due to changes in dam’s milk
what is the diagnosis and treatment of foal heat diarrhoea
diagnosed on history and clinical signs
no treatment required
which foals are affected by rotavirus
all (highly infectious, common cause of diarrhoea). especially those housed in large groups with their dams
usually 7-28days old
what is the pathogenesis of rotavirus
invade epithelial cells lining the intestinal villi
cell death and blunting of villi
maldigestion through loss of intestinal enzymes
malabsorption through loss of surface area
what are the clinical signs of rotavirus
- anorexia
- depression
- profuse, watery diarrhoea
- hypovolaemia (not all)
- electrolyte derangements (not all)
how is rotavirus diagnosed
faeces - PCR, EM, ELISA
all low sensitivity, virus will be diluted if faeces is largely water
how is rotavirus treated
vaccination of mares supportive therapy - IVFT (sometimes oral) - PPN - sucralfate - vaseline/sudocreme around perineum - plasma and antibodies in young foals to prevent secondary infection
how is rotavirus prevented
colostrum - use a SNAP test to check IgG concentrations in outbreak scenario
what are the most common bacterial causes of diarrhoea in foals and adults
Clostridium perfringens and difficile
what are the clinical signs of bacterial diarrhoea in foals
colic hypovolaemia profuse, smelly, watery diarrhoea - sometimes red-tinged, haemorrhagic diarrhoea particularly with C perfringens A --> hypovolaemia and hypoproteinaemia anorexia depression SIRS ventral oedema eventually due to low protein low Na, K and Cl metabolic acidosis
how is bacterial diarrhoea diagnosed
in foals <7 days always rule out sepsis with blood culture
faecal ELISA or PCR for toxin (bacteria is ubiquitous)
ultrasound of SI
how is bacterial diarrhoea in foals treated
IVFT
broad spectrum parenteral antibiotics (IV TMPS/oxytet/penicillin)
hospitalisation
vaseline around perineum
occasional - whole blood transfusion or plasma if lots of protein lost through GIT
faecal transfaunation - anecdotally effective
steroids if no improvement in diarrhoea
what percentage of sick foals with diarrhoea will be septic
50% - always assume they are
other than clostridia, what other bacterial agent causes diarrhoea in foals
E coli - not as important as in farm animals and hard to know if pathogenic or commensal
describe a Strongyloides westeri infection in foals
transmammary transmission close to birth
signs at 8-12 days old
mild, self-limiting diarrhoea
often ignore
responds to deworming with BZ or avermectins but unnecessary
list the differentials for diarrhoea in weanlings
Lawsonia intracellularis
Rhodococcus equi
strongylus vulgaris
all adult diseases
how does lawsonia intracellularis (proliferative enteropathy) present in weanlings
2-8months old depression rapid and significant weight loss subcutaneous oedema diarrhoea colic poor hair coat pot-belly severe hypoalbuminaemia increased WBCs anaemia of chronic disease
describe the diagnosis of lawsonia intracellularis
difficult to get a definitive diagnosis
clinical signs, low albumin, rule out other causes
marked SI thickening on abdominal US
faecal PCR is insensitive
how is lawsonia intracellularis treated
oxytetracycline IV BID
if brighter and diarrhoea not as severe can use doxycycline PO BID
other - erythromycin, clarithromycin, azithromycin PO +/- rifampin to intracellularise antibiotic
colloidal support - plasma
describe the presentation of strongylus vulgaris in weanlings
6mo and over (lifecycle = 6-9m)
rare due to avermectin use
signs due to L4 migration through arterioles of caecum and descending colon - colic, SIRS, sick horse
how is strongylus vulgaris diagnosed and treated
difficult unless taken to surgery
clinical exam, history clinical pathology, FEC (but can’t rule out if negative)
treatment = avermectins when foals start to be exposed to eggs
how does rhodococcus equi present in weanlings
2-4mo
enteric infection - fever and diarrhoea
intra-abdominal abscess (bastard form) - fever and colic
respiratory form (more common) - high RR, cough, ill-thrift
describe the lifecycle of rhodococcus equi
excreted in dam’s faeces
build up on pasture in warm, dry or wet conditions
ingested by weanling
colonises white blood cells intracellularly
abscessation occurs primarily in the lungs
how is rhodococcus equi treated and what are the side effects
rifampin PO plus macrolide or erythromycin estolate PO side effects - hyperthermia (erythromycin) - diarrhoea in dam (macrolides cause severe C difficile infection in adults)
what are the differentials for acute diarrhoea in adult horses
larval cyathastomosis clostridial diarrhoea right dorsal colitis secondary to NSAIDs grain overload idiopathic dietary changes rare - salmonellosis - antibiotic induced - peritonitis - sand colic - strongylosis - duodenitis - proximal jejunitis - congestive heart failure - liver disease (hyperlipaemia)
what is the most prevalent and severe equine parasitic disease and what are its signs
cyathostominosis (80% prevalence)
severe acute or chronic diarrhoea and colic
describe the life cycle of cyasthastomes
direct cycle:
- adults adhere to mucosa of caecum and colon
- pre-patent period 6-14 weeks if no hypobiosis
- eggs produced and excreted
hypobiosis
- larvae encyst and development arrested in large intestinal mucosa unaffected by any anthelmintic
- emerge in spring
what percentage of a cyasthastome population do larvae make up
90%
50% encysted
what is the epidemiology of cyathastominosis
all ages affected, more commonin young or unexposed horses
egg shedding highest in spring
re-infection in june-sept/oct if not too dry
larvae at maximum number in horse in autumn
how is cyathastominosis diagnosed
FEC allows you to rule in but not out
history and clinical signs (young, poor worming history, sudden change)
larvae in faeces/on glove after rectal if acute
clinical pathology - neutrophilia, hypoalbuminaemia, hyperglobulinaemia
what are the clinical signs of cyathastominosis
spring syndrome (mucosal damage due to L3 emergence) - colic - weight loss - ventral oedema - diarrhoea (acute usually and chronic) - wasting - death - secondary neurological signs autumn syndrome (larvae entering intestinal wall) - colic (milder) - diarrhoea (less severe)
how is cyathostominosis treated
intensive care if acute
- IVFT
- parenteral antibiotics depending on age
- colloidal support (plasma)
- foot supports
- polymixin B
- dobutamine infusion
- NSAIDs
- other analgesia (lidocaine, ketamine drip)
- pre-treatment with steroids before anthelmintics to reduce inflammation
- moxidectin is larvicidal
how is cyathostominosis prevented
moxidectin during spring/autumn pick up faeces keep different ages of horses separate avoid overgrazing rotate pastures (harrowing if hot weather - not effective in England)
what is the prognosis for cyathostominosis
guarded, around 30-40% survive without treatment. may take months to re-gain weight as colonic wall takes time to heal
what is the prognosis for clostridial diarrhoea
30-50%
first losses occur due to the client running out of money to fund IVFT
second bout of losses often due to severe and fatal laminitis (after horse producing normal faeces)
where is antibiotic induced diarrhoea common and which drugs are indicated
uncommon in UK, common in USA penicillin ceftiofur TMPS doxycycline oxytetracycline (any antibitotic which targets gram negative or anaerobic bacteria) erythromycin in mares which ingest drug from foal's faeces
what are the clinical signs of antibiotic induced diarrhoea
- variable
- mild transient diarrhoea with no systemic effects
- severe fulminant enterocolitis
how is antibiotic induced diarrhoea diagnosed
history
faecal ELISA or PCR for clostridial perfringens enterotoxin and C difficile toxins A and B
how is antibiotic induced diarrhoea treated
stop antibiotics
faecal transfaunation
metronidazole - rarely used now
if severe - treat as for clostridiosis
describe the pathogenesis of grain overload diarrhoea
horse gains access to large quantity of hard feed
SI digestion overwhelmed and soluble CHO enters LI
rapid fermentation by lactic acid producing bacteria lowers pH
gram negative enterobacteriaceae die, other bacteria overgrow, gull wall is compromised and bacteria enter the circulation
what are the clinical signs and diagnosis of grain overload diarrhoea
SIRS
osmotic diarrhoea due to lactic acid being poorly absorbed
severe, often fatal laminitis
diagnosis based on history
how is grain overload diarrhoea treated
IVFT analgesia broad spectrum parenteral antibiotcs oral laxatives - liquid paraffin coats what is eaten to allow it to pass through the LI anti-endotoxic agents - polymixin B frog supports, ice feet PPN to rest gut surgery if severe to decontaminate GIT before they get too sick
describe the pathogenesis of right dorsal colitis
secondary to NSAIDs often if higher than licensed doses administered (not always).
ponies more susceptible to horses.
changes in GI blood flow affects protective mechanisms
what are the clinical signs of right dorsal colitis
anorexia lethargy/depression colic diarrhoea fever SIRS if chronic - weight loss - intermittent colic - depression - anorexia - ventral oedema - soft/less formed faeces
what clinical pathology is seen in right dorsal colitis
hypoproteinaemia hypovolaemia electrolyte abnormalities neutropenia occasional anaemia increased creatinine
how is right dorsal colitis diagnosed
presumptive based on history
more common with oral phenylbutazone (and suxibuzone) use, possibly less common with more COX2 selective drugs
transabdominal ultrasound - thickening of RDC wall
how is right dorsal colitis treated
stop NSAIDS (use paracetamol if analgesia needed)
supportive care
PGE2 analogue - misoprostol to increase GI blood flow and protective factors but has side effects
describe idiopathic diarrhoea in horses
persistent diarrhoea remains normovolaemic bright demeanour can become hypoproteinaemic over time possibly caused by dietary intolerance e.g. haylage
how is idiopathic diarrhoea diagnosed
rule everything else out history FEC faecal culture (3 over 1 week) toxin ELISA exclusion diet for 4-6 weeks
how is idiopathic diarrhoea treated
if exclusion diet doesn’t work, codeine phosphate PO BID to reduce LI motility
describe salmonellosis diarrhoea in horses
rare cause in UK syndromes - acute fulminant diarrhoea - sepsis in foals - depression, fever, anorexia - small colon impaction can get latent/carrier state
how is salmonellosis diagnosed
bacterial culture.
3 negative to rule out
5 negative to declare no longer infected after positive
how is salmonellosis treated and prevented
supportive care as for cyathostominosis
antibiotics to manage bacteraemia rather than kill salmonella
isolation - personnel and equipment
phenolics and fumigation of environment
when should horses/foals be isolated
two out of
- pyrexia
- neutropenia
- diarrhoea
– (except when 24-48 hours after LCV surgery)
neurological disease - decreased tail tone and dog sitting (EHV1)
suspected strangles
what are the aims of investigating acute diarrhoea
determine
- likely cause
- need for specific therapy
- need for supportive therapy
- risk to in-contact horses and personnel
how is the likely cause of diarrhoea and need for specific therapy determined
history physical exam haematology and biochemistry FEC Faecal PCR/ELISA faecal culture and sensitivity
how is the need for suppportive therapy determined
major body system assessment basic bloodwork - PCV/TP - lactate - blood gas and electrolytes - clotting profiles
what does supportive therapy consist of for diarrhoea
IVFT plasma dobutamine infusions - haemodynamic support analgesia lidocaine infusions polymixin B - anti-endotoxic drug antibiotics (controversial) foot supports/ice monitor jugular veins ensure eating or consider PPN within 48 hours of anorexia steroids (controversial) transfaunation
list the causes of weight loss
dental disease intestinal disease parasites liver disease renal disease neoplasia GI infection chronic systemic infection malnutrition
why may a horse have reduced feed intake
malnutrition due to owner
competition for feed
dental disorders
anorexia due to pain or dysphagia
what may lead to reduced digestion, absorption or assimilation of nutrients
dental disorders
malabsorption syndromes specific to the intestine
- parasitic disease
- idiopathic
- infiltrative bowel disease (inflammtory or neoplastic)
liver disease
what may cause increased loss of nutrients
PLE
PLN
squestration to body cavity - peritonitis or pleuritis
what may cause a horse’s energy requirements to increase
pregnancy lactation sepsis neoplasia other systemic disease
what factors may be associated with liver disease in horses
maldigestion (rare) anorexia hypoalbuminaemia (rare) increased energy consumption infection/sepsis
how is liver damage evaluated in horses
damage - serum enzyme activities - SDH/GLDH - hepatocellular - GGT - biliary function - bilirubin (mild increase with anorexia) - bile acids (pre vs post prandial doesn't really change) - ammonia
describe renal disease in horses
rare PLN may occur assess using - serum creatinine - urine SG BUN not helpful
what may lead to primary peritonitis in horses
haematogenous - strep equi - actinobacillus - R equi migrating parasites
what may cause secondary peritonitis in horses
sepsis - rupture of GI tract - uterine tear reactive - abscess - neoplasia - ruptured bladder
what are the clinical signs of sepsis in horses
pyrexia depression ileus +/- reflux pain on walking anorexia
how is peritonitis diagnosed in horses
abdominocentesis
- copious volumes of fluid
- cloudy sample
- high numbers of degenerate neutrophils
what is the prognosis for peritonitis in horses
depends on cause
may may chronic diarrhoea occur with malabsorption/protein losing enteropathies
- primary large colon dysfunction
- abnormal energy substrates to hind gut flora
what are the potential aetiologies of infiltrative bowel disease
- parasites (no direct link)
- genetic
- food allergy
- mycobacterium spp
- histoplasma
how is infiltrative bowel disease diagnosed
- rectal biopsy
- duodenal biopsy
- laparoscopy
how is infiltrative bowel disease treated
- anti-inflammatory doses of steroids
- anthelmintics if parasites may be a factor
- diet of highly digestible foods and high fibre
how is infiltrative bowel disease classified
- granulomatous enteritis
- lymphocytic-plasmocytic enteritis
- multisystemic eosinophilic epitheliotrophic disease
- eosinophilic enteritis
name the types of equine lymphoma
alimentary - 2-5yo and aged horses generalised - aged horses solitary - any age cranial mediastinal - any age cutaneous - any age
what paraneoplastic syndromes may occur with equine lymphoma
- hypercalcaemia
- haemolytic anaemia
name the types of malabsorption in horses
- anthelmintic responsive
- steroid responsive
- non-steroid responsive
how dose right dorsal colitis usually present
protein losing enteropathy
hypovolaemia
alongside NSAID administration
how is right dorsal colitis diagnosed and treated
ultrasound - thickened RDC >5mm
stop NSAIDs
supportive care
misoprostol to increase intestinal blood flow
what obvious causes of weight loss should be ruled out when taking a history
diet
parasites
what should be looked for on clinical exam when investigating weight loss
BCS - is weight loss genuine jaundice oedema - PLE fever oral/dental exam rectal exam - thickening/mass
what further tests should be used when investigating weight loss
liver, renal and inflammatory markers
repeat blood tests
abdominocentesis
FEC (won’t find tapeworm)
what non-specific changes may be seen on H&B when investigating weight loss
leucocytosis - peritonitis/cyathastominosis
neutrophilia - peritonitis
eosinophilia (sometimes parasites but uncommon in horses)
anaemia of chronic disease
increased liver enzymes
how may total protein be altered with weight loss
decrease
may be masked by concurrent hypovolaemia
how may hypoalbuminaemia be interpreted
GI loss more common than renal
peritoneal/pleural effusions
liver disease (rare)
how may hypoglobulinaemia or hyperglobulinaemia be interpreted
hypo - GI loss
hyper - chronic inflammatory disease (cyathostominosis)
how may hyperfibrinoginaemia be interpreted
infection
inflammation
neoplasia
when does serum amyloid A increase
inflammatory response
describe the interpretation of serum protein electrophoresis
a - infection, inflammation, neoplsaia (acute phase protiens)
b - parasitism, chronic infection, neoplasia (C reactive protein)
g
- polyclonal - chronic infection, abscesses, neoplasia
- monoclonal - tumours of reticuloendothelial system
what may oral glucose tolerance test be used for
test if there is an issue with sugar absorption
what are the issues with an oral glucose tolerance test
- only assesses sugars (not proteins or fats)
- doesn’t only assess SI function
- D-xylose absorption test more reliable but expensive
what may paritial malabsorption in the oral glucose tolerance test indicate
parasitism
localised lesions
rapid GI transit
what may a delayed flat curve on an oral glucose tolerance test indicate
delayed gastric emptying
poor starvation
what can be assessed on intestinal ultrasonography
wall thickness (should be 2-3mm)
lumen diameter
motility
anatomy
what methods may be used for GI biopsy in the horse
midline exploratory celiotomy UGA
flank laparotomy - reduced recovery time
laparoscopy - further reduced recovery time
rectal mucosal biopsy using uterine biopsy instrument
duodenal biopsy via gastroscopy
