Equine 5 Flashcards
(100 cards)
1
Q
What broad age groups are horses classed into
A
neonatal foals <1mo
older foals and weanlings 1-9mo
adults >9mo
2
Q
list the differentials for diarrhoea in foals
A
- foal heat diarrhoea
- necrotising enterocolitis
- neonatal sepsis
- viral diarrhoea (rotavirus)
- bacterial diarrhoea (clostridia)
- parasitic diarrhoea (s. westeri)
- cryptosporidium
3
Q
what is the presentation of foal heat diarrhoea
A
5-14 days old
mild, self limiting diarrhoea
foal remains bright and suckling
normothermic (mean 38.3 degrees)
4
Q
what is the pathogenesis of foal heat diarrhoea
A
likely a change in GI function or diet
unlikely that it is due to changes in dam’s milk
5
Q
what is the diagnosis and treatment of foal heat diarrhoea
A
diagnosed on history and clinical signs
no treatment required
6
Q
which foals are affected by rotavirus
A
all (highly infectious, common cause of diarrhoea). especially those housed in large groups with their dams
usually 7-28days old
7
Q
what is the pathogenesis of rotavirus
A
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
8
Q
what are the clinical signs of rotavirus
A
- anorexia
- depression
- profuse, watery diarrhoea
- hypovolaemia (not all)
- electrolyte derangements (not all)
9
Q
how is rotavirus diagnosed
A
faeces - PCR, EM, ELISA
all low sensitivity, virus will be diluted if faeces is largely water
10
Q
how is rotavirus treated
A
vaccination of mares supportive therapy - IVFT (sometimes oral) - PPN - sucralfate - vaseline/sudocreme around perineum - plasma and antibodies in young foals to prevent secondary infection
11
Q
how is rotavirus prevented
A
colostrum - use a SNAP test to check IgG concentrations in outbreak scenario
12
Q
what are the most common bacterial causes of diarrhoea in foals and adults
A
Clostridium perfringens and difficile
13
Q
what are the clinical signs of bacterial diarrhoea in foals
A
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
14
Q
how is bacterial diarrhoea diagnosed
A
in foals <7 days always rule out sepsis with blood culture
faecal ELISA or PCR for toxin (bacteria is ubiquitous)
ultrasound of SI
15
Q
how is bacterial diarrhoea in foals treated
A
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
16
Q
what percentage of sick foals with diarrhoea will be septic
A
50% - always assume they are
17
Q
other than clostridia, what other bacterial agent causes diarrhoea in foals
A
E coli - not as important as in farm animals and hard to know if pathogenic or commensal
18
Q
describe a Strongyloides westeri infection in foals
A
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
19
Q
list the differentials for diarrhoea in weanlings
A
Lawsonia intracellularis
Rhodococcus equi
strongylus vulgaris
all adult diseases
20
Q
how does lawsonia intracellularis (proliferative enteropathy) present in weanlings
A
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
21
Q
describe the diagnosis of lawsonia intracellularis
A
difficult to get a definitive diagnosis
clinical signs, low albumin, rule out other causes
marked SI thickening on abdominal US
faecal PCR is insensitive
22
Q
how is lawsonia intracellularis treated
A
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
23
Q
describe the presentation of strongylus vulgaris in weanlings
A
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
24
Q
how is strongylus vulgaris diagnosed and treated
A
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
25
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
26
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
27
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)
```
28
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)
```
29
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
30
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
31
what percentage of a cyasthastome population do larvae make up
90%
| 50% encysted
32
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
33
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
34
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)
```
35
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
36
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)
```
37
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
38
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)
39
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
```
40
what are the clinical signs of antibiotic induced diarrhoea
- variable
- mild transient diarrhoea with no systemic effects
- severe fulminant enterocolitis
41
how is antibiotic induced diarrhoea diagnosed
history
| faecal ELISA or PCR for clostridial perfringens enterotoxin and C difficile toxins A and B
42
how is antibiotic induced diarrhoea treated
stop antibiotics
faecal transfaunation
metronidazole - rarely used now
if severe - treat as for clostridiosis
43
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
44
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
45
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
```
46
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
47
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
```
48
what clinical pathology is seen in right dorsal colitis
```
hypoproteinaemia
hypovolaemia
electrolyte abnormalities
neutropenia
occasional anaemia
increased creatinine
```
49
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
50
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
51
describe idiopathic diarrhoea in horses
```
persistent diarrhoea
remains normovolaemic
bright demeanour
can become hypoproteinaemic over time
possibly caused by dietary intolerance e.g. haylage
```
52
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
```
53
how is idiopathic diarrhoea treated
if exclusion diet doesn't work, codeine phosphate PO BID to reduce LI motility
54
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
```
55
how is salmonellosis diagnosed
bacterial culture.
3 negative to rule out
5 negative to declare no longer infected after positive
56
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
57
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
58
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
59
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
```
60
how is the need for suppportive therapy determined
```
major body system assessment
basic bloodwork
- PCV/TP
- lactate
- blood gas and electrolytes
- clotting profiles
```
61
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
```
62
list the causes of weight loss
```
dental disease
intestinal disease
parasites
liver disease
renal disease
neoplasia
GI infection
chronic systemic infection
malnutrition
```
63
why may a horse have reduced feed intake
malnutrition due to owner
competition for feed
dental disorders
anorexia due to pain or dysphagia
64
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
65
what may cause increased loss of nutrients
PLE
PLN
squestration to body cavity - peritonitis or pleuritis
66
what may cause a horse's energy requirements to increase
```
pregnancy
lactation
sepsis
neoplasia
other systemic disease
```
67
what factors may be associated with liver disease in horses
```
maldigestion (rare)
anorexia
hypoalbuminaemia (rare)
increased energy consumption
infection/sepsis
```
68
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
```
69
describe renal disease in horses
```
rare
PLN may occur
assess using
- serum creatinine
- urine SG
BUN not helpful
```
70
what may lead to primary peritonitis in horses
```
haematogenous
- strep equi
- actinobacillus
- R equi
migrating parasites
```
71
what may cause secondary peritonitis in horses
```
sepsis
- rupture of GI tract
- uterine tear
reactive
- abscess
- neoplasia
- ruptured bladder
```
72
what are the clinical signs of sepsis in horses
```
pyrexia
depression
ileus +/- reflux
pain on walking
anorexia
```
73
how is peritonitis diagnosed in horses
abdominocentesis
- copious volumes of fluid
- cloudy sample
- high numbers of degenerate neutrophils
74
what is the prognosis for peritonitis in horses
depends on cause
75
may may chronic diarrhoea occur with malabsorption/protein losing enteropathies
- primary large colon dysfunction
| - abnormal energy substrates to hind gut flora
76
what are the potential aetiologies of infiltrative bowel disease
- parasites (no direct link)
- genetic
- food allergy
- mycobacterium spp
- histoplasma
77
how is infiltrative bowel disease diagnosed
- rectal biopsy
- duodenal biopsy
- laparoscopy
78
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
79
how is infiltrative bowel disease classified
- granulomatous enteritis
- lymphocytic-plasmocytic enteritis
- multisystemic eosinophilic epitheliotrophic disease
- eosinophilic enteritis
80
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
```
81
what paraneoplastic syndromes may occur with equine lymphoma
- hypercalcaemia
| - haemolytic anaemia
82
name the types of malabsorption in horses
- anthelmintic responsive
- steroid responsive
- non-steroid responsive
83
how dose right dorsal colitis usually present
protein losing enteropathy
hypovolaemia
alongside NSAID administration
84
how is right dorsal colitis diagnosed and treated
ultrasound - thickened RDC >5mm
stop NSAIDs
supportive care
misoprostol to increase intestinal blood flow
85
what obvious causes of weight loss should be ruled out when taking a history
diet
| parasites
86
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
```
87
what further tests should be used when investigating weight loss
liver, renal and inflammatory markers
repeat blood tests
abdominocentesis
FEC (won't find tapeworm)
88
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
89
how may total protein be altered with weight loss
decrease
| may be masked by concurrent hypovolaemia
90
how may hypoalbuminaemia be interpreted
GI loss more common than renal
peritoneal/pleural effusions
liver disease (rare)
91
how may hypoglobulinaemia or hyperglobulinaemia be interpreted
hypo - GI loss
| hyper - chronic inflammatory disease (cyathostominosis)
92
how may hyperfibrinoginaemia be interpreted
infection
inflammation
neoplasia
93
when does serum amyloid A increase
inflammatory response
94
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
95
what may oral glucose tolerance test be used for
test if there is an issue with sugar absorption
96
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
97
what may paritial malabsorption in the oral glucose tolerance test indicate
parasitism
localised lesions
rapid GI transit
98
what may a delayed flat curve on an oral glucose tolerance test indicate
delayed gastric emptying
| poor starvation
99
what can be assessed on intestinal ultrasonography
wall thickness (should be 2-3mm)
lumen diameter
motility
anatomy
100
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
