Equine 6 Flashcards
(104 cards)
1
Q
what are the predisposing factors to hyperlipidaemia in the horse
A
- 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
2
Q
summarise the pathophysiology of hepatic lipidosis
A
- 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
3
Q
what will blood from an animal with elevated triglyceride look like in a serum tube
A
serum will be turbid and cloudy in moderately-severely affected animals (>5.5mmol/L)
4
Q
what is the treatment for hyperlipaemia if anorexic
A
- 5% dextrose/glucose at maintenance rate (short term)
- enteral nutrition if primary disease allows
- partial parenteral nutrition if enteral not possible
5
Q
what is the treatment for hyperlipaemia if also hyperglycaemic
A
- introduce insulin therapy
- insulin zinc suspension 0.15 IU/kg
dubious efficacy with insulin resistance
6
Q
what may be used to inhibit fat metabolism in hyperlipaemia
A
nicotinic acid - unproven efficacy
7
Q
what may be used to increase triglyceride uptake by peripheral tissues in hyperlipaemia
A
heparin - stimulates lipoprotein lipase to remove triglycerides. however LPL already at maximum so benefit is questionable
8
Q
list the parasites in the horse
A
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
9
Q
how is gasterophilus diagnosed
A
gastroscopy
not seen on faecal analysis
10
Q
what is the significance of gasterophilus infestation
A
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
11
Q
how is gasterophilus prevented and treated
A
can’t control flies
remove eggs in summer months using bot knife/topical insecticides
sensitive to ivermectin and moxidectin (not worth using)
12
Q
describe habronemiasis infection
A
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)
13
Q
how is habronemiasis diagnosed
A
faecal analysis difficult due to fragile eggs rupturing
gastroscopy - see lesions
14
Q
how is habronemiasis prevented
A
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
15
Q
describe parascaris equorum infection
A
disease usually affects horses under 2yo (immune response not yet developed)
prevalence 10-50%
adult horses act as reservoirs
16
Q
briefly describe the life cycle of parascaris equorum
A
involves migration through the liver, vena cava, alveoli, bronchi and trachea.
adults 4cm long, cream and round
eggs coughed up and swallowed
17
Q
what are the clinical signs of parascaris equorum infestation
A
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
18
Q
describe the diagnosis of parascaris equorum
A
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
19
Q
how is parascaris equorum treated and prevented
A
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
20
Q
what are the clinical signs of S westeri infection
A
very mild
dematitis - fenzy behaviour
enteritis - profuse, non-fetid diarrhoea in foals with no temperature
occasional cough due to migration
21
Q
how is S westeri prevented
A
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
22
Q
describe anoplocephala perfoliata infestation
A
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
23
Q
describe the life cycle of anoplocephala
A
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
24
Q
how is anoplocephala diagnosed
A
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
25
what are the clinical signs of anoplocephala infection
```
ileal impaction
intussusceptions
caecal impaction and motility disorders
spasmodic colic
diarrhoea - less common
```
26
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
27
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
28
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
29
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
30
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
31
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
```
32
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
33
which equine parasite disease is the most important in terms of prevalence and severity of clinical signs
cyathostominosis
34
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
35
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
36
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
37
describe autumn syndrome in cyathostominosis
occurs when larvae enter the intestinal wall
less common than spring syndrome
- colic
- diarrhoea due to inflammation
38
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
```
39
describe the clinical signs of pinworm
anal pruritus
skin excoriation
myiasis
rarely colic if huge burden
40
how is pinworm diagnosed
eggs in perianal region on examination
| sellotape test
41
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
42
describe the resistance of parasites to ivermectins
emerging in cyathastomes
large strongyles sensitive
widespread resistance in ascarids
43
describe the resistance of parasites to moxidectin
emerging in cyathostomes
large strongyles sensitive
widespread resistance in ascarids
44
describe the resistance of parasites to fenbendazole
widespread in cyathastomesand
probably ok in large strongyles
anecdotal in ascarids
45
describe the resistance of parasites to pyrantel
some resistance in cyathostomes
large strongyles sensitive
some cases of resistance in ascarids in USA
46
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
```
47
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
```
48
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
49
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
50
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)
51
list potential oesophageal congenital abnormalities in foals
```
Stenosis
Persistent right aortic branch
Vascular abnormalities
Duplication cysts
Idiopathic megaoesophagus
```
all rare
52
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
```
53
list some causes of colic in foals
meconium impactions - most common
gastric ulceration
parascaris equorum infestation
intestinal obstruction
54
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)
55
what aspects of the history are important in a colic investigation in foals
parturition process
colostrum consumption
meconium production
faecal/urinary production
56
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
57
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
58
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
59
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
60
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
61
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
62
what are the signs of meconium impaction
tenesmus without defaecation
sometimes see moderate pain signs
gas distension due to obstruction
63
how is meconium impaction diagnosed
digital palpation per rectum
manual abdominal palpation
abdominal ultrasound
abdominal radiography
64
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
65
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)
66
what are the clinical signs of EGUS in foals
```
may be none
colic
diarrhoea
excessive salivation
teeth grinding (bruxism)
perforation is a concern
```
67
how is EGUS/GDUS (gastroduodenal ulcer syndrome) diagnosed in foals
clinical signs
endoscopy
- EGUS, smaller scope than adults
- GDUS
68
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
69
how is EGUS treated
```
acid suppression - omeprazole? + sucralfate or misoprostol. other: ranitidine, Al/Mh hydroxide
supportive care
- IV FT
- antibiotics
- NSAIDs
```
70
how is GDUS treated
acid suppression
supportive care
gastrojujunostomy in selected cases (difficult to perform)
71
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
72
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
```
73
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
74
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
75
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
```
76
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)
```
77
what metabolic disturbances occur due to foal diarrhoea
```
hypovolaemia
hypoalbuminaemia
metabolic acidosis
sepsis, SIRS
endotoxaemia
lactose intolerance
```
78
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
```
79
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
80
describe perinatal asphyxia syndrome
decreased oxygen supply and ischaemia-reperfusion injury during birth
results in decreased GI function (ileus or diarrhoea)
81
what are the clinical signs and treatment of PAS
signs
- dullness
- inappetence
- colic
- hypothermia/pyrexia
- tachycardia
- tachypnoea
treatment
- supportive/nursing care
- antimicrobials
- hyperimmune plasma
82
describe necrotising enterocolitis in foals
bacterial mediated
pathophysiology is multifactorial - GI immaturity, hypovolaemia, inflammation, genetics, dysbiosis, diet
controverisl role of clostridia/salmonella
83
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
84
what is the treatment and prognosis of necrotising enterocolitis in foals
supportive care
BS antimicrobials +/- metronidazole
poor prognosis
85
describe the presentation of rotavirus in foals
5-35 days old
| pyrexia, anorexia, depression, profuse watery diarrhoea, hypovolaemia
86
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
```
87
how does coronavirus present in foals
```
usually adults, occasionally foals
co-infection with rota or Cl perfingens
hypovolaemia
pyrexia, anorexia, lethargy
neutropenia, hypoalbuminaemia
```
88
how is coronavirus diagnosed, treated and prevented
faecal PCR
supportive treatment
prevent with strict biosecurity
89
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
90
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
```
91
how is clostridial diarrhoea diagnosed
positive toxin ELISA or RT-PCT (difficile)
| faecal gram stain - high count gram positive rods/spores (perfringens)
92
how is clostridial diarrhoea treated
supportive care
| metronidazole
93
describe rhodococcus equi infection
primarily respiratory pathogen
foals 1-4 months old show signs but infection from birth
33% develop diarrhoea
94
how is rhodococcus equi diagnosed
uniquitous - hard to prove significance
VapA-PCR
thoracic US screening due to common subclinical infection
95
how is rhodococcus equi treated
supportive care
| macrolide and rifampin
96
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
97
what are the signs of proliferative enteropathy
```
oedema
lethargy
diarrhoea
weight loss
pyrexia
colic
hypoalbuminaemia
severe SI thickening on US
```
98
how is proliferative enteropathy diagnosed
clinical signs
serology
faecal PCR
99
how is proliferative enteropathy treated
lipophilic antimicrobials for 3 weeks (oxytet, doxycycline, macrolides)
good prognosis
100
how is bacterial diarrhoea diagnosed and treated
blood culture with sepsis
faecal culture
haematology
treat with antibiotics and supportive care
101
describe cryptosporidium parvus infection in foals
```
1-4 weeks old
diarrhoea
weight loss
may have concurrent disease
zoonotic
```
102
how is C parvus diagnosed and treated in foals
```
faecal analysis (flotation/staining, ELISA, RT-PCR)
self limiting so just supportive care
```
103
describe strongyloides westeri infection in foals
trans-mammary infection
diarrhoea only if in high numbers
responds to ivermectins
104
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
