Horses 2 Flashcards
acute colitis how bad, success rate, how often get diagnosis and complications
- Emergency - due to possible cardiovascular collapse due to fluid loss into the gut
- Expensive to treat
- ISOLATION
- Treatment can be unsuccessful - 70% success rate
- Definitive diagnosis in 20-30% cases
- Complications
○ SIRS
○ Laminitis
○ DIC, MODS, death
what are the 7 main differential diagnosis for acute colitis
1) salmonella
2) clostridium
3) antimicrobia-assoacited colitis
4) potomac horse fever
5) viral - coronavirus
6) cyasthostomiasis (parasite)
7) non-pathogenic - grain overload and right dorsal colitis (NSAID toxicosis)
Salmonella and clostridium causing acute colitis what types, how infectious
- Salmonella ○ Many serovars, groups B and C most common (horses) - not clinically important which serotype present ○ Highly contagious -> important ○ Invade mucosa, produce enterotoxins - Clostridium ○ C. perfringens § Types A and C most common in horses § Produce α toxin (type A), β and β2 toxins (type C) ○ C. difficile § Two main toxins: A & B
What occurs with antimicrobial-associated colitis and potomac horse fever in terms of causing acute colitis
- Antimicrobial-associated colitis
○ Overgrowth of pathogens due to disruption of normal colonic flora
○ ANY antimicrobial, some more likely than others - Potomac Horse Fever (Neorickettsia risticii)
○ North America – certain geographical locations, spreading. Seasonal, complex life cycle.
○ Within the bloodstream - leads to bi-phasic fever
○ Organism invades monocytes; evades immune response, travels to colon
○ Predilection for large colon mucosal epithelial cells → loss of microvilli
in terms of acute colitis how does viral, parasites and non-pathogenic disease cause
- Viral
○ Coronavirus
§ Cell invasion → necrotizing enteritis (crypt and tip necrosis), villus attenuation, fibrin deposition (pseudomembrane formation), microthrombosis and haemorrhage - Cyathostomiasis (parasite) – mass emergence
○ Physical disruption of mucosa due to larval cyst rupture, inflammatory response - Non-pathogenic
○ Grain overload
§ Overgrowth of lactate-producing species, physical damage of acid on mucosa
○ Right dorsal colitis – NSAID toxicosis
§ Lack of protective PGs, vasoconstriction, ischaemia, ulceration, (necrosis)
acute colitis how important is the diagnosis
REGARDLESS OF THE CAUSE, CLINICAL APPEARANCE IS THE SAME - smell, haemorrhagic, non-haemorrhagic
YOU CANNOT MAKE A DIAGNOSIS BASED ON CLINICAL SIGNS ALONE
Pathogenis in the colon what are the 4 main effects
1. Disruption to caecal and colonic mucosa → abnormal fluid and ion transport ○ Malabsorption ○ Hypersecretion ○ Combination ○ Inflammatory cells – release inflammatory mediators → stimulate direct and indirect secretory responses 2. Inflammatory response in colon ○ “Leaky” capillaries § Colonic oedema § Loss of albumin into colon § Leakage of bacterial toxins into circulation – COMMENSALS + pathogens ○ Infiltration of leukocytes § Produce inflammatory mediators 3. Fluid shifts ○ Secretion, malabsorption → fluid sequestered in colon, lost in diarrhoea →cardiovascular effects § Hypovolaemia § Poor perfusion 4. Electrolyte loss -> Na+, K+, Cl
SIRS when/how occurs
- Gut and blood in close alignment
○ Gut - gram negative and gram positive bacteria
○ Blood - albumin and white blood cells - Inflammation of the layer
○ Bacteria can move into blood (not common) more common is the endotoxins moving into the blood
○ Albumin moving into gut from blood
○ Loss of blood
In SIRS after bacteria moves into the blood what occurs
- Toxins interact with white blood cells -> cascade within WBC resulting in inflammatory cytokines -> activate coagulation -> loss of platelets
- Neutrophils express L selection molecules and endothelial cells produce E selection molecules
- White blood cells attach to the endothelial lining and move into the gut
○ Blood sample -> low albumin, low white blood cell
Problem list for acute enteritis cases
- Diarrhoea ○ Infectious (vs. noninfectious) - Hypovolaemia/ haemoconcentration ○ Fluid loss in diarrhoea - Hypoproteinaemia ○ Protein-losing enteropathy - SIRS (“endotoxaemia”) Secondary to GI compromis - Thrombocytopenia ○ Hypercoagulable state - Leukopenia/neutropenia ○ SIRS - Mild azotaemia ○ Pre-renal/renal/post-renal ○ Probably pre-renal - Hyperglycaemia ○ Stress ○ Severe disease
Acute enteritis diagnostic plan what need to submit
- WILL need to start treatment before results back
○ OFTEN don’t get an answer, need to tell the owners - Samples to submit
○ Faeces
§ Clostridial toxins
§ Salmonella PCR/culture (series of 5) -> one negative doesn’t indicate horse is negative
□ Shed in varied quantities, intermittently
§ Parasitology
○ If PHF season/area
§ EDTA blood – PHF PCR
§ Serum – PHF IFAT
+/- Ultrasound - can help assess oedema
What are the 4 main complications of acute colitis and when at risk
- Laminitis - most common - ANY CASE ○ All colitis cases at risk ○ PHF, grain overload big risks - Coagulopathy ○ Thrombophlebitis – consequence of SIRS - Hypertriglyceridaemia - Rectal prolapse - really oedematous rectums straining to pass large amounts of diarrhoea
Acute enteritis treatment plan, what is generally needed and not needed
- Largely supportive, VERY EXPENSIVE
- Referral generally required
- ISOLATION
- Long-term IV catheter
○ IV crystalloid fluids
○ Anti-inflammatory treatments - Antimicrobials – generally NO
Supportive - reduce laminitis, anti-diarrhoeals, anaglesia, anti-endotoxin treatment
Acute enteritis describe the supportive/preventative measures needed
○ Reduce risk laminitis
§ Ice boots (how long?) -> a few days after white cell count normalises
○ Anti-diarrhoeals
§ Di-tri-octahedral smectite (Biosponge®)
○ Probiotic?
§ Saccharomyces boulardii
○ Analgesia
§ Control colic pain
□ Usually due to ileus, dysmotility, (colon infarction)
§ NSAIDs (not in right dorsal colitis (RDC)- caused by NSAIDS)
□ Look a lignocaine and opioids
○ Anti-endotoxin treatment??
§ (Hyperimmune plasma) -> 50:50 in literature, risks that have with transfusions
§ Flunixin meglumine (not RDC) -> works on the clinical effects -> WORKS
acute enteritis prevention and monitoring plan
Prevention - Isolation - Separate at-risk groups - Don’t mix horses and cattle (Salmonella) - Feed roughage ASAP following GI compromise e.g. colic - Don’t use antimicrobials when unnecessary Monitoring plan - Regular monitoring is essential ○ Cardiovascular parameters ○ PCV/TP ○ Lactate ○ Diarrhoea frequency, volume ○ Electrolytes ○ CBC Monitor for complications
foal diarrhoea difference to adults, result, treatment and how to balance referral and management on farm
- Easier to diagnose - generally higher identification of the pathogen
- Neonates do become bacteraemia (useful to take blood culture)– consequences
○ Sepsis
○ Septic joints/other synovial structures
○ Omphalitis - umbilical structures - Treatment largely supportive, still expensive
- Referral vs. management on farm
○ Severity of disease (i.e. intensity of required treatment)
○ Ability and knowledge of owners/farm managers
What are the 3 initial things need to do to diagnose a foal with diarrhoea
- Signalment – age esp. important
- History
○ Farm size
○ Gestation and birth
○ Post-partum period
○ Adequate passive transfer?
○ Duration of diarrhoea?
○ What is it doing now?
§ Is it up and nursing or dull and not nursing - Physical exam
○ Mentation
○ Cardiovascular status
○ Signs of sepsis/bacteraemia
§ Joints
§ Umbilicus
§ Petechiae
○ Evidence of not nursing well
○ Colic? - distention of small intestine, colon or disruption to movement
Foal diarrhea what is the general problem list and clinical pathology findings
Problem list - Dull/lethargic - Not nursing - Diarrhoea - Colic - Petechiae - Injected mucous membranes, slow CRT - Cold extremities - Slow jugular refill Clinical pathology findings - CBC - Fibrinogen - Biochemistry - Venous blood gas - IgG (neonates) - may be normal at 24 hour mark but if septic may use as energy so then begin to decrease
What are the 9 main differentials for neonatal foal diarrhoea
- Salmonellosis
- Clostridiosis – usually perfringens – often haemorrhagic - can be so severe than become anaemic
- Coronavirus
- Rotavirus
- Cryptosporidium
- Enterococcus durans***
○ New discovery in terms of being pathogenic - Nutritional – orphans especially
- FOAL HEAT
- Parasitic – Strongyloides
What are the 4 main differentials for older foals/weanlings
- Strongyles
- Ascarids
- Rhodococcus
- Equine proliferative enteropathy/Lawsonia (weanling age, usually chronic)
Foal diarrhoea diagnostics what needed and what differentials can it rule in or out
- Blood culture as become bacteriaemic
- Ultrasound
○ Colicky foals
○ Intussusception
○ Intestinal wall thickening, Intestinal contents
○ Umbilical infection
○ Surgical lesion? - Diagnostic faecal samples – slightly more rewarding in foals than adults
○ Salmonella PCR/culture
○ Clostridial toxin assay
§ +/- Gram stain
○ Rotavirus ELISA or LAT
○ Parasitology
§ acid fast (protozoal diarrhoea) - cryptosporidium
Foal diarrhoea diagnostic what to add for older foals and why
○ Rhodococcus – culture, PCR for VapA
§ PCR Good at ruling out but not ruling things in
Rotavirus how common in what age, clinical signs and what does it cause
- Most common in foals 5 days – 4 weeks old
- Clinical signs variable – diarrhoea usually watery, yellowish/greenish, non-fetid
- Causes denuded villi, crypt hyperplasia, and combined secretory/malabsorptive enteritis
○ Temporary lactase deficiency - need lactase replacement therapy
Cryptosoridium how host-specific, importance, causes, diagnosis, treatment and prevention
- Non-host specific protozoa
○ ZOONOSIS! - Implicated as cause of foal diarrhoea
○ BUT isolated with same frequency from normal and diarrhoeic foals - Generally self-limiting, resolves in 5-14 days
- Diagnosis: acid fast stain (faecal sample)
- Treatment generally supportive
- Strict hygiene!
Nutritional diarrhoea what foals generally occurs in, causes and best treatment options
- Usually orphan foals
- Incorrectly mixed milk replacer
- Too much milk replacer
- Electrolyte abnormalities
- Correct feeding practices
- Nurse mare if available - best, otherwise goat milk is a good replacer
Foal heat diarrhoea what age group, why, results and treatment
- Foals aged approx. 7-9 days (may be 4-14 days)
○ Occurs around same time mare’s “foal heat”
○ Generally when foals are coprophagic (normal) - Foal remains systemically healthy
- Diarrhoea self-limiting
- Usually no treatment required
○ monitor
Rhodoccus equi what cause in foals and 2 other causes of diarrhoea
- Usually pneumonia (pulmonary abscesses), but many extrapulmonary manifestations ○ Ulcerative colitis 1) Sepsis, neonatal encephalopathy ○ Period of poor perfusion to GI tract ○ Treat primary problem, supportive care 2) Intestinal nematode parasites ○ Older foals/weanlings
What are the treatment options for foal diarrhoea
- Long term IV catheter
- IV fluids – replacement crystalloids
○ Care – electrolyte disturbances
○ Colloids? Generally not - Plasma – FPT, sepsis
- Systemic antimicrobials – broad spectrum, parenteral, preferably IV
○ Cephalosporin – 2nd or 3rd generation
○ Penicillin + aminoglycoside (if renal function OK)
○ Add metronidazole (PO) if concerned Clostridial - Anti-diarrhoeals
○ Di-tri-octahedral smectite
○ Bismuth subsalicylate - Gastroprotectants? - not done
○ Omeprazole - Allow to nurse vs. withholding from mare
○ Lactase enzyme replacement if villous damage suspected - Topical barrier Tx (minimise scalding) - like nappy san for babies
In general what are more likely colic causes in young horses (neonates) and immature horses
Young horses
- First manure getting stuck (meconium impaction)
- congenital abnormalities of the gut (atresia coli)
Immature
- Prone to infectious problems
- Enteritis (small intestinal)
- Parasitic
○ Ascarid impactions of the small intestine (foal lecture)
○ Intussusception (association with worms)
Aged horses and colic what breds, what type of lesions and why
- Often quite stoic- esp pony breeds
- Consider lesions that take time to develop (>15 years old)
○ Tumours
§ Benign: pedunculated lipoma: strangulate SI**
§ Malignant (uncommon)
□ Lymphoma
□ Adenocarcinoma
Aged horses with colic what looking for and what often related to especially in what species
- Look for evidence of previous, more severe abdo pain
○ Trauma/skin off head - Or related to poor dentition
○ Impactions
○ Esp donkeys: (long lived) -> generally lose multiple teeth leading to impaction
§ Donkeys very stoic - generally just lay down -> DON’T IGNORE IF GO OFF FEED
§ Rarely roll or paw
§ Note subtle behavioural changes
§ Metabolism of NSAIDs is faster -> lasts half the time of horses
□ BUT: be careful masking signs
aged horses with colic does it change their prognosis
Age does not reduce prognosis if in good health
- BUT: Consider concurrent dx
- Cushings syndrome inhibits healing
Previous laminitis?
stallion colic what need to consider and some diagnostics
- Consider reproductive organs: check testicles
- Enlargement (with colic) is either:
○ Testicle itself: testicular torsion
○ Something else in the tunic with it: herniation (SI) - Both ischaemic + painful
○ Ddx with palpation /ultrasound /rectal
○ Palpate small intestine through internal inguinal rings
Broodmare colic what need to consider and main differentials
- Broodmare: pre or post-partum?
- Pre-partum -> Pregnant causes
a. Foal movement can result in low gr colic
b. foaling/ate term abortion
c. uterus can twist: uterine torsion (last 2 months)
Post-partum
a. rupture of uterine artery
b. foal can damage uterus during foaling
c. can also damage GI tract
Foaled within 3 months - HIGH RISK - most common large colon volvulus (this until proven otherwise
Broodmare pre-partum what are the 3 common causes of colic how common and diagnosis
a. Foal movement can result in low gr colic
§ More common in maiden mares
§ Present as low grade /intermittent colic
b. Foaling / late term abortion
§ Vaginal discharge /open cervix -> ASSESS RECTALLY
§ (colic) More likely in later gestation when foal large
c. Uterus can twist: uterine torsion (last 2 months)
§ Relatively uncommon
§ Diagnosis: rectal palpation of broad ligaments - EASILY IDENTIFIED
□ Ligament crosses uterus obliquely in direction of torsion
□ Left ligament horizontal and heading cranial
□ Right ligament vertical and heading below uterus (less reliable)
® =clockwise torsion ( Counter clockwise also possible)
Uterine torsion leading to colic in broodmares pre-partum and what are the 2 main options for correction and what must be confident on
1) Surgical
® Standing flank laparotomy
® Midline caeliotomy - preferred for shorter people
2) Non-surgical
® GA (triple drip)
® Roll in opposite direction to torsion
® Advantages of non-surgical correction
◊ Financial
◊ Less invasive /no risk of incisional problems - especially when late in pregnancy - increase pressure on that surgical incision
- Must be confident in diagnosis and direction of torsion -> Risk uterine rupture
What is the most common cause of colic in broodmare that has recently foals, when occur, presentation and results
Rupture of uterine artery**- common
§ Moderate- violent colic (hemorrhage is painful)
□ Soon after foaling: up to 48hrs
□ BUT- have very pale mmbs (ddx GI cause)
□ Most often bleed into broad ligament (contained)
® Can bleed into abdomen/uterine lumen
◊ Can bleed out quickly -> not able to save generally
Rupture of uterine artery leading to colic in recently foaled broodmare what is the treatment options
□ NSAIDs, careful sedation to calm -> don’t want to drop blood pressure too dramatically
® Detomidine and top up if needed
□ Tranexamic acid: antifibrinolytic (10mg/kg in 1L IV) - stabilises the clot
□ +/- blood transfusion (indications below)
® Decided by: lactate>4, HR 80, Hb<8g/dL, PCV<15% (unreliable in acute stage)
® Can lose approx 11L without need to transfuse
® (1/3 of blood volume: b.vol = 8% body weight)
What are the 2 main things foals can do during birth that can lead to colic in broodmares post-partum, what occurs and treatment
1) Foal can damage uterus during foaling
§ Uterine tear
§ Uterine fluid (sterile) in abdomen
□ Present as peritonitis 1-3d after foaling: low grade fever, dull, mild colic, inflammatory abdo tap
§ May require surgical closure and abdominal lavage - place abdominal drains
2) Or can damage GI tract
§ Necrosis or rupture of GI tract (high bacterial load)
§ Present as peritonitis BUT: severe inflammation and endotoxemia
§ Cannot be treated effectively: euthanise
What is the highest risk period for broodmares, what generally occurs and most common cause, treatment
Highest risk period for broodmares -> Foaled within 3 months
- Moderate- severe colic (ischemia/signif distension)
- CV compromise (ischaemia)
- Abdominal distension (LI)
- MOST COMMON CAUSE -> Large colon volvulus until proven otherwise
○ Surgical emergency
Travelling colicky broodmares how should be done, and what do if in severe or mild-moderate pain
- Separating mare and foal is stressful for both
- Judgement based on safety for foal
- Severe pain - dangerous for the foal
○ Mare doesn’t worry about foal if in severe pain
○ Safer to transport separately - Mild-moderate pain
○ Mare stressed if foal taken
○ Travel them together
○ Sedate mare for trip
What are the 4 main causes of colic based on geographical location
1) sandy soil - sand impactions - SA,WA, VIC
2) enteroliths - WA,NSW,QLD (NOT VIC)
3) infectious agents - QLD, northern NSW
4) swim colic - racehorse swum for excercise
Sandy soil how can that result in colic, treatment, diagnosis, prevention and location
○ Sand impactions
○ Clients often aware of risk
○ Sometimes surgical if sand doesn’t move through well
○ Auscultate sand on ventral abdomen
§ Hear what sounds like ‘Sea washing over sand’
○ Sand in manure or loose manure due to mucosal irritation
○ Prevention -> Feed off ground, drench / feed psylium (little evidence)
○ SA, WA, occasionally in VIC
Enteroliths causing colic where form, result, treatment and locations common
○ Form in large colon
○ Luminal obstruction when large
○ Chronic +/- acute colic
○ Ingesta and gas build up oral to obstruction, pressure necrosis possible
○ Require surgical removal
○ WA, NSW, QLD - don’t learn just not VIC commonly
Infectious agents causing colic what common location, why, disease, transmission and presentation
○ QLD /Northern NSW (or shipped in past 2 weeks)
○ Flying foxes
○ Hendra virus can present as colic
§ Uncommon but 100% mortality (Seropositive euthanised)
§ No horse –horse transmission
§ Passed to humans in resp secretions /blood
□ Do not suck on NG tubes during work up of QLD/NSW horses
§ Presentation
□ Respiratory, neurological (depression, ataxia)
□ More recently presenting as colic
□ Straining to pass manure/ urinate
□ Fever not reliable
□ Concurrent resp /neuro unreliable
□ Limited details on ‘colic’ signs as yet
§ Take precautions with sick, unvaccinated horses from high risk locations
□ PPE
Swim colic when occur, treatment, why occur and what is important
○ “Swim colic”: racehorses swum for exercise
§ Typically severe colic within 30 minutes of swim
○ Treatment - 95% respond to NSAID + sedative
§ +/- Gas on stomach tube
○ Dysmotility induced during swim
§ Can have severe distension
○ 5% surgical** - not always medical situation - should respond quickly
○ Distension: SI or LI +/- displacement/volvulus
○ Some repeat offenders
§ Client education*
Febrile colic what is generally the cause types of pathogen within large intestine, small intestine and abdominal cavity
- Febrile suggests infectious (most commonly)
○ Bacterial
§ Large intestine= Colitis (Salmonella/Clostridia)
§ Small intestine= Anterior Enteritis (Clostridia)
§ Abdominal cavity=
□ Peritonitis (Actinobacillus equuli)
□ Peritonitis due to GI catastrophe
○ Viral
§ Hendra
Analyse situation and give diagnosis - General history ○ 8yo TB, Quiet /lying down approx 12 hrs ○ Little manure passed today No drugs given so far - Physical exam ○ Occasional flank watching/dull ○ HR 48 ○ Mmbs salmon pink ○ Hasn’t passed much manure ○ Temp 39.0 ○ NGTube: no reflux ○ Abdominocentesis: Turbid, yellow WCC 210x109 cells/L TP 30 g/dL Lactate <2 mmol/L
No drugs - know that pain is the actual level
PE
- Low grade abdominal pain consistent with MMbs salmon pink
- hasn’t passed much manure -> § Reduced LI motility? - Large colon impaction - know if rectal
FEVER NARROWS DOWN
§ Narrows ddx down: SI / LI / peritoneal cavity - no longer routine LC impaction
□ Ddx Colitis, Anterior Enteritis, Peritonitis
- no reflex - NOT ANTERIOR ENTERITIS
- abdominocentesis - peritonitis
Peritonitis leading to colic treatment and monitoring
- Bacterial infection ○ Abx: penicillin +/- gentamicin - Low grade colic ○ NSAID - Little manure (inflammation in abdomen slows motility) ○ Enteral fluids - Expect normal physical exam within hours - Re-evaluate after 5 days with abdo tap ○ Not necessary in many cases
What findings for colic would rule out GI catastrophe, colitis and anterior enteritis
Not GI catastrophe - Would be CV collapse - Massive bacterial load- mixed population - Endotoxaemia - HR, RR, Poor perfusion due to CV collapse Not colitis - GS often increased early on - Loose manure/dxa on rectal - Peritoneal fluid rules out Not AE - No reflux
In general what is the cause of colic in broodmares with severe colic or moderate colic in aged pony
- Broodmares with severe colic = large colon volvulus OR uterine artery haemorrhage
- Moderate colic in aged pony = strangulating lipoma
Chronic dirrhoea in horses what are important higns in history to ask
○ Duration? ○ Severity? ○ Recent or ongoing treatments (especially NSAIDs)? ○ Deworming? ○ Conditions the horse is kept in? ○ Weight loss? (Appetite?) ○ Acute worsening?
physical examination and clinical pathology for chronic diarrhea horse what generally presents
○ Usually no signs of systemic inflammation ○ Usually not febrile ○ Often not hypovolaemic ○ Diarrhoea cowpie to liquid, variable volume and frequency ○ Often accompanied by weight loss ○ +/- Colic signs ○ Ventral oedema - Clinical pathology findings ○ CBC § Normal, any changes possible § PCV may be ↑ (hypovolaemia), ↓ (anaemia of chronic disease) or normal § TP often ↓ ○ Biochemistry § Triglycerides
What are the 6 main differentials diagnosis for chronic diarrhoea in horses
a. Right dorsal colitis (NSAID toxicity)
b. Sand enteropathy
c. Cyathostomiasis
d. Inflammatory bowel diseases
e. Alimentary lymphosarcoma
f. Equine proliferative enteropathy (Lawsonia intracellularis)
Right dorsal colitis what is the most common cause, other cause
- NSAID toxicosis - common ○ Prolonged administration ○ High doses - Individuals – idiosyncratic sensitivity ○ Inhibition COX-1 ○ Ulcerative lesions – RDC, stomach ○ Renal disease ○ ↑ risk if NSAIDs used when dehydrated, endotoxaemic, or combination NSAIDs used
Right dorsal colitis common problem list and diagnosis
- Common problem list ○ History of NSAID administration § Prolonged § High doses § Normal doses ○ Hypoproteinaemia § Hypoalbuminaemia - ventral oedema, distal limb oedema ○ Colic ○ Diarrhoea - CHRONIC - Diagnosis ○ History ○ Hypoproteinaemia (hypoalbuminaemia) - oedema ○ Ultrasound § Just because you don’t see thickening, doesn’t mean it isn’t there
Right dorsal colitis treatment and prevention
- Treatment
○ NO NSAIDs – use alternative analgesics to control colic pain
○ Supportive, esp. colloids
○ +/- misoprostol (Prostaglandin replacement)
§ No good evidence surrounding use
§ Need to wear gloves -> nothing that is pregnant
○ Omeprazole, sucralfate for concurrent gastric ulceration
○ Low roughage diet - finely chopped chaff, off hay
○ Surgical resection in severe cases - Prevention
○ Monitor TP in cases receiving prolonged NSAID treatment
Sand enterpathy generally when occur and presentation
- Horses fed on bare ground with minimal/no vegetation
- Accumulation sand (or gravel) in ventral colon, transverse colon causes inflammation
- Presentation
○ Often accompanied by weight loss
○ Chronic diarrhoea, often not severe
sand enteropathy common problem list and diagnostic tests
- Common problem list
○ History – kept in paddock with no/minimal vegetation, fed hay off ground
○ Weight loss
○ Diarrhoea
○ +/- Hypoproteinaemia
○ Colic - Sand directly irritating to the colon
○ Often multiple locations - Diagnostic tests
○ “Sand test”
§ Place diarrhoea and water into rectal glove and hold upside down for awhile
§ The sand will settle into the fingers
○ Auscultation - may hear sand moving across sand?
○ Imaging – radiographs (referral), (ultrasound)
Sand enteropathy treatment and prevention
- Treatment ○ Remove horse from sand!! ○ Medical management - managing colic pain via NSAIDS ○ Psyllium – NOT if colicking § Combine with probiotics? ○ Some require surgical correction § Enterotomy to empty sand from colon § Good prognosis - Prevention ○ Remove horse from sand!! ○ Feed off ground, in tubs, on concrete, indoors ○ Psyllium, commercial products available
Cyathostomiasis which causes issues, what are those issues and diagnosis
- Encysted larval stages – L3
- Commonly causes chronic diarrhoea, assoc. with ill thrift
- Acute severe diarrhoea associated with mass emergence of encysted larvae
- Diagnosis
○ FEC – but won’t tell you about encysted larvae
§ Useful for herd management but not individual management
○ Hypoalbuminaemia
○ Response to treatment
○ Rectal mucosal biopsy - generally not done -> lucky to get piece of tissue with encysted larvae
Cyathostomiasis treatment and prevention
- Treatment ○ Anthelmintics - larvicidal § Fenbendazole – 10 mg/kg PO SID for 5 days □ Resistance problems § Moxidectin – 0.4 mg/kg PO once (usual dose) ○ Supportive - Prevention ○ Good de-worming protocol
Inflammatory bowel disease what is it and common problem list
- Malabsorption, maldigestion due to infiltration of inflammatory cells into GI tract
- Common problem list
○ Chronic diarrhoea, often cowpie rather than watery
○ Chronic weight loss (good appetite, at least initially)
○ Intermittent colic
○ Poor haircoat
○ Ventral oedema
○ Hypoproteinaemia
Inflammatory bowel disease what are the 4 recognized types how common in what age group, main presentation and prognosis
1) Granulomatous enteritis (GE)
○ Young horses, idiopathic, low % have diarrhoea
2) Lymphocytic-plasmacytic enterocolitis (LPE)
○ Rare, no specific identifying features
3) Eosinophilic enterocolitis (EE)
○ Colic primary sign, not weight loss; better prognosis
4) Multisystemic eosinophilic epitheliotropic disorder (MEED)
○ Young horses, skin lesions, other organs affected (liver, spleen)
Inflammatory bowel disease diagnosis
○ Glucose absorption test
§ Prior fasting, feed withheld during test (water OK)
§ 1 g/kg glucose (as 20% solution) administered via NGT
§ Blood glucose measurements taken at baseline, then q 30 min for 3-4 hours, then q 60 min for another 2-3 hours (total 6 hours)
§ Glucose should peak (>85% of baseline value) by 120 minutes.
§ D-xylose absorption test alternative
○ Abdominal ultrasound
○ Rectal biopsy
○ Intestinal biopsy (if colic surgery)
○ Abdominocentesis
○ Can be elusive
Inflammatory bowel disease treatment and prognosis
○ Often palliative
§ EE may gain long-term success
○ Often ongoing
○ Corticosteroids – tapering until find lowest dose that controls clinical signs
§ Some horses may have periods of not needing corticosteroids at all
- Prognosis generally poor
Alimentary lymphosarcoma presentation, age, rectal exam
- Similar history and presentation to IBD
- Often young horses
- May have multiple organ involvement (overlapping types)
- Enlarged mesenteric lymph nodes on rectal exam
Alimentary lymphosarcoma diagnosis, treatment and prevention
- Diagnosis as for IBD ○ Partial to complete malabsorption - glucose absorption test ○ Abdominal ultrasound ○ Rectal exam ○ Abdominocentesis ○ +/- Rectal biopsy ○ Can be elusive - Treatment as for IBD - Prognosis generally poo
Equine proliferative enteropathy what caused by, age, presentation adn diagnosis
- Lawsonia intracellularis (bacteria)
- Weanling age foals - 5 months old
- Proliferative enteropathy
- Presentation
○ Signs: lethargy, weight loss, colic, diarrhoea, severe hypoproteinaemia, oedema
○ Usually not febrile - Diagnosis
○ Faecal PCR
○ Serology – Serum IPMA (immunoperoxidase monolayer assay)
○ Ultrasound
Equine proliferative enteropathy treatment and prognosis
- Treatment
1) Supportive
§ May require colloids
2) Antimicrobials: choice does not affect survival.
§ Oxytetracycline - needs to penetrate
§ Macrolide + rifampin - can use macrolides in foals NOT ADULTS
§ (Chloramphenicol – NOT in VIC)
Prognosis generally good with prompt Tx
○ Sell for less as yearlings
Equin proliferative enteropathy prevention/control
- Prevention/control ○ Difficult ○ No vaccine for horses (yet) ○ Don’t mix horses with pigs § Other species – wildlife reservoirs ○ Start Treatment early
parasitic disease what are the 3 main parasites causing disease, resistance and what not done anymore
- Main disease-causing culprits ○ Small strongyles (cyathostomins - high resistance) ○ Ascarids (Parascaris spp; foals) ○ Tapeworms (Cestodes; Anoplocephala spp.) - Resistance ○ Benzimidazoles (54-98% farms) ○ Pyrantel (41% farms) ○ Macrocyclic lactones (0% farms) - ROTATIONAL GRAZING - not done anymore
Small strongyles what is the main one, what is pathogenic and how pathogenic
cyathostomins
- Adults non-pathogenic, larvae are the issue
- Larvae encyst to develop from early L3 to late L4 stage - can stay for up to 2 years
- Can arrest development at early L3 stage
- Mass emergence - COLIC
○ Late winter to early spring
○ Late summer to early autumn
○ Severe weight loss, diarrhoea, hypoproteinaemia, passage large numbers larvae in faeces
Cestodes main issue, where mainly found and diagnosis
- No acquired immunity develops
- Attach at ileocaecal valve - can do this in large numbers - can lead to intussusception -> colic
- Diagnosis difficult - proglottids intermediately shed - may not be present and can break down
Saturated sugar float is the easiest way but not always present
What are some other GI parasites (not small strongyles or cestodes) and what can cause
- Large strongyles
- Strongyloides westerii
- Oxyuris spp. (pinworms) - cause discomfort not large issue
- Gasterophilus spp. (bots) - bot larvae
- Ascarids (foals) - cause life threatening disease
Available anthelmintics for horses what are the types and drugs within
- Benzimidazoles ○ Fenbendazole ○ Oxfendazole ○ Oxibendazole - Macrocyclic lactones ○ Ivermectin ○ Abamectin ○ Moxidectin - Tetrahydropyrimidines ○ Pyrantel ○ Morantel - Praziquantel - Cestodes only
cyathostomum how to reduce anthelmintic resistance, what horses do for, and what need to acknowledge
SELECTIVE DEWORMING - for Cyathostomum
- In ADULT horses only NOT foals - doesn’t work for ascarids
- Acknowledge the problem
○ Convince clients!
- Accept that completely parasite-free horses are neither possible nor desirable
what are the goals for selective deworming
○ Prevent parasitic disease
○ Reduce pasture contamination
○ Preserve refugia = prevent anthelmintic resistance
§ Refugia? Where? -> worms that we don’t put selective pressure on by not
□ In horses that don’t get dewormed
□ Encysted larvae
□ In the environment at the time of deworming
How to perform selective deworming
○ PERFORM FAECAL EGG COUNTS
§ Select only high (and maybe some moderate) shedders for deworming - leaving the others with a refugia population
□ This is the one shedding onto the pasture
□ Interpreting FEC results
® Low shedders: less than 150 EPG
® Moderate shedders: 150-500 EPG
® High shedders: over 500 EPG
In terms of selective deworming how do you know if the farm already has resistance before introduction
Perform FECRTs (faecal egg count reduction test) (on at least 6 horses)
§ When beginning selective deworming program
§ Every 2-3 years afterwards - to ensure still no resistance
○ FECRT
§ Pre-treatment egg count and post-treatment (14 days) egg count
§ Pre-treatment EPG (egg count) - Post-treatment EPG ÷pretreatment EPG x 100
§ Results
□ >90% reduction – no significant resistance
□ 80-90% reduction – suspect resistance
□ <80% reduction – resistance
□ Macrocyclic lactones – <98% reduction raises suspicion - because so effective
What to do after first selective deworming
○ Repeat FECs just after ERP (egg reappearance period) of anthelmintic used
§ Dosing interval determined by ERP (varies between anthelmintics
§ Egg reappearance periods
□ Vary between anthelmintics
® Moxidectin: 12 weeks (now what we have) (16-22 weeks - when first came on the market)
◊ Becomes less and less effective on the luminal larval (late L4) so ERP gets shorter -> this can indicate early resistance
® Ivermectin: 4-8 weeks (9-13 weeks)
® Oxfendazole: 4 weeks (6 weeks)
® Fenbendazole: 4 weeks (6 weeks)
® Pyrantel: 4 weeks (5-6 weeks)
what are the limitation of FECs and therefore why bother doing them
○ Egg shedding, distribution
○ FECs do not reflect presence of encysted larvae
○ FECs often don’t correlate with numbers of adults
○ Technique – detection limit
○ Why bother doing them?
§ To identify horses that are contaminating the pasture for everyone - to reduce parasite populations as much as possible without increasing resistance
Should you combine anthelmentic and what if once a high shedder
- Combination products?
§ Exposes parasite population to >1 anthelmintic
§ If resistance present? - for now not a good idea
§ Evidence needed - Once a high shedder?
○ FEC consistency over time generally
○ Do you need to keep doing FEC on these?
§ Do it for a year to ensure consistent - establish a pattern and deworm the ones that need it
What worming to do with other parasites that aren’t cyathostomum
○ Once yearly deworming recommended in Autumn
○ Ensure praziquantel combination or pyrantel
○ Unable to test for large burdens at the moment
What environmental management is done to reduce parasite resistance
○ Long time when the larvae are OUT of the horses
§ Address the pasture stages
○ Very sensitive -> Extreme heat or cold
§ <6ºC – no hatching or development
□ Will survive if above freezing
§ >45ºC – larvae hatch but rapidly die -> don’t need to deworm in these temperatures
§ 25-33ºC – optimal development and hatching
□ 3-5 days to destroy larvae numbers
□ Survival shortened (weeks)
○ Reduce larval numbers
§ Remove manure from paddocks every 3-5 days
§ Don’t advise dragging/harrowing -> horses generally don’t tend to graze where manure is anyway -> not advised UNLESS VERY HOT -> expose eggs and larvae to these conditions
How to convince your clients to undergo selective deworming
- Widespread, indiscriminate moxidectin use
○ 80-90% used larvicidal anthelmintics regularly - Concerned about resistance, BUT
○ Extra work
○ Extra costs
○ Want guaranteed results - Cost-benefit
○ Investment in the future…
○ Reduction anthelmintic use by 75-82% -> in large farms large money saver - Get them to tell their friends!
○ This works best if everyone does it
Deworming foals which parasite of most concern, what management is needed, what ersult in
- Ascarids of greatest concern
- Adults cause disease
- Pasture not required
- Eggs containing L2 larvae - very persistent in the environment, will stay there for years
- Failure to thrive - small, poor haircoat
Ascarids how pathogenic in foals, what results in and the worse presentation with prognosis
- Migratory larvae – liver, lungs - why adults have good immunity (6months of age)
○ Larvae in lungs can cause respiratory signs - Large burdens – failure to thrive
○ Small intestinal impactions - Ascarid impactions
○ Recent history of deworming
○ Prognosis guarded if surgical
○ Risk of SI rupture - doesn’t need to have a large burden for this to occur
○ Adult numbers not correlated with rupture
○ Whole worms in faeces, reflux
○ FEC
Ascarids resistance and can you use selective deworming?
- Resistance in ascarids
○ Greater resistance to macrocyclic lactones than benzimidazoles (US)
○ Australia
§ Resistance to all classes reported
§ Multiple resistance
○ Base anthelmintic choice on FECRT - Cannot currently use selective approach
-> No easy way to identify foals with large adult burdens
○ FECs don’t reflect adult numbers
○ Ultrasound? Cannot image the whole intestines
Deworming foals what is the main objective and current recommendations
- Main objectives:
○ Remove adults
○ Reduce eggs in environment - Traditional recommendations likely overkill
○ Increase in resistance - Current recommendations:
○ Deworm ALL foals at 2 and 5 months and then at weaning as stressful event
○ Then use selective deworming targeted at cyathostomin control at 6 months
○ Don’t deworm before 2 months
§ Larval and juvenile adult population
Foals what to do is suspect high adult burdens
○ Macrocyclic lactone vs. benzimidazole?
○ Consider mechanism of action
§ Paralytic - macrocyclic lactones - all die and being passes at the same time -> higher risk of impaction
§ β-tubulin binding - disrupt energy mechanism - die of starvation -> generally more broad distribution in death time -> less likely to impact
○ Treatment
§ Current lack of evidence
what do most medical colics respond to, if not
MOST MEDICAL COLICS RESPOND TO FLUNIXIN AND DETOMADINE
- If not - SURGERY - REFERRAL
- If have to dose at 12 hours for flunixin (should last 24 hours for mild pain) then again refer
if presented with horse what do next
- rolling repeatedly at 4am, trainer gave 2ml Ace into vein no change at 10mins, 10ml flunixin horse lying in box and repeatably rolling
ace - (not good for pain, ALSO dilates blood vessels - NOT GOOD IF WANT TO GO TO SURGERY)
flunixin - good for visceral pain but only just administered it, probably not on board yet
NEXT
- Get history -> NOT YET
- Physical exam -> HARD TO DO
- Refer dt pain -> MORE INFORMATION NEEDED
- Give PBZ -> Flunixin generally better for visceral pain over PBZ
○ Right dorsal colitis, will be dehydrated so reduced renal blood flow -> if adding more drugs may compromise renal function - NO
- Give detomidine -> alpha-2 sedative, analgesia for visceral pain - GOOD DO THIS
○ Will reduce heart rate and GI sounds
○ Will give 1 hour acting sedation (flunixin should be on board at this point)
Anaemia how to measure and what need to consider and define
- Absolute reduction in RBC mass ○ PCV § Need to consider □ Excitement or pain □ Breed (hot vs cold blooded horses) □ Age (changes in neonates) □ Hydration status ○ Haematocrit ○ Red blood cell count ○ Haemoglobin concentration Functionally defined as a decrease in the blood's O2 carrying capacity
How to classification anaemia via bone marrow response, the two main ones, what indicates and signs
a. Regenerative (responsive) § Blood loss, haemolysis § Signs of regenerative □ Reticulocytosis □ Macrocytosis and anisocytosis □ Polychromasia □ Basophilic stippling □ THESE CHANGES DO NOT OCCUR IN HORSES - may see macrocytosis ® To determine need to do bone marrow biopsy § When are these signs absent □ Acute anaemia - 2-3 days required for bone marrow response □ Protein malnutrition □ Chronic external blood loss (GI parasitism (loss of protein and iron) b. Non-regenerative (non-responsive) □ Indicates abnormal bone marrow □ Other cell lines often affected
Haemorrhage leading to anaemia, clinical signs and what else also generally associated
§ Mucous membrane pallor
□ Icterus not usually a feature -> unless internal haemorrhage
§ Clinical signs of decrease D02
□ Tachycardia, tachypnoea etc
§ Hypovolaemic
§ Anaemia accompanied by hypoproteinaemia
□ PCV and (protein) normal acutely - lost all at the same rate
® Until blood is diluted through fluids or movement of fluids within the animal
□ Splenic contraction may obscure anaemia acutely in horses
□ Protein may be normal with haemorrhage into a body cavity
Where can you internal and external haemorrhage
§ Internal haemorrhage where
□ Pleural cavity
□ Peritoneal cavity -> splenic/hepatic trauma
□ Uterine artery rupture -> post-foaling
□ Muscle bellies -> longbone/rib fractures
§ External haemorrhage where
□ External wounds
□ Gastrointestinal tract - Parasites and ulceration
□ Uterus
□ Urinary tract
□ Guttural pouch mycosis - Carotid artery
Haemolysis what signs generally seen and other indications
§ Icteric/jaundice (hyperbilirubinaemia)
□ R/O liver disease
□ R/O anorexia in horses
§ Signs of an inflammatory reaction - fever (intravascular causes inflammatory and could be secondary to infection), neutrophilia
§ Anaemia with a normal or slightly increase (protein)
§ Erythrocyte morphology can suggest etiology - heinz body
§ Hyperbilirubinaemia (unconjugated)
§ Anti-RBC antibodies (cooms test or flow cytometry)
Urogenital haemorrhage which artery generally assocaited with, when occur and clinical signs
- Middle uterine artery ○ May occasionally involve iliac artery - Almost always post-partum ○ Usually affects multiparous mares - Clinical signs include ○ Sweating ○ Trembling (muscle weakness) ○ Signs of abdominal pain ○ Whinnying and flehman response - Mares often markedly tachycardic (60-140/min) Tachycardia is inappropriate for level of discomfort
Urogenital haemorrhage diagnosis
Diagnosis difficult -> history and clinical impression - COLIC AND ANAEMIA - brrodmare after foaling
- Rectal palpation
○ May be able to palpate haematoma within broad ligament
○ Often unremarkable
○ May exacerbate bleeding by increasing blood pressure
- Transcutaneous ultrasonography
○ Haemorrhage within broad ligament
○ Hemoperitoneum (confirm with abdominocentesis)
Urogenital haemorrhage treatment plan
- Rupture of the middle uterine artery with intra-abdominal haemorrhage
○ CANNOT FIX - just hope that she clots
Supportive
1. IV fluids
§ Restore vascular volume
§ Isotonic fluids
§ Require 3-4 times estimated blood loss
§ Hypertonic saline (7 to 7.5% @ 4-6m/kg)
§ Fluid administration will decrease PCV but improves perfusion -> usually improves DO2 (oxygen delivery)
2. Broad-spectrum antimicrobials
§ Bacterial culture medium in abdomen. cannot exclude uterine rupture
3. Analgesics/anti-inflammatory drugs
4. Keep mare quiet
§ Acepromazine: may cause mild hypotension
§ Rectal examination
5. Anti-fibrinolytic (formalin, amino-caproic acid) - STOP THE CLOT FROM BREAKING DOWN
6. blood transfusion if doesn’t respond to above
