VIN Class 3 - Equine Info Flashcards
Define the term Colic. What are the most common clinical signs of colic recognized by an owner. Is colic always GI in origin?
Colic is a generic term used to describe abdominal pain in horses. It’s most often
attributed to true gastrointestinal pain but horses can also act “colicky” due to non-GI causes. The most common colic signs recognized by an owner are frequent pawing, kicking at abdomen with hind legs, stretching out as if to urinate, laying down, rolling, anorexia, sweating, muscle fasciculations, and Flehman response.
Topic: Colic - Small Intestinal Disease
- Describe the pathogenesis of small intestinal disease.
- List the different causes of the above pathogenesis.
- There are several different ways the SI can be affected. Most cause strangulation, cutting off blood supply of affected intestine, and quickly devitalizing tissue.
- A - Mesenteric lipoma: Typically seen in older horses (20+), twists around one or more pieces of SI –> strangulation.
B. Volvulus: twist within the SI –> strangulation.
C. Intussusception: Typically seen in younger horses @ ileocecal junction most commonly. Occurs due to diet changes, parasites (tapeworms).
D. Herniation Inguinal, umbilical, or incisional.
E. Mesenteric defect: piece of SI entrapped through a rent in mesentery causing strangulation. Rarely epiploic foramen entrapment.
F. Anterior/proximal enteritis: will mimic SI obstruction. Pain usually less severe but significant GI reflux, medical management.
Topic: Colic - Small Intestinal Disease cont.
1. What are the clinical signs?
2. How is this disease diagnosed?
3. What is the treatment?
4. Prognosis?
1 & 2. Severe pain, poorly responsive to analgesics.
- Gastric reflux.
- Transabdominal ultrasound will show
dilated/non-motile loops of SI.
- As it progresses, abdominal fluid will become serosanguinous with elevated proteins/WBC.
- Rectal exam: rarely palpable distended loops of SI depending on duration.
3. surgical; resection and anastomosis if bowel devitalized already, surgical reduction only if caught early (rare)
4. guarded; Poor prognosis if longer duration before
surgery or large amount dead bowel (i.e., >15 feet), frequent post-op ileus if resection required
Topic: Colic - Large Intestinal Volvulus/Torsion
1. This form of colic happens in horses of what age?
2. Describe the pathogenesis.
3. What are the major clinical signs/diagnostics?
4. How is this treated?
5. Prognosis?
6. List the risk factors
- This form of colic can happen in horses of any age.
- A portion of colon twists and rapidly becomes ischemic and begins to necrose
- Severe pain, poorly responsive to analgesics. Elevated HR; systemic shock. NO gastric reflux, Peritoneal fluid may be normal initially.Rectal exam: palpable diffuse gas distension in LI.
- surgical correction, nearly impossible to resect LI.
- good/fair if early surgical correction, poor if more than a few hours
- older broodmares, just before parturition or up to 4 months postpartum; larger horses (more room for LI to twist), any age.
Why is there no gastric reflux seen in horses with LI volvulus/torsion?
B/c the lesion is too caudal to allow fluid to back up to the stomach.
What is a major risk of correcting a LI volvolus in a horse?
Risk of endotoxic shock when volvulus is corrected
Topic: Colic - Colonic Impaction
1. Etiology
2. Risk factors
3. Describe the clinical signs/diagnostics
4. Treatment
5. Prognosis
- This type of colic results from backup of fecal material.
- Older horses w/ poor dentition, fed hay or coarse feed; decreased water intake, stress; Mini horses - small colon impaction common; frequently grooming self/others OR feed material OR poor dentition
- Mild/intermittent colic signs initially and worsen with prolonged duration w/o treatment. May seem “normal” with analgesics. Decreased appetite.
○ Decreased manure production.
○ Palpable firm feed impaction on rectal exam.
○ Increased HR, pain, dehydration, etc. only if progresses without being treated - analgesics; oral fluids with laxatives via intermittent or indwelling nasogastric tube (mineral oil, psyllium, Epsom salts), main goal is to hydrate impaction; IV fluids.
- good. Surgical intervention only if severe pain or several days duration.
Topic: Colic - Colonic Tympany
- What is the traditional cause of colonic tympany?
- What are the C/S and diagnosis?
- Treatment?
- Prognosis
- Traditionally caused by a diet change or diet upset but can happen anytime in
any age animal.
2.
Topic: Colic - Colon Displacement
Topic: Colic - Enteroliths/Sand Colic
Topic: Colic - Gastric Ulcers
Topic: Colic - Parasite Associated Colic
Topic: Acute Colitis
Topic: Urolithiasis
Topic: Uterine Torsion
Equine Infectious Anemia
West Nile Virus
Tent Caterpillar Toxicity
Rhodoccocus equii pneumonia in foals
Equine herpesvirus 1
Equine herpesvirus 4
African Horse Sickness
Hoof Abscess
Topic: CEM
1. Etiology:
2. Considered what type of disease?
3. Is it found in the U.S? Canada?
4. With mares, you would see what grossly?
4. Are there any C/S in stallions typically?
5. Is this disease reportable?
- Taylorella equigenitalis
- Considered an exotic disease, CEM did not appear in the
U.S. until 1978.
- An outbreak occurred in multiple states in 2008.
- Several cases diagnosed since 2010 by USDA.
- CEM has not yet been detected in Canada. - Mares: mucopurulent vaginal discharge in up to 40%, abortion, infertility.
- Stallions: NO clinical signs, typically.
- CEM is a REPORTABLE disease!
Topic: Laminitis
1. Etiology/Risk factors
2. Pathogenesis
3. C/S
- Metabolic disease: obese or overweight horses, metabolic-prone breeds (Morgans, ponies,
miniatures, etc.), Equine Cushing’s disease, excess grass intake (especially in springtime). - Endotoxemic diseases: grain overload, colitis, retained fetal membranes.
- Support limb laminitis.
- Iatrogenic steroid-induced
- Metabolic disease: obese or overweight horses, metabolic-prone breeds (Morgans, ponies,
- Regardless of initial cause, an inflammatory cascade is set off –> laminar projections
(lamellae, i.e., “velcro”) in hoof capsule become inflamed and weaken.
○ Deep digital flexor tendon attaches to coffin bone at palmar aspect. Pull of the flexor tendon
on weak laminae causes the coffin bone to rotate toe palmar towards ground. Alternatively, coffin bone may “sink” lower in hoof due to weight-bearing force on weak laminae - All feet can be affected but usually just fronts or fronts significantly worse.
- Increased digital pulse, heat in hooves.
- Rocked back stance, “walking on eggshells”
- Total or significantly increased recumbency.
- Hoof testers: positive to pressure at toe
Topic: Laminitis cont.
4. Diagnostics
5. Treatment
- No effective tx. Treat inciting cause.
- * Therapy is varied & controversial. Most equine clinicians agree Rx should include:
- Gastric lavage (in cases of grain overload)
- NSAIDs or other analgesics
- IV fluids if shock, dehydration present
- Anti-endotoxemics if indicated
- Deeply bedded stalls
- Avoid corticosteroids
* Chronically, laminitis may result in forelimb lameness, laminitic rings on hooves, and pedal bone rotation.
* Special shoes may help horses with chronic laminitis.
Vet prep tx info: Initial stages: icing or cooling feet, anti-inflammatories.
○ Traditionally horses were given phenoxybenzamine to cause vasodilation and improve
circulation to hooves; true benefit unknown, not used as frequently now.
■ Deeply bedded stall, sand bedding. Cushioned boots or styrofoam on hooves for
extra cushion.
■ Trimming over time to “derotate”: bring back toe and square off, decrease heel angle.
■ Chronic cases not responding well to traditional treatment: deep digital flexor tendon
tenotomy to relieve pull of tendon on coffin bone.
■ Long term: weight loss, diet changes for low sugar and low starch hay and grain,
soaking hay in water to remove sugars before feeding
Topic: Navicular Disease
Horses with a long toe and short heel are prediposed
palmar digital nerve block –> horse goes sound
radioluscent abnormalities in navicular bone
regardless of tx disease progresses and prognosis is guarded
In a salivating, tooth-grinding foal, rule out what first?
Ulcers (the common disease)
Poorly understood pathogenesis
* NSAID use has been associated with development of ulcers.
* Treatment is to reduce/neutralize gastric acid:
- Omeprazole, a proton pump inhibitor, is most effective
- Histamine receptor antagonists ( cimetidine) are also useful.
Topic: Right Dorsal Colitis
Topic: Failure of Passive Transfer
Foals are born without circulating immunoglobulins (IgG) and depend on colostral IgG for immunocompetency. Adequate colostral intake must happen as soon as possible after birth.
Ideally, ~ 1 liter of colostrum within the first 90 min of life.
Serum IgG concentrations in the foal should be 800 mg/dI.
- Gut “closure” virtually complete by 24 hours
- After 24 hours, must give plasma IV. (Frozen equine plasma is readily available.)
Topic: Neonoatal Isoerythrolysis
- Signalment
- Pathogenesis?
- Treatment
- Most common in horses, pigs, cattle, and cats.
- Happens only in foals of mares that have developed anti-RBC antibodies during a previous pregnancy. Foal swallows colostrum containing maternal antibodies to the neonate’s erythrocyte antigens.
- Type II hypersensitivity reaction causes neonate RBC lysis
- Normal neonates become weak & icteric 2-3 days after birth. - Rx:
- STOP ingestion of colostrum and
- Give blood transfusions (often washed maternal RBCs).
* In large animals, Ni does not occur in maiden dams.
* But cats can have anti-RBC antibodies without prior exposure, and first litters may be affected by NI.
Is a continuous murmur normal in a neonatal foal?
- A continuous murmur on left side is normal in
newborn foals. - Due to a slight opening of the ductus arteriosus,
- Usually closes within a week
What is the most common cause of equine pregnancy loss? When do these losses occur? When does the mare com back into heat?
Twinning is the most common cause of equine pregnancy loss.
Most losses occur too early to be classified as abortion.
If pregnancy ends before
day 38, the mare will come into heat on the next cycle and may be rebred.
Topic: EHV-1
1. This is the most common cause of?
2. This, along with what other herpes virus cause?
3. Weeks to months later, you may see what?
4. Clinical signs?
5. With some EHV-1 strains you can see what C/S after what particular incidiences?
6. What is the cause of coital xanthema?
- Equine herpes: most common cause of equine infectious abortion.
- EHV-1 & EHV-4 both cause acute, febrile, upper respiratory disease and both may result in latent infection.
- With EHV-4 see respiratory disease more in weanlings.
- Weeks to months later, you may see 3rd trimester abortions in mares.
- Aborting mares seldom show premonitory signs.
- With some EHV-1 strains, you can see neurological symptoms in mares after abortion storms or in other horses.
- FYI: EHV-3 causes coital exanthema.
Topic: EHV-1
1. EHV-1 and what other herpesvirus can recrudesce during times of stress? What are the C/S?
2. How can this be prevented?
3. Is infection with EHV common? Which strains are horses most commonly exposed to?
4. What is a major DDx for EHV-1?
- EHV-1 and EHV-4 infections can recrudesce in times of stress
- Affected horses cough, are febrile, lymphopenic, and neutropenic +/- retropharyngeal/submandibular lymphadenopathy
- Vaccination at 5, 7, and 9 months of gestation helps prevent abortion.
- EHV-1 and EHV-4 are ubiquitous:
- > 85% of adult horses thought to be exposed to, or latently infected with EHV-1, so…
- Even with regular vaccination,
- No horse is absolutely protected.
- Equine viral arteritis (EVA): not common but can cause abortion and should be a DDx for abortion due to EHV-1
Topic: Viral resp disease
1. What is a major clue that avirus is responsible?
2. Key diagnostics?
3. Equine viral rhinopneumonitis is caused by?
4. EVA is transmitted via?
5. Equine influenza is or is not contagious?
6. Major clinical signs?
7. Is there a carrier state for EVA?
8. Consequences
- Leukopenia is a clue that a virus may be responsible.
- Real-time polymerase chain reaction (PCR) testing of nasopharyngeal (NP) swabs
- Equine viral respiratory pathogens are NOT distinguishable based on clinical signs.
- Equine viral rhinopneumonitis is usually caused by EHV-4.
- Equine viral arteritis (EVA) transmitted resp. & venereal routes
- Equine influenza is very contagious.
- Rapid onset of high fever, depression, and cough.
- No carrier state is known.
- Influenza virus destroys tracheal & bronchial epithelium.
- During epithelial regeneration (3 wks), horse susceptible to secondary bacterial infection cause norm. mucociliary defense mech. are not functioning well.`
Topic: Strangles
1. Etiology
2. What are the major clinical signs?
3. Does it require a primary viral infection to cause disease?
4. Is this disease contagious?
5. What is the source of infection?
6. Bacteria can survive for how long outside host?
7. Treatment?
8. Control?
9. see other info
- Streptococcus equi equi - Gram-positive
- Fever, mucopurulent nasal discharge, dramatic neutrophilia
- +/-abscessation & drainage of submandibular, parotia, and retropharyngeal lymph nodes - Does NOT require a primary viral infection to cause disease.
- Highly contagious; trans. by direct contact and fomites.
- Carrier animals a source of infection
- Bacteria may survive 9 weeks outside the host.
- Wait until abscess goes away/ drained to give ABX. see vet prep n otes for this
- Isolate affected horses
- Monitor rectal temperatures of REST of horses
- Pyrexic horses should be separated from the herd.
- Sick horses shed bacteria ~1 month after clinical recovery.
- Affected horses should have 3 negative nasopharyngeal swab cultures taken 2 weeks apart before release from quarantine.
- Isolate affected horses
- Post-exposure immunity is good
- Early ABX (w/in 24 hr of initial fever) may
PREVENT immunity from developing.
- Vaccination may help control; intranasal and intramuscular vaccines avail.
- IM vaccines do not stimulate mucosal immunity, but they reduce clinical attack rate.
- Post-exposure immunity is good
Topic: Rhodococcus equi
1. Signalment
2. Transmission
3. C/S
4. Diagnostics
5. Treatment
6.
- Primary invader of lower respiratory tract, foals less than 5 months old.
- “Nearly ubiquitous” in soil.
- Infection via inhalation of bacteria-laden dust.
- Foals swallow bacteria in the sputum, it replicates in Gl tract.
- Their manure then contaminates the environment.
- Slowly progressive pulmonary lesions (suppurative bronchopneumonia, pulmonary abscesses, and lymphadenitis) probably follow early infection < 2 weeks of age.
- See lethargy, fever with pulmonary consolidation; may have diarrhea.
- Degree of neutrophilia and/or lymphocytosis &
hyperfibrinogenemia = prognostic indicator. - Mediastinal lymphadenopathy and nodular lung lesions on radiographs puts
R. equi at the top of the differential diagnosis list. - Treatment is Rifampin plus ONE of the following drugs:
- Erythromycin, or
- Clarithromycin, or
- Azithromycin.
What is a threat the mother of a R. equi foal takes ? How is the mother treated? How is this controlled on a farm?
- Clostridium difficile enterocolitis: a threat to dams of treated foals.
- Foal’s antibiotics given for lengthy periods: 4 to 9 weeks.
- Dam ingests antibiotics when cleaning foal: affects her gut flora.
- Case fatality rate without treatment ~ 80%.
- Rhodococcus equi control
- On farms with endemic R. equi, control strategies include:
- Isolation of pneumonic foals,
- Avoidance of dust and overcrowding,
- Close monitoring of foals <5 months old, including,
- Monthly checks of fibrinogen concentration and CBC.
- Hyperimmune plasma administration to young foals may reduce the incidence of disease in endemic situations.
Topic: Pleuropneumonia
1. Similar to ?
2. Signalment
3. Risk factors?
4. Etiologic agents
5. C/S
6. Diagnostics
7. Tx
8. Prognosis
Like “shipping fever” but in horses
* Most common in young, athletic horses.
* Induced by stressors (viral respiratory infection, surgery, shipping).
- Pleural fluid often contains mixed bacterial populations:
- Strep. equi zooepidemicus E. coli, Actinobacillus; sometimes anaerobes like Bacteroides, Clostridium
* Signs: Non-specific fever, depression, anorexia, lethargy, colicky
- Pleuropneumonia is painful; horses reluctant to move.
- May adopt an elbow-abducted stance to ease breathing.
- May have sternal edema.
* Diagnose by clinical signs, plus ultrasound and thoracocentesis
- To ID specific bacteria, transtracheal wash may be a higher-yield procedure.
- Management:
Daily ultrasounds to monitor progress, plus - Intermittent or continuous thoracic drainage,
- Antibiotics,
Analgesics, and NSAIDS. - Prognosis for return to performance is fair to good.
Topic: Equine Asthma
1. AKA?
2. Etiology
3. C/S
4. Diagnostics
5. Tx
6. Signalment
- Allergic etiology
- High dust concentration in the environment is a predisposing factor.
- (NOT a hypersensitivity reaction from the classic types I -
IV classification.) - Signs: coughing older horse, tachypnea at rest, no fever
- Large amount of mucus in the airways, severe bronchospasm
- Heave line
- Wheezing and prolonged expiratory effort on auscultation.
- Neutrophilic inflammation in airways, +/- neutrophilia.
- No cure, but Rx includes:
- Avoid allergens (moldy hay, overhead hay racks, round hay bales, straw bedding, indoor housing).
- Corticosteroids and bronchodilators.
- In 2016, Equine Asthma Syndrome described: range of airway disorders from milder inflammatory airway disease (IAD) to more severe RAO.
- IAD usually seen in younger, athletic horses.
- Often present with exercise intolerance and coughing, but no tachypnea at rest.
- Full recovery expected.
Topic: Lungworms
1. Etiology
2. C/S
3. Diagnostics
4. Tx
- Dictyocaulus arnfieldi
* Donkeys are often the source of that infect horses.
- Donkeys have patent infections.
- So testing donkeys is a higher-yield approach.
- Most adult horses DO NOT have patent infections (a few can but not all).
* Coughing is common in adult horses.
* Donkeys usually asymptomatic.
* Prepatent period is 2 to 3 months.
* Treatment is moxidectin or ivermectin.
Six yearlings on a breeding farm have experienced a sudden onset of severe diarrhea and weight loss.
On exam, the affected horses are thin with ventral edema.
Bright red larvae are evident in the feces of some affected horses.
Which choice is the most likely diagnosis?
A. Stomach worms (Habronema spp.)
B. Ascarids (Parascaris equorum)
C. Cyathostomes (small strongyles)
D. Strongyloides westeri
E. Cryptosporidiosis (Cryptosporidium parvum)
Topic: Cyathostomiasis
Missed first slide on this ~ 1 hr inx
1. Etiology
2. C/S
3. Dx
4. Tx
5. Prevention
Dx: Eggs may not be apparent on fecal exams;
- Rectal palpation is normal BUT at necropsy, large intestinal wall may feel gritty, due to the presence of encysted larvae
- Passage of adult cyathostomes does not necessarily indicate illness
- Symptoms are due to the emergence of hypobiotic larvae into the intestinal lumen.
Major Gl parasite of concern in U.S. horses.
- 3rd-stage larvae can undergo hypobiosis (arrested development) and encyst in gut wall.
- Hypobiotic larvae can emerge en masse from intestinal wall in late winter and spring.
- They cause severe weight loss and diarrhea.
- Prognosis is guarded if this occurs.
- Rx: Hypobiotic larvae harder to eradicate than adult worms.
- Moxidectin or high dose fenbendazole are the most effective way to control hypobiotic larvae.
- Ivermectin NOT reliably effective.
- Resistance increasingly an issue
- Adults susceptible to common dewormers: benzimidazoles, avermectins, pyrantel salts.
- Prevention
- Regular deworming of all horses on premises
- Removing fecal material regularly from living spaces helps.
Topic: Ethmoid Hematoma
- Intermittent unilateral epistaxis in older horses
- Usually visible in nasal passages on endoscopy
- Etiology unknown
- Initial Rx: formalin injection directly into hematoma mass, using endoscopy to guide placement.
- Electrocautery is indiscriminate
- Damages surrounding anatomic structures
- Recurrence is common
- Manage recurrence surgically
Topic: EIPH
1. Signalment
2. Main clinical sign? One of these C/S is also seen in what other disease process?
3. Diagnostics
4. Tx
Common in Thoroughbred, Standardbred racehorses
More common than guttural pouch mycosis (which also may cause epistaxis).
Many horses with EIPH don’t actually have epistaxis Dx: Post-exercise endoscopy/bronchoalveolar lavage
(BAL) is diagnostic.
Rx: Furosemide and nasal dilator strips lessen bleeding but do not prevent it.
Furosemide enhances performance in both EIPH-affected and EIPH-unaffected horses. (Mechanism unknown)
Topic: Dorsal Displacement of Soft Palate
1. Describe this disease process.
2. Etiology
3. C/S
4. Diagnostics
5. Tx
Epligottis is completely hidden. Normally triangular shaped epiglottis would be visible but in these horses the dorsally displaced soft palate is getting in the way. Makes it hard for horse to breathe properly.
- Common
- Gurgling expiratory sound during exercise
- Caudal border of soft palate DORSAL to epiglottis and the epiglottis not visible on endoscopy
- Often caused by problem with the pharyngeal branch of cranial nerve 10, the vagus
- May be secondary to upper respiratory infections in young horses
- In chronic cases the treatment of choice is the “tie-forward” surgery with about an 80% success rate.
Topic: Laryngeal Hemiplegia
1. AKA
2. Signalment
3. Characterized by
4. C/S
5. Diagnostics
6. Tx
- Roaring
Exercise intolerance and noisy breathing.
* Distinctive roaring noise during inspiration.
* Characterized by axonal dystrophy of the left recurrent laryngeal nerve.
* Causes partial or complete failure of abduction of the left arytenoid cartilage during inspiration.
* Most common in males and large breeds.
* Endoscopic observation of complete or partial immobility of the arytenoid cartilage and vocal fold is diagnostic.
* Surgical Rx:
- “Tie-back” or laryngoplasty
- Fixes affected arytenoid cartilage in abducted (open) position.
Topic: Eplglottic Entrapment
1.
- Less common.
- Epiglottic mucosa covers the lateral margin and apex of the epiglottis,
- Reduced performance with inspiratory and expiratory noise.
- Endoscopy is diagnostic:
- Outline of epiglottis is visible; but mucosa covers epiglottis, so normal crenated margin is hidden.
- Surgical correction is effective.
Myopathy Types To Know:
- Exertional rhabdomyolysis (“Tying up”), COMMON
* If sporadic, may be due to simple overexertion
* Chronically may be polysaccharide storage myopathy [PSSM] or
abnormal regulation of calcium in skeletal muscle - Toxicities, and various other etiologies.
- Hyperkalemic periodic paralysis (HYPP, inherited mutation)
Topic: Exertional Rhabdomyolysis
(“Tying up”)
1. C/S
2. Diagnostics
3. Confirmatory diagnostic? What does this test also do?
4.
- Signs after intense exercise
- Profuse sweating
- Reluctance to move
- Tachypnea
- Tachycardia - Creatine kinase & aspartate aminotransferase elevated after episodes
- Muscle biopsies (semimembranosus, usually) both confirm and differentiate recurrent exertional rhabdomyolysis from polysaccharide storage myopathy (PSSM).
Topic: Hyperkalemic Periodic Paralysis (HyPP)
1. Categorized as?
2. Onset is?
3. Etiology
4. Signalment
5. C/S
6. Diagnostics
7. Treatment
- Technically, NOT an exertional myopathy (genetic mutation)
- Onset is unpredictable
- Not induced by exercise
- Heritable
- Affected horses are commonly descended from the quarterhorse stallion “Impressive.
- Usually diagnosed in young horses (<3 years old),
- Muscle fasciculations, weakness (sometimes leading to recumbency).
- Horses appear normal after episodes
- Diet changes can trigger episodes (especially high-potassium foods) and other stressors.
- Diagnosis by DNA testing of hair.
- Management
- Mild episodes controlled by exercise or ingestion of grain or corn syrup.
- IV dextrose is preferred therapy for severely affected animals.
- Avoid high-potassium feeds (alfalfa, molasses).
- High-fat, low-carbohydrate diets seem to help control symptoms.
Topic: Nosocomial Salmonellosis
Nosocomial Salmonellosis:
Severe Acute Colitis
* Nosocomial infection=patient was infected in a clinic or hospital.
- Lots of horses are inapparent carriers of
Salmonella
- Because stressed animals are more susceptible to infection, horses hospitalized for other reasons are at risk for salmonellosis.
* Most common types: Salmonella enterica serovar
Typhimurium and S. enterica Agona.
* ZOONOTIC
- Signs: Some adult horses develop acute colitis
- High fever and watery diarrhea.
- Rapid dehydration, +/- hypovolemic shock
- Horse can die within 24 hours.
- СВС (complete blood count) shows neutropenia. ***
- Acidosis and hyponatremia
- Horses need intensive fluid therapy and correction of acidosis.
- Laminitis can be a sequela to Salmonella septicemia.
- Rx is mainly supportive
- IV fluids and electrolytes.
- Gl protectants (e.g., biosponge, bismuth subsalicylate, activated charcoal) may help to bind bacterial toxins.
- NSAIDs like flunixin meglumine (Banamine) help counteract endotoxin effects, control pain, may help prevent laminitis.
- Low-dose polymyxin B (3,000 units/kg, BID) has been advocated to bind circulating endotoxin.
- Systemic antimicrobial Rx is controversial
- Antibiotics do NOT appear to alter course of colitis or to decrease shedding of Salmonellae.
- In horses with extremely low WBC, broad-spectrum IM antibiotics may be given to prevent secondary infections.
Topic: Potomac Horse Fever Enterocolitis
1. Etiology
2. Transmission
3. C/S
4. Diagnostics
5. Tx
- Caused by Neorickettsia risticii
- Carried by trematodes in a snail vector
- Horses pastured near water at risk.
- Related to Neorickettsia helminthoeca, agent of salmon poisoning in dogs.
- Acute enterocolitis syndrome
- Mild colic, fever, and diarrhea
- Horses of all ages
- Laminitis and abortion may follow.
- Diagnosed by PCR of blood or feces
- Rx = oxytetracycline,
- If given early in disease, response usually w/in 12 hr
- Overall case fatality rate 5%-30%.
Topic: Equine Tetanus
1. Etiology
2. Transmission
3. C/S
4. Diagnostics
5. Treatment
6. Prevention
- Caused by a neurotoxin produced by Clostridium tetani.
- Anaerobic inhabitant of the soil and of animal intestinal tracts.
- Horses are very sensitive to the neurotoxin.
- C. tetani grows in necrotic tissue.
- Disease is usually preceded by a puncture wound.
- Tetanus signs
- Prolapse of the third eyelid
- Erect tail and ears
- Dilation of the nares
- “Sawhorse” stance
- Diagnose by clinical signs and history
- Treatment
- Tranquilization/sedation
- 5,000-50,000 IU tetanus antitoxin bid
- Wound drained, penicillin
- Tetanus immunization and booster annually
- Mortality is high (80%)
- Prevention: Immunize broodmares with tetanus toxoid 4 to 6
weeks PRE-partum.
Topic: Theiler’s Disease:
Acute Equine Hepatitis
1. Caused by?
2. C/S
3. Dx
4. Tx
- Most common cause of acute equine liver disease.
- Associated with biologics, e.g. tetanus antitoxin
- Mares that receive tetanus antitoxin at foaling at risk of acute hepatitis.
- See icterus, anorexia, hepatic encephalopathy.
- Dx: Hepatic biopsy
- Mortality is high (up to 88%).
- Routine administration of tetanus antitoxin to recently foaled mares is NOT a good idea.
- Recent research indicates a parvovirus is a possible cause.
Mortality in horses showing clinical signs from eastern equine encephalitis virus (EEEV) is ?
50%- 90% .
Topic: Arboviruses
1. Arboviruses is a portmanteau for?
2. Spread via?
3. List the enzootic arboviruses affecting horses
4. Diagnostics
- Arbovirus is a portmanteau word (arthropod-borne virus)
- Spread by mosquitoes or other hematophagous arthropods (e.g., sandflies, ticks)
- Enzootic arboviruses affecting horses:
- Eastern Equine Encephalitis
- Western Equine Encephalitis
- Venezuelan Equine Encephalitis
- West Nile Virus
- By the time horses are neurologic, they are no longer viremic. So the blood of febrile stable mates is best way to isolate EEE virus at this point.
- You could do a CSF tap (difficult in a neurologic horse), BUT Diagnosis requires virus isolation, not just cytology. CSF cytology and protein levels might suggest severe CNS inflammation.
Which togaviruses can you not differentiate between based on clinical signs alone?
What is the definitive diagnostics method?
- CANNOT differentiate these togaviruses based on clinical Sx.
- Eastern equine encephalitis (EEE)
- Western equine encephalitis (WEE)
- Venezuelan equine encephalitis (VEE)
- Definitive diagnosis requires virus isolation.
List the regions in which EEE, WEE, and VEE occur
- EEE, WEE, & VEE usually occur in specific geographic regions.
- EEE: all states EAST of Mississippi river and a few states west of it.
- WEE: WEST of Mississippi river.
- VEE: enzootic in Florida, the Rockies, and northern plain. (rarely causes disease in horses or people in the U.S.).
- EEE and WEE have a bird-mosquito cycle:
- People and horses are dead-end hosts.
- People and horses have low levels of viremia.
- No direct spread among infected horses, people, birds.
- EEE is the most dangerous to people
- WEE & VEE usually cause only mild human disease.
- VEE usually has a rodent-mosquito cycle;
- Horses and people are incidental hosts.
- UN-like EEE and WEE,
horses infected with VEE can amplify virus; i.e., they can transmit the virus to biting mosquitoes.
Topic: West Nile Virus
1. You must always consider WNV when evaluating a horse with ?
2. C/S
3. Diagnostics
4. Prevention
5. Zoonotic risk?
- Must consider WNV when evaluating a horse with neurologic symptoms.
- WNV kills ravens, crows, jays, and other birds
- Neurologic disease in horses, people.
- Equine clinical signs
- General: Depression, low-grade fever, anorexia
- Neurologic: Head-pressing, visual impairment,
ataxia
(often hind-end weakness or paralysis) - Today, vaccination helps keep equine WNV cases low,
~ 100 to 300 cases/r. - In 2002 more than 15,000 equine cases were detected in the U.S.
- Canada has relatively little West Nile virus activity, only a handful of equine & human cases per year.
- ZOONOSIS: Human cases
- No symptoms in 8 out of 10 WNV-infected people
- Febrile illness ~ 1 in 5 (headache, body aches, joint pains, vomiting, diarrhea, rash).
- Serious encephalitis or meningitis in ~ 1 in 150
- ~2000 human case-patients reported annually in
U.S. and Canada
Topic: Angular Limb Deformities in Foals
1. What valgus deviation is normal in foals? How can it be treated?
2.
3. Tx options
- Valgus deviation up to 6 degrees is normal in foals
- Does not require treatment.
- Stall rest allows mild valgus deformity to correct on its own.
- Corrective hoof trimming also therapeutic
- More severe valgus deformities may be corrected by surgery
- Periosteal transection SPEEDS growth on side where you do it.
- Transphyseal bridging SLOWS growth on side where you do it..
Surgical options:
- Hemi-circumferential periosteal transection on lateral (concave) aspect of radius
-Or-
- Transphyseal bridging of medial (convex) side of radius
-Or-
- Some combination of both techniques.
Topic: Septicemia in the Neonatal Foal
- What is the biggest risk factor leading to septicemia?
- Etiology
- Clinical signs
- Treatment
- Failure of passive transfer of maternal antibodies is biggest risk factor.
- Gram-negative infections are common.
- But gram-positive bacteria are often contributing factors.
- Endotoxin release from gram-negative bacteria contributes to septic shock.
- Clinical signs: initially depression, but progress to septic shock.
- Recumbency
- Muddy mucous membranes
- Hypotension
- Dehydration
- Tachycardia
- Treatment
- Broad-spectrum antibiotics, usu. penicillin and amikacin
- IV fluids and plasma transfusions are routine
- Hyperimmune plasma administration should be considered
- Nutritional support is very important
- Intensive care of up to one month is typical
- Survival rates >50% are expected at referral hospitals
Topic: Tyzzer’s Disease
1. Etiology
2. Signalment
3. C/S
4. Diagnostics
- What is seen on necropsy?
5. Treatment
Clostridium piliforme
* Acute focal hepatitis with multisystemic consequences:
- Colitis, lymphoid and focal myocardial necrosis.
- Convulsions caused by profound hypoglycemia.
- Clostridium piliforme is a gram-negative, spore-forming, intracellular organism
- Affects wide range of mammals, devastating in horses.
* Clinical findings:
- Neonatal foals ~1 - 2 weeks of age most often affected.
- Sporadic.
- Route of infection is assumed to be by ingestion.
- Affected foals usually become comatose and die rapidly.
Topic: Equine Corneal Ulcers and atropine
- Corneal ulcers very common in horses.
Image courtesy of Dr. Den - Often Rx ulcers with topical antibiotic and atropine.
- Atropine causes mydriasis, inhibits ciliary muscle spasm, and minimizes synechiae formation.
- Colic is a possible adverse effect of topical atropine.
- Atropine affects intestinal motility, even to the point of causing cecal impaction.
- Monitor all horses treated w/ topical atropine for colic.
- STOP atropine if:
- Intestinal sounds diminish -or-
- Intestinal transit time is prolonged.
Topic: Foaling Related Perineal Laceration
DEscribe grades of perinela lac
Foaling-Related Perineal Laceration
* Common foaling-related injury.
* 1st, 2nd, or 3rd degree.
- 1st-degree tears=mildest: involve only skin and mucous membrane of the dorsal commissure of vulva.
- 2nd-degree lacerations extend to muscle of perineal body but not to anal sphincter or wall of the rectum.
- 3rd-degree tears=worst: extend through rectovestibular shelf and penetrate rectum (rectovestibular fistulas).
- 1st- and 2nd-degree lacerations predispose mare to pneumovagina, due to disruption of the vulvar lips.
- 2nd- and some 1st-degree tears need Caslick’s to prevent pneumovagina and urine pooling.
- 3rd-degree lacerations always require surgical
repair, - Should delay repair from 3 weeks post-foaling to weaning.
- Allows maximal healing before surgery.
Bonus Q
Three weaner pigs in a group of 30 died yesterday. Four more pigs were found dead this morning. A few animals are down and paddling. Some are blind, others are uncoordinated. These pigs have been off-feed for 3 days.
Cultures from necropsy tissue of dead pigs:
* Lungs: Hemophilus parasuis, Streptococcus suis,
Pasteurella multocida;
* Pharynx: Hemophilus parasuis, Streptococcus suis,
Pasteurella multocida;
* Brain: Streptococcus suis;
* Heart: Streptococcus suis; and
* Pleura: Mixed growth, including Proteus spp.
Which choice is the most likely cause of illness in
these pigs?
A. Actinobacillus suis
B. Hemophilus parasuis
C. Pasteurella multocida
D. Proteus spp.
E. Streptococcus suis
C ??? answer on dashboard
