Disease of the equine neonate pt 4 Flashcards
Infectious Diarrhea - Foals
- common agents
l Rotavirus
l Salmonellosis
l Clostridiosis
l Cryptosporidiosis
l Septicemia
l Rhodococcus equi
l Lawsonia intracellularis
l Strongyloides westeri
l Most common viral cause of diarrhea in foals
Rotavirus
pathogenesis of rotaviral diarrhea
Small intestine: invades villus epithelial cells → villus atrophy → crypt cell proliferation → ↑fluid secretion, malabsorption, maldigestion → diarrhea
rotavirus morbidity, mortality
l High morbidity, low mortality, farm outbreaks
- rotavirus affects foals of what age?
- Dx?
- how common in diarrheic foals?
- vaccine?
- Reported in foals 5-35 days of age, but older (>1mo) foals may be at increased risk
- Diagnosis by immunoassay or electron microscopy of feces
- Can be isolated in 20-40% of diarrheic foals
- Vaccine available – efficacy against field strains?
Salmonellosis - Foals
- how common?
- generally what type of syndrome?
- what type is problematic?
- shedding increased in what animals?
- Common pathogen in foals with GI disease
- More likely sepsis syndrome vs purely diarrhea
- Enteroinvasive Salmonellas (ie S. typhimurium) carry higher risk for bacteremia and sepsis
- Shedding is significantly increased in hospitalized foals with GI disease compared to hospitalized adult horses with GI disease (Ernst et al 2004)
Clostridiosis
- type of bacteria, characteristics, where found
l Gram positive bacilli
l Obligate anerobe to aerotolerant
l Spore-forming
l Spores are ubiquitous in environment
Clostridiosis
- most common types implicated
- common associations
- normal inhabitants of where?
- C. difficile and C.perfringens most common, but C. septicum, C. cadaveris, C. sordelli have also been isolated from horses with colitis
- Commonly associated with anti-microbial administration or nosocomial
- Normal inhabitants of GI tract in low numbers and non-toxin producing
Clostridiosis - Foals
- only found in sick?
- primary pathogen or opportunist
- type of C. perfringens most common? mortality rate?
- C. difficile prevalence?
- Can be isolated from both healthy and sick/diarrheic foals
- Can act as primary pathogen in foals
- C. perfringens – types A & C most common, C has significantly higher mortality rate
- C. difficile prevalence in healthy foals reportedly higher than adult horses
C. perfringens
- types and their toxins, what they do?
Types A, B, C, D, & E (classified by exotoxin)
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* A → α-toxin (phosphlipase C), disrupts glucose uptake/energy production & activates AA pathway in enterocytes
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* B & C → β-toxin (cytotoxin), enterocyte necrosis/ulceration
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* A & C → enterotoxin (cytotoxin), membrane pores in enterocytes, altered permeability, enterocyte necrosis, desquamation/inflammation etc
C. difficile
l 3 large toxins, what they do
- A → enterotoxin, recruitment/activation of PMNs → vasodilation, secretory, inflammatory response
<><> - B → cytotoxin (in vitro), interacts with toxin A
<><> - Binary toxin (cdT) → ADP-ribosylation, cytotoxic
<><><><> - Varying toxin profiles exist in pathogenic strains
Clostridiosis - Epidemiology
- risk factors
- spores
l Antimicrobials
l Hospitalization, stress, withholding roughage l +/-PPIs
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Spores are very persistent in environment
> 16.7% in veterinary hospitals
> more common on breeding farms vs. farms with only mature horses (Baverud 2002)
Clostridiosis - Diagnosis for C. perfringens
– fecal culture, enterotoxin ELISA (CPE), PCR for toxin production
Clostridiosis - Diagnosis for C. difficile
- what are the best tests?
– fecal culture, cytotoxicity tissue culture assay, toxin ELISA, PCR
- Approx 25% of isolates are non-toxin producing
- Cytotoxicity assay is gold standard
- PCR higher Sn & Sp than ELISA
Cryptosporidiosis
- agent characteristics
- symptoms
- apthogenesis
- shedding
- Dx
- Non-host specific protozoa, zoonotic
- Causes diarrhea in many species
- Invades enterocytes of distal SI → villus atrophy & fusion → malabsorption → diarrhea
- Oocyst shedding concurrent with diarrheic phase
- Diagnosis – sucrose wet mount of feces to identify oocysts
Cryptosporidiosis
- significance in foal diarrhea
- when is it found?
- Questionable role in foal diarrhea
- Has been isolated with similar frequency in healthy and diarrheic foals
- Co-infection with other putative diarrheal pathogens in foals with GI disease (Slovis et al 2013)
- More studies needed
Rhodococcus equi
- agent characteristics
- where its found, type of pathogen
- affects what age
- primary disease caused
- Gram positive pleomorphic coccobacillus
- First described (pneumonia) in foals in 1923
- Endemic in environment, opportunistic pathogen
- Affects foals 1-6 months of age
- Primarily bronchopneumonia, but extrapulmonary disease occurs in up to 74% of foals
Rhodococcus equi
- how often detected in diarrhea from foals?
- treatment connection with diarrhea?
- Variable detection in feces of healthy and diarrheic foals (8-14% in one study, Slovis et al 2013)
- Treatment with a macrolide & rifampin may also cause diarrhea
<><><><> - Role as a causative agent of diarrhea alone (without pulmonary signs)?
Proliferative enteropathy
- agent
- pathogenesis
- age affected
- Lawsonia intracellularis – obligate intracellular bacterium
- Apical cytoplasm of proliferative crypt epithelial cells in intestinal mucosa → chronic thickening and malabsorption with protein loss → diarrhea
- Foals affected at 3-7 months of age, onset of clinical signs has been associated with recent weaning
Proliferative enteropathy
- clinical signs
- Dx, ante and post mortem
- Depression, ill thrift, weight loss, edema, diarrhea, rough hair coat, potbelly appearance
- Severe hypoproteinemia/hypoalbuminemia, anemia, leukocytosis
- Antemortem diagnosis by fecal PCR, serology, signalment and clinical signs, exclusion of other causes of diarrhea
- Post-mortem diagnosis by silver stain of intracellular bacteria in crypt epithelial cells
Strongyloides westeri
- what is it?
- transmission?
- age affected?
- signs?
- Tx
- Common parasitic infection of foals
- Transmammary transmission
- Patent infection in foals by 8-12 days of age
- Generally mild diarrhea
- Treatment – deworming with benzimidazole or ivermectin
Strongylus vulgaris
- pathogenesis?
- when it causes problems
- Tx
- 4th stage larvae may cause diarrhea/colic in foals
- Migration through arterioles of cecum & descending colon
- Pre-patent period 6 months – not a cause of diarrhea in neonatal foals
- Treatment – appropriate deworming
Non-infectious Diarrhea - Foals
- causes, generally
- Foal heat diarrhea
- Antimicrobial-associated
- Nutritional causes
- Gastric ulcers
Foal heat diarrhea
- what does it look like? what age?
- coincides with what
- etiology
- should look for what?
- Mild, self-limiting diarrhea in foals 5-14 days of age
- Coincides with mare’s foal heat
- Etiology remains unknown
- Foals are not sick – if not nursing, dehydrated, etc another cause should be investigated for diarrhea
Nutritional causes of diarrhea in foals
- pathogenesis of each
Overingestion of milk or overfeeding
- Overwhelms capacity of SI → milk into colon → fermentation → ↑sugars and acids → osmotic diarrhea
- May occur when feeding milk replacer or non-equine products
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Lactase deficiency
- Damage to mucosal epithelial cells → ↓production of lactase → ↓ability to digest milk → diarrhea as above
- Treatment – lactase, allow mucosa to recover
Gastric ulcers
- cause, generally
Imbalance between:
* protective:
> (mucosal blood flow, mucus/bicarb production, prostaglandins, gastroduodenal motility) and
* aggressive factors
> (gastric acid, pepsin, enzymes) in gastric +/- duodenal mucosa
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- Causes include NSAIDs, hypoxia, sepsis
gastric ulcers in foals clinical signs
- Clinical signs in foals include abdominal pain, bruxism, lying in dorsal recumbency, diarrhea
- Can be clinically normal or only mildly depressed/anorexic
Pathophysiology of foal gastric ulcers
* Imbalance between aggressive and protective factors:
- what are they
Aggressive factors
* HCl-
* pepsin
* Heliobacter pylori??
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Protective factors
u Mucus layer and mucosal blood flow
u PGE2
u Cellular restitution
u Epidermal growth factor
u Gastroduodenal motility
Clinical Signs of gastric ulcers in Foals
- Poor appetite or intermittent nursing.
- Colic
- Poor body condition.
- Frequently lies on back.
- Bruxism (grinding of teeth).
- Ptyalism (excessive salivation).
- Diarrhea or history of diarrhea.
Gi ulceration risk factors
- stress
- transportation
- high grain diet
- stall confinement
- intermittent feeding
- intense exercise
- racing
- illness
- NSAID use
- management changes
in what region of the stomach are GI ulcers in horses commonly found
Endoscopic surveys indicate that ~80% of these lesions are found in the nonglandular squamous mucosa of the stomach (equine squamous gastric ulcer disease), especially on the lesser curvature just proximal to the margo plicatus.
scoring for equine gastric ulcers
Grade 0: epithelium is intact throughout; no hyperemia, no hyperkeratosis (yellowish color, sloughing)
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Grade 1: mucosa is intact, but there are areas of hyperemia and/ or hyperkeratosis
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Grade 2: small, single or multi-focal erosions or ulcers
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Grade 3: large, single or multi focal ulcers, or extensive erosions and sloughing
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Grade 4: extensive ulcers, with areas of deep submucosal penetration
equine gastric ulcers - comlications
- perforation
- stricture
equine gastric ulcer prevalence in
- foals
- others
Foals:
* 25-50%
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* TBandSTB * 88%
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* Swedish Standardbred racehorses in race training
* 70%
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* Danish Pleasure horses
* 53%
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* Old horses
* 56%
GI ulcers Dx, tests available
- History, clinical signs and physical examination
- Gastroscopy
- lower red blood cell counts (RBC) counts and hemoglobin concentrations
- fecal occult blood test: ppv 90%; npv 17%;
- “SUCCEED-Equine fecal blood test
> equine monoclonal antibodies to both albumin and hemoglobin (ppv 77%; npv 72%)
GI ulcer treatment options - types of drugs, generally
- Acid-suppressive drugs
- Non-Acid-suppressive drugs
Acid-suppressive drugs for GI ulcer treatment
H2-receptor antagonists
* Ranitidine
* Famotidine
* Nizatidine etc
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H+/K+-ATPase inhibitors (proton pump inhib.) * Omeprazole (Gastrogard paste)
* Pentoprazole
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Antacids
Non-Acid-suppressive drugs for GI ulcer treatment
- Sucralfate
<> - Synthetic PG analogues
> Misoprostol (PGE1)
> Enprostol, arbaprostol (PGE2)
<> - Colloidal bismuth (Pepto-Bismol®)
<> - Gastric emptying stimulants
> Metoclopramide
> Bethanechol
> Anti-cholinergic drugs: Not recommended due to side effects
Congenital hypothyroidism and dysmaturity syndrome (CHD)
- what is this disorder? what do we observe?
- what happens to the thyroid gland
- gestation length
- congenital musculoskeletal abnormalities
- Dysmaturity
- Thyroid gland hyperplasia
- Increased gestational length
- Multiple congenital musculoskeletal abnormalities:
> mandibular prognathism, flexural limb deformities, rupture of the common digital extensor tendons, incomplete closure of the abdominal wall, incomplete ossification of the tarsal and carpal cuboidal bones - Dysmaturity:
> soft, silky hair coat, domed forehead and floppy ears, weak at birth, hypothermic and not able to stand up normally.
Congenital hypothyroidism and
dysmaturity syndrome
* Etiology
is still under debate
- dietary deficiencies, excess dietary nitrate, toxic substances, and infectious agents have all been suggested
Congenital hypothyroidism and
dysmaturity syndrome Tx
no effective treatment
Congenital hypothyroidism and
dysmaturity syndrome
- prognosis
- long-term survival and a future athletic performance is grave.
- Most foals that are die or are subjected to euthanasia soon after birth.
- In the few cases that have survived for longer, tend to develop a variety of orthopaedic disorders and rarely go on to have a normal athletic career
Junctional Epidermolysis Bullosa (JEB)
- signalment
- inheritance pattern
- signs
- carriers
- Belgian Draft horses and derivatives of that breed
<> - Inherited as a recessive trait (homozygous recessive)
> causes moderate to severe blistering of the skin and mouth epithelia, and sloughing of hooves in newborn foals.
<> - Carriers
> 50% chance of passing on the mutation to their offspring.
Severe Combined Immunodeficiency (SCID)
- inheritance, signalment
- how it arises?
- outcome
- prevalence
- Lethal genetic (Arabian foals), inherited autosomal recessive disorder
- Mutation in the coding for the enzyme DNA-protein kinase catalytic subunit (DNA-PKcs) on chromosome 9
> Responsible for the formation of key immune defense molecules.
> Lymphopenia and hypogammaglobulinemia - Foals die of an opportunistic infection (such as
pneumonia) or they are euthanized - Prevalence of 2.3% in USA
Lavender Foal Syndrome (LFS), also known as Coat Color Dilution Lethal
- how it arises, outcome
- signs
- looks like?
- Lethal neurologic disorder caused by a mutation of the MYO5A gene on chromosome 1
- coat color can appear to be pale lavender, pale pink or silver
- affected foals are unable to stand and will have episodes of tetany where the foal will lay on its side rigidly extending its limbs, neck and back.
- Tetanic episodes, the foal will also frequently make paddling motions.
- Foals are often large and have a difficult delivery (dystocia).
- Affected foal may be initially misdiagnosed with neonatal maladjustment syndrome
Overo lethal white syndrome
- inheritance
- signs
- treatment
- Autosomally inherited disease associated with horse breeds that register white coat patterns.
- single amino acid substitution at residue 118 on the endothelin-B receptor gene
- ileocolonic agangliosis
- White foals born to American paint horses of overo lineage,
specifically the frame overo subtype. - There is no treatment for this condition
