Disease of the equine neonate pt 4 Flashcards

1
Q

Infectious Diarrhea - Foals
- common agents

A

l Rotavirus
l Salmonellosis
l Clostridiosis
l Cryptosporidiosis
l Septicemia
l Rhodococcus equi
l Lawsonia intracellularis
l Strongyloides westeri

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2
Q

l Most common viral cause of diarrhea in foals

A

Rotavirus

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3
Q

pathogenesis of rotaviral diarrhea

A

Small intestine: invades villus epithelial cells → villus atrophy → crypt cell proliferation → ↑fluid secretion, malabsorption, maldigestion → diarrhea

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4
Q

rotavirus morbidity, mortality

A

l High morbidity, low mortality, farm outbreaks

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5
Q
  • rotavirus affects foals of what age?
  • Dx?
  • how common in diarrheic foals?
  • vaccine?
A
  • 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?
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6
Q

Salmonellosis - Foals
- how common?
- generally what type of syndrome?
- what type is problematic?
- shedding increased in what animals?

A
  • 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)
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7
Q

Clostridiosis
- type of bacteria, characteristics, where found

A

l Gram positive bacilli
l Obligate anerobe to aerotolerant
l Spore-forming
l Spores are ubiquitous in environment

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8
Q

Clostridiosis
- most common types implicated
- common associations
- normal inhabitants of where?

A
  • 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
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9
Q

Clostridiosis - Foals
- only found in sick?
- primary pathogen or opportunist
- type of C. perfringens most common? mortality rate?
- C. difficile prevalence?

A
  • 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
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10
Q

C. perfringens
- types and their toxins, what they do?

A

Types A, B, C, D, & E (classified by exotoxin)
<><><><>
* A → α-toxin (phosphlipase C), disrupts glucose uptake/energy production & activates AA pathway in enterocytes
<><>
* B & C → β-toxin (cytotoxin), enterocyte necrosis/ulceration
<><>
* A & C → enterotoxin (cytotoxin), membrane pores in enterocytes, altered permeability, enterocyte necrosis, desquamation/inflammation etc

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11
Q

C. difficile
l 3 large toxins, what they do

A
  • 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
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12
Q

Clostridiosis - Epidemiology
- risk factors
- spores

A

l Antimicrobials
l Hospitalization, stress, withholding roughage l +/-PPIs
<><>
Spores are very persistent in environment
> 16.7% in veterinary hospitals
> more common on breeding farms vs. farms with only mature horses (Baverud 2002)

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13
Q

Clostridiosis - Diagnosis for C. perfringens

A

– fecal culture, enterotoxin ELISA (CPE), PCR for toxin production

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14
Q

Clostridiosis - Diagnosis for C. difficile
- what are the best tests?

A

– 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

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15
Q

Cryptosporidiosis
- agent characteristics
- symptoms
- apthogenesis
- shedding
- Dx

A
  • 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
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16
Q

Cryptosporidiosis
- significance in foal diarrhea
- when is it found?

A
  • 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
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17
Q

Rhodococcus equi
- agent characteristics
- where its found, type of pathogen
- affects what age
- primary disease caused

A
  • 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
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18
Q

Rhodococcus equi
- how often detected in diarrhea from foals?
- treatment connection with diarrhea?

A
  • 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)?
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19
Q

Proliferative enteropathy
- agent
- pathogenesis
- age affected

A
  • 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
20
Q

Proliferative enteropathy
- clinical signs
- Dx, ante and post mortem

A
  • 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
21
Q

Strongyloides westeri
- what is it?
- transmission?
- age affected?
- signs?
- Tx

A
  • 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
22
Q

Strongylus vulgaris
- pathogenesis?
- when it causes problems
- Tx

A
  • 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
23
Q

Non-infectious Diarrhea - Foals
- causes, generally

A
  • Foal heat diarrhea
  • Antimicrobial-associated
  • Nutritional causes
  • Gastric ulcers
24
Q

Foal heat diarrhea
- what does it look like? what age?
- coincides with what
- etiology
- should look for what?

A
  • 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
25
Q

Nutritional causes of diarrhea in foals
- pathogenesis of each

A

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
<><><><>
Lactase deficiency
- Damage to mucosal epithelial cells → ↓production of lactase → ↓ability to digest milk → diarrhea as above
- Treatment – lactase, allow mucosa to recover

26
Q

Gastric ulcers
- cause, generally

A

Imbalance between:
* protective:
> (mucosal blood flow, mucus/bicarb production, prostaglandins, gastroduodenal motility) and
* aggressive factors
> (gastric acid, pepsin, enzymes) in gastric +/- duodenal mucosa
<><><>
- Causes include NSAIDs, hypoxia, sepsis

27
Q

gastric ulcers in foals clinical signs

A
  • Clinical signs in foals include abdominal pain, bruxism, lying in dorsal recumbency, diarrhea
  • Can be clinically normal or only mildly depressed/anorexic
28
Q

Pathophysiology of foal gastric ulcers
* Imbalance between aggressive and protective factors:
- what are they

A

Aggressive factors
* HCl-
* pepsin
* Heliobacter pylori??
<><><><>
Protective factors
u Mucus layer and mucosal blood flow
u PGE2
u Cellular restitution
u Epidermal growth factor
u Gastroduodenal motility

29
Q

Clinical Signs of gastric ulcers in Foals

A
  • 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.
30
Q

Gi ulceration risk factors

A
  • stress
  • transportation
  • high grain diet
  • stall confinement
  • intermittent feeding
  • intense exercise
  • racing
  • illness
  • NSAID use
  • management changes
31
Q

in what region of the stomach are GI ulcers in horses commonly found

A

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.

32
Q

scoring for equine gastric ulcers

A

Grade 0: epithelium is intact throughout; no hyperemia, no hyperkeratosis (yellowish color, sloughing)
<><>
Grade 1: mucosa is intact, but there are areas of hyperemia and/ or hyperkeratosis
<><>
Grade 2: small, single or multi-focal erosions or ulcers
<><>
Grade 3: large, single or multi focal ulcers, or extensive erosions and sloughing
<><>
Grade 4: extensive ulcers, with areas of deep submucosal penetration

33
Q

equine gastric ulcers - comlications

A
  • perforation
  • stricture
34
Q

equine gastric ulcer prevalence in
- foals
- others

A

Foals:
* 25-50%
<><><><>
* TBandSTB * 88%
<>
* Swedish Standardbred racehorses in race training
* 70%
<>
* Danish Pleasure horses
* 53%
<>
* Old horses
* 56%

35
Q

GI ulcers Dx, tests available

A
  • 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%)
36
Q

GI ulcer treatment options - types of drugs, generally

A
  • Acid-suppressive drugs
  • Non-Acid-suppressive drugs
37
Q

Acid-suppressive drugs for GI ulcer treatment

A

H2-receptor antagonists
* Ranitidine
* Famotidine
* Nizatidine etc
<><><>
H+/K+-ATPase inhibitors (proton pump inhib.) * Omeprazole (Gastrogard paste)
* Pentoprazole
<><><>
Antacids

38
Q

Non-Acid-suppressive drugs for GI ulcer treatment

A
  • 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
39
Q

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

A
  • 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.
40
Q

Congenital hypothyroidism and
dysmaturity syndrome
* Etiology

A

is still under debate
- dietary deficiencies, excess dietary nitrate, toxic substances, and infectious agents have all been suggested

41
Q

Congenital hypothyroidism and
dysmaturity syndrome Tx

A

no effective treatment

42
Q

Congenital hypothyroidism and
dysmaturity syndrome
- prognosis

A
  • 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
43
Q

Junctional Epidermolysis Bullosa (JEB)
- signalment
- inheritance pattern
- signs
- carriers

A
  • 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.
44
Q

Severe Combined Immunodeficiency (SCID)
- inheritance, signalment
- how it arises?
- outcome
- prevalence

A
  • 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
45
Q

Lavender Foal Syndrome (LFS), also known as Coat Color Dilution Lethal
- how it arises, outcome
- signs
- looks like?

A
  • 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
46
Q

Overo lethal white syndrome
- inheritance
- signs
- treatment

A
  • 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