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3. Equine > Equine entero-typhylo-colitis pt 2 > Flashcards

Equine entero-typhylo-colitis pt 2 Flashcards

1
Q

Sepsis - Endotoxemia
criteria for diagnosis of SIRS in horses

A
  • atleration in body temp
  • alteration in the leukogram
  • tachycardia, tachypnea

<><><>
Systemic inflammatory response syndrome

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2
Q

endotoxemia signs

A
  • Lethargy
  • Pyrexia
  • Tachycardia
  • Tachypnea
  • Hyperemic mucus membranes
  • Prolonged CRT
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3
Q

Thrombophlebitis
- what does it feel like?
- can we ‘milk’ it out?
- signs?
<>
- how to stop it

A
  • Painful
  • Hot
  • Thickened
  • Cannot be milked out
  • Head edema
    <><>
  • Remove catheter!
  • Cold/warm packing
  • Don’t continue injecting in that vein.
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4
Q

Laminitis Clinical signs

A
  • Increased digital pulses
  • Warm hooves
  • Coronary sinking
  • Pain
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5
Q

Laminitis treatment

A
  • Fluid therapy to dilute toxins
  • NSAIDs
  • Cryotherapy
  • Pain control (lidocaine, butorphanol, feet blocks)
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6
Q

Dehydration clinical assessment
4-6%
7-9%
>9%
- skin tent
- mucous membrane moisture
- CRT
- PCV
- TP

A

4-6%
- Skin tent: 2-3s
- Mucous membrane moisture: fair
- CRT: 1-2s
- PCV: 40-50%
- TP: 6.5-7.5
<><><><>
7-9%
- Skin tent: 3-5s
- Mucous membrane moisture: sticky
- CRT: 2-4s
- PCV: 50-65%
- TP: 7.5-8.5
<><><><>
>9%
- Skin tent: >5s
- Mucous membrane moisture: dry
- CRT: >4s
- PCV: >65%
- TP: >8.5

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7
Q

what factors may affect PCV and TP readings when trying to assess dehydration?

A

splenic contraction and hypoproteinemia

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8
Q

dehydration treatment
- what are the losses?
- formula?

A
  1. Replacement of fluid and electrolyte losses
    <><><>
    Maintenance + Dehydration + Losses
    <><><>
    50-60ml/kg/day + 5% dehydration + ?
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9
Q

Crystalloids
- volume to give
- capillary leakage

A
  • Large volume
  • Leaks out of abnormal capillaries
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10
Q

hypertonic fluids
- effect on intravascular volume
- purpose / use
- must be followed with?

A
  • ↑ intravascular volume
  • Initial rehydration in severe cases
  • Has to be followed with crystalloids
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11
Q

Colloids
- volume to give
- properties / purpose
- side effect
- max dose
- price
- possible disadvantage in endotoxemia?

A
  • Small volume
  • Large molecules that stay in IV space
    and attract fluid to IV space
  • Coagulopathy – side effect
  • Maximum dose 10ml/kg/day
  • Expensive

> controversial: we have leaky vessels, molecules can end up in subQ and attract fluid there

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12
Q

dehydration - what are common electrolyte imbalances? how do we correct?

A
  • Hyponatremia & hypokalemia is common
  • Oral supplementation
  • Salt block
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13
Q

ileus can be caused by what electrolyte imbalance?

A

hypocalcemia

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14
Q

issues with fluids in a case of severe hyponatremia

A
  • brain edema > seizure
    <><>
  • concentration of sodium in our fluids is higher than in the body > creates osmotic pressure
  • rise in plasma sodium provokes osmotic water movement out of the cell > brain shrinkage
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15
Q

Control of inflammation and pain
- issues with NSAIDs in dehydrated patients
- good alternative? another risk?

A
  • NSAIDs (side effects – nephrotoxicity)
    > blocks vasodilator PGs via COX-2 inhibition
    > reduced GFR
    <><>
  • lidocaine is a good alternative
    > with hypoproteinemia we have a greater risk of lidocaine toxicity
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16
Q

ways to reduce fluid secretion
- possible drawback with one of these?

A
  • Bismuth subcylicate
  • Di-tri-octahedral smectite (Biosponge)
    > impactions*
  • Activated charcoal
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17
Q

methods to control endotoxemia

A
  • Plasma transfusion
  • Systemic antibiotic therapy
  • Polymyxin B > binds to toxins
    <><>
  • Pentoxifylline
  • DMSO
    > these scavenge reactive oxygen species, not used often
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18
Q

methods: Control of sepsis
- watch out for what?

A
  • Systemic antibiotic therapy
    > Can cause further disruption of GI flora!
  • Indicated in severe cases, especially if neutropenia is present
19
Q

how do we re-establish normal gut flora in a diarrhea / endotoxemia case?

A

> All of these are Disappointing in studies :(
* Fecal transfaunation (give oral anti-acids first)
* Probiotics
* Feed supplements containing live organisms that exert a benefit beyond inherent basic nutrition

20
Q

what we need to do to treat a diarrhea / endotoxemia case (6 steps) - summary

A
  1. Replacement of fluid and electrolyte losses
  2. Control of inflammation and pain
  3. Reduction of fluid secretion
  4. Control endotoxemia
  5. Control of sepsis
  6. Reestablishment of normal flora
21
Q

salmonella
- bacterial properties
- virulence properties

A
  • Enterobacteriacea
  • Gram-negative
  • Kauffman-White taxonomy
    > O = somatic
    > H = flagella
    <><><><>
  • Name: place of isolation
  • i.e. Dublin, Montevideo, etc.
22
Q

Clinical syndromes associated with salmonella

A
  1. Inapparent infection
    <><>
  2. Acute colitis
    * Profuse diarrhea
    * Abdominal pain
    * Sepsis
    <><>
  3. Fever and leukopenia
    <><>
  4. Proximal enteritis
    * Gastric reflux
23
Q

Salmonellosis
- where is it found?
- prevalence?
> with lameness
> with GI
> ICU

Dont really need to know numbers

A
  • Ubiquitous in the environment
    <><>
    Prevalence:
    Overall: <1%
  • Culture (1-5%)
  • PCR
    > 17% lameness
    > 60% GI disorders
  • ICU: 5-6.3%
  • GI disease: 5-13%
  • Increase to 4% during hospitalization
24
Q

Salmonellosis – risk factors

A
  • Transportation,
  • Gastrointestinal tract disorders
  • Change in or withholding of feed
  • Abdominal surgery
  • High ambient temperature
  • Antimicrobial therapy
25
Q

Salmonellosis
- transmission
- pathogenesis

A

Fecal-oral transmission
> Invasion and replication (pharyngeal, intestinal and colonic mucosa)
> Toxins and virulence factors production
> Immune response

26
Q

Salmonellosis - pathophysiology
- what type of diarrhea?
- why?

A

Diarrhea
* Hypersecretion
* Inflammation mediated malabsorption
> Not fully understood
> Toxin + inflammatory reaction > induce pro- inflammatory transduction factors and cytokines (IL-1, IL-6- IL-8, TNF-a and g-interferon

27
Q

Salmonellosis - diagnosis

A

Culture
* 20-50% Sensitivity
* 3-5 fecal samples collected 12 to 24 hours
<><>
PCR
<><>
Rectal mucosa biopsy sample – culture
<><>
Lateral flow immunoassay and DNA hybridization

28
Q

Salmonellosis – prevention

A

Biosecurity is crucial for preventing an outbreak
* Isolation
* Removal of organic debris (stalls, including water buckets, drains, and cracks in the floors and wall; and nasogastric tubes and pumps).
* Restricted personnel PPI (gloves, disposable coveralls, and disposable plastic boots).
* Footbaths with disinfectant are effective only if they are kept clean and fresh.
* Vacated stalls should be thoroughly cleaned, allowed to dry, and disinfected, and cultured.

29
Q

The two most important clostridial species affecting the equine intestinal tract are:

A

C. difficile and C. perfringens

30
Q

What agent appears to be the most common cause of antibiotic-associated diarrhea?
- a very significant cause of what other category of diarrhea?

A

C. difficile appears to be the most common cause of antibiotic-associated diarrhea and is a very significant cause of nosocomial diarrhea in horses

31
Q

Clostridial diarrhea - presentation in foals

A
  • hemorrhagic diarrhea with sepsis.
  • Classic necrotizing enterocolitis
    > gas- or fluid-distended
    > intestines and thickened intestinal mucosa.
32
Q

Clostridial diarrhea - presentation in adults

A
  • diarrhea, abdominal discomfort or fever
  • spectrum of clinical signs exists, from moderate illness to severe toxemic colitis
33
Q

C. difficile properties
- gram
- spore
- aerobe/anaerobe
- normal flora?
- virulence factors

A
  • Gram positive
  • Spore-former
  • Strict anaerobic
  • Not part of normal GI flora (prevalence in normal horses < 2%)
    <><>
    Virulence factors
  • Toxin A
  • Toxin B
34
Q

C. difficile toxin A effects

A

Toxin A has intestinal secretory and cytotoxic effects, increases intestinal permeability, and can elicit a pronounced inflammatory response in the bowel

35
Q

C. difficile toxin B effects

A

Toxin B exhibits enterotoxigenic (secretory) activity and has also been shown to have potent cytotoxic effects on human colonic epithelium.

36
Q

C. difficile toxins A and B
- how often are these found in diarrheaic adults? foals? what about those with normal feces?

Fun Facts- no need to know percentages

A

Weese et al., 2001.
* 12/55 (21.8%) diarrheic adults
– 5/30 (16.7%) diarrheic foals
– 1/83 adults (1.2%) 0/21 foals with normal faeces
<><><><>
Donaldson & Palmer, 1999.
– Tox A: 8/57 (14%) Diarrheic adults
– Enterotoxin + Tox A 3/57 (5%) Diarrheic adults

37
Q

C perfringens properties
- gram
- spores
- found where
- hosts
- what it causes, generally

A
  • Gram-positive anaerobe
  • Spore forming
  • Ubiquitous bacterium
  • Multiple hosts
  • Gastroenteritis
  • Non-enteric diseases
38
Q

C. perfringens
- types and their toxins

A

Types A, B, C, D, E
Toxins alpha, beta, epsilon, iota
<><><>
Type A: alpha
Type B: alpha, beta, epsilon
Type C: alpha, beta
Type D: alpha epsilon
Type E: alpha, iota
<><><><><>
<><><><><>
* Production of both major and minor toxin
* Classical toxinotyping (major toxins)
* New toxins: Enterotoxin, Beta2, NetB, TpeL

39
Q

disease caused by C. perfringens type A?

A

Type A (alpha toxin)
- food poisoning

40
Q

disease caused by C. perfringens type B?

A

Type B (alpha, beta, epsilon)
- lamb dysentery

41
Q

disease caused by C. perfringens type C?

A
  • Type C (alpha, beta)
    Hemorrhagic gastroentritis calves, foals, piglets; “Struck” adult sheep; “Darmbrand”, “Pig-Bel” of humans
42
Q

disease caused by C. perfringens type D?

A

Type D (alpha, epsilon)
- Pulpy kidney disease of sheep and goats (cattle)

43
Q

disease caused by C. perfringens type E?

A

Type E (alpha, iota)
- Bovine neonatal enterotoxemia

3. Equine (17 decks)

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