Equine entero-typhylo-colitis pt 2 Flashcards
Sepsis - Endotoxemia
criteria for diagnosis of SIRS in horses
- atleration in body temp
- alteration in the leukogram
- tachycardia, tachypnea
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Systemic inflammatory response syndrome
endotoxemia signs
- Lethargy
- Pyrexia
- Tachycardia
- Tachypnea
- Hyperemic mucus membranes
- Prolonged CRT
Thrombophlebitis
- what does it feel like?
- can we ‘milk’ it out?
- signs?
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- how to stop it
- Painful
- Hot
- Thickened
- Cannot be milked out
- Head edema
<><> - Remove catheter!
- Cold/warm packing
- Don’t continue injecting in that vein.
Laminitis Clinical signs
- Increased digital pulses
- Warm hooves
- Coronary sinking
- Pain
Laminitis treatment
- Fluid therapy to dilute toxins
- NSAIDs
- Cryotherapy
- Pain control (lidocaine, butorphanol, feet blocks)
Dehydration clinical assessment
4-6%
7-9%
>9%
- skin tent
- mucous membrane moisture
- CRT
- PCV
- TP
4-6%
- Skin tent: 2-3s
- Mucous membrane moisture: fair
- CRT: 1-2s
- PCV: 40-50%
- TP: 6.5-7.5
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7-9%
- Skin tent: 3-5s
- Mucous membrane moisture: sticky
- CRT: 2-4s
- PCV: 50-65%
- TP: 7.5-8.5
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>9%
- Skin tent: >5s
- Mucous membrane moisture: dry
- CRT: >4s
- PCV: >65%
- TP: >8.5
what factors may affect PCV and TP readings when trying to assess dehydration?
splenic contraction and hypoproteinemia
dehydration treatment
- what are the losses?
- formula?
- Replacement of fluid and electrolyte losses
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Maintenance + Dehydration + Losses
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50-60ml/kg/day + 5% dehydration + ?
Crystalloids
- volume to give
- capillary leakage
- Large volume
- Leaks out of abnormal capillaries
hypertonic fluids
- effect on intravascular volume
- purpose / use
- must be followed with?
- ↑ intravascular volume
- Initial rehydration in severe cases
- Has to be followed with crystalloids
Colloids
- volume to give
- properties / purpose
- side effect
- max dose
- price
- possible disadvantage in endotoxemia?
- 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
dehydration - what are common electrolyte imbalances? how do we correct?
- Hyponatremia & hypokalemia is common
- Oral supplementation
- Salt block
ileus can be caused by what electrolyte imbalance?
hypocalcemia
issues with fluids in a case of severe hyponatremia
- 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
Control of inflammation and pain
- issues with NSAIDs in dehydrated patients
- good alternative? another risk?
- 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
ways to reduce fluid secretion
- possible drawback with one of these?
- Bismuth subcylicate
- Di-tri-octahedral smectite (Biosponge)
> impactions* - Activated charcoal
methods to control endotoxemia
- Plasma transfusion
- Systemic antibiotic therapy
- Polymyxin B > binds to toxins
<><> - Pentoxifylline
- DMSO
> these scavenge reactive oxygen species, not used often
methods: Control of sepsis
- watch out for what?
- Systemic antibiotic therapy
> Can cause further disruption of GI flora! - Indicated in severe cases, especially if neutropenia is present
how do we re-establish normal gut flora in a diarrhea / endotoxemia case?
> 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
what we need to do to treat a diarrhea / endotoxemia case (6 steps) - summary
- Replacement of fluid and electrolyte losses
- Control of inflammation and pain
- Reduction of fluid secretion
- Control endotoxemia
- Control of sepsis
- Reestablishment of normal flora
salmonella
- bacterial properties
- virulence properties
- Enterobacteriacea
- Gram-negative
- Kauffman-White taxonomy
> O = somatic
> H = flagella
<><><><> - Name: place of isolation
- i.e. Dublin, Montevideo, etc.
Clinical syndromes associated with salmonella
- Inapparent infection
<><> - Acute colitis
* Profuse diarrhea
* Abdominal pain
* Sepsis
<><> - Fever and leukopenia
<><> - Proximal enteritis
* Gastric reflux
Salmonellosis
- where is it found?
- prevalence?
> with lameness
> with GI
> ICU
Dont really need to know numbers
- Ubiquitous in the environment
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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
Salmonellosis – risk factors
- Transportation,
- Gastrointestinal tract disorders
- Change in or withholding of feed
- Abdominal surgery
- High ambient temperature
- Antimicrobial therapy
Salmonellosis
- transmission
- pathogenesis
Fecal-oral transmission
> Invasion and replication (pharyngeal, intestinal and colonic mucosa)
> Toxins and virulence factors production
> Immune response
Salmonellosis - pathophysiology
- what type of diarrhea?
- why?
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
Salmonellosis - diagnosis
Culture
* 20-50% Sensitivity
* 3-5 fecal samples collected 12 to 24 hours
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PCR
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Rectal mucosa biopsy sample – culture
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Lateral flow immunoassay and DNA hybridization
Salmonellosis – prevention
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.
The two most important clostridial species affecting the equine intestinal tract are:
C. difficile and C. perfringens
What agent appears to be the most common cause of antibiotic-associated diarrhea?
- a very significant cause of what other category of diarrhea?
C. difficile appears to be the most common cause of antibiotic-associated diarrhea and is a very significant cause of nosocomial diarrhea in horses
Clostridial diarrhea - presentation in foals
- hemorrhagic diarrhea with sepsis.
- Classic necrotizing enterocolitis
> gas- or fluid-distended
> intestines and thickened intestinal mucosa.
Clostridial diarrhea - presentation in adults
- diarrhea, abdominal discomfort or fever
- spectrum of clinical signs exists, from moderate illness to severe toxemic colitis
C. difficile properties
- gram
- spore
- aerobe/anaerobe
- normal flora?
- virulence factors
- Gram positive
- Spore-former
- Strict anaerobic
- Not part of normal GI flora (prevalence in normal horses < 2%)
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Virulence factors - Toxin A
- Toxin B
C. difficile toxin A effects
Toxin A has intestinal secretory and cytotoxic effects, increases intestinal permeability, and can elicit a pronounced inflammatory response in the bowel
C. difficile toxin B effects
Toxin B exhibits enterotoxigenic (secretory) activity and has also been shown to have potent cytotoxic effects on human colonic epithelium.
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
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
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Donaldson & Palmer, 1999.
– Tox A: 8/57 (14%) Diarrheic adults
– Enterotoxin + Tox A 3/57 (5%) Diarrheic adults
C perfringens properties
- gram
- spores
- found where
- hosts
- what it causes, generally
- Gram-positive anaerobe
- Spore forming
- Ubiquitous bacterium
- Multiple hosts
- Gastroenteritis
- Non-enteric diseases
C. perfringens
- types and their toxins
Types A, B, C, D, E
Toxins alpha, beta, epsilon, iota
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Type A: alpha
Type B: alpha, beta, epsilon
Type C: alpha, beta
Type D: alpha epsilon
Type E: alpha, iota
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* Production of both major and minor toxin
* Classical toxinotyping (major toxins)
* New toxins: Enterotoxin, Beta2, NetB, TpeL
disease caused by C. perfringens type A?
Type A (alpha toxin)
- food poisoning
disease caused by C. perfringens type B?
Type B (alpha, beta, epsilon)
- lamb dysentery
disease caused by C. perfringens type C?
- Type C (alpha, beta)
Hemorrhagic gastroentritis calves, foals, piglets; “Struck” adult sheep; “Darmbrand”, “Pig-Bel” of humans
disease caused by C. perfringens type D?
Type D (alpha, epsilon)
- Pulpy kidney disease of sheep and goats (cattle)
disease caused by C. perfringens type E?
Type E (alpha, iota)
- Bovine neonatal enterotoxemia
