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how is calf scours classified?
complicated or uncomplicated, depending on whether lesions extend beyond the superficial GI tract
in general, what is the approach to treating calf scours?
because the causative agent is rarely determined, we address treatment of undifferentiated calf diarrhea
which animals is uncomplicated scours seen in?
calves <3 weeks old
what are the mechanisms of uncomplicated scours?
hypersecretion and malabsorption/maldigestion
what is the end result of hypersecretion and malabsorption in calves?
result of either of these mechanisms is loss of body water, sodium chloride, bicarbonate, potassium and impaired absorption of nutrients
is bicarbonate lost more through secretion or malabsorption?
bicarb is lost more thru malabsorption
what are clinical signs of uncomplicated scours?
-profuse, watery diarrhea
-depression
-weakness
-anorexia
-loss of skin turgor and eye luster
-severely affected calves usually comatose
-death if calf is not treated appropriately
what do the clinical signs of uncomplicated scours relate to?
signs are progressive and relate to the degree of dehydration and acidosis
signs may resolve in 1-2 days or progress over 1-3 days
what is the epidemiology of uncomplicated scours?
scours can affect individual calves or occur in outbreaks
what clinpath changes are seen with uncomplicated scours?
-hyponatremia/hypochloremia
-metabolic acidosis
-azotemia (prerenal)
-hypo-, normo-, hyperkalemia (depending on acidosis, anorexia)
-hyperphosphatemia (renal)
-CBC should be normal, or stress leukogram
what are the direct mechanisms of acid-base disturbances?
loss of bicarbonate in the feces- most important
what are secondary mechanisms of acid-base disturbances? (4)
1. lactic acidosis (circulatory compromise w/ dehydration)
2. retention of organic acids normally excreted by kidney
3. absorption of VFAs from colon
4. release of organic acids from dying cells (bad signs)
what are respiratory mechanisms of acid-base disturbances?
1. respiratory alkalosis (compensatory in strong animals)
2. respiratory acidosis (hypovolemia due to weakness with severe, advanced dz)
what are the 4 classifications of scours?
1. mild/non-clinical
2. moderate
3. severe
4. very severe
what is mild/non-clinical scours characterized by?
profuse diarrhea, but minimal systemic signs
calf is bright and alert
what are the clinical signs of mild/non-clinical scours?
-minimal skin tent
-able to stand and eat readily
-strong suckle reflex
what is the blood pH, dehydration status, and bicarbonate deficit of mild/non-clinical scours?
blood pH: 7.35-7.5
dehydration: <5%
bicarb deficit: 0mEq/L
what is moderate scours characterized by?
profuse diarrhea, dull but responsive
what are the clinical signs of moderate scours?
-prolonged skin tent, normal eye luster
-able to stand and eat, but eats slowly
-weak suckle reflex
-holds head down
what is the blood pH, dehydration status, and bicarbonate deficit of moderate scours?
blood pH: 7.1 - 7.25
dehydration: 7%
bicarb deficit: 5mEq/L
what is severe scours characterized by?
profuse diarrhea, dull and minimally responsive
what are the clinical signs of severe scours?
-very long skin tent
-eyes sunken and dull
-can only stand with assistance
-able to stay in sternal with head up when recumbent
-eats very slowly if at all
-minimal suckle reflex
what is the blood pH, dehydration status, and bicarbonate deficit of severe scours?
blood pH: 6.9 - 7.1
dehydration: 8-10%
bicarb deficit: 10mEq/L
what is very severe scours characterized by?
profuse diarrhea and 'smell of death'
what are the clinical signs of very severe scours?
-skin tents forever
-eyes very sunken and dull
-non-responsive and no suckle
-unable to maintain sternal recumbency (lateral)
what is the blood pH, dehydration status, and bicarbonate deficit of very severe scours?
blood pH: 6.8 - 7.0
dehydration: 10-12%
bicarb deficit: 15-20mEq/L
how do older calves with scours differ from younger calves with scours?
older calves are stronger and have diseases that result in more bicarb loss
what are the causes of scours in calves <3 weeks old?
1. e. coli (enterotoxic- ETEC)
2. rotavirus
3. coronavirus
4. cyrptosporidium parvum and ubiquitum
why are calves under 3 weeks old more susceptible to e. coli infections causing diarrhea?
enterotoxigenic e. coli (ETEC) has a virulence factor (adhesion pilus K99) which has an affinity for immature enterocytes, which are gradually shed by the calf in the 1st week of life
what does ETEC cause in calves leading to scours?
hypersecretion
how is ETEC diagnosed in calves?
fecal culture with PCR, antibody testing or gene probes to confirm presence of K99 pilus antigen
culture alone is insufficient- there are many benign e. coli
how does rotavirus cause scours?
rotavirus divides within and destroys villus tip enterocytes, mainly in the small intestine
what lesions are seen in the intestine due to rotavirus?
blunting and clubbing of villi
how is rotavirus diagnosed?
electron microscopy of feces, ELISA, PCR, protein A-gold immunoelectron microscopy
virus is stable and easy to identify
how does coronavirus scours?
similar to rotavirus, except that more of the villus and the colon is affected
may lead to hematechezia and tenesmus (may also spread thru respiratory tract)
how is coronavirus diagnosed?
electron microscopy of feces, ELISA, PCR
virus is not stable and may be difficult to identify
how do cryptosporidium species (parvum and ubiquitum) cause scours?
pathogen colonizes just inside the brush border membrane of villus tip enterocytes of the small and large intestine (ileum is the primary site)
is cryptosporidium zoonotic?
yes
how does autoinfection of cryptosporidium occur?
due to sporulation of oocysts within the gut, leading to relapses
how long can cryptosporidium persist in the environment?
up to 6 months
what is the most common agent causing diarrhea in calves under 4 days old?
e. coli
e. coli rarely affects calves over 5 days old
what is the most common overall agent causing scours in calves under 3 weeks old?
rotavirus (esp. ages 4-14 days old)
what are the immediate treatment goals for scours?
1. rehydration
2. replace lost electrolytes
3. restore acid-base balance
less immediate: +/- provide nutrition, provide for ongoing losses
how are hydration deficits calculated?
10% dehydration in a 40kg calf:
0.1 (10% dehydrated) x 40kg x 1kg/L = 4L deficit
how are electrolytes replaced in calves?
Na, Cl, HCO3, and K are lost roughly in proportion to ECF, replace in roughly the same proportions
ie replace with ECF-like fluid
what are the different routes fluids can be administered to calves?
oral
subcutaneous
intravenous
(intraosseus and intraperitoneal in rare cases)
when is it indicated to rehydrate calves with oral fluids?
in calves with good appetites and those that have recently lost their appetites
when is it indicated to rehydrate calves with intravenous fluids?
calves that are inappetent with severe dehydration
what should you do if administration of oral fluids has not led to a response within 2-4 hours?
administer IV fluids
what is a common cause of diarrhea in calves over 3 weeks old?
coccidiosis (eimeria spp.)
how long does it take for a calf to develop clinical disease of coccidiosis?
around 21 days (minimum 14 days)
where does the most severe damage due to coccidiosis in calves occur?
in the distal small intestine and colon
what are clinical signs of coccidiosis in calves over 3 weeks old?
diarrhea
because the colon is affected, water loss may be severe and hematochezia and tenesmus may be present
animals are usually fairly bright
what lesions will be seen due to coccidiosis in calves?
effacement of villi, presence of organisms
how is coccidiosis in calves diagnosed?
direct smear of feces
what is the treatment for coccidiosis in calves?
1. fluids for severely affected animals
2. anticoccidial drugs
3. prophylactic treatment (control rather than kill, to create immunity)
what anticoccidial drugs are used to treat coccidiosis in calves?
-sulfas
-amprolium (drug of choice)
what prophylactic treatment is used to control coccidiosis in calves?
-decoquinate
-monensin, lasalocid (ionophore, growth promoter)
-amprolium
how is coccidiosis in calves prevented?
prevented thru good hygiene and not mixing animals of different ages
what is the difference between cows ('mountain ruminants') and sheep/goats ('desert ruminants')?
main difference is the spiral colon, which has much fewer loops and less capacity to absorb water in cattle
what is the difference between the feces of cattle and sheep/goats?
cattle feces are normally soft (75-85% water in cattle, 55% water in sheep/goats)
increased water load to the large intestine is poorly handled
what is osmotic diarrhea?
increased delivery of solutes to the large intestine resulting in diarrhea
what are 2 causes of osmotic diarrhea in cattle?
1. gastric maldigestion
2. grain overload
how does gastric maldigestion lead to osmotic diarrhea in cattle?
any disruption of gastric fermentative or acid digestion of food leads to delivery of large, poorly digestible feed particles to the colon
these particles then draw in water to the colon
what are causes of gastric maldigestion leading to osmotic diarrhea in cattle?
DA
feed change
period of anorexia
oral medications
rumen acidosis
ulcers
how is gastric maldigestion diagnosed?
-knowledge of concurrent condition
-cow is otherwise bright
-normal labwork
-undigested large feed particles (corn) in feces
-this diarrhea is rarely profuse
what is the treatment for gastric maldigestion?
none- correct other conditions, transfaunation
how can grain overload lead to osmotic diarrhea?
cattle which survive peracute rumen acidosis have increased delivery of poorly absorbed lactate (especially D-form) to the intestine
also, changes in rumen flora and pH alter rumination frequency and inhibit digestion of large particles
when is osmotic diarrhea due to grain overload typically seen?
diarrhea seen 1-2 days after acute event
how is grain overload causing osmotic diarrhea diagnosed?
rumen or blood pH, knowledge of exposure to high energy feed
what is the treatment for grain overload causing osmotic diarrhea?
-correct rumen pH (usually too late tho)
-transfaunation
-maintain systemic electrolyte and acid-base balance
what are the most common causes of infectious diarrhea in cattle? (8)
1. salmonella
2. bovine viral diarrhea (BVDV)
3. winter dysentery
4. rinderpest (eliminated)
5. malignant catarrhal fever
6. schmallenberg virus
7. eimeria
8. adenovirus
A Sad Bovine Wins Really Malignant, Effusive, S***
what are the 2 main diseases of bovine viral diarrhea virus (BVDV)?
1. acute BVD
2. mucosal disease
what is acute BVD?
infection of an immunocompetent cow with either cytopathic or non-cytopathic strains
how is acute BVD transmitted?
primarily thru the respiratory system, where it gains access to the blood (first fever w/ viremia) and carried to other susceptible tissues
which animals are susceptible to acute BVD?
all ages are susceptible, but vaccinated cattle and calves with good colostral antibody have better protection
can occur as individual cases or outbreaks depending on immunity
what lesions are seen with acute BVD?
virus multiplies in and kills epithelial cells and other cells:
-WBCs: neutropenia and necrosis of peyer's patches
-epithelium: GI ulcers, necrosis of crypt cells
affects GIT from mouth to colon, nasal and ocular mucosa, coronary band, resp. tract in some cases
what are the clinical signs of acute BVD?
-depression
-anorexia (decreased production)
-high biphasic fever
-panleukopenia
-diarrhea
-oculonasal discharge
how is acute BVD diagnosed?
-isolation,
-PCR
-FA of virus from blood, secretions, tissues (not feces)
-rising antibody titer (serum neutralization)
how is acute BVD treated?
supportive care
how is acute BVD prevented?
vaccination (reduces morbidity and mortality)
2-shot series is necessary to initiate immunity, esp. against severe type-2 strains, and annual boosters recommended to enhance colostral protection
what may decrease BVD vaccine efficacy?
antigenic diversity
what 2 vaccines are available for BVD?
1. modified live vaccines: give better immunity with one shot, but cause immunosuppression and viral replication
2. killed vaccines: do not cause immunosuppression, but protection is short lived (3-4 months)
what animals can modified live vaccines of BVD be used for? which animals should they not be used for?
modified lives BVD vx's are good for calves (6 months old) or synchronized herds (pre-bred beef cattle)
do not use on or near pregnant cows
which animals are killed BVD vaccines good for?
safe for pregnant cows
also herds with constant calving (dairies)
what is BVD-mucosal disease?
infection of a persistently-infected cow with a cytopathic strain or mutation of a non-cytopathic strain to cytopathic
what are the clinical signs of BVD-mucosal disease?
looks like acute BVD but often has more severe coronary band, eye, and mouth lesions (blunted papillae)
how is BVD-mucosal disease diagnosed?
-virus isolation
-FA/IHC from blood, secretion, tissues (ear notch)
how is BVD-mucosal disease prevented?
prevention of carrier state: good immunity of dams, prevention of infection/live virus vaccination during pregnancy
identification and culling of PI animals (virus isolation, IHC)
what causes winter dysentery?
enteric coronavirus
-potentially same strains as affected calves
-low titers in adults appear to increase susceptibility, as does using same equipment to provide feed and remove manure
-may spread thru respiratory tract
what lesions are seen with winter dysentery?
coronavirus kills villus tip cells in most of the small and large intestine, resulting in shortened and clubbed villi and malabsorption/maldigestion
what are the clinical signs of winter dysentery?
-profuse, acute watery diarrhea, often with frank blood
- +/- recent history of respiratory disease
-fever occurs very early or not at all
-often occurs in outbreaks in cattle housed for winter
-high morbidity, low mortality
what is the treatment for winter dysentery?
self-limiting (days for cow/weeks for herd)
-fluids for severely affected cows
how is winter dysentery diagnosed?
-electron microscopy of feces
-rising antibody titer (for coronavirus)--> Ag-capture, ELISA, PCR
what is the morbidity/mortality of rinderpest?
extremely contagious, high morbidity and high mortality
what diseases does rinderpest appear similar to?
acute BVD, MCF
what is the cause of malignant catarrhal fever (MCF)?
sheep associated and wildebeast associated caused by ovine herpesvirus-2 and alcelaphine herpesvirus-1 and 2
cattle, bison, and other exotics get dz from asymptomatic sheep, usually around lambing time
what lesions are seen with malignant catarrhal fever?
cytotoxic t-cell mediated vasculitis of most epithelial surfaces
what are the clinical signs of malignant catarrhal fever?
-crusting oral and nasal ulcers
-conjunctivitis with corneal edema
-high fever
-diarrhea
-hematuria
-coronitis
-encephalitis
-lymphadenopathy
what is the treatment for MCF?
symptomatic
but most affected animals die within 96 hours