Diarrhoea in calves Flashcards
Types of diarrhoea in calves
Osmotic
Secretory
Osmotic diarrhoea in calves
- Diffuse intestinal disease causing malabsorption
- CHO malabsorption
- Ingestion of poorly absorbed electrolytes (saline laxatives)
- Overfeeding of normally digestible CHOs
The volume increase less than for secretory diarrhoea and acidic faecal pH
Secretory diarrhoea
- bacterial enterotoxins
- Mucosal inflammation
- Elevated hydrostatic pressure
Stool osmolality normal, can be very large volumes of fluid and electrolytes, normal or alkaline faecal pH
What is diarrhoea?
An increase in faecal waterloss due to an increase in water content or an increase in volume
Causative mechanisms of diarrhoea
Altered ion transport
Passive malabsorption
Intestinal motility
Osmotic effects
Tissue hydrostatic pressure and permeability (inflammation)
Which type of diarrhoea does not cause damage to the mucosal structure?
Enterotoxin production (intestinal hypersecretion)
Mechanism of diarrhoea caused by ETEC
Enterotoxin production -> intestinal hypersecretion
Mechanism of diarrhoea caused by Salmonella
Enterotoxin production and inflammation -> intestinal hypersecretion and maldigestion/malabsorption
Mechanism of diarrhoea caused by Cryptosporidia
Inflammation and villous atrophy causing intestinal hypersecretion and maldigestion/malabsorption
Mechanism of diarrhoea caused by rotavirus/coronavirus
Villous atrophy causing malabsorption/maldigestion
Normal function of the villous cells
Depends on the presence of disaccharides and peptidases for digestion, and on specific transport processes on the apical membrane
Crypt cells secrete Cl or HCO3 which can be accompanied by Na and fluid - underlying secretion in basal state but can be stimulated to hypersecretion
Under normal conditions villous absorption outweighs crypt secretion and net absorption occurs
Secretion caused by bacterial enterotoxins
ETEC hypersecretion mediated by
- heat labile toxin (LT) activating cAMP
- heat stable toxin (ST) activating cGMP
Absorptive capacity of large intestine is overwhelmed
Metabolic acidosis and dehydration occur -> circulatory collapse and death
Requires attachment of organism to mucosal cells in large numbers
Does not affect substrate linked Na absorption, so can use oral glucose electrolyte solutions for rehydration
Secretion and malabsorption caused by inflammation
Effects of chemical mediators of inflammatory response
Glucose linked Na absorption impaired due to destruction of mucosa (salmonellosis) so glucose-electrolyte solutions don’t work so well
Maldigestion and malabsorption caused by villous atrophy
Maldigestion due to loss of hydrolytic enzymes
Malabsorption due to passage of fermentable sugars to the large intestine, and loss of the transport system
Glucose-electrolyte solutions less use due to destruction of mucosa
What is the predilection site for rotavirus?
Top third of villus and proximal small intestine
What is the predilection site for coronavirus?
Attacks both large and small intestine
E. coli
Fimbrial antigens enable gross attachment: K99 and F41 in cattle
Toxigenic strains, ahdesive strains, enterohaemorrhagic strains, verotoxin producing lesions
Infective causes of calf diarrhoea
E. coli
- ETEC
- EPEC
- EIEC
Salmonella
Clostridium perfringens (Types C (most commonly), B and possibly D)
Cryptosporidium
BVD
Rotavirus
Coronavirus
Epidemiology of bovine enteric colibacillosis
Very common
Commonly first week of life
Cow management, colostral quality, housing conditions all important
Aetiopathogenesis of bovine enteric colibacillosis
Pathogenic strains have ability to produce toxin (only ST in the calf) - ETEC
Must have ability to adhere to small intestinal mucosa and proliferate so are also EPEC
K99 is important adherence factor in calves and lambs - K99 antibodies are prophylactic
Age related resistance develops in first few days of life
Clinical signs of bovine enteric colibacillosis
Effortless, fluid, malodorous diarrhoea
Dehydration -> depression -> anorexia -> weakness -> weight loss
Death in 3-5d in severe untreated cases
morbidity 30% in dairy calves, mortality 5-50%
Mixed infections more common than single agent
Diagnosis of bovine enteric colibacillosis
History: <1wk (viral 1d-1mo, crypto >1wk)
Bacterial culture accompanied by demonstration of K99 antigen
Slide agglutination
ELISA
Fluorescent antibody (FA)
Histopath - integrity of mucosal structure
FA of ileum and ileal impression smears for K99
Direct rapid test of faeces for K99
Prevention of bovine enteric colibacillosis
Management of pregnant cow
Maximise colostral intake and absorption
Use of monoclonal K99 product in face of outbreak with unvaccinated herds
Vaccination of herd in dry period with K99 antigens
Septicaemic colibacillosis
Calves <2wks (usually first 3-4d)
Diarrhoea is not a primary component of disease but a secondary consequence
Pathogenesis of septicaemic colibacillosis
Two determinants for occurence:
- complete or partial FPT
- exposure to invasive serotypes of E. coli
Not seen in calves with high serum immunoglobulin levels at 24hrs old
Invasion primarily nasal and oropharyngeal mucosa (also navel and intestinal)
Bacteraemia > overwhelming septicaemia > endotoxaemia
Diarrhoea only in their last 3-4hrs of life
Can die in 6-8hrs
Clinical signs of septicaemic colibacillosis
Can be found dead - normally 24-96hr course
Depression, anorexia, increasing weakness > prostrate
Pyrexia then subnormal T when prostrate
Shock (increased pulse and resp rate, cold extremities)
Diarrhoea if survives long enough
If chronic localised infection: polyarthritis, meningitis, panopthalmitis
Clin path results of septicaemic colibacillosis
FPT or PFPT
Neutropaenia
Thrombocytopaenia
Azotaemia
Hypoglycaemia
Joint fluid/CSF exam
Blood culture
Post mortem of septicaemic colibacillosis
Petechial and echymotic haemorrhages, joint effusions, and fibrin tags
Culture internal organs/heart blood
Therapy of septicaemic colibacillosis
Intensive care, often unrewarding
IV antibiotics: penicillin/aminoglycoside, TMPS
Plasma from immunocompetent donor
IV fluid support
Prevention of septicaemic colibacillosis
Avoidance of FPT or PFPT (good calf management)
Isolation
Vaccination unnecessary
Salmonellosis in calves
> 14-21 days of age
Principle serotypes: S. typhimurium, S. Dublin, S. muenchen, S. copenhagen
Hard to eradicate as can survive and multiply in a variety of hosts
Aetiopathogenesis of salmonellosis in calves
Oral infection, aerosol less common
Rumen and abomasum are barrier to infection but toung calves have no rumen and higher abomasal pH
Penetration in ileum/caecum, spread to LNs and subsequent bacteraemia
Only invasive strains cause diarrhoea
Inflammation, increased secretion, malabsorption and maldigestion
Can reside in mesenteric LNs, liver, and gall bladder
Clinical signs of salmonellosis in calves
All ages, principally young 10d-3mo
Three forms: peracute (septicaemic), acute (enteric), and chronic
Peracute: depression then death
Acute (enteric): diarrhoea watery initially, then dysonturic casts, frank blood. Dehydration, pyrexia followed by hypothermia
Chronic: 6-8wk olds, loose faeces, scruffy hair coat, undersized
Clin path of salmonellosis in calves
Leukpaenia in peracute and enteric forms
Rebound neutrophilia and hyperfibrinogenaemia in surviving enteric forms
Electrolyte/acid-base deficits
How can S. dublin differ from other serotypes?
May only show fever, depression, unthriftiness and death.
Meningioencephalitis, osteomyelitis leading to a polyarthritis, and pneumonia are more common
Pathology of salmonellosis in calves
Non specific in peracute forms - septicaemic
Acute typhimurium: fibrin tags in abdo, congested distended intestines, swollen haemorrhagic LNs, mucous/fluid faeces
Chronic: catarrhal enteritis, hyperplastic mesenteric LNs
Diagnosis of salmonellosis in calves
Culture fresh large faecal samples using enrichment techniques
Sample repeatedly
Culture bile and mesenteric LNs at PM
Serology useful for identifying serotype
Control of salmonellosis in calves
Antibiotic use dubious in acute cases - TMPS or ampicillin if used at all
Difficult to prevent spread and expensive to identify carriers
Clinical cases may shed for a few days to 70 days
Idividual calf housing and hygiene
Clostridial diarrhoea (enterotoxaemia) in calves
Rare cause of outbreaks - usually individal
Due to proliferation of Cl. perfringens and toxin elaboration in the gut. Types C, B, and D.
Types of Cl. perfringens causing diarrhoea in calves
Type C most widespread cause of haemorrhagic enterotoxaemia or necrotic enteritis.
Also types B, and possibly D (with neuro symptoms due to epsilon toxin)
Aetiopathogenesis of clostridial diarrhoea in calves
Very young animals, 2-10d
Less enzyme activity, trypsin inhibitor in gut?
Normal gut organism that multiplies and can produce toxins in conditions of high energy diet, diet change, indigestion/over eating
Ideal conditions are high energy diet with some normal flora disturbance, especially if gut stasis - some of this can be caused by viral infection
Clinical signs of of clostridial diarrhoea in calves
Diarrhoea
Dysentery
Colic
Sometimes opisthotonus and tetany
Severe cases may show colic and no diarrhoea prior to death
Pathology of clostridial diarrhoea in calves
Haemorrhagic enteritis, ulceration, and necrosis if severe
Diagnosis of clostridial diarrhoea in calves
Clinical signs and PM
Definitive if toxins identified, but often inactivated - store intestinal contents at 4 degrees, or add 0.5% formalin and rush
Therapy for clostridial diarrhoea in calves
Rarey feasible
Use of type B, C, and D antitoxins in early clinical case or prophylaxis (3wk protection)
Oral antibiotics
Prevention of clostridial diarrhoea in calves
Multivalent clostridial vaccines, boosters prior to calving
Vaccinate calf at 8, 12, and possibly 16wks if high nutrition
Boost at 4-5mo or weaning
Lifecycle of cryptosporidiosis in calf diarrhoea
Attaches and develops within microvillar brush border
Sporulated infective oocysts in faeces, immediately infective
Oocyte ingested, sporozoite penetrates microvillus, asexual phase with two generations of meronts.
Released merozoites reinvade microvillus developing as trophzoite, microgametocyte or macrogametocyte. Microgametes fertilize macrogametes producing zygotes
Complete lifecycle is within the host
Route of infection of cryptosporidiosis in calf diarrhoea
Faeco-oral transmission with no intermediate host
Opportunity for autoinfection, possibly bearing on overwhelming infections in immunosuppressed hosts
Aetiology of cryptosporidiosis in calf diarrhoea
More common in calves 1-3wks
2-7d incubation
Very significant in mixed infections e.g. with rotavirus
Clinical signs of cryptosporidiosis in calf diarrhoea
Enterocolitis: diarrhoea, anorexia, weight loss, depression, occasional dehydration
Morbidity can be high, mortality low
Symptoms not pathognomic
More common in immunodeficiency
Pathology of cryptosporidiosis in calf diarrhoea
Gut pathology only
Principally distal SI
Fluid distended gut, shortened villi, microvillar pathology
Diagnosis of cryptosporidiosis in calf diarrhoea
Acid fast techniques to identify on smears
Floatation concentration (ZnSO4)
Smear fresh PM mucosa
Management of cryptosporidiosis in calf diarrhoea
Supportive care only, no good therapy
Uncomplicated cases are self limiting
Disinfection, isolation
Zoonotic!
Epidemiology of rotaviral diarrhoea in calves
Not zoonotic
Exposure up to 100%, morbidity 20-40%, mortality <10% when uncomplicated infection
Sub-clinical infections common during outbreak
Survive several days in wastewater/faeces, resistant virus
Oral infection, environmental contamination important
Pathogenesis of rotaviral diarrhoea in calves
Target cell is enterocyte covering villus
Primarily proximal 1/3 of SI - not large bowel
Large amounts of viral antigen accumulate within initially in tact cell - exfoliated - viral antigen in faeces
Atrophy of villusand covered with immature cells from crypts
Mixed infections (ETEC) very common
Clinical signs of rotaviral diarrhoea in calves
Sudden onset, rapid spread
Often under 10 days old
24-48hr incubation
Diarrhoea mild to severe/death
High levels of rotavirus antibody in colostrum prevents infection while fed
Pathology of rotaviral diarrhoea in calves
No gross lesions except fluid filled gut
Typical microscopic appearance
Diagnosis of rotaviral diarrhoea in calves
Needs to be less than 24hrs after onset of diarrhoea
Faeces/mid-ileum for immunofluorescence
EM - cheap, broad spectrum, low sensitivity
ELISA - rapid, accurate, more sensitive
Important facts in rotaviral diarrhoea
DsRNA virus
Calf isolates - type A
‘White scour’
Peak incidence at 10 days old
Disease course 4-8d
Lesions from upper jejunum to ileum
To prevent keep away from adult cattle and ensure good colostrum
Epidemiology of coronavirus in calf diarrhoea
Not zoonotic!
Exposure up tp 100%, morbidity 15-25%, mortality 5-10% in uncomplicated disease
Epizootics have affected adults
Oral infection
Pathogenesis of coronavirus in calf diarrhoea
Small intestine AND colon affected
Starts in cranial intestine and progresses caudally - crypt cells spared
Functional change causing diarrhoea, then lose epithelial cells and villi shorten. Atrophy of colon ridges
Atrophy of villus and covered in immature cells from crypt
Clinical signs of coronavirus in calf diarrhoea
Sudden onset, rapid spread
Often under 20do
Like rotavirus but more severe
30-60hr incubation
After 2-4d diarrhoea can become very depressed/dehydrated and death may follow
Diagnosis of coronavirus in calf diarrhoea
Needs to be less than 24hrs after onset of diarrhoea
Faeces/mid-ileum for immunofluorescence
EM - cheap, broad spectrum, low sensitivity
ELISA - rapid, accurate, more sensitive
Prevention and control of viral diarrhoea in calves
Vaccination in late pregnancy
- Multivalent ETEC/rota/corona products with modern adjuvants
Important facts about coronavirus in calf diarrhoea
ssRNA virus
More severe than rotavirus
Water, yellow with clots and mucus
1-3wks old
4-5d course of disease
LI involvement
No vaccine available (?)
Villous atrophy resulting from viral infection
Impaired digestion
Impaired absorption
Crypt epithelium undergoes hyperplasia to regenerate villi
Increased secretion not excessive in abscence of toxin
Non-infectious/unknown pathogen causes of calf diarrhoea
Persistent peri-weaning calf diarrhoea
Necrotising enteritis in beef suckler calves
Epidemiology of persistent peri-weaning calf diarrhoea
Affects dairy calves
High morbidity (>50%)
Low mortality
Aetiology unknown but giardia often present
Clinical signs of persistent peri-weaning calf diarrhoea
Chronic grey-brown diarrhoea
Starts between 3-10wks old
Persists for at least 1 month
Appetite unaffected
Growth checked
Treatment and prevention of persistent peri-weaning calf diarrhoea
Careful reconsiderations of management diet etc
Poor response to diet changes
Only transient response to antimicrobials in some cases
Epidemiology of necrotising enteritis in beef suckler calves
Affects spring born suckler calves
Aged 2-4mo
Low morbidity, high mortality
Aetiology unknown
Often reccurs in same herd
Clinical signs of necrotising enteritis in beef suckler calves
Acute stages: depression and pyrexia
Diarrhoea often profuse and haemorrhagic, then becomes more scant muco-haemorrhagic
Tenesmus
Resp signs (not always)
Anaemia - pale MM
Occasional oral and nasal ulcers
Progressive depression and dehydration with death in 7-10d
Treament and prevention of necrotising enteritis in beef suckler calves
Purely symptomatic
Systemic antibiotic coverage
Oral or IV fluid therapy
Multivitamins
Blood transfusion if severely anaemic
Possible electrolyte imbalances in calf diarrhoea
Dehydration
Hyponatraemia
Acidosis
Potassium (usually raised but may be low/normal)
SYstemic consequences of diarrhoea in calves
Loss of ECF
Contraction of plasma volume
Decreased arterial pressure
Decreased renal function, decreased H excretion, acidosis
Decreased tissue perfusion, increased anaerobic metabolism, acidosis
Intracellular H-K exchange
Hyperkalaemia
Death
Difference between younger (<1wk) and older calves (>1wk) that have diarrhoea
Acidosis more pronounced in older depressed calves than young depressed calves
Acidosis in older calves not necessarily accompanied by severe dehydration
How to reliably determine acid-base abnormalities
Blood gas measurement or at least total CO2 determination (halerco apparatus)
Halerco apparatus
Allows immediate and accurate estimation of the acid-base status
Uses single venous blood sample
Measures displacement of CO2 from blood with lactic acid
Which diarrhoea calves require IV fluid therapy?
Unwilling to suck
Depressed
> 8% dehydrated
What to do if a diarrhoea calf has acidic faecal pH
Osmotic diarrhoea
Withdraw milk for 24hrs (??) - dont think we still do this. Definitely don’t if they are alert and willing to suck
Offer oral fluids
What to do if a diarrhoea calf has alkaline faecal pH
Absorptive mechanisms in tact
Rehydrate with oral fluids
IV correction of acidosisIV fluid therapy in calves
Hypoglycaemia is an important consideration if cachectic - 5% glucose in fluids
Nutritional support only if emaciated or off milk for >3d
Potassium may be of less concern in calves, can just use saline and bicarb as composite therapy
Overadministration of IV fluids to calves
Beware of CNS oedema, congestive heart failure, or severe respiratory disease - may be exacerabted with high sodium fluids
Hard to overload an adult but not a calf
Protein levels and IV fluid therapy in calves
When less than 4 g/dl back off and give plasma
Hypokalaemia and IV fluid therapy
Frequent complication in large animals if not supplemented in advance of signs
Fluid administration with increase renal excretion and can increase losses
Correction of hypoglycaemia or acidosis will precipitate hypokalaemia in animals with decreased whole body potassium
Bicarbonate and IV fluid therapy in calves
Overadministration can cause metabolic alkalosis, together with paradoxic cerebrospinal fluid acidosis
Hypertonic bicarb can cause hyperosmolality, hypernatraemia, and CNS haemorrhage due to hypernatraemia
Never mix with calcium containing fluids
IV fluids to correct acidosis
Traditionally Hartmanns but this is inadequate for severe cases
Normal saline + bicarb
