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Diarrhoea in calves Flashcards

1
Q

Types of diarrhoea in calves

A

Osmotic
Secretory

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2
Q

Osmotic diarrhoea in calves

A
  • 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

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3
Q

Secretory diarrhoea

A
  • bacterial enterotoxins
  • Mucosal inflammation
  • Elevated hydrostatic pressure

Stool osmolality normal, can be very large volumes of fluid and electrolytes, normal or alkaline faecal pH

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4
Q

What is diarrhoea?

A

An increase in faecal waterloss due to an increase in water content or an increase in volume

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5
Q

Causative mechanisms of diarrhoea

A

Altered ion transport

Passive malabsorption

Intestinal motility

Osmotic effects

Tissue hydrostatic pressure and permeability (inflammation)

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6
Q

Which type of diarrhoea does not cause damage to the mucosal structure?

A

Enterotoxin production (intestinal hypersecretion)

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7
Q

Mechanism of diarrhoea caused by ETEC

A

Enterotoxin production -> intestinal hypersecretion

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8
Q

Mechanism of diarrhoea caused by Salmonella

A

Enterotoxin production and inflammation -> intestinal hypersecretion and maldigestion/malabsorption

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9
Q

Mechanism of diarrhoea caused by Cryptosporidia

A

Inflammation and villous atrophy causing intestinal hypersecretion and maldigestion/malabsorption

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10
Q

Mechanism of diarrhoea caused by rotavirus/coronavirus

A

Villous atrophy causing malabsorption/maldigestion

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11
Q

Normal function of the villous cells

A

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

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12
Q

Secretion caused by bacterial enterotoxins

A

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

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13
Q

Secretion and malabsorption caused by inflammation

A

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

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14
Q

Maldigestion and malabsorption caused by villous atrophy

A

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

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15
Q

What is the predilection site for rotavirus?

A

Top third of villus and proximal small intestine

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16
Q

What is the predilection site for coronavirus?

A

Attacks both large and small intestine

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17
Q

E. coli

A

Fimbrial antigens enable gross attachment: K99 and F41 in cattle

Toxigenic strains, ahdesive strains, enterohaemorrhagic strains, verotoxin producing lesions

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18
Q

Infective causes of calf diarrhoea

A

E. coli
- ETEC
- EPEC
- EIEC

Salmonella

Clostridium perfringens (Types C (most commonly), B and possibly D)

Cryptosporidium

BVD

Rotavirus

Coronavirus

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19
Q

Epidemiology of bovine enteric colibacillosis

A

Very common

Commonly first week of life

Cow management, colostral quality, housing conditions all important

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20
Q

Aetiopathogenesis of bovine enteric colibacillosis

A

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

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21
Q

Clinical signs of bovine enteric colibacillosis

A

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

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22
Q

Diagnosis of bovine enteric colibacillosis

A

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

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23
Q

Prevention of bovine enteric colibacillosis

A

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

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24
Q

Septicaemic colibacillosis

A

Calves <2wks (usually first 3-4d)

Diarrhoea is not a primary component of disease but a secondary consequence

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25
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
26
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
27
Clin path results of septicaemic colibacillosis
FPT or PFPT Neutropaenia Thrombocytopaenia Azotaemia Hypoglycaemia Joint fluid/CSF exam Blood culture
28
Post mortem of septicaemic colibacillosis
Petechial and echymotic haemorrhages, joint effusions, and fibrin tags Culture internal organs/heart blood
29
Therapy of septicaemic colibacillosis
Intensive care, often unrewarding IV antibiotics: penicillin/aminoglycoside, TMPS Plasma from immunocompetent donor IV fluid support
30
Prevention of septicaemic colibacillosis
Avoidance of FPT or PFPT (good calf management) Isolation Vaccination unnecessary
31
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
32
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
33
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
34
Clin path of salmonellosis in calves
Leukpaenia in peracute and enteric forms Rebound neutrophilia and hyperfibrinogenaemia in surviving enteric forms Electrolyte/acid-base deficits
35
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
36
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
37
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
38
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
39
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.
40
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)
41
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
42
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
43
Pathology of clostridial diarrhoea in calves
Haemorrhagic enteritis, ulceration, and necrosis if severe
44
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
45
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
46
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
47
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
48
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
49
Aetiology of cryptosporidiosis in calf diarrhoea
More common in calves 1-3wks 2-7d incubation Very significant in mixed infections e.g. with rotavirus
50
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
51
Pathology of cryptosporidiosis in calf diarrhoea
Gut pathology only Principally distal SI Fluid distended gut, shortened villi, microvillar pathology
52
Diagnosis of cryptosporidiosis in calf diarrhoea
Acid fast techniques to identify on smears Floatation concentration (ZnSO4) Smear fresh PM mucosa
53
Management of cryptosporidiosis in calf diarrhoea
Supportive care only, no good therapy Uncomplicated cases are self limiting Disinfection, isolation Zoonotic!
54
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
55
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
56
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
57
Pathology of rotaviral diarrhoea in calves
No gross lesions except fluid filled gut Typical microscopic appearance
58
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
59
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
60
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
61
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
62
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
63
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
64
Prevention and control of viral diarrhoea in calves
Vaccination in late pregnancy - Multivalent ETEC/rota/corona products with modern adjuvants
65
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 (?)
66
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
67
Non-infectious/unknown pathogen causes of calf diarrhoea
Persistent peri-weaning calf diarrhoea Necrotising enteritis in beef suckler calves
68
Epidemiology of persistent peri-weaning calf diarrhoea
Affects dairy calves High morbidity (>50%) Low mortality Aetiology unknown but giardia often present
69
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
70
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
71
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
72
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
73
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
74
Possible electrolyte imbalances in calf diarrhoea
Dehydration Hyponatraemia Acidosis Potassium (usually raised but may be low/normal)
75
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
76
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
77
How to reliably determine acid-base abnormalities
Blood gas measurement or at least total CO2 determination (halerco apparatus)
78
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
79
Which diarrhoea calves require IV fluid therapy?
Unwilling to suck Depressed >8% dehydrated
80
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
81
What to do if a diarrhoea calf has alkaline faecal pH
Absorptive mechanisms in tact Rehydrate with oral fluids
82
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
83
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
84
Protein levels and IV fluid therapy in calves
When less than 4 g/dl back off and give plasma
85
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
86
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
87
IV fluids to correct acidosis
Traditionally Hartmanns but this is inadequate for severe cases Normal saline + bicarb

Cattle I (33 decks)

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