acute diarrhoea Flashcards
what is the pathophysiology of accute diarrhoea?
- osmotic
◦ maldigestion (eg EPI, damage to the brush border)
◦ malabsorption (eg mucosal damage, villus atrophy, infiltrative disease such as lymphoma) - secretory
◦ toxin
◦ infection related - inflammatory (altered permeability)
◦ inflammatory bowel disease (eg adverse food reaction, idiopathic chronic enteropathy)
◦ motility disorder
How is canine parvovirus spread?
in what dogs is it seen? what occurs?
- Virus stable in environment for years
- Faecal-oral – 3-6 days incubation
- Generally see in young puppies with low maternal immunity (pre-vaccination), older unvaccinated dogs (breed predisposition – black and tan?)
- Infects rapidly dividing cells
◦ Gut crypts, bone marrow, lymphoid tissue, (myocytes and CNS in some neonates)‣ Vomiting ‣ Haemorrhagic diarrhoea – profuse and foetid, mucosal sloughing ‣ Rapid dehydration ‣ Panleucopaenia (as infects the bone marrow, get sepsis) ‣ Depressed, anorexic, pyrexic ‣ Loss of mucosal barrier – septicaemia/endotoxaemia and shock/DIC ‣ Ileus
what are the differentials for canine parvovirus?
- HGE - including neoplasia and idiopathic HGE (AHDS)
- Salmonella, enteric infections
- Intussusception
- FB
- Hypoadrenocorticism
- Acute intoxication
how is canine parvovirus diagnosed?
- Signalment and clinical signs strongly supportive
- Faecal analysis – EM for virus, Ag tests (SNAP) or PCR
- Care with positive results after MLV vaccination (SNAP ok….)
- Severe necrosis of GIT can lead to false negative Ag tests
- Haematology and biochemistry – consequences of disease
- Panleucopenia – consequence of viral replication
- Azotaemia, acid-base disturbance, electrolyte disturbances, liver enzymes abnormal, possibly low total protein
- Clotting times may be prolonged if severe systemic consequences present
what is the managemet of canine parvovirus?
- Fluid therapy
◦ LRS – be aggressive, maintain electrolytes via supplementation – requires monitoring of blood pressure, and regular assessment of weight
◦ Acid-base status assessment – can be severe imbalance
◦ Colloid/plasma/whole blood - Antibiotics
◦ Broad spectrum due to GI translocation of bacteria - Clav-amox, +/- quinolone –care with age of patient, gram negative coverage is difficult in young animals - Anti-emetics
◦ important as marked nausea – metoclopramide, maropitant and ondansetron/dolasetron - Pro-motility medication
◦ Metoclopramide – enteritis reduces GI motility, major consequences - Antacid drugs and ulcer coating medication
◦ severe gastritis can develop along with reflux oesophagitis and stricturesBegin oral fluid/nutrients ASAP - Enteric support is crucial
- Aggressive anti-emetic use
- May require assisted feeding, care with reflux and aspiration
◦ E.g.Naso-oesophageal tubes
what is the prevention of canine parvovirus?
- Vaccination – various protocols
◦ Early vaccination and late vaccination in susceptible breeds and environments - Cleaning and disinfection – bleach/Virkon
◦ Resistant to some disinfectants
what is the aetiology of acute haemorrhagic diarrhoea syndrome (AHDS)?
what are the ddx?
AKA haemorrhagic gastroenteritis
* Idiopathic in most cases
◦ DDx parvovirus enteritis/intussusception/pancreatitis
◦ Aetiology may be type I intestinal hypersensitivity reaction or the result of Clostridium perfringens enterotoxin production
what are the clinical signs and laboratory findings of dogs affected with acute haemorrhagic diarrhoea syndrome?
- Small breed dogs usually
- Vomiting +/- blood
- Foetid diarrhoea – inc protein loss – brown water
- Depression, anorexia – very poorly
- Haemoconcentration –
◦ fluid shift into GIT means severe hypovolaemia before clinical dehydration is apparent
◦ PCV high
◦ TP not so high as GI loss
◦ No leucopenia (c.f. parvo)
what is the treatment and prognosis for acute haemorrhagic diarrhorea syndrome?
- Fluid therapy – must be aggressive as with CPV
- Colloid/plasma/whole blood
◦ Depends on degree of haemorrhage and complications - Antimicrobial –
◦ Potential for clostridial infection and sepsis
◦ Four quadrant cover only if signs consistent with sepsis – G+, G-, aerobes and anaerobes
‣ Clav-amox, metronidazole, fluoroquinolone - Prognosis is good in most cases however severe cases where proteins are low and systemic inflammatory response develops is guarded
◦ These cases are most critical in the acute presentation stage
◦ take a while to get better so don’t PTS too early
what is the feline ‘parvovirus’?
how is it spread?
what does it cause?
Feline panleucopaenia
* Transmission and signs as CPV
◦ Kittens/colonies
◦ Widespread in feral cats
◦ Cats can be infected by CPV-2
◦ Diagnosis same as for CPV
* Feline vaccine used in early CPV outbreaks as there seems to be cross protection
- Reproductive failure/cerebellar hypoplasia (infections in-utero)
what dogs does coronavirus affect?
what is the pathogenesis and what does it cause?
what is the treatment?
what does coronavirus cause in cats?
Dog
* Young dogs (age related immunity?), highly contagious
* Mild villus destruction – enterocytes at tips
* Usually subclinical but strain related and co-infection can worsen disease
* Predominantly small bowel but can be mixed
◦ If severe – v+ and watery/mucoid d+
◦ Treatment – supportive IVFT and nutritional support for GI tract
Cat – FECV
* Signs as dog
* NB link to FIP – mutates to FIP-causing coronavirus
what campylobacter species are commensals in dogs, what is the issue with this?
what disease canthey cause in dogs?
Campylobacter jejuni and upsaliensis - zoonotic
* Clinical disease in young, immunocompromised animals or those with additional infectious agents (giardia, parvo etc)
- Acute enterocolitis (NOT CHRONIC LOW-GRADE DIARRHOEA)
◦ d+ +/- blood/mucus
◦ Vomiting
◦ Straining – large intestinal “type” d+
◦ Fever, abdominal pain
◦ Can become enteroinvasive due to host stress (IFN and noradrenaline mediated)
how is campylobacter diagnosed and treated in dogs?
- Diagnosis
◦ Faecal stain/culture
‣ Fragile therefore best isolated from fresh faeces
‣ slender motile seagull-shaped bacteria
‣ Standard culture may be misleading as speciation is not performed,
◦ PCR - Treat underlying disease if present – e.g. CE/IBD
- Treatment most frequently with 4-fluoroquinolones (can use erythromycin, can lead to vomiting)
Salmonella has a similar aetiopathogenesis to campylobacter
* Mainly seen in young and immunocompromised animals or those with concomitant infections
* Is a commensal in many dogs
it poses a potential zoonotic risk to owners
what are the 4 scenarios after infection?
◦ Transient asymptomatic diarrhoea
◦ Acute Gastroenteritis
◦ Carrier state
◦ Bacteraemia
salmonella infections can be mild or severe what are the clinicla signs of sever infection?
what are the negative prognostic indicators?
when should you treat salmonella infection?
haemorrhagic diarrhoea, pyrexia and sepsis (due to translocation across gut wall)
◦ Negative prognostic indicators – hypoglycaemia, temp > 40C, degenerate left shift
◦ SIRS and DIC – RIP
- Only treat if severe sepsis and shock and only on basis of culture results
◦ NOT if patient is well/mild d+ as unlikely to be significant if found on diagnostic testing
