Acute diarrhoea in dogs and cats

Cards (65)

  • Causes of acute diarrhoea
    Diet - acute gastroenteritis
    • Change, allergy, intolerance, scavenging.
    • Food poisoning - suggests infectious agent.
    • Toxins - usually through dietary indiscretion.
    Drugs - antimicrobials, chemotherapy etc.
    Infections - viral, bacterial, parasitic.
    inflammatory disease - CE/IBD, pancreatitis.
    Metabolic disease - hypoadrenocorticism
    Anatomic disease - intussesception/ FB
    Neoplasia - peracute lymphoma, paraneoplasia (only likely to give diarrhoea if diffuse, not focal).
    Anomalous - stress/anxiety - usually mixed/large bowel.
  • Acute infectious diarrhoea - viruses
    Parvovirus
    Coronavirus
    Adenovirus
    (FeLV, FIV - chronic enteritis, weight loss, lymphoma on FeLV).
    Rotavirus
    (Norovirus).
  • Acute infectious diarrhoea - bacteria
    Salmonella
    Campylobacter
    E.coli - ETEC, EHEC, EPEC
    Clostridium perfingens, C.difficile
    Shigella
    Yersinia enterocolitica - rarely reported.
    Mycobacteria in cats - granulomaotus enteritis - not acute disease.
  • Acute infectious diarrhoea - parasitic
    Helminths
    Protozoa - Giardia, Tritrichomonas
  • Canine parvovirus - over view
    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).
    Infects rapidly dividing cells
    • Gut crypts, bone marrow, lymphoid tissue, (myocytes and CNS in some neonates).
  • Canine parvovirus - clinical signs
    Vomiting
    Haemorrhagic diarrhoea - profuse and foetid, mucosal sloughing.
    Rapid dehydration
    Panleucopenia
    Depressed, anorexic, Pyrexic.
    Loss of mucosal barrier - septicaemia/endotoxaemia and shock/ DIC.
    Ileus - start to get disruption of the bacterial combinations and makes everything more complcated.
  • Canine parvovirus - differentials
    HGE - including neoplasia and idiopathic HGE (AHDS - acute haemorrhagic diarrhoea syndrome).
    Salmonella, enteric infections.
    Intussesception
    Foreign body
    Hypoadrenocorticism (Addison’s).
    Acute intoxication
  • Canine parvovirus - diagnosis
    Signalment and clinical signs strongly supportive.
    Faecal analysis - EM fir virus, Ag tests (SNAP) or PCR.
    • Care with positive results after MLV vaccination.
    • Severe necrosis of GIT can leaf to false negatives Ag test.
    Haemotology and biochemsitry - consequences of disease.
    • Panleucopenia - consequence of viral replication.
    • Azotaemia, acid-base disturbances, electrolytes disturbances, liver enzymes abnormal, possibly low total protein.
    Clotting times may be prolonged if severe systemic consequence present.
  • Canine parvovirus - management with fluid therapy
    LRS - be aggressive, maintain electrolytes via supplementation, requires monitoring of blood pressure, COP if Necessary and regular assessment of weight.
    Acid-base status assessment - can be severe imbalance.
    Colloid/ plasma/ whole blood.
  • Canine parvovirus - management with antibiotics
    Broad spectrum due to GI translocations of bacteria - clav-amox, +/- quinolone - care with age of patient, gram negative coverage is difficult in young animals.
  • Canine parvovirus - management with anti-emetics
    Important as marked nausea - metoclopramide, maropitant and ondansetron/ dolasetron.
  • Canine parvovirus - management with pro-motility medication
    Metoclopramide - enteritis reduces GI motility, major consequences.
  • Canine parvovirus - management with antacid and ulcer coating medication
    Severe gastritis can develop along with reflux oesophagitis and strictures.
  • Canine parvovirus - management with immunomodulators and ancillary therapies
    Recombinant feline interferon (Virbagen Omega)
    • For the reduction in mortality and clinical signs of parvovirus (enteric form) in dogs from one month of age.
    • Treatment of cats infected with FeLV and/or FIV, in non-terminal in clinical stages, from the age of 9 - evidence for this is lacking.
    CSFs to encourage BM recovery.
    Unclear benefit and are expensive. Not a substitute for supportive therapy.
    Faecal matter transplant is an option
  • Canine parvovirus - management begin oral fluids/nutrients ASAP
    Enteric support is crucial
    Aggressive anti-emetic use.
    May require assisted feeding, care with reflux and aspiration.
    • e.g. Naso-oesophageal tubes.
  • Canine parvovirus - prevention
    Vaccination - various protocols
    • Early vaccination and late vaccination in susceptible breeds and environments.
    Cleaning and disinfection - bleach/ Virkon
    • Resistant to some disinfectants
    • A major reason for not taking unvaccinated puppies outside.
    • This is a key step in controlling ANY infectious cause of diarrhoea in small animals.
  • Haemorrhagic gastroenteritis - overview
    Syndrome of acute haemorrhagic diarrhoea (AHDS)
    Idiopathic in most cases:
    • Diagnosis parvovirus enteritis/ intussusception/pancreatitis.
    • Aetiology may be type I intestinal hypersensitivity reaction or the result of Clostridium perfringens enterotoxin production.
  • Haemorrhagic gastroenteritis - clinical signs
    Usually small breed dogs.
    Vomiting +/- blood.
    Foetid diarrhoea - including protein loss - brown water.
    Depress ion, 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
  • Haemorrhagic gastroenteritis - Treatment
    Fluid therapy - must be aggressive as with CPV
    Colloid/ plasma/ whole blood.
    • Depends on degree of haemorrhage and complication.
    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
  • Haemorrhagic gastroenteritis - prognosis
    Prognosis is good in most cases however severe cases where proteins are low and systemic inflammatory response develops is guarded.
    • There cases are most critical in the acute presentation stage.
  • Feline panleucopaenia - feline parvo
    Transmission and signs as CPV.
    • Kittens/ colonies
    • Widespread in feral cats
    • Cats can be infected by CPV-2 (canine).
    • 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).
  • Coronavirus - 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 - vomiting and watery/ mucoid diarrhoea
    • Treatment - supportive IVFT and nutritional support for GI tract.
  • Coronavirus - cat FECV
    Signs as dog
    Note link to FIP - mutates to FIP - causing coronaviruses
  • Bacterial enteritis - dilemmas
    Zoonotic - so kill it/ ignore it?
    But … resistance/ health implications of treating.
    Could it become a carrier.
    Occurs in young animals and colonies/ kennels/ homes.
    Sampling - take Multiple samples.
    Dysbiosis - historically SIBO
    • Histiocytic ulcerative colitis in boxers.
  • Campylobacter (jejuni and upsaliensis) - overview
    Commensal in dogs therefore potential long-term zoonosis.
    Clinical disease in young, immunocompromised animals or those with additional infectious agents (Giardia, parvo).
  • Campylobacter (jejuni and upsaliensis) - clinical signs
    Acute enterocolitis - not chronic low grade diarrhoea.
    • Diarrhoea +/- blood/mucosa.
    • Vomiting
    • Straining - large intestinal ‘type’ diarrhoea
    • Fever, abdominal pain.
    • Can become enteroinvasive due to host stress (IFN and noradrenaline mediated).
  • Campylobacter (jejuni and upsaliensis) - 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
  • Campylobacter (jejuni and upsaliensis) - treatment
    Treat underlying disease if present - e.g. CE/IBD
    Treatment most frequently with 4-fluoroquinolones (can use erythromycin, can lead to vomiting).
  • Salmonella - aetiopathogenesis
    Similar to campylobacter.
    • Mainly seen in young and immunocompromised animals or those with concomitant infections.
    • Is a commensal in many dogs.
    • Reports suggest isolated from up to 30% of normal dog faeces and 18% of cats.
    • More commonly is around 2% unless on raw diets when carriage is higher and up to 20%.
  • Salmonella - scenarios after infection
    Transient asymptomatic diarrhoea.
    Acute gastroenteritis
    Carrier state
    Bacteraemia
  • Salmonella -indicators and signs
    Infection can be mild or severe with haemorrhagic diarrhoea, pyrexia and sepsis (due to translocation across gut wall).
    • Negative prognostic indicators - hypoglycaemia, temperature >40C, degenerate left shift.
    • SIRS and DIC - RIP.
    • Cats - usually mild diarrhoea but songbird fever whe ingest birds (migration season) can lead to acute febrile illness with diarrhoea.
  • Salmonella - treatment
    Only treat if severe sepsis and shock and only on basis of culture results:
    • Not if patient is unwell/mild diarrhoea as unlikely to be significant.
  • Clostridial enteritis
    C.perfringens, C.difficile - normal anaerobic flora!
    • Diarrhoea generally due to enterotoxin production
    • Relationship with kennels and both acute and chronic diarrhoea but causation still unclear.
    Large intestinal type diarrhoea/HGE(AHDS)
    Mange complications, treat with metronidazole as first choice ampicillin and tylosin alternatives (less effective).
    Environmental spores are very resistant
  • E.coli enteritis
    Common gut commensal and faecal isolate.
    Histiocytic ulcerative colitis in boxers newly discovered attaching and invasive islolate.
    • Can develop rapid resistacne however 4-fluoroquinolone treatment or metronidazole is effective in many cases.
    Various strains present - clear that plasmid genes code for pathogenicity (labs are able to test for these).
  • Helminth infestation - Ascarids
    Puppies/kittens mostly - adults have low burdens and worm migration patterns and are different (adults have mainly somatic migration which generally leads to cyst formation in tissues).
    Fail to gain weight
    Pot bellied appearance
    Vomiting and small bowel diarrhoea
    Obstruction of GIT if large burdens along with respiraoty disease when migrating.
  • Helminth parasites of dogs - hookworms
    Kennelled dogs most commonly identified.
    Diarrhoea
    Weight loss
    Anaemia with Ancylostoma
    Interdigital dermatitis/ perineal irritation.
  • Helminth infestations - cestodes
    D caninum, taenia sp. and Echinococcus sp.
    Signs rare in adults - zoonotic aspect necessitates control.
  • Helminth infestations - diagnosis
    Clinical signs and history
    Faecal examination
  • Helminth infestations - treatment
    Heavy importance for treatment due to public health consideration (VLM and OLM).
    • Toxocara and cestodes.
    Treatment does not remove encysted larvae.
    Occult parasitic infestation should be considered in animals being investigated for IBD.
    This treatment for intestinal parasites should form part of the initial therapy in these cases.
  • Protozoa - Coccidian (faecal-oral) overview
    Isospora canis (dog), I. felis, I.rivolta (cat).
    Pups/kittens, poor conditions etc lead to most severe clinical signs.
    Diarrhoea in experimental dogs (I.canis) suggest primary pathogen - can see chronic intermittent shedding by carriers during stress or concomitant disease.
    Can be severe and mortality can occur. Diagosis with faecal exam (direct or flotation for oocysts).