Canine Infectious Disease Flashcards
Describe Canine Parvovirus (CPV2).
Severe haemorrhagic vomiting/diarrhoea (haemorrhagic gatroenteritis) with leukopenia
Faeco-oral spread
Inactivated by formalin and hypochlorite disinfectants
Part of core canine vaccination
Infects rapidly diving tissue (neonatal myocardium, intestinal crypt, bone marrow)
What is the signalment for CPV?
Inadequately protected puppy - immunity gap
Unvaccinated adult
What are the clinical signs of CPV?
Haemorrhagic diarrhoea +/- vomiting
Anorexic, depressed, abdominal pain
Neutropenia
Pyrexia, cardiovascular compromise, death
How do we diagnose CPV?
Test every puppy with haemorrhagic diarrhoea and/or neutropenia
Faecal parvovirus antigen ELISA test (in-house)
Post-mortem (various tissues)
How do we treat CPV?
Fluid therapy (IV crystalloids) - Monitor K+ and supplement glucose as necessary
Naso-oesophageal tube trickle feeding
Control emesis - maropitant/metoclopramide
Antibiotics - amoxicillin clavulanate IV
What nursing care can we provide to CPV patients?
Bottom hygiene, diarrhoea scald Hypersalivation - mandibular lip scald Ensure warm, euhydrated/euvolaemic Notify if pyrexic/hypothermic Early nutrition essential to recovery! Dedicated nurse/nurse last
How can we prevent CPV?
Barrier nursing/disinfection with hypochlorite
Vaccination
Describe Leptospirosis in the environment.
Infected urine - contamination
Cannot replicate outside of host
Exposure to heat/frosts, UV irradiation = readily inactivated
Can survive for weeks-months in warm/wet months
Describe the pathogenesis of leptospirosis.
Infection via contaminated urine contacting MMs or compromised skin
Replication within bloodstream (leptospiraemia)
Renal infection and shedding in urine (leptospiruria)
Incubation period approx. 1 week
What is the clinical presentation of leptospirosis?
Typically acute
Lethargy, inappetence, vomiting/diarrhoea, pyrexia
Hepatic injury +/- jaundice
Renal injury +/- failure
What do find on examination of a leptospirosis patient?
Lethargic, dull Frequently pyrexic \+/- jaundice \+/- petechial haemorrhages \+/- mild generalised lymphadenomegaly
What are the common laboratory findings of leptospirosis patients?
Thrombocytopenia (mild-moderate)
Hepatic injury +/- jaundice
Renal injury (azotemia) - anuria/polyuria
How do we diagnose leptospirosis?
Demonstration of serological conversion
Organism identification - before antibiotic therapy (PCR most commonly used)
How do we treat leptospirosis?
When suspicious, start before results available
Doxycycline (2 weeks) required +/- in-contact animals
Frequently use amoxicillin clavulanate IV
Supportive treatment for affected organs
What nursing care can we provide for leptospirosis patients?
Hygiene and barrier nursing
Disinfect appropriately - chlorine/phenol-based
Appropriate cage signage
Designated urine area - monitor urine output roughly
Consider phlebotomy
What human considerations do we have regarding leptospirosis?
ZOONOTIC!
Avoid contact with bodily fluids, especially urine and blood
‘Weil’s disease’ - typically mild and flu-like, less typically severe multisystemic life-threatening illness (+/- abortions)
Describe Canine Distemper Virus.
Survives <1 day in environment - rapidly inactivated by heat, drying, disinfectants
Rare in UK due to vaccination
Shed in all body secretions/excretions BEFORE clinical signs
Tendency for epithelial localisation e.g. respiratory, GI, CNS, urinary, skin, RBC/WBC
What is the acute presentation of distemper?
Highly variable - host, pathogenicity, dose etc.
Pyrexia, lethargy
Respiratory = cough, naso-ocular discharge +/- pneumonia
GI = vomiting, diarrhoea
+/- neurological
Secondary infections common
What is the chronic/other manifestations of distemper?
CNS signs = seizures, ataxia, myoclonus
Ocular signs = inflammatory +/- blindness
Dental = enamel and dental hypoplasia
Dermatological - foot pad and nasal planum hyperkeratosis (‘hardpad’)
How do we diagnose distemper?
No specific screening lab findings (although lymphopenia common)
Identifying organism - swabs/samples
Cytology - viral inclusions (leukocytes, conjunctival cells, fluid samples etc)
Antigen (ELISA) assays/PCR detection
Antibody detection (serology, paired)
Post-mortem - histopathology (inclusions +/- in situ hybridisation)
How do we treat distemper?
Isolation/barrier nursing
Supportive nursing and management of secondary infections
Antiviral therapy not currently available
Surviving, apparently recovered dogs are at risk of future CNS signs
What are the two presentations of Canine Adenovirus?
CAV-1 = Infectious Canine Hepatitis CAV-2 = respiratory pathogen, part of Kennel Cough complex
Describe CAV-1.
Survives at room temp. for months, readily inactivated by disinfectants
Affected dogs usually juvenile or unvaccinated (rare in UK)
Also causes disease in other dog-like species (not ferrets)
How is CAV-1 transmitted?
Shed in saliva, urine, faeces for months post-infection
Direct dog-dog contact or via fomites
4-9 day incubation before clinical signs
What are the 4 disease syndromes of CAV-1?
Mild/subclinical = immunological competence
Per-acute = circulatory collapse and death (1-2 days)
Sub-acute to chronic = partially immune, hepatic failure and death
Acute = severe disease lasting 1-2 weeks, mortality up to 30%, most commonly seen
What are the clinical signs of CAV-1?
Hepatic injury (icterus uncommon)
Petechial/ecchymotic haemorrhages +/- GI haemorrhage
Conjunctivitis +/- uveitis +/- corneal oedema (‘Blue Eye’) - NOT all
+ non-specific pyrexia, lethargy, inappetence, vomiting, diarrhoea, tachypnoea
+/- glomerular +/- tubular damage - may persist
Robust antibody response at ~7 days - limited injury beyond this timeframe
How do we diagnose CAV-1?
Leukopenia/neutropenia +/- pancytopenia
Biochem reflects hepatocellular injury and dysfunction - coagulopathic
Serologic - rising titre
Virus identification - PCR (nasal/ocular/rectal swabs, body fluids/tissues)
Post-mortem characteristic intranuclear inclusion bodies
How do we treat and nurse CAV-1 patients?
Isolate/barrier nurse
Supportive (esp. hepatic) - fluid/nutrition, nausea, encephalopathic, painful?
+/- specific ophthalmic care
What is the prognosis for CAV-1 survivors?
Chronic hepatitis/glomerulonephritis possible
Describe Canine Herpesvirus infection (CHV-1).
Latent infection of neural ganglia = reactivation/shedding at times of stress
Typically venereal transmission in adults - subclinical URT/genital disease + latency
Replicates < 37 degrees C so usually only in puppies - ‘fading puppy syndrome’
Which three canine infectious respiratory pathogens are considered part of the Kennel Cough complex?
Bordetella bronchiseptica
Canine parainfluenza virus
Canine adenovirus 2 (CAV-2)
Describe Kennel Cough.
Multiple pathogens, usually causing acute and self-limiting URT cough (harsh and hacking)
May also cause concurrent oculo-nasal signs + progression to pneumonia
Highly contagious (aerosol, direct and fomite transmission) - high unvaccinated population density risk
How do we manage a KC coughing dog who is otherwise well and non-pyrexic?
Give time (1-2 weeks), environmental management
+/- NSAIDs
+/- cough suppressants
How do we manage a KC coughing dog who is pyrexic with lower respiratory or systemic signs?
Antibiotics - doxycycline (and/or guided by culture/sensitivity)
Lower respiratory signs = ideally radiography
Systemic signs = consider other infectious diseases/diagnostics etc.
What challenges do we face from bacterial infections?
Can be isolated from healthy dogs’ faeces
Zoonoses and reverse zoonoses
Knowing the significance/proving causality
What are the risk factors for a bacterial canine infection?
Raw-fed
Young
Unsanitary/crowded environment
Immunocompromised owners
What are the clinical signs of bacterial enterocolitis?
Haemorrhagic vomiting +/- diarrhoea Pyrexia Sepsis \+/- abdominal pain Enterotoxaemia is possible
Describe Campylobacter spp. infection.
Present in faeces of (>50%) healthy dogs/cats (young/kennelled)
If faecal culture +ve, speciate with PCR
C. jejuni related to disease in dogs, C. coli related to disease in cats
C. upsaliensis likely a canine commensal
First line therapy (off-licence) = erythromycin
Describe Salmonella spp. infection.
Subclinical carriage - up to 30% healthy dogs and 18% healthy cats
In cats, clinical signs do not always include GI - pyrexia +/- leukocytosis +/- GI signs (‘songbird fever’)
How do we diagnose Salmonella spp. infection?
Faecal culture and/or blood culture/PCR
How do we treat Salmonella spp. infection?
Treat only if systemically unwell
Antibiotics may encourage carrier state - least likely with fluoroquinolones (10 days then reculture)
Describe Escherichia coli infection.
Various pathogenic types, may be commensal
May cause acute or chronic diarrhoea - often in combo with other pathogens
How do we diagnose E. coli?
Positive faecal culture
Can evaluate for pathogenicity genes
How do we treat E. coli infection?
Antimicrobials
Others (vaccination, oral Ig’s) not proven
Describe Clostridium perfringens infection.
Can isolate from >80% healthy dogs
Subtyped based on various toxins
Clostridium perfringens enterotoxin (CPE)
netF toxin likely associated with canine Acute Haemorrhagic Diarrhoea Syndrome
How do we diagnose Clostridium perfringens infection?
Dogs more typically have lower intestinal diarrhoea (SI or mixed also common)
Ideally - CPE (ELISA) in faeces and CPE gene PCR
In reality rely on faecal culture - HUGE limitations
How do we treat Clostridium perfringens infection?
No rationale for treating systemically well dogs with diarrhoea
Treat if systemically ill (haemorrhagic gastroenteritis, pyrexia, inflammatory leukogram) - ampicillin / metronidazole
Describe Acute Haemorrhagic Diarrhoea Syndrome (AHDS).
Acute haemorrhagic diarrhoea (+/- vomiting) and marked haemoconcentration
Increasing evidence for C. perfringens netF in pathogenesis - pore in enterocytes
Most commonly affects small breed dogs, any age
Some suffer repeated events
What is the clinical presentation of Acute Haemorrhagic Diarrhoea Syndrome?
Acute onset
Acute haemorrhagic diarrhoea +/- vomiting
Abdominal pain, obtundation
Extreme fluid losses into gut lumen = hypovolaemic shock, marked haemoconcentration
How do we diagnose AHDS?
Consistent clinical signs
Marked elevation in PCV (often >60%) without commensurate increase in proteins
Exclude other causes
How do we treat AHDS?
IV crystalloid therapy for hypovolaemia (boluses, ongoing CRI)
Amoxicillin clavulanate when indicated, i.e. pyrexic, septic
Describe Clostridium difficile infection.
Small proportion healthy animals carry asymptomatically
Disease likely secondary to toxin production
How do we diagnose Clostridium difficile infection?
Faecal culture and/or common antigen test
+ ELISA for toxins (TcdA and TcdB)
Negative culture = good NPV
How do we treat Clostridium difficile infection?
Metronidazole, where clinically indicated
If antibiotic-induced, stop antibiotics
What nursing care can we provide in bacterial enterocolitis?
Barrier nursing
Hygiene
Attention - fluid balance, severity of haemorrhagic component, abdominal pain, nausea, appetite, changes in body temp.
