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Canine Infectious Disease Flashcards

1
Q

Describe Canine Parvovirus (CPV2).

A

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)

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2
Q

What is the signalment for CPV?

A

Inadequately protected puppy - immunity gap

Unvaccinated adult

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3
Q

What are the clinical signs of CPV?

A

Haemorrhagic diarrhoea +/- vomiting
Anorexic, depressed, abdominal pain
Neutropenia
Pyrexia, cardiovascular compromise, death

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4
Q

How do we diagnose CPV?

A

Test every puppy with haemorrhagic diarrhoea and/or neutropenia
Faecal parvovirus antigen ELISA test (in-house)
Post-mortem (various tissues)

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5
Q

How do we treat CPV?

A

Fluid therapy (IV crystalloids) - Monitor K+ and supplement glucose as necessary
Naso-oesophageal tube trickle feeding
Control emesis - maropitant/metoclopramide
Antibiotics - amoxicillin clavulanate IV

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6
Q

What nursing care can we provide to CPV patients?

A 
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
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7
Q

How can we prevent CPV?

A

Barrier nursing/disinfection with hypochlorite

Vaccination

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8
Q

Describe Leptospirosis in the environment.

A

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

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9
Q

Describe the pathogenesis of leptospirosis.

A

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

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10
Q

What is the clinical presentation of leptospirosis?

A

Typically acute
Lethargy, inappetence, vomiting/diarrhoea, pyrexia
Hepatic injury +/- jaundice
Renal injury +/- failure

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11
Q

What do find on examination of a leptospirosis patient?

A 
Lethargic, dull
Frequently pyrexic
\+/- jaundice
\+/- petechial haemorrhages
\+/- mild generalised lymphadenomegaly
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12
Q

What are the common laboratory findings of leptospirosis patients?

A

Thrombocytopenia (mild-moderate)
Hepatic injury +/- jaundice
Renal injury (azotemia) - anuria/polyuria

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13
Q

How do we diagnose leptospirosis?

A

Demonstration of serological conversion

Organism identification - before antibiotic therapy (PCR most commonly used)

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14
Q

How do we treat leptospirosis?

A

When suspicious, start before results available
Doxycycline (2 weeks) required +/- in-contact animals
Frequently use amoxicillin clavulanate IV
Supportive treatment for affected organs

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15
Q

What nursing care can we provide for leptospirosis patients?

A

Hygiene and barrier nursing
Disinfect appropriately - chlorine/phenol-based
Appropriate cage signage
Designated urine area - monitor urine output roughly
Consider phlebotomy

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16
Q

What human considerations do we have regarding leptospirosis?

A

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)

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17
Q

Describe Canine Distemper Virus.

A

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

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18
Q

What is the acute presentation of distemper?

A

Highly variable - host, pathogenicity, dose etc.
Pyrexia, lethargy
Respiratory = cough, naso-ocular discharge +/- pneumonia
GI = vomiting, diarrhoea
+/- neurological
Secondary infections common

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19
Q

What is the chronic/other manifestations of distemper?

A

CNS signs = seizures, ataxia, myoclonus
Ocular signs = inflammatory +/- blindness
Dental = enamel and dental hypoplasia
Dermatological - foot pad and nasal planum hyperkeratosis (‘hardpad’)

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20
Q

How do we diagnose distemper?

A

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)

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21
Q

How do we treat distemper?

A

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

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22
Q

What are the two presentations of Canine Adenovirus?

A 
CAV-1 = Infectious Canine Hepatitis
CAV-2 = respiratory pathogen, part of Kennel Cough complex
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23
Q

Describe CAV-1.

A

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)

24
Q

How is CAV-1 transmitted?

A

Shed in saliva, urine, faeces for months post-infection
Direct dog-dog contact or via fomites
4-9 day incubation before clinical signs

25
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
26
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
27
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
28
How do we treat and nurse CAV-1 patients?
Isolate/barrier nurse Supportive (esp. hepatic) - fluid/nutrition, nausea, encephalopathic, painful? +/- specific ophthalmic care
29
What is the prognosis for CAV-1 survivors?
Chronic hepatitis/glomerulonephritis possible
30
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'
31
Which three canine infectious respiratory pathogens are considered part of the Kennel Cough complex?
Bordetella bronchiseptica Canine parainfluenza virus Canine adenovirus 2 (CAV-2)
32
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
33
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
34
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.
35
What challenges do we face from bacterial infections?
Can be isolated from healthy dogs' faeces Zoonoses and reverse zoonoses Knowing the significance/proving causality
36
What are the risk factors for a bacterial canine infection?
Raw-fed Young Unsanitary/crowded environment Immunocompromised owners
37
What are the clinical signs of bacterial enterocolitis?
``` Haemorrhagic vomiting +/- diarrhoea Pyrexia Sepsis +/- abdominal pain Enterotoxaemia is possible ```
38
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
39
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')
40
How do we diagnose Salmonella spp. infection?
Faecal culture and/or blood culture/PCR
41
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)
42
Describe Escherichia coli infection.
Various pathogenic types, may be commensal | May cause acute or chronic diarrhoea - often in combo with other pathogens
43
How do we diagnose E. coli?
Positive faecal culture | Can evaluate for pathogenicity genes
44
How do we treat E. coli infection?
Antimicrobials | Others (vaccination, oral Ig's) not proven
45
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
46
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
47
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
48
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
49
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
50
How do we diagnose AHDS?
Consistent clinical signs Marked elevation in PCV (often >60%) without commensurate increase in proteins Exclude other causes
51
How do we treat AHDS?
IV crystalloid therapy for hypovolaemia (boluses, ongoing CRI) Amoxicillin clavulanate when indicated, i.e. pyrexic, septic
52
Describe Clostridium difficile infection.
Small proportion healthy animals carry asymptomatically | Disease likely secondary to toxin production
53
How do we diagnose Clostridium difficile infection?
Faecal culture and/or common antigen test + ELISA for toxins (TcdA and TcdB) Negative culture = good NPV
54
How do we treat Clostridium difficile infection?
Metronidazole, where clinically indicated | If antibiotic-induced, stop antibiotics
55
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.

Veterinary Nursing (65 decks)

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