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Veterinary Nursing > Canine Infectious Disease > Flashcards

Canine Infectious Disease Flashcards

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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
Q

What are the 4 disease syndromes of CAV-1?

A

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
Q

What are the clinical signs of CAV-1?

A

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
Q

How do we diagnose CAV-1?

A

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
Q

How do we treat and nurse CAV-1 patients?

A

Isolate/barrier nurse
Supportive (esp. hepatic) - fluid/nutrition, nausea, encephalopathic, painful?
+/- specific ophthalmic care

29
Q

What is the prognosis for CAV-1 survivors?

A

Chronic hepatitis/glomerulonephritis possible

30
Q

Describe Canine Herpesvirus infection (CHV-1).

A

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
Q

Which three canine infectious respiratory pathogens are considered part of the Kennel Cough complex?

A

Bordetella bronchiseptica
Canine parainfluenza virus
Canine adenovirus 2 (CAV-2)

32
Q

Describe Kennel Cough.

A

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
Q

How do we manage a KC coughing dog who is otherwise well and non-pyrexic?

A

Give time (1-2 weeks), environmental management
+/- NSAIDs
+/- cough suppressants

34
Q

How do we manage a KC coughing dog who is pyrexic with lower respiratory or systemic signs?

A

Antibiotics - doxycycline (and/or guided by culture/sensitivity)
Lower respiratory signs = ideally radiography
Systemic signs = consider other infectious diseases/diagnostics etc.

35
Q

What challenges do we face from bacterial infections?

A

Can be isolated from healthy dogs’ faeces
Zoonoses and reverse zoonoses
Knowing the significance/proving causality

36
Q

What are the risk factors for a bacterial canine infection?

A

Raw-fed
Young
Unsanitary/crowded environment
Immunocompromised owners

37
Q

What are the clinical signs of bacterial enterocolitis?

A 
Haemorrhagic vomiting +/- diarrhoea
Pyrexia
Sepsis 
\+/- abdominal pain
Enterotoxaemia is possible
38
Q

Describe Campylobacter spp. infection.

A

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
Q

Describe Salmonella spp. infection.

A

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
Q

How do we diagnose Salmonella spp. infection?

A

Faecal culture and/or blood culture/PCR

41
Q

How do we treat Salmonella spp. infection?

A

Treat only if systemically unwell

Antibiotics may encourage carrier state - least likely with fluoroquinolones (10 days then reculture)

42
Q

Describe Escherichia coli infection.

A

Various pathogenic types, may be commensal

May cause acute or chronic diarrhoea - often in combo with other pathogens

43
Q

How do we diagnose E. coli?

A

Positive faecal culture

Can evaluate for pathogenicity genes

44
Q

How do we treat E. coli infection?

A

Antimicrobials

Others (vaccination, oral Ig’s) not proven

45
Q

Describe Clostridium perfringens infection.

A

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
Q

How do we diagnose Clostridium perfringens infection?

A

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
Q

How do we treat Clostridium perfringens infection?

A

No rationale for treating systemically well dogs with diarrhoea
Treat if systemically ill (haemorrhagic gastroenteritis, pyrexia, inflammatory leukogram) - ampicillin / metronidazole

48
Q

Describe Acute Haemorrhagic Diarrhoea Syndrome (AHDS).

A

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
Q

What is the clinical presentation of Acute Haemorrhagic Diarrhoea Syndrome?

A

Acute onset
Acute haemorrhagic diarrhoea +/- vomiting
Abdominal pain, obtundation
Extreme fluid losses into gut lumen = hypovolaemic shock, marked haemoconcentration

50
Q

How do we diagnose AHDS?

A

Consistent clinical signs
Marked elevation in PCV (often >60%) without commensurate increase in proteins
Exclude other causes

51
Q

How do we treat AHDS?

A

IV crystalloid therapy for hypovolaemia (boluses, ongoing CRI)
Amoxicillin clavulanate when indicated, i.e. pyrexic, septic

52
Q

Describe Clostridium difficile infection.

A

Small proportion healthy animals carry asymptomatically

Disease likely secondary to toxin production

53
Q

How do we diagnose Clostridium difficile infection?

A

Faecal culture and/or common antigen test
+ ELISA for toxins (TcdA and TcdB)
Negative culture = good NPV

54
Q

How do we treat Clostridium difficile infection?

A

Metronidazole, where clinically indicated

If antibiotic-induced, stop antibiotics

55
Q

What nursing care can we provide in bacterial enterocolitis?

A

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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