Infectious Diseases - Dogs Flashcards

1
Q

What is parvovirus?

A

A virus causing severe haemorrhagic vomiting and/or diarrhoea with leukopenia

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2
Q

How is canine parvovirus transmitted?

A

Faeco-oral spread - large quantities shed in diarrhoea

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3
Q

How can parvovirus particles be inactivated?

A

Formalin and hypochlorite disinfectants (bleach-based)

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4
Q

What is the pathogenesis of canine parvovirus?

A

Infects rapidly dividing tissue (neonatal myocardium, intestinal crypts, bone marrow) and causes ulcerations

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5
Q

What are the clinical signs of canine parvovirus?

A

Intestinal - haemorrhagic diarrhoea +/- vomiting - depressed, anorexic, abdominal pain
Bone marrow - neutropenia
Risk of sepsis - pyrexia, CVS compromise

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6
Q

How is canine parvovirus diagnosed?

A

Clinical suspicions should lead to faecal parvovirus antigen ELISA test

May be anaemic/hypoproteinaemic

Electrolyte imbalances

Post-mortem (various tissues)

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7
Q

What is the treatment for canine parvovirus?

A

Aggressive fluid therapy - IV crystalloids

Monitor electrolytes and glucose

NG tube trickle feeding (once vomiting controlled)

Anti-emetics (Maropitant, metoclopramide)

Antibiotics (amoxicillin clavulanate IV)

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8
Q

What nursing considerations should be made when caring for a parvovirus puppy?

A

Dedicated nurse/nurse last

Ensure comfortable (reduce diarrhoea/salivation scalds)

Ensure warm and euhydrated/euvolaemic

Notify if pyrexic/hypothermic

Early nutrition essential to recovery

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9
Q

How can canine parvovirus infection be prevented?

A

Vaccination

Recovery from natural infection gives life-long protection (not ideal)

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10
Q

Can cats get parvovirus?

A

Yes - feline panleukopenia, feline infectious enteritis

Closely related to canine PV

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11
Q

What is the typical presentation of a dog with leptospirosis?

A

Acute or chronic hepatic and/or renal insult

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12
Q

Is leptospirosis zoonotic?

A

Yes

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13
Q

How is leptospirosis transmitted?

A

Environmental contamination with infected urine - cannot replicate outside host

Infection when contaminated urine contacts mucous membranes/compromised skin

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14
Q

What are the 2 phases of pathogenesis involving leptospirosis?

A

Replicates within the bloodstream (leptospiraemia)

Renal infection and shedding in urine (leptospiruria)

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15
Q

What is the incubation period for leptospirosis?

A

Approx 1 week - varies between animals

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16
Q

What is the clinical presentation of leptospirosis infection?

A

Typically acute

Hepatic injury +/- jaundice
Renal injury +/- failure

Lethargy, pyrexia, inappetence, vomiting, diarrhoea

Signs related to affected organ system(s)

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17
Q

What might you find upon examination of a dog with leptospirosis?

A

Dog is lethargic, dull, frequently pyrexic

+/- jaundice, petechial haemorrhages, mild generalised lymphadenomegaly

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18
Q

What laboratory findings might be seen with leptospirosis infection?

A

Varies considerably between patients

Thrombocytopenia common

Raised liver enzymes (hepatic injury)

Azotemia (renal injury) - anuria/polyuria possible, monitor UOP

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19
Q

How is leptospirosis diagnosed?

A

Demonstration of serologic conversion (antibodies in blood)

Organism identification via PCR

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20
Q

How is leptospirosis treated?

A

If suspected, start treating BEFORE confirmed diagnosis

Doxycycline (2 weeks)

Amoxicillin clavulanate

Supportive treatment for affected organs

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21
Q

What is the prognosis for leptospirosis infection?

A

> 50% full recovery

Others turn into chronic disease which is ultimately fatal despite treatment

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22
Q

What nursing care considerations should you take with leptospirosis?

A

Careful hygiene, barrier nursing

Disinfect appropriately (chlorine/phenol based)

Appropriate cage signage

Designated urination area - roughly monitor UOP (do not handle - zoonotic)

Consider location of phlebotomy if thrombocytopenic

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23
Q

What considerations should be taken to avoid zoonotic infections of leptospirosis?

A

Avoid contact with bodily fluids (urine and blood esp)

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24
Q

What is canine distemper virus?

A

Virus causing multi-systemic disease, including respiratory, GI, neurological and dermatological disease

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25
Q

What type of virus is canine distemper virus?

A

Enveloped RNA morbillivirus

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26
Q

How is canine distemper virus inactivated?

A

Rapidly via heat, drying, disinfectants

Survives <1 day in environment

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27
Q

What is the pathogenesis of canine distemper?

A

Replicates in tonsils/lymphoid tissues of upper respiratory tract

Invades and travels in monocytes and disseminates to entire reticuloendothelial system

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28
Q

How is canine distemper transmitted?

A

Transmitted via oro-nasal secretions - direct contact or large-particle aerosol

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29
Q

What is the clinical presentation of acute canine distemper infection?

A

Highly variable - can be sub-clinical or rapidly progressive and fatal

Pyrexia, lethargy, vomiting +/- diarrhoea

Cough, naso-ocular discharge

Neurological signs

Secondary infections common

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30
Q

What are the common neurological signs of canine distemper?

A

Seizures, ataxia, myoclonus

‘Old dog encephalitis’

31
Q

What clinical signs can be seen with chronic distemper infection?

A

Ocular - various inflammatory manifestations +/- blindness

Dental - enamel and dentin hypoplasia

Dermatological - foot pad and nasal planum hyperkeratosis

32
Q

How is canine distemper diagnosed?

A

Lymphopenia common

Identification of organism via cytology, ELISA/PCR, post-mortem

Serology (antibody detection)

33
Q

What is the management for canine distemper?

A

Isolate/barrier nurse

Supportive nursing and management of secondary infections

Vitamin A?

34
Q

are anti-virals available for canine distemper?

A

not currently

35
Q

How can canine distemper infection be prevented?

A

Recovery from natural infection gives life-long immunity

Immunity requires cell-mediated immunity and antibodies

36
Q

What are the 2 types of canine adenovirus?

A

CAV-1 - infectious canine hepatitis

CAV-2 - respiratory pathogen, causes mild disease, part of the kennel cough complex

37
Q

What type of adenovirus do we vaccinate dogs with?

A

Modified live CAV-2

38
Q

Why don’t we vaccinate dogs with CAV-1?

A

Vaccination with CAV-1 can lead to glomerulopathy and corneal oedema (‘blue eye’) - CAV-2 gives protection against both types

39
Q

How long does CAV-1 survive in the environment? How is it inactivated?

A

Survives at room temperature for months but readily inactivated by disinfectants

40
Q

How is CAV-1 transmitted?

A

Shed in saliva/urine/faeces for months post-infection

Direct dog-dog contact or via fomites

41
Q

What is the pathogenesis of CAV-1?

A

First picked up by oro-nasopharynx/conjunctiva –> tonsillar replication –> lymphatic spread –> lymph nodes and bloodstream

Cell injury and lysis causes widespread tissue damage

42
Q

What is the incubation period for CAV-1?

A

4-9 days (average, can vary)

43
Q

What are the 4 classifications of CAV-1 infection?

A

Mild/subclinical (vaccinated dogs)

Per-acute (circulatory collapse and death in 1-2 days)

Acute (severe disease, 1-2 weeks)

Sub-acute (hepatic failure)

44
Q

What are the clinical signs of CAV-1 infection?

A

Hepatic injury

Petechial haemorrhages +/- GI haemorrhage

Conjunctivitis +/- uveitis and oedema

Pyrexia, lethargy, inappetence, V+/D+, tachypnoea

Glomerular/tubular damage

45
Q

How is CAV-1 infection diagnosed?

A

Leukopenia/neutropenia +/- pancytopenia

Serology - rising titre

Virus identification through PCR

Characteristic intranuclear inclusion bodies

46
Q

What is the treatment for CAV-1 infection?

A

No specific treatment - supportive nursing (barrier)

Fluid/nutritional support

Anti-emetics and analgesia if required

Ophthalmic care

47
Q

How is canine herpesvirus transmitted?

A

Latent infection of neural ganglia –> reactivation/shedding at times of stress

Typically venereal transmission

48
Q

Why are signs of canine herpesvirus usually only apparent in puppies?

A

Canine herpesvirus only replicates <37°C - puppies have lower internal body temperature than adults

49
Q

Why is it important to have pregnant bitches vaccinated against herpesvirus?

A

Exposure of pregnant bitch in last trimester leads to abortions/neonatal deaths (up to 100% of litter)

50
Q

Which respiratory pathogens are considered part of the canine kennel cough complex?

A

Bordetella bronchiseptica
Canine parainfluenza virus
CAV-2

51
Q

What is the lay term for infectious tracheobronchitis?

A

kennel cough

52
Q

What are the clinical indications of kennel cough?

A

Self-liming acute URT cough, harsh and hacking
Concurrent oculo-nasal signs
Progression to pneumonia (not common)

53
Q

How is kennel cough transmitted?

A

Highly contagious aerosol, direct and fomite transmission

54
Q

How should kennel cough be treated if there are no other significant clinical findings?

A

Usually self limiting - don’t walk on collar, keep well away from other dogs

+/- NSAIDs
+/- Cough suppressants (only if non-productive coughing)

55
Q

How should kennel cough be treated if there are also lower respiratory/systemic signs?

A

Antibiotics - doxycycline

Radiography

56
Q

What are the symptoms of bacterial enterocolitis?

A

Haemorrhagic vomiting +/- diarrhoea
Pyrexia
Sepsis
+/- abdominal pain

57
Q

Why is diagnosis of bacterial enterocolitis often a challenge?

A

Most culprit bacteria can be isolated from faeces of healthy dogs - challenge is proving causality

58
Q

What are the risk factors for bacterial enterocolitis?

A

Raw fed
Young dogs
Unsanitary/crowded environments

59
Q

How is bacterial enterocolitis diagnosed?

A

Consider faecal culture but remember to evaluate for parvovirus as signs can be very similar

60
Q

How would you diagnose and treat campylobacter spp.?

A

If faecal culture positive, speciate with PCR (C. jejuni related to disease in dogs)

First line treatment is erythromycin (not licensed)

61
Q

How would you diagnose and treat a salmonella spp. infection?

A

Faecal and/or blood culture and PCR

Treat with antibiotics (fluoroquinolones) but only if systemically unwell

62
Q

How would you diagnose a Escherichia coli. infection?

A

Positive faecal culture

Can then evaluate for pathogenicity genes but this still does not prove causality - may be commensal

63
Q

How would you treat an Escherichia coli infection?

A

Antimicrobials

64
Q

How would you diagnose a Clostridium perfringens infection?

A

Test for clostridium perfringens enterotoxin (CPE) in faeces (ELISA)
Identify CPE gene via PCR

65
Q

How would you treat a Clostridium perfringens infection?

A

Ampicillin or metronidazole

Only treat if systemically ill (haemorrhagic gastroenteritis, pyrexia, inflammatory leukogram)

66
Q

What is acute haemorrhagic diarrhoea syndrome?

A

Syndrome of acute haemorrhagic diarrhoea and marked haemoconcentration (+/- vomiting)

67
Q

Which bacteria most commonly causes AHDS?

A

Increasing evidence for C. perfringens NetF in pathogenesis (causes pore in enterocytes)

68
Q

What is the clinical presentation of AHDS?

A

Acute onset haemorrhagic vomiting +/- diarrhoea

Abdominal pain

Obtundation

Hypovolaemic shock

Marked haemoconcentration

69
Q

How would you diagnose AHDS?

A

Consistent clinical signs

Marked elevation in PCV (>60%) without commensurate increase in proteins

Exclusion of other causes (parvo, dietary toxins, pacreatitis, hypoadrenocorticism)

70
Q

How would you treat a case of AHDS?

A

IV crystalloids (boluses and CRI)

Amoxicillin clavulanate (not indicated unless systemically unwell)

71
Q

How would you diagnose a Clostridium difficile infection?

A

Faecal culture and/or common antigen test

ELISA for toxins

72
Q

How would you treat a Clostridium difficile infection?

A

Metronidazole (where clinically indicated)

If antibiotic-induced, stop antibiotics

73
Q

With which overall symptoms should you consider the cause to be a bacterial pathogen?

A

Acute haemorrhagic vomiting and/or diarrhoea

With signs of sepsis, pyrexia, inflammatory leukogram

74
Q

What nursing considerations should you take with a bacterial enterocolitis infection?

A

Barrier nursing
Fluid balance - euvolaemia, euhydration
Consider abdominal pain, nausea, appetite, and severity of haemorrhagic component