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Veterinary Nursing > Feline Infectious Disease > Flashcards

Feline Infectious Disease Flashcards

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1
Q

Define zoonosis.

A

A disease that can be passed from animals to humans.

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2
Q

Define reverse zoonosis.

A

A disease that can be passed from humans to animals.

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3
Q

Define community-acquired disease.

A

A disease that is acquired in the community.

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4
Q

Define hospital-acquired (nosocomial) disease.

A

A disease that is acquired in hospital.

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5
Q

Define pathogen.

A

A disease-causing organism.

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6
Q

Define commensal.

A

An organism that inhabits a specific mucosal surface in the body and is a normal finding.

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7
Q

What are the 3 main shapes of bacteria?

A

Coccoid (spherical) e.g. Staphylococcus
Bacillus (rods) e.g. Escherichia coli
Spiral e.g. Leptospirosis

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8
Q

How do we diagnose bacteria?

A

Organism detection - microscopy and/or culture

Demonstration of antibody

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9
Q

How do we diagnose viruses?

A

Demonstration of virus (antigen or DNA) - may need special transport medium
Demonstration of antibody

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10
Q

How do we diagnose fungi?

A

Organism identification - microscopy, fungal culture, antigen, DNA
Demonstration of antibody

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11
Q

What are 3 examples of parasites?

A

Helminths (worms)
Protozoa
Ectoparasites (e.g. fleas)

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12
Q

How do we diagnose parasites?

A

Usually diagnose by identification of organism - microscopy/gross visualisation - antigen/DNA

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13
Q

In what ways are infectious diseases spread?

A

Hygiene in practice
Contamination of inanimate objects
Transmission between animals (grooming, fighting)
Blood transfusions/contact
Ectoparasite transmission
Aerosol transmission (sneezing, yawning etc.)
Vomiting/diarrhoea in environment

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14
Q

How long do cats have Feline Herpesvirus-1 and what triggers it later on?

A

Latent lifelong carriers

Stressful events = reactivation of shedding 4-12 days later, shed for ~1 weeks with/out clinical signs

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15
Q

How long is a cat infected with Feline Calicivirus?

A

Persists in oropharyngeal tissues for >1 month
‘Carrier state’ - in small % this may be lifelong
Continuous shedding during this time
May be asymptomatic

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16
Q

How is Feline Herpesvirus-1 spread?

A

Direct/indirect contact

Respiratory secretions - oculo-nasal discharge, saliva

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17
Q

How is Feline Calicivirus spread?

A

Direct/indirect contact
Respiratory secretions - oculo-nasal discharge, saliva
Urine / faeces

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18
Q

What is the incubation period of FHV-1/FCV?

A

Incubation period 2-6 days

Viral shedding from 1 day post-infection (BEFORE clinical signs)

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19
Q

What are the clinical signs of FHV-1/FCV?

A

2-6 days post-infection
Range from mild to severe/life-threatening (worse in kittens/immunocompromised patients)
Exacerbated by secondary opportunistic infections
Oral
Nasal
Ocular
Systemic

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20
Q

How do we diagnose feline upper respiratory tract infections?

A

Swabs (conjunctival, pharyngeal)
PCR - FCV, FHV-1, C. felis, B. bronchiseptica
Virus isolation - FVC/FHV-1, requires viral transport medium
Culture - C. felis, B. bronchiseptica

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21
Q

How do we treat feline URT infections?

A

Supportive - fluid therapy, nutrition

Specific meds - antivirals?, antibiotics for secondary infections, analgesia, appetite stimulants

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22
Q

What nursing care can we provide to feline URT infection patients?

A

Clean face - warm, wet, soft wipes
Barrier creams to prevent scald
Ocular lubricant
Nebulisation to loosen secretions

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23
Q

What nutritional considerations should we have for feline URT infection patients?

A

Correct dehydration and electrolyte imbalances first (24-48hrs)
Oral preferable
Small volume, palatable, warm foods
Offer fresh 4-6x/day, remove if uneaten after 20-30 mins
Gentle handfeeding, owner engagement
Anti-emetics, appetite stimulants
Severe cases may need tube feeding

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24
Q

What specific drugs can we use for FHV-1 patients?

A

Antivirals, e.g. Famciclovir (oral) - clinical improvement and reduced shedding
Lysine (oral) - improves conjunctivitis and reduces shedding

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25
Q

What specific drugs can we use for FCV patients?

A

Recombinant feline interferon-omega (IFN-omega) - improves refractory stomatitis

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26
Q

How do we treat secondary bacterial infections in feline URT patients?

A

Ideally culture and sensitivity

Antibiotics - Doxycycline (C. felis and B. bronchiseptica) / Amoxycillin clavulanate

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27
Q

How can we manage FHV in the environment?

A

Survives 18hrs at room temperature

Inactivated by most disinfectants and drying

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28
Q

How do we manage FCV in the environment?

A

Greater environmental persistence, up to 1 month (longer in dry conditions)
Bleach (sodium hypochlorite), potassium peroxymonosulfate or accelerated hydrogen peroxide
Resistant to quaternary ammonium compound (routine disinfection)

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29
Q

How do we handle feline URT infection patients?

A

Isolation facilities
Barrier nurse - single staff member, handle last, disposable gloves/apron/over-shoes
Hygiene of hands and arms

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30
Q

What is the incubation period of Chlamydia felis?

A

2-5 days.

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31
Q

Describe the typical Chlamydia felis patient.

A

From a multi-cat household

Typically young cats (<1 year old)

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32
Q

What are the main clinical signs of Chlamydia felis?

A

Feline conjunctivitis (acute and chronic/recurrent)
+/- upper respiratory signs
Corneal ulceration rare

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33
Q

How do we diagnose Chlamydia felis?

A

PCR (conjunctival swabs)

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34
Q

How do we treat Chlamydia felis?

A

Oral doxycycline

For at least 4 weeks and at least 2 weeks beyond clinical resolution

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35
Q

Where is Bordetella bronchiseptica most prevalent and how do we treat the environment?

A

High density populations e.g. boarding kennels/catteries, shelters etc.
Highly contagious
Persists in environment for ~10 days
Susceptible to most disinfectants

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36
Q

What is the incubation period of Bordetella bronchiseptica?

A

2-10 days.

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37
Q

What are the clinical signs of Bordetella bronchiseptica infection in cats?

A

Sneezing, mucoid/mucopurulent nasal discharge
Harsh cough
Kittens susceptible to bronchopneumonia

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38
Q

How do we diagnose Bordetella bronchiseptica in cats?

A

Bronchoalveolar lavage fluid
Culture and sensitivity (may not grow readily)
PCR

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39
Q

How do we treat Bordetella bronchiseptica in cats?

A

When required = doxycycline (1-4 weeks)

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40
Q

How is FIV transmitted?

A

Bite wounds (saliva)
From mother -> 1/3rd of kittens
Infected blood products
Venereal rare

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41
Q

What does FeLV stand for>

A
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41
Q

What does FeLV stand for?

A

Feline Leukaemia Virus

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42
Q

How is FeLV transmitted?

A 
Allogrooming, fomites (bowls)
Prolonged oronasal salivary exposure
Very frequently from mother -> kittens
Infected blood products
Venereal rare
43
Q

What are the signalments for FIV?

A

Fighters
Outdoor access
Older, male
More common in feral cats

44
Q

What are the signalments for FeLV?

A

Close-contact cats
Outdoor access
Young (3 years median age)
Entire

45
Q

What are the three phases of FIV infection?

A 
Acute phase (8-12 weeks)
Asymptomatic phase (years - life)
Terminal phase
46
Q

How is FIV diagnosed?

A

Screening tests detect antibodies against FIV

Assuming no history of vaccination and > 6months old

47
Q

What secondary infections can we see with FIV?

A 
Chronic gingivostomatitis
Opportunistic infections
Atypical infections
Neurological disease
Neoplasia
Myelosuppression
48
Q

Why may we see a false negative result for FIV?

A

Early disease (takes up to 8 weeks for antibodies to be detectable)
Terminal disease (antibody production may be impaired)
Kittens with rapidly progressive disease (may have huge viral load with minimal antibody response
If suspicious, recheck 2 months after initial check / use PCR (blood)

49
Q

When else should we test for FIV?

A

Known exposure to FIV+ cat
Before rehoming to multi-cat household/environment
Blood donor screening
Before vaccinating for FIV (available in some countries)

50
Q

What are the three types of FeLV infection?

A 
Abortive infection (strong immune response, immunity)
Regressive infection (effective immune response)
Progressive infection (inadequate immune response, established bone marrow infection)
51
Q

What are the clinical manifestations of FeLV infection?

A

Anaemia/bone marrow disorders
Immunosuppression
Neoplasia
Other

52
Q

Describe FeLV associated immunosuppression.

A

Various infections - opportunistic
Specific infections, e.g. upper respiratory, Mycoplasma haemofelis
Impaired response to vaccinations

53
Q

Describe FeLV anaemia/bone marrow disorders.

A

Typically non-regenerative but macrocytic
Regenerative also possible, e.g. IMHA +/- secondary to Mycoplasma haemofelis
Neutropenia
Thrombocytopenia
Various severe and pre-malignant/leukaemic bone marrow disorders

54
Q

Describe FeLV related neoplasia.

A

Most commonly lymphoma, leukaemia
Thymic lymphoma
FeLV lymphoma cats are often young, less prevalent due to vaccination

55
Q

What are the other FeLV associated diseases?

A 
Ocular signs (aniscoria)
Uncommon - reproductive failure, neurological signs, immune-mediated diseases, GI signs
56
Q

How do we diagnose FeLV?

A

Screening blood tests - ELISA for FeLV antigen (capsid protein p27)
Confirmed with immunofluorescent antibody/PCR

57
Q

Why might we get false negative FeLV results?

A

May take up to 1 month for FeLV Ag to be detectable
Maternal antibody not tested for, therefore less complicated than FIV in kittens
If suspicious, retest in 1-2 months

58
Q

What are the treatment options for FIV and FeLV?

A

Hydration, nutrition, management of manifestation of disease (antibiotics, dental hygiene etc.)
Antiviral drugs may help gingivostomatitis / neurological signs in FIV cats
Interferons (alpha, omega) may provide some limited benefit

59
Q

How do we manage FIV/FeLV cats at home?

A

Indoor only - prevent transmission, limit risk of opportunistic infections
Ideally separate positive and negative cats
No hunting / raw food
Regular health checks - body weight, oral health
Vaccinate against core diseases - only inactivated vaccines!

60
Q

How can we prevent FIV?

A

Inactivated vaccine, not fully protective

Not usually vaccinated for in this country

61
Q

How can we prevent FeLV?

A

Non-core vaccine, not 100% effective

Vaccinate outdoor cats, multi-cat households

62
Q

What is the prognosis for FIV+ cats?

A

Sick positive cats usually survive <1 year
Healthy positive vs negative cats do not have significant difference in survival time
Median survival 4-6 years post-diagnosis
More rapid deterioration to feline AIDS in kittens/geriatrics

63
Q

What is the prognosis for FeLV infected cats?

A

Regressive infection, usually leads to FeLV associated disease within 3-5 years
Survival time is less than half that of non-FeLV cats
Once sick (anaemias, neoplasia) prognosis/quality of life is usually poor

64
Q

Describe Feline Coronavirus (FCoV).

A

Faeco-orally transmitted virus
High prevalence of infection, low prevalence of clinical disease
Potential to mutate to Feline Peritonitis

65
Q

Describe FCoV infection.

A

Replicates in intestines, frequently without signs
1 week later, shed virus faecally (some cats become lifelong shedders)
Most cats are transiently infected, with phases of recurrent infection

66
Q

Is Feline Peritonitis Virus (FIPV) contagious?

A

Not usually considered to spread between cats.

67
Q

What is ‘wet’ FIP?

A

Up to 80% of cases
Development of effusions and associated clinical signs - abdominal (distension), pleural (tachy/dyspnoea), pericardial (right-sided heart failure)
Frequently jaundiced
Lethargy, inappetance, weight loss and pyrexia

68
Q

What is ‘ dry’ FIP?

A

Development of pyo/granulomatous lesions within multiple organs - dysfunction +/- organomegaly
(lymph nodes, brain, eyes, intestines, liver, kidneys)
No effusions - may develop over time
May be jaundiced
Lethargy, inappetence, weight loss and pyrexia
Often more chronic than ‘wet’

69
Q

How do we diagnose FCoV/FIP?

A

No perfect test for FIP, no test to distinguish FCoV from FIPV
Only testable difference is ability to infect macrophages/cause multi-systemic disease

70
Q

What is the signalment for FIP?

A

Young, purebred cats from multi-cat households
Can occur at any age but commonly <1 year old/peak at geriatric
Recent stressor may be identifiable (e.g. rehoming, vaccination, neutering)

71
Q

What might we find on examination of a FIP patient?

A 
Weight loss, poor body condition
Often jaundiced
\+/- effusions
\+/- ocular changes
\+/- neurological signs
\+/- palpably enlarged lymph nodes / liver / kidneys
72
Q

What might we see on haematology analysis of an FIP patient?

A

May be normal

Often lymphopenia / anaemia (non-regenerative)

73
Q

What might see on serum biochemistry of an FIP patient?

A

Increased globulin - hyperproteinaemia
Decreased albumin : globulin ratio (often < 0.4)
Increased bilirubin (+/- clinical icterus)

74
Q

How can we check for FIP using imaging?

A

Keep looking for fluid, may develop after fluid therapy
Abdominal ultrasound (effusion / lymphadenomegaly)
Thoracic ultrasound (pleural/pericardial effusion)
MRI (CNS) if neurological signs

75
Q

How can we analyse an effusion from an FIP patient?

A

Thick, yellow, proteinaceous exudate
Increased protein, due to increased globulin
Moderate cellularity (often neutrophils, macrophages)

76
Q

What further FIP effusion fluid tests can we run?

A

FCoV reverse transcriptase polymerase chain reaction (RT-PCR) - looking for FCoV nucleic acid in effusions
Immunocytochemistry - use of fluorescent labelled probes to demonstrate FCoV within macrophages (FIP)

77
Q

How can we test an FIP patient if they are not ‘wet’?

A

Wait and see if effusion develops OR
Sample grossly abnormal (pyo/granulomatous lesions) organs
Immunohistochemistry (same principle as immunocytochemistry)
These are usually used for post-mortem diagnosis

78
Q

Is FIP treatable, and if so, how?

A

FIP is uniformly fatal - aims to improve quality of life, but most cats warrant euthanasia within weeks of diagnosis
Prednisolone may palliate signs transiently in mild cases
Dry cases may survive slightly longer
Various therapies trialled without convincing success

79
Q

How does FIP immunity work?

A

Cell-mediated immunity required for protection
Kittens born with maternally derived antibody, wanes after 6 weeks then become infected from mum/environment
Immunity to FCoV is short-lasting

80
Q

How can we manage a FCoV-contaminated environment?

A

May survive a few days in environment, up to 7 weeks in faeces
Susceptible to most disinfectants, including bleach (1:32)

81
Q

Describe post-FIP infection management of a household.

A

If cat dies of FIP - inform breeder
Single-cat household = wait 2 months before acquiring another cat
Multi-cat household = reduce stress/overcrowding, ensure cleanliness

82
Q

What additional considerations should breeders have concerning FIP?

A

Queens should kitten away from other cats
Avoid repeat mating that have resulted in multiple FIP kittens - breed/lineage susceptibility demonstrated
FIP case within breeding household = quarantine, avoid breeding (6 months)

83
Q

What preventative strategies can we have for FIP?

A

Minimise stress - temporally separate major events, avoid introducing new cats to household
Aim for single/small-group cat households to avoid overcrowding
Hygiene - FCoVs are spread faecally!

84
Q

Define definitive host.

A

The host in which parasitic sexual maturity and reproduction occurs

85
Q

Define intermediate host.

A

The host in which one (or more) stage(s) of parasitic development occurs

86
Q

Define transport host.

A

A host in which the parasite may survive but no parasitic development occurs. This host may be a vector/vehicle for transmission to other hosts

87
Q

Describe how Toxoplasma gondii acts within the definitive host (cats).

A

Typically infected during hunting (ingestion of bradyzoites in prey tissues)
Within intestinal epithelial cells
Schizogony (asexual reproduction) - merozoites, transform - macro- (female) and micro- (male) gametes - sexual reproduction - zygote
Zygote shed faecally as unsporulated oocyst

88
Q

Describe how Toxoplasma gondii acts within the intermediate host.

A

Sporulated oocyst/tissue bradyzoite (raw meat) ingestion
Release sporozoites into intestinal tract, penetration = systemic spread (blood, lymph)
Can infect most types of mammalian cell - rapid asexual reproduction (tachyzoites) within cells, production of bradyzoites, may persist indefinitely (may be reactivated at times of stress/pregnancy/immunosuppression)
Particular sites of replication include CNS, skeletal muscle, organs

89
Q

What are the risk factors for T. gondii exposure?

A

Outdoor lifestyle - faecal ingestion, hunting

Age (increased opportunity for exposure)

90
Q

What are the clinical signs of T. gondii infection?

A 
Non-specific, lethargy, anorexia
Ocular - uveitis, chorioretinitis
Neurological - CNS signs, neuromuscular disease
Hepatic, pancreatic
Pulmonary, dyspnoea
Rarely GI signs
91
Q

How can we diagnose T. gondii infection?

A

Serum biochemistry may indicate organ involvement, e.g. hepatic/muscle enzymes
Thoracic radiographs - pulmonary parenchymal disease
Faecal oocysts NOT helpful - do not indicate clinical disease
Look for response - use IgM > 1:64 for clinical disease, or demonstrate 4-fold rise in IgG

92
Q

What do we see in serology of T. gondii infection?

A

IgG usually detectable by 3-4 weeks post-infection, commonly remain elevated for years
IgM usually elevated by 2-4 weeks post-infection, usually negative by 16 weeks post-infection

93
Q

How can we use cytology/histology to diagnose T. gondii infection?

A

Fluid analysis - CSF, aqueous humour, bronchoalveolar lavage, effusions
Parenchymal fine needle aspiration/biopsy
If found = diagnostic, if not found = does not exclude disease

94
Q

How do we treat T. gondii infection?

A

Clindamycin - 4 weeks, oesophageal stricture risk
Analgesia
Anti-inflammatories (prednisolone)
Nutritional/fluid support/anti-emetics

95
Q

What is the prognosis for T. gondii infection?

A 
Treatment suppresses replication, improves clinical signs, does not eliminate infection
Poor prognosis, esp if CNS, pulmonary or hepatic involvement
Concurrent disease (e.g. FIV/FeLV) or immunosuppression increases risk of poor outcome
Survivors may be left with residual dysfunction or full recovery
96
Q

How do humans catch T. gondii?

A

Ingestion of raw meat
Lambing - contact with infected sheep placentae/lambing discharges
Sporulated oocysts

97
Q

What are the three species of haemotropic mycoplasmas?

A

Mycoplasma haemofelis
Candidatus Mycoplasma haemominutum
Candidatus Mycoplsma turicensis

98
Q

How are haemoplasmas transmitted?

A 
??? Remains elusive
Iatrogenic (blood transfusions)
Various arthropod vectors, including fleas
Bite/fight wounds?
Vertical transmission?
99
Q

What are the risk factors for haemoplasma infection?

A

Outdoor access
Male
Non-pedigree
Young / FIV and/or FeLV positive

100
Q

Describe the pathogenesis of Mycoplasma haemofelis.

A

Incubation period 2 days - 1 month
Acute disease typically lasts ~2-4 weeks - rapid replication and removal by immune system
Survival (treatment or natural recovery) = recovery phase, complete removal or sub-clinical clearance of organism from blood

101
Q

What are the clinical signs of M. haemofelis anaemia?

A 
Non-specific, weak, lethargic, inappetant
Pallor, tachypnoea, possible icterus
Tachycardia, heart murmurs
\+/- splenomegaly
\+/- pyrexia
Pica
102
Q

What do we find on haematology with M. haemofelis infection?

A

Regenerative/pre-regenerative anaemia

+/- autoagglutination, antibodies on surface of RBCs

103
Q

How do we diagnose M. haemofelis infection?

A

PCR - blood sample (EDTA), species specific, good sensitivity and specificity

104
Q

Why can we not use blood smears to diagnose M. haemofelis infection?

A

Cyclic nature, haemoplasmas not always visible on RBCs
Haemoplasmas may ‘fall off’ ex vivo erythrocytes following collection
Many other features cannot be differentiated from haemoplasmas, e.g. Howell-Jolly-bodies

105
Q

How do we treat M. haemofelis infection?

A 
Doxycycline - 2 weeks
Clinical remission, may not eradicate organism
\+/- blood transfusions
(+/- prednisolone, uncommonly needed)
Usually respond within a few days

Veterinary Nursing (65 decks)

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