Feline Infectious Disease Flashcards

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
What specific drugs can we use for FCV patients?
Recombinant feline interferon-omega (IFN-omega) - improves refractory stomatitis
26
How do we treat secondary bacterial infections in feline URT patients?
Ideally culture and sensitivity | Antibiotics - Doxycycline (C. felis and B. bronchiseptica) / Amoxycillin clavulanate
27
How can we manage FHV in the environment?
Survives 18hrs at room temperature | Inactivated by most disinfectants and drying
28
How do we manage FCV in the environment?
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)
29
How do we handle feline URT infection patients?
Isolation facilities Barrier nurse - single staff member, handle last, disposable gloves/apron/over-shoes Hygiene of hands and arms
30
What is the incubation period of Chlamydia felis?
2-5 days.
31
Describe the typical Chlamydia felis patient.
From a multi-cat household | Typically young cats (<1 year old)
32
What are the main clinical signs of Chlamydia felis?
Feline conjunctivitis (acute and chronic/recurrent) +/- upper respiratory signs Corneal ulceration rare
33
How do we diagnose Chlamydia felis?
PCR (conjunctival swabs)
34
How do we treat Chlamydia felis?
Oral doxycycline | For at least 4 weeks and at least 2 weeks beyond clinical resolution
35
Where is Bordetella bronchiseptica most prevalent and how do we treat the environment?
High density populations e.g. boarding kennels/catteries, shelters etc. Highly contagious Persists in environment for ~10 days Susceptible to most disinfectants
36
What is the incubation period of Bordetella bronchiseptica?
2-10 days.
37
What are the clinical signs of Bordetella bronchiseptica infection in cats?
Sneezing, mucoid/mucopurulent nasal discharge Harsh cough Kittens susceptible to bronchopneumonia
38
How do we diagnose Bordetella bronchiseptica in cats?
Bronchoalveolar lavage fluid Culture and sensitivity (may not grow readily) PCR
39
How do we treat Bordetella bronchiseptica in cats?
When required = doxycycline (1-4 weeks)
40
How is FIV transmitted?
Bite wounds (saliva) From mother -> 1/3rd of kittens Infected blood products Venereal rare
41
What does FeLV stand for>
41
What does FeLV stand for?
Feline Leukaemia Virus
42
How is FeLV transmitted?
``` Allogrooming, fomites (bowls) Prolonged oronasal salivary exposure Very frequently from mother -> kittens Infected blood products Venereal rare ```
43
What are the signalments for FIV?
Fighters Outdoor access Older, male More common in feral cats
44
What are the signalments for FeLV?
Close-contact cats Outdoor access Young (3 years median age) Entire
45
What are the three phases of FIV infection?
``` Acute phase (8-12 weeks) Asymptomatic phase (years - life) Terminal phase ```
46
How is FIV diagnosed?
Screening tests detect antibodies against FIV | Assuming no history of vaccination and > 6months old
47
What secondary infections can we see with FIV?
``` Chronic gingivostomatitis Opportunistic infections Atypical infections Neurological disease Neoplasia Myelosuppression ```
48
Why may we see a false negative result for FIV?
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
When else should we test for FIV?
Known exposure to FIV+ cat Before rehoming to multi-cat household/environment Blood donor screening Before vaccinating for FIV (available in some countries)
50
What are the three types of FeLV infection?
``` Abortive infection (strong immune response, immunity) Regressive infection (effective immune response) Progressive infection (inadequate immune response, established bone marrow infection) ```
51
What are the clinical manifestations of FeLV infection?
Anaemia/bone marrow disorders Immunosuppression Neoplasia Other
52
Describe FeLV associated immunosuppression.
Various infections - opportunistic Specific infections, e.g. upper respiratory, Mycoplasma haemofelis Impaired response to vaccinations
53
Describe FeLV anaemia/bone marrow disorders.
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
Describe FeLV related neoplasia.
Most commonly lymphoma, leukaemia Thymic lymphoma FeLV lymphoma cats are often young, less prevalent due to vaccination
55
What are the other FeLV associated diseases?
``` Ocular signs (aniscoria) Uncommon - reproductive failure, neurological signs, immune-mediated diseases, GI signs ```
56
How do we diagnose FeLV?
Screening blood tests - ELISA for FeLV antigen (capsid protein p27) Confirmed with immunofluorescent antibody/PCR
57
Why might we get false negative FeLV results?
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
What are the treatment options for FIV and FeLV?
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
How do we manage FIV/FeLV cats at home?
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
How can we prevent FIV?
Inactivated vaccine, not fully protective | Not usually vaccinated for in this country
61
How can we prevent FeLV?
Non-core vaccine, not 100% effective | Vaccinate outdoor cats, multi-cat households
62
What is the prognosis for FIV+ cats?
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
What is the prognosis for FeLV infected cats?
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
Describe Feline Coronavirus (FCoV).
Faeco-orally transmitted virus High prevalence of infection, low prevalence of clinical disease Potential to mutate to Feline Peritonitis
65
Describe FCoV infection.
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
Is Feline Peritonitis Virus (FIPV) contagious?
Not usually considered to spread between cats.
67
What is 'wet' FIP?
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
What is ' dry' FIP?
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
How do we diagnose FCoV/FIP?
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
What is the signalment for FIP?
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
What might we find on examination of a FIP patient?
``` Weight loss, poor body condition Often jaundiced +/- effusions +/- ocular changes +/- neurological signs +/- palpably enlarged lymph nodes / liver / kidneys ```
72
What might we see on haematology analysis of an FIP patient?
May be normal | Often lymphopenia / anaemia (non-regenerative)
73
What might see on serum biochemistry of an FIP patient?
Increased globulin - hyperproteinaemia Decreased albumin : globulin ratio (often < 0.4) Increased bilirubin (+/- clinical icterus)
74
How can we check for FIP using imaging?
Keep looking for fluid, may develop after fluid therapy Abdominal ultrasound (effusion / lymphadenomegaly) Thoracic ultrasound (pleural/pericardial effusion) MRI (CNS) if neurological signs
75
How can we analyse an effusion from an FIP patient?
Thick, yellow, proteinaceous exudate Increased protein, due to increased globulin Moderate cellularity (often neutrophils, macrophages)
76
What further FIP effusion fluid tests can we run?
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
How can we test an FIP patient if they are not 'wet'?
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
Is FIP treatable, and if so, how?
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
How does FIP immunity work?
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
How can we manage a FCoV-contaminated environment?
May survive a few days in environment, up to 7 weeks in faeces Susceptible to most disinfectants, including bleach (1:32)
81
Describe post-FIP infection management of a household.
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
What additional considerations should breeders have concerning FIP?
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
What preventative strategies can we have for FIP?
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
Define definitive host.
The host in which parasitic sexual maturity and reproduction occurs
85
Define intermediate host.
The host in which one (or more) stage(s) of parasitic development occurs
86
Define transport host.
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
Describe how Toxoplasma gondii acts within the definitive host (cats).
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
Describe how Toxoplasma gondii acts within the intermediate host.
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
What are the risk factors for T. gondii exposure?
Outdoor lifestyle - faecal ingestion, hunting | Age (increased opportunity for exposure)
90
What are the clinical signs of T. gondii infection?
``` Non-specific, lethargy, anorexia Ocular - uveitis, chorioretinitis Neurological - CNS signs, neuromuscular disease Hepatic, pancreatic Pulmonary, dyspnoea Rarely GI signs ```
91
How can we diagnose T. gondii infection?
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
What do we see in serology of T. gondii infection?
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
How can we use cytology/histology to diagnose T. gondii infection?
Fluid analysis - CSF, aqueous humour, bronchoalveolar lavage, effusions Parenchymal fine needle aspiration/biopsy If found = diagnostic, if not found = does not exclude disease
94
How do we treat T. gondii infection?
Clindamycin - 4 weeks, oesophageal stricture risk Analgesia Anti-inflammatories (prednisolone) Nutritional/fluid support/anti-emetics
95
What is the prognosis for T. gondii infection?
``` 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
How do humans catch T. gondii?
Ingestion of raw meat Lambing - contact with infected sheep placentae/lambing discharges Sporulated oocysts
97
What are the three species of haemotropic mycoplasmas?
Mycoplasma haemofelis Candidatus Mycoplasma haemominutum Candidatus Mycoplsma turicensis
98
How are haemoplasmas transmitted?
``` ??? Remains elusive Iatrogenic (blood transfusions) Various arthropod vectors, including fleas Bite/fight wounds? Vertical transmission? ```
99
What are the risk factors for haemoplasma infection?
Outdoor access Male Non-pedigree Young / FIV and/or FeLV positive
100
Describe the pathogenesis of Mycoplasma haemofelis.
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
What are the clinical signs of M. haemofelis anaemia?
``` Non-specific, weak, lethargic, inappetant Pallor, tachypnoea, possible icterus Tachycardia, heart murmurs +/- splenomegaly +/- pyrexia Pica ```
102
What do we find on haematology with M. haemofelis infection?
Regenerative/pre-regenerative anaemia | +/- autoagglutination, antibodies on surface of RBCs
103
How do we diagnose M. haemofelis infection?
PCR - blood sample (EDTA), species specific, good sensitivity and specificity
104
Why can we not use blood smears to diagnose M. haemofelis infection?
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
How do we treat M. haemofelis infection?
``` Doxycycline - 2 weeks Clinical remission, may not eradicate organism +/- blood transfusions (+/- prednisolone, uncommonly needed) Usually respond within a few days ```