cats Flashcards

1
Q

aetiology of feline panleukopenia

A
  • Feline panleukopenia virus, non-enveloped single stranded DNA
  • Very stable, survives 1y at room temp on solid fomites. Only inactivated by bleach + 90oC for 10 mins. Similar to CPV
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2
Q

SOI of feline pan

A

infected animals/ contaminated fomites

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3
Q

MOT of panleuko

A

oronasal (in secretions + faeces). In utero

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4
Q

host suscetibility of pan

A

non-vaccinated, kittens most severe. Free roaming susceptible cats exposed within 1st y only shed for 1-2 d but up to 6w post recovery

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5
Q

pathogenesis of pan

A
  • PO  replicates in oropharynx  rapidly dividing cells in bone marrow, lymphoid tissue + GI epithelium + cerebellum + retina in v. young
  • Lymphoid tissue  cellular depletion  panleukopenia
  • GI  damages immature cells  malabsorptive diarrhoea
  • Destroys germinal epithelium of cerebellum in perinatal period  cerebella hypoplasia, tremors (feline ataxia syndrome)
  • Queens  early fetal death, mummified foetuses
  • Cerebellum damaged as it is in still developing in late gestation + neonatal period in cats
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6
Q

signs of pan

A
  • Subclinical (75% healthy have antibody titres) ‘fading kitten syndrome’, 3-5 m old, death in <12h
  • Acute = fever, depression, anorexia, biley vomit, maybe diarrhoea, extreme dehydration
  • Terminal = hypothermic, septic shock, DIC
  • Abdo palpation = thickened intestinal loops + enlarged mesenteric LN
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7
Q

diagnosis of pan

A
  • Signs in unvaccinated cat with leukopenia
  • ELISA for CPV faeces but false negative common
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8
Q

treatment of pan

A
  • Isolation, fluids, FFP, atb (ampicillin/cephalosporin), maropitant, food ASAP. Feline interferon (food for CPV, unknown for FPV)
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9
Q

differentials of pan

A
  • Salmonellosis, FeLV, FIV, concurrent infections = worse
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10
Q

prevention of pan

A
  • MLV vaccine at 6-9w + 16w then 26-52w then q3y
  • MLV not to pregnant, immunosuppressed or <4w old kittens (adjuvant inactivated vaccine available)
  • Vaccinate FeLV+, FIV+ only if high risk and with killed
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11
Q

prognosis of pan

A
  • Worse than CPV
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12
Q

Feline Upper Infectious Respiratory Tract Disease (URTD) =

A

FHV + FCV, chlamydia, bordetella

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13
Q

feline herpes

A

feline viral rhinotracheitis

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14
Q

aetiology of herpes

A
  • FHV type 1. Enveloped DNA
  • fragile outside host, survives 18h in damp environment, unstable in aerosol
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15
Q

SOI of herpes

A

infected/ sick + subclinical carriers

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16
Q

MOT of herpes

A

direct contact with carrier cat (shed intermittently), sneeze can travel 1-2m environemt + aerosol not normally SOI. Shed in ocular + oronasal secretion

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17
Q

HS of herpes

A

all Felidae animals. Recovered cats become lifelong carriers (in trigeminal ganglia) reactivated by stress – shed 1w after stress for 1-2w

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18
Q

micro herpes

A
  • Acidophilic intranuclear inclusion bodies in tongue, tonsils, trachea + nictitating membrane
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19
Q

signs of herpes

A

2-6d incubation + signs lasts 10-20days
- Depression, anorexia, fever, sneezing, conjunctivitis, lacrimation, oral ulceration
- Ulcerative keratitis, epiphora, blepharospasm
- Often 2ndary bacterial infection
- Osteolytic changes to nasal turbinates predisposes to bacterial infection
- Abortion

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20
Q

diagnosis of herpes

A
  • Signs FHV = conjunctiva + nasal passages most of effected
  • PCR of ocular/nasal secretions. Can be difficult because virus sheds intermittently + seroprevalence similar to Ill + clinically normal cats
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21
Q

treatment of herpes

A
  • ¬symptomatic + supportive
  • Atb if symptoms of 2ndary bacterial infection
  • Remove/wipe discharges, nebulisation of saline
  • palatable feed if anorexic
  • topical antiviral if herpetic keratitis. Lysine
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22
Q

prevention of herpes

A
  • core vaccine >9w old = 2x with 3w interval
  • adults = q1-3y
  • usually MLV, FHV + FCV with inactivated MLV FPV vaccine all together
  • asymptomatic carriers + recovered still need to be vaccinated
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23
Q

aetiology of chlamydia

A
  • Cp. Felis, C. psittaci
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24
Q

signs of chlamydia

A
  • ¬conjunctivitis, maybe sneezing, fever, acute-chronic, epithelial hyperplasia
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25
Q

diagnosis of chlamydia

A
  • PCR on conjunctival swab (dry), early in course can find organism in Giemsa stained smear
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26
Q

treatment of chlamydia

A
  • Atb- doxy for 4 weeks to ensure elimination of organism
  • Systemic atb better than topical local
  • Young = 4w therapy + clavulanic acid/amocillin
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27
Q

aetiology of calicivirus

A
  • feline calicivirus, small enveloped RNA virus
  • many strains with variable pathogenicity (all 1 serotype), more resistant than FHV1, survives for d-1 on dry surfaces at room temp
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28
Q

SOI of calicivirus

A

sick/carrier animal. Maybe contaminated environment. Shed continually

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29
Q

MOR of calicivurs

A

contact with sick cats

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30
Q

POE of calivirus

A

nasal, oral or conjunctival mm

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31
Q

HS of calivirus

A

carriers widespread 10% household pets + 25-75% of shelter cats

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32
Q

pathogenesis of calicivurs

A
  • Predilection for epithelium of oral epithelium + deep tissues of lungs
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33
Q

signs of calivirus

A
  • Salivation, ulceration of oral cavity (heal over 2-3w) maybe sneezing, conjunctivitis
  • Some strains = pulmonary oedema + interstitial pneumonia
  • 2 strains cause ‘limping syndrome’ with no ulcers or pneumonia – fever, alternating limp, pain on palpation, usually 8-12w + resolves on its own. Can occur in vaccinated
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34
Q

diagnosis of calicivirus

A
  • Clinically hard to differentiate from FHV-1 (more likely oval ulcerations in FCV)
  • RT-PCR of conjunctival/ oral swabs, blood interpret + result clinically as could be due to carrier state or vaccine
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35
Q

treatment of calivirus

A
  • Supportive + symptomatic, food-warm + palatable
36
Q

prevention of calicivurs

A
  • ¬core vaccine (MLV), combined with FHV-1 + feline panleukopenia
  • Recommended to vaccinate recovered as not protected for life (esp because of different strains)
37
Q

aetiology of bordetella

A
  • ¬Bordetella bronchiseptica, G- aerobic coccobacillus
38
Q

MOT of bordetella

A

aerosol (oronasal cavity)

39
Q

HS of bordetella

A

dogs, cats, swine, rodents.

40
Q

risk of bordetella

A

stress + pre-existing viral infection

41
Q

pathogenesis of bordetella

A
  • Unclear. Usually primary viral infecetion
  • Virulence factors to adhere to cilia of resp epithelium  cilicostasis  decrease mucus ciliary clearance + persistence of bacteria
  • Toxins  damage mucosa of trachea + bronchi  bronchitis
  • Sometimes lower resp tract affected  bronchopneumonia
42
Q

signs of bordetella

A
  • Sneezing, coughing, oculonasal discharge
  • Dyspnoea, cyanosis, death, cough less marked in cats, pneumonia in kittens <10w
43
Q

diagnosis of bordetella

A
  • Any coughin in cat should be suspicious of B. bronchiseptica
  • Bacterial culture or PCR (maybe commensal)
  • ID from BAL in cats = diagnostic
  • Isolation for atb susceptibility
  • Cytology of tracheal wash = polymorphonuclear leukocytes, macrophages + bacteria
44
Q

treatment of bordetella

A
  • ¬atb – tetracyclines if severe – supportive care, fluids, Oxygen etc
45
Q

prevention of bordetella

A
  • ¬non-core MLV vaccine 1x q/y. recommended for cats living in high density +/or high risk population with history of b.bronchiseptica
  • Cats receiving vaccine will shed bacteria – warn owners
  • Potentially zoonotic in immunocompromised
46
Q

incubation of FIA

47
Q

aetiology of FIA

A
  • ¬Mycoplasma haemofilis, candidatus mycoplasma haemominutum (in older cats) + Ca mycoplasma turicenesis bacteria that parasite RBC
48
Q

MOT of FIA

A

not completely understood. Blood transfers, fleas + ticks, vertical to kittens, fighting (in saliva + claw beds of infected cats)

49
Q

HS of FIA

A

male, outdoor intact cats most likely, association with retrovirus infections

50
Q

signs of FIA

A
  • Lethargy, decreased appetite, weight loss, intermittent fever, pallor, splenomegaly
  • Severe = increased HR + RR, bounding pulse
  • Haemolytic anaemia in ‘healthy’ cats – severe
  • Chronic asymptomatic carriers possible
  • Coombs test positive
51
Q

diagnosis of FIA

A
  • PCR of whole blood or spleen aspirates
  • Microscopy of blood smear – small, round, basophilic rods/rings on RBCs but parasitaemia can be cyclic and disappear from circulation in 2 hr
  • Cannot be grown in vitro culture
52
Q

treatment of FIA

A
  • Doxy 10mg/kg SID PO for 3 w
  • No need for glucocorticoids as antibodies appear due to haemolysis rather than medicating it
  • Maybe blood transfusion
  • Once controlled, protective immunity develops (not sure for how long or against other species)
53
Q

prevention of FIA

A
  • PCR screen donors, sterilised equipment, control fleas + ticks. Keep cats indoors
54
Q

zoonotic of FIA

A
  • Potentially in immunocompromised people exposed to lots of cats
55
Q

aetiology of FeLV

A
  • FeLV – retrovirus (enveloped, single-stranded RNA) lipid layer
  • Easily destroyed by soap, can survive outside of host if moist + at room temp
  • A-T subtypes. A = original + most infected with it, B= neoplastic, C= erythroid hypoplasia, T = tropism for T lymphocytes (immunodeficiency)
  • Exogenous is the causative agent for FeLV
    o Endogenous gamma-retroviruses (enFeLV, RD-114, ERV, DCs) (all cats have it, but it’s not the infective form)
56
Q

SOI of FeLV

A

FeLV viraemic cats (in saliva, faeces, milk nasal secretions)

57
Q

MOT of FeLV

A

oronasal contact, bite wounds (mutual grooming, shared equipment). In utero

58
Q

HS of FeLV

A

young = higher risk of progressive (more severe FeLV)

59
Q

types of FeLV

A
  1. Abortive infection
    - Replication in oropharyngeal lymphoid tissue stopped by immune response
    - No viraemia – best outcome
  2. Regressive infection
    - FeLV carried in monocytes + lymphocytes systemically but viraemia stopped just before (after bone marrow infection)
    - Transient symptoms (some affected precursor cells). Normal lifespan. Viral DNA dormant
  3. Progressive infection
    - Viraemia not stopped so extensive replication in lymphoid tissue + bone marrow etc
    - Persistent viraemia + disease development
  4. Atypical infection
    - Rare in natural conditions – persistent replication in 1 place eg mammary gland, eyes, bladder
60
Q

signs of FeLV

A
  • Non-regenerative normochromic anaemia, lymphoma, leukaemia, fading kitten syndrome, feline panleukopenia like syndrome, neuro problems (due to tumours compression) immune suppression: increased infection risk, immune mediated diseases, chronic gingivostomatitis
61
Q

diagnosis of FeLV

A
  • POC ELISA then confirm with lab test
  • PCR (but can’t know if pro or regressive
  • RT-PCR to know stage of disease
  • Cats with antigen + can clear viraemia. Retest healthy after 6+w. antigen detected 30d PI
62
Q

treatment of FeLV

A
  • No cure – supportive therapy, good nutrition, antivirals?
63
Q

prognosis of FeLV

A
  • With disease usually survive 3 years, age at infection = important (older = more resistant)
64
Q

manage of FeLV

A
  • Keep indoors, good hygiene. Routine vaccines + antiparasitic. Neuter animals, separate from others, semi annual check-ups. No raw food (parasites), vaccinate asymptomatic with inactivated vaccines (no benefit of FeLV one)
65
Q

prevention of FeLV

A
  • Lots of different vaccines – preferably recombinant at 8-9w old then 3-4w 1 after then q 2-3y
  • Vaccinate based on risk (chance of sarcoma from vaccines)
66
Q

FeLV test interpretation

A
  • PCR = detects proviral DNA (Could be dormant, regressive stage)
  • RT-PCR = detects viral RNA (means virus is there so progressive stage)

LOOK AT TABLE

67
Q

aetiology of FIV

A
  • FIV – lentivirus from the retroviridae family
  • 5 subtypes or clades (designated A to E) (A+B most common)
  • Only survives mins outside host + susceptible to all disinfectants and soap
68
Q

MOT of FIV

A

biting (in saliva) + blood

69
Q

HS of FIV

A

older, free roaming, intact male cats (increased fighting tendencies)

70
Q

transmission FIV

A

to kittens depend on viral load in queen during pregnancy + birth if queen asymptomatic: kittens okay queen has clinical signs: 70% infected

71
Q

pathogenesis of FIV

A
  • viremia peak at 8-12 weeks PI then decreases in viral load  asymptomatic phase that can last years/lifelong virus targets lymphocytes  gradual loss of CD4+ T lymphocytes  widespread immunodeficiency
72
Q

signs of FIV

A
  • acquired immunodeficiency syndrome (AIDS)– related complex (ARC)
  • transient fever, lymphadenopathy + neutropenia lasting d-w. then asymptomatic for years
  • acquired immunodeficiency leads to chronic secondary/opportunistic infections of resp, GI (mouth), urinary tract + skin
  • immune mediated disease – chronic gingivostomatitis, rhinitis, weight loss etc
  • increase incidence of FeLV neg lymphoma of B type
73
Q

diagnosis of FIV

A
  • western blot = gold standard
  • POC ELISA or immunochromatography but in low prevalence population, positive POC should be confirmed by western blot
  • PCR but serology better
74
Q

treatment of FIV

A
  • Supportive according to clinical signs
  • Antivirals, AZT, subcut feline interferon, PO human interferon
75
Q

management of FIV

A
  • Testing, decrease aggression/stress, keep indoors/decrease outdoor access, periodic check up
  • vaccination – questionable result - not registered in Europe
76
Q

aetiology of FIP

A
  • feline coronavirus, large enveloped single strand RNA. High rats of mutation – injected cats shed ‘mutant cloud’. Serotype 1= cats, serotype 2= recombinant with CCoV.
  • FCoV mutates to FIPV in cats
77
Q

MOT of FIP

A

feco-oral or fomites. Queens to kittens (FCoV), Shed in faeces for w/m  life, stress increase shed

78
Q

HS of FIP

A

domestic + wild cats (cheetahs, bobcats)

79
Q

Risks of FIP

A

= <2y or 10y+, multicat households, male, purebred (Bengal ,ragdoll, rex), stress

80
Q

pathogenesis of FIP

A
  • FeCoV infection – resistant, transient, persistent or FIP mutation
  • Primary replication in mature SI epithelial cells  persistent in cells  shedding
  • FeCoV mutates to FPV – tropism changes from enterocytes to monocyte/macrophage
  • Monocytes attach to endothelium  extravasation  differentiate to macrophages  plasma leak
  • Acute = lots of vessels damaged  (wet) effusion
  • Chronic = less vessels damage but pyogranulomatous inflam (Dry)
81
Q

signs of FIP

A
  • FeCoV = mild self-limiting, vomiting/diarrhoea. Subclinical
  • FIP = insidious onset + progressive, wet or dry form
  • Wet = most common, vasculopathy – ascites, pleural effusion, increased HR + RR, muffled heart, blue mm, icterus, Lymphadenomegaly, lameness
  • Dry = granuloma formation, anterior uveitis, neuro signs, vomiting, diarrhoea, palpable abdo masses, granulomatous pneumonia, necrotising dermal phlebitis or vasculitis
82
Q

PM of FIP

A
  • Perivascular pyogranulomatous lesions on serosal surfaces
83
Q

diagnosis of FIP

A
  • ¬AM = difficult, PM = definitive – histo path to detect intracellular FeCoV antigen with immunohistochem test effusion. Rivalta test, US, X-ray, RT-PCR but false + can occur
  • Very difficult to diagnose FIP especially dry form
84
Q

differentials of FIP

A
  • septic peritonitis, retroviruses, lymphoma, pyothorax, CHF
85
Q

treatment of FIP

A
  • ¬supportive – drain fluid, steroids, antivirals, interferons
86
Q

prevention of FIP

A
  • Good hygiene, decrease stress, enough litter trays, only introduce new animals to FeCoV seronegative cats
  • No vaccine as causes antibody dependent increases infection