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LCB2 > Viral diseases of lymphoid system > Flashcards

Viral diseases of lymphoid system Flashcards

1
Q

What are the main mechanisms by which feline leukaemia virus causes disease?

A

Immunosuppression, neoplasia, anaemia

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2
Q

What are the main mechanisms by which feline immunodeficiency virus (FIV) causes disease?

A

Immunosuppression, neoplasia, anaemia

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3
Q

What are the main mechanisms by which equine infectious anaemia causes disease?

A

Immunecomplexes

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4
Q

What are the main mechanisms by which infectious bursal disease virus causes disease?

A

Immunosuppression

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5
Q

What are the main mechanisms by which aleutian disease virus causes disease?

A

Immune complexes

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6
Q

What are the main mechanisms by which malignant catarrhal fever causes disease?

A

Hyperimmune disease

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7
Q

Give examples of apharetoviruses that cause immune disease

A
  • Avian luekosis

- Rous sarcoma

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8
Q

What genus does Jaagsiekte sheep retrovirus belong to?

A

Betaretrovirus

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9
Q

What genus does feline leukaemia virus belong to?

A

Gammaretrovirus

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10
Q

What genus does bovine leukaemia virus belong to?

A

Deltaretrovirus

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11
Q

What genus do fish tumour viruses belong to?

A

Epsilonretroviruses

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12
Q

List lentiviruses that affect the immune system

A
  • Human immunodeficiency virus
  • Feline immunodeficiency virus
  • Equine infectious anaemia virus
  • Caprine arthritis-encephalitis virus
  • Maedi-Visna virus
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13
Q

Identify the notifiable retroviruses that affect the immune system

A
  • Bovine leukaemia virus

- Equine infectious anaemia virus

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14
Q

Outline how cats can become persistently infected with feline leukaemia virus

A
  • Most will clear virus and recover, some do not
  • PI cats are usually younger and mount less robust immune response, realistically die within 1-2 years
  • More at risk if born to unvaccinated dams
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15
Q

Describe the clinical signs of feline leukaemia virus

A
  • Leukaemia
  • Lymphoma
  • Anaemia
  • Immunosuppression
  • Enteritis
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16
Q

Explain the viral migration of feline leukaemia virus

A
  • Oronasal infection
  • Infects lymphocytes in oropharynx, then to local LNs-
  • Virus infects local LNs, travels to bone marrow and other lymphoid tissues, then to mucosal tissues
  • Incubation period 3-6 weeks until virus found in blood and excreted in saliva
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17
Q

In a cat infected with FeLV, the Ag, viral culture and PCR are all negative. What stage is the cat at regarding the viral migration and describe this stage

A
  • Has invaded local lymphoid tissue, but not invaded bone marrow yet
  • Inapparent, local infection
  • “Abortive infection”
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18
Q

In a cat infected with FeLV, the Ag is -ve, viral culture -ve and PCR +ve. What stage is the cat at regarding the viral migration and describe this stage

A
  • Has invaded the bone marrow but not the mucosal tissue yet
  • May be hard to find on PCR
  • Latent infection aka “regressive infection”
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19
Q

In a cat infected with FeLV, the Ag is +ve (may also be -ve), viral culture -ve and PCR+ve (may also be -ve). What stage is the cat at regarding the viral migration and describe this stage

A
  • Has left bone marrow and invaded mucosal tissue, leading to focal infection
  • Transient viraemia, “regressive infection”
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20
Q

In a cat infected with FeLV, the Ag, viral culture and PCR are all positive. What stage is the cat at regarding the viral migration and describe this stage

A
  • Virus is shed
  • Persistent viraemia, progressive infection
  • Do not develop a proper antibody response
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21
Q

Explain the pathogenesis of equine infectious anaemia virus

A
  • Immune complex formation
  • Complement activation leads to anaemia, thrombocytopaenia, pyrexia
  • Episodic pyrexia/illness associated with emergence of viral variants
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22
Q

Explain the pathogenesis of Aleutian disease of mink

A
  • Parvo
  • Viral antibody complexes formed but not eliminated
  • Leads to immune complex disease
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23
Q

List the viral infection associated with disorders of haematopoiesis

A
  • Feline leukaemia virus

- Lentiviruses (FIV, EIA, BIV)

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24
Q

Outline the prevalence of FeLV

A
  • Variable

- Decreased due to vaccination and test/removal schemes

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25
Q

Explain the pathogenesis of FeLV

A

Immunosuppression probably due to virus replication in cell progenitors in BM

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26
Q

What are the different subtypes of FeLV and how are these classified?

A

A, B, C and T, classified based on viral envelope protein sequence

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27
Q

Describe FeLV A

A

Isolated in all infected animals

28
Q

Describe FeLV B (development and consequences)

A
  • Arises due to homologous recombination between A envelope and endogenous FeLV related DNA
  • Increases rate of tumour formation
29
Q

Describe FeLV C (development and consequences)

A
  • Arises, rarely, de novo due to point mutations in the envelope
  • Causes severe rapid fatal aplastic anaemia
  • All blood cells fall in the animal affected
30
Q

Describe FeLV T

A
  • Targets T lymphocytes

- Causes severe immunosuppression

31
Q

Describe the transmission of FeLV

A
  • Close contact required (labile in environment)
  • Transmitted by milk, saliva of dam, transplacental infection
  • Transplacental usually die in uterua
  • Response to infection determines PI or not
32
Q

Outline the diagnosis of FeLV

A
  • Aim to identify persistently viraemic cats
  • NO antibody to virus so detect antigen
  • Can use in house ELISA
  • Confirm positive results wih virus isolation or immunofluorescence
  • qPCR
33
Q

Discuss the interpretation of the ELISA of FeLV

A
  • Negative results reliable, NPV >99% (but still consider clinical signs and retest if no other cause found after 12 weeks)
  • Positive results may be false (PPV 70-90%)
  • All positive results should be tested by virus isolation or immunofluorescence
34
Q

What may cause false positives when testing for FeLV?

A
  • Blood haemolysis
  • Incorrect test use-
  • Antigen cross reaction
35
Q

How is FeLV definitively confirmed?

A
  • qPCR
  • Detects provirus in circulating WBCs, not viraemia
  • NPV very high, but need to consider viral load
36
Q

Outline the control and management of FeLV

A
  • Correct diagnosis of PI cats
  • Test and removal
  • Symptomatic and supportive treatment
  • Impact on chemotherapy of cancers
  • Vaccination of at risk cats
37
Q

Explain how Lentiviruses evade the host immune responses

A
  • Virus accessory genes

- Decrease MHC expression so less lymphocyte recognition of infected cells

38
Q

Describe the pathogenesis of Lentiviruses

A
  • Persist via cycles of cell killing, viral release and re-infection (waves of disease - high viral load early, then drops as immune response mounted, then rises once immune response depleted)
  • Cell destruction leads to disease
  • Infect macrophages/monocytes +/- lymphocytes
  • No chance of recovery following infection
39
Q

Describe the immunopathogenesis of FIV

A
  • Infection of CD4 Th lymphocytes
  • Decreased CD4 cell count
  • Marked lymphadenopathy
  • Virus also targets CD8 T cells, B cells, macrophages and glial cells
  • Lymphoid tissues of intestine may also be affected
  • Follicular destruction/dysplaisa seen in later stages of disease
40
Q

Describe the signs of FIV

A
  • Acute transient illness severel weeks after exposure
  • Long asymptomatic carrier state
  • Chronic disease with secondary infections e.g. respiratory, oronasal, enteric, urinary
  • Severe disease in terminal stages: anaemia, cachexia, diarrhoea, leukopaenia, opportubistic infections
  • Uveitis, gingivitis, CNS infection
41
Q

Describe the formation of tumours in FIV

A
  • Rare compared to FeLV
  • B cell lymphomas
  • Extranodal: gut, liver, spleen
42
Q

Which cats are more at risk of FIV?

A

Older male entire strays/free ranging cats

43
Q

Describe the transmission of FIV

A
  • Horizontal, mainly by biting
  • Rarely transplacental, may be associated with biting through umbilicus
  • Kittens born to infected dams receive MDAs which persist until 16 weeks of age
44
Q

Describe the prognosis for FIV

A

Longer than FeLV

45
Q

Describe the diagnosis of FIV

A
  • Detection of antiviral Ab using snap test/ELISA
  • Cats may be Ab negative up to 12 weeks post infection
  • Young kittens born to FIV + dams will have maternally derive antibody, wait or test with PCR based test
46
Q

Describe the control of FIV

A
  • Control feral cat population
  • Prevent transmission from known FIV positive cats (reduce fighting e.g. no new cats in household, but may entire through gum abrasions, allogrooming)
  • Vaccination not available in UK
47
Q

Outline the treatment of FIV

A
  • Palliative

- Dental care, antibiotics etc.

48
Q

Describe the transmission of equine infectious anaemia

A

Transmitted by biting insects e.g. horseflies

49
Q

Describe the clinical signs in the acute phase of equine infectious anaemia infection

A
  • Fever, diarrhoea, lethargy, restlessness, colic, rapid breathing, naal and ocular discharge, emaciation, oedema, paralysis of hindquarters
  • Anaemia
  • High levels circulating virus
50
Q

Describe the diagnosis of equine infectious anaemia virus

A
  • Confirm negative by Coggins test - agar gel immunodiffusion test detects antibody
  • Test plasma of all imported horses
51
Q

Outline the treatment and control of EIA

A
  • NO vaccines

- Poor treatment options

52
Q

Describe infectious bursal disease virus

A
  • Highly resistant and contagious
  • Affects 2-6 week old chicks
  • Tropism for lymphocytes in bursa and thymus
53
Q

Describe the clinical signs of infectious bursal disease

A
  • Watery diarrhoea
  • Cloacal inflammation
  • Secondary infection
  • Oedematous bursa
54
Q

Describe the histopathological appearance of a bursa affected by infectious bursal disease virus

A
  • Loss of lymphocytes leads to loss of purple rings of follicles
  • Cysts in chronic infection
55
Q

Explain the pathogenesis of infectious bursal disease

A
  • Tropism for lymphocytes

- Viral protein VP2 induces apoptosis of lymphocytes

56
Q

Outline the treatment of infectious bursal disease

A

No treatment

57
Q

Outline he control of infectious bursa disease

A
  • Emergency of very virulent (VV) strains makes control difficult
  • Difficult to eliminate
  • Attenuated or recombinant vaccines used with variable efficacy
  • Controlled by vaccination of breeding stock adngood biosecurity
58
Q

Describe the pathology and signs of Aleutian mink disease

A
  • Glomerulonephritis
  • Splenomegaly
  • Areritis
  • Ferrets: ascending paralysis
59
Q

Describe the clinical findings in malignant catarrhal fever

A
  • Single animals
  • Depressed, anorexic, mild drop, weight loss
  • Nasal and ocular discharges
  • Corneal oedema
  • Marked pyrexia (>41°C), sweating
  • Oral, nasal ulceration
  • Lymphadenopathy
60
Q

Outline the diagnosis of malignant catarrhal fever

A
  • Clinical signs highly suggestive

- Confirm by antiviral (OHV-2) Ab detection or PCR

61
Q

Outline the management of malignant catarrhal fever

A
  • No effective treatment
  • No vaccine
  • Avoid mixing sheep/cattle around lambing time
  • Management systems in zoo collections (Wildebeest are reservoirs)
62
Q

Outline the transmission of malignant catarrhal fever

A
  • Sheep (and Wildebeest) are natural hosts, not affected

- Cattle are dead end hosts

63
Q

Outline the effect of feline infectious peritonitis on the immune system

A

Immune complex formation

64
Q

Outline the effect of bovine viral diarrhoea on the immune system

A

Immunosuppression predisposes to respiratory disease complex in calf or calf diarrhoea

65
Q

Outline the effect of parvovirus on the immune system

A
  • Panleukopaenia: decrease white blood cell count

- Killing of lymphoid and myeloid stem cells

66
Q

Describe a logical testing protocol for a shelter to test for FeLV and FIV

A
  • Isolate/quarantine when arrive (although can carry FeLV and FIV for life so not useful for these diseases specifically)
  • Selective testing of at risk cats: stray, entire,
  • FIV positive cats: advise indoor lifestyle
  • FeLV positive on second test: do not rehome, poor prognosis

LCB2 (14 decks)

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