Viral diseases of the lymphoid system Flashcards
Immunosuppressed vs immunocompromised vs immunodeficient
immunocompromised = any aspect of host defences is deficient
immunosuppressed = immune defences are specifically impaired
immunodeficient = body’s immune response is compromised or absent
Specific (immune) host defences
- PMNs (polymorphonuclear leukocytes) – phagocytosis
- Cell-medicated immunity (monocytes/macrophages, T-lymphocytes)
- Humoral immunity (B-lymphocytes)
- Complement cascade
Non-specific (immune) host defences
- e.g. integument
Interaction of a virus with a cell
Productive
-> lytic infection
-> persistent infection
Non-productive
-> latent infection
-> oncogenic transformation
-> viral destruction
How does a virus enter a cell?
- Utilisation of naturally occurring and useful receptors on the cell surface
- Endocytosis: both enveloped and non- enveloped viruses
- Direct injection (bacteriophages)
- Fusion of the envelope (some enveloped viruses)
Canine distemper
- type of virus
- survival in the environment
- which cells in infects
- route of infection
- spread of infection in the animal
- Morbillivirus related to Measles
- RNA enveloped virus
- poor survival in the environment
- particular tropism for lymphocytes (causes their destruction
- oro-nasal infection (inhalation of aerosol)
- replication in local lymphoid tissue -> macrophages -> dissemination to local LN -> spread to other haemopoieitc organs ( spleen, bone marrow, etc)
Canine parvovirus 2 & Feline panleukopaenia virus (CPV & FPV)
- type of virus
- which cells in infects
- spread of infection in the animal
- non-enveloped DNA virus
- tropism for fast dividing cells (GIT crypts, bone marrow, lymphoid tissue)
- destruction of WBC precursors within bone marrow, sequestration of neutrophils within GIT, damage to barrier leading to bacterial translocation
Feline leukaemia virus (FeLV)
- type of virus
- survival in the environment
- which cells in infects
- route of infection
- prevalence
- risk factors
- subtypes
- retrovirus
- RNA virus
- worldwide distribution
- 4 subtypes: A, B, C, T (all closely related antigenically)
- exogenous as well as endogenous FeLV (incorporated into DNA long time ago)
- transmission through mutual grooming, rarely through bites -> can be transmitted by any secretions
- risk factors: young age, increased population density, poor hygiene
- in many areas low prevalence due to testing and vaccination
- vertical transmission, transplacental transmission & horizontal transmission
FeLV pathogenesis
Mouth and nose contact with virus-containing saliva (or litter trays, bowls, bite wounds, mutual grooming)
-> replication in the draining LN
-> lymphoid tissue -> peripheral blood, leukocytes
OR -> bone marrow -> peripheral blood, leukocytes, platelets
-> epithelial cells
-> saliva, nasal secretion, urine
FeLV pathophysiology
- Each cat can present differently
- Much more severe and less selective than FIV (lymphopenia, neutropenia,
impaired neutrophil function, loss of CD4+ and CD8+ cells). - Anaemia: regenerative (usually through secondary causes e.g.
Mycoplasma haemofelis or immune-mediated destruction) or non-
regenerative (direct effect of the virus on bone marrow). - Neoplasia (lymphoma and leukaemia) though these days uncommonly
associated
Feline immunodeficiency virus (FIV)
- type of virus
- route of infection/transmission
- prevalence
- subtypes
- Retrovirus, RNA virus, Lentivirus genus
– closely related to HIV but humans aren’t susceptible to this virus - 5 genetically distinct subtypes (important for PCR testing)
- seroprevalence highly variable between regions (1-14% in cats with no clinical signs and up to 44% in sick cats
- Transmission via deep wounds inoculation with saliva.
- Transmission in stable households -> uncommon
- Kittens born to persistently infected queens-rarely infected but antibodies may be present
FIV pathophysiology
- Infects CD4+ T lymphocytes ( T helper cells) which are crucial for humoral and cell-medicated immunity.
- Invades dendritic cells, macrophages and CD4+ T-cells – can be detected in circulation, slow increase in viral particles and proviral DNA up to 12 weeks (clinical signs related to initial infection).
- Seroconversion within 2-4 weeks
- Decrease in viral load –> entering asymptomatic phase.
- Latency –> protection from immune system.
- Functional immunodeficiency through decline of CD4+ cells leading to AIDS-like deterioration.
- Late in the disease, antibodies level may decline and animal may test
negative
FIV - cats at risk
- un-neutered
- old
- male
- stray (free-ranging)
What behaviour is FIV related to?
- aggressive behaviour
Feline infectious peritonitis (FIP)
- type of virus
- what is is / develops from
- Enveloped RNA virus
- FCoV = enteric virus, ubiquitous in feline population
- only small proportion of cats will develop FIP, biphasic peak (weaning then >10y/o)
- mutation that allows the virus to infect monocytes (-> macrophages)
2 forms of FIP
Effusive (wet FIP)
- any body cavity including pleural and pericardial cavities, as well as abdominal cavity
Non-effusive (dry FIP)
- usually ocular and neurological presentation
But consider it a continuum (a spectrum) from non- effusive to effusive form
Effusion is not related to peritonitis, it is multi systemic inflammatory vasculitis (pyogranulomatous vasculitis)
FIP pathophysiology
Activated monocytes express cytokines and adhesion molecules which facilitate interactions with small-medium veins -> Endothelial barrier dysfunction -> Extravasation of monocytes -> Increased vascular permeability leading to effusions
What are produced by monocytes/macrophages and what do they do?
- IL-6 = stimulates hepatocytes to release AGP (acute phase glycoprotein)
- TNF-α = part of inflammatory response (lymphopaenia)
- IL-1 = pyrogenic, activates B and T cells
- Matrix metalloproteinases = increase ‘leakiness’ of the vessels
