Virology 3 Flashcards
Rhabdoviridae shape and enveloped or non-enveloped
- bullet shaped virions
- enveloped virus
List 3 main genera of Rhabdoviridae and example of disease within
1) Lyssavirus - rabies, Australia bat Lyssavirus (epidemiology different from rabies but vaccination effective against)
2) Vesiculovirus - vesicular stomatitis virus
3) Ephemerovirus - bovine ephemeral fever
Rabies, family and genus what are the 3 generally host species
Family Rhabdoviridae Genus Lyssavirus 1) Dog rabies 2) Cattle rabies 3) Wildlife rabies
Rabies what animals at risk, incubation period, why?, main clinical sign
- All warm blooded animals at risk
- Variable incubation period: 14-90 days (years: depends on species, virus strain, site, inoculum)
○ Due to pathogenesis, strain of virus, species of animal, site of the bite -> children often bitten on the face - Change in mentation - aggressive or passive change
Rabies what are the 3 types in terms of clinical signs, what leads to and pathogenesis
1) Prodromal period: confused, disoriented
2) Furious rabies: increased aggressiveness hyper-excitable, roam long distance, bite inanimate objects
3) Dumb rabies: muscle weakness, inability to swallow (choke), salivation (hydrophobia) - mainly with livestock cattle rabies
- Invariably fatal
○ Terminally, seizures, coma, respiratory arrest and death within two weeks of onset of clinical signs
Pathogenesis…
- Transmission usually occurs through bites (although scratching and licking can transmit virus)
What are the steps in rabies movement within the host and results, when is post-exposure prophylaxis effective and what ultimately leads to death
1) Virus replicates in muscle cells
○ Binds to acetylcholine receptors
○ Before crosses the neuromuscular junction -> post-exposure prophylaxis is effective, once get into nerves DEAD
2) Very little virus replication in nerve cells
○ Virus infects peripheral nerve endings
○ Virus travels to CNS by retrograde axonal transport
- Variable incubation period (weeks – years) - Bites around face, deep bites = shorter incubation period
3) Virus travels to brain via spinal cord
○ Clinical signs reflect extent and site of neuronal damage by virus replication within neurones
○ Within CNS: infection of lymbic system
§ reduced cortical control of behaviour = Furious Rabies
○ Further spread within CNS (neocortex)
§ reduced CNS function = Dumb Rabies (death due to resp arrest)
How does Rabies infect other animals, the 2 important infectious cycles, where major issue and control
How get out and infect others
- Centrifugal spread in nerves – release from axon terminal
Infection of non-nervous tissue – Salivary glands -> transmission
1. Urban rabies in dogs (developing countries)
- >95% of human cases of rabies are from dog bites
○ Urban rabies in dogs: stray dog control and vaccination programs
- stray dog control and vaccination programs
2. Sylvatic rabies in wildlife (North America, Europe, Africa)
- Focus of public health in more developed countries
- More difficult where multiple species involved
○ Bat rabies in South American cattle (in cavers in N America)
○ Increased reporting of cases in USA (raccoon rabies)
- ONE VACCINATION PROTECTS AGAINST ALL RABIES WTIHIN DIFFERENT SPECIES
Rabies when does increase in cases occur, what does vaccine coverage need to reach to protect dog population, what is the most effective treatment and what is the issue with this treatment
- Incidence of rabies in people increases proportionately with the dog population density.
- Vaccination coverage needs to reach 60-80% of the dog population before significant reduction in human cases is seen.
- Parenteral vaccination is more effective than oral baits in protecting dogs against rabies.
- Accessibility to vaccine is not uniform for all dogs (~10% of dogs could be caught and vaccinated
What are the 2 ways to diagnosis, immune response and controls
Diagnosis
1) Post mortem diagnosis - immunofluorescence, Histological -> H and E stains looking for negri bodies
- Need to get the brain -> now at risk of rabies
2) Behavioural changes
Immune response…
- Protective immunity involves both humoral and CMI
- Immune hosts will clear virus from site of entry BEFORE virus enters the nervous system (post-exposure vaccination and RIG)
Control strategies for rabies and what depends on
Control
- Inactivated and attenuated vaccine available and effective
- Population control (desex and vaccinate) and vaccination
- Attenuated vaccine bait
- Requirements vary between countries depending on the species of reservoir hosts (fox, mongoose, dog…)
Vesicular stomatitis famile and genus, what is important about it, is it present in australia, clinical signs and athropods
Family Rhabdoviridae
Genus Vesiculovirus
- Clinically indistinguishable from FMD expect in HORSES AS WELL
- Exotic to Australia
- Vesicular lesions: (heal within 7-10 days)
Oral mucosa, teats, coronary band of cattle (XS salivation)
○ Snout and coronary bands of swine - Lesions of tongue of horses
- Spread by arthropod vectors
Bovine ephemeral fever family and genus, what spread by, where found, mortality and morbidity and when is mortality common
Family Rhabdoviridae
Genus Ephemerovirus
- Spread by Culicoides midges and Mosquitos
○ Outbreaks when conditions favour vector movement or movement of susceptible animals into an endemic area
○ In tropical regions, outbreaks occur after rainfall
○ In temperate regions, outbreaks in Summer
- High morbidity and low mortality -> high mortality involved with large animals (bull becoming recombinant -> myositis -> death)
Bovine ephemeral fever clinical signs, site of replication, incubation period and immune response
Clinical signs
- 3 day sickness -> get sick go down, get up and over it
- Sudden onset of fever and reduced milk yield
- Depression, lameness, recumbency
- Primary site of replication unknown -> local replication at site of the bite and then viremia
○ 4 – 7 day incubation
○ 3 – 4 day duration of viraemia associated with neutrophil fraction
Immune
- Neutrophilia: vasoactive amines cause increased permeability of serous membranes
- Neutralising antibodies by day 3 after clinical signs -> 3 day sickness
Diagnosis and control of Bovine ephemeral fever
- Solid immunity post infection (cases in unexposed animals)
○ if outbreak couple of years, the following year just the young animals - Diagnosis by clinical signs (majority of herd affected) - down and sick for 3 days
- Treatment with anti-inflammatories effective -> when the larger animals go down such as bulls as higher risk of mortality
- Inactivated vaccine available
National arbovirus monitoring program what is the main goal, what important for
- Monitors the distribution of economically important arboviruses:
- Important in proving to trade partners proof of disease free status of diseases especially Bluetongue (sheep not near vectors)
○ Infectious disease is a barrier to trade
National arbovirus monitoring program list 3 ways they monitor
1) Sentinel cattle herds (serology) -> regular bases bleed certain animals and test to see whether antibody positive
○ If seasonally happening on annual basis want to bleed the younger animals to know if the disease is present recently
2) Serological surveillance
3) Insect traps -> where are the vectors? Are they causing the disease in certain areas, which species?
National arbovirus monitoring program what are the 3 main viruses that are monitored, what lead to and vector
- Bluetongue virus (BTV) that causes bluetongue disease in sheep and other ruminant animals
- Culicoides brevitarsis
- NT, aren’t allowed to have sheep as vectors do come into the NT - Akabane virus that causes congenital abnormalities in ruminant animals
- Culicoides brevitarsis - bovine ephemeral virus that causes bovine ephemeral fever (BEF, or three-day sickness) in cattle and water buffalo.
- Culicoides and mosquitoes
Bunyaviridae what are the 2 main genus and the main disease within
Family Bunyaviridae Genus Bunyavirus Akabane Family Bunyaviridae Genus Hantavirus Haemorrhagic fever
Akabane how transmitted, what hosts and general transmission
- Arbovirus (Culicoides brevitarsis) of sheep and cattle
○ Most other Bunya viruses are mosquito borne - Vertical transmission: foetal death, abortion, hydrancephaly, arthrogryposis
Akabane family and genus and epidemiology
Family Bunyaviridae
Genus Bunyavirus
- Widespread throughout tropical and subtropical regions in Middle East, Asia, Australia and Africa
- Sporadic epidemics correspond with movement of vectors (or movement of susceptible animals into endemic areas)
- Disease is seen in cattle, sheep, goats and deer
Akabane Pathogenesis
- Previously unexposed dam is bitten by infected vector
- Virus crosses placenta from maternal circulation without producing other clinical signs in mother
- Severity of clinical signs in the foetus depends on stage of gestation when infected
- Primary foetal infection is an encephalomyelitis and polymyositis, curly leg
○ Severely affected foetuses die and are aborted or if infected early in gestation
- Survivors develop large cavitations in the cerebrum, hydrancephaly and neurogenic arthrogryposis
○ Torticollis, Kyphosis, Scoliosis
Why is Akabane hard to diagnose
○ don’t notice when pregnant just during calving -> cannot do acute and convalescent as occurred within the mother many months before
○ No virus circulating in the foetus once born -> cannot detect there -> HARD TO DIAGNOSE
Diagnosis and control of Akabane
- Diagnosis usually by gross pathological examination
○ Virus is difficult to isolate from foetus/newborn - caesarean - Inactivated vaccine available in Japan and Australia
○ Not cheap as not widely used
Hantaviruses transmission and hosts
- No arthropod vector established
- Unique among genera of Bunyaviridae
- Rodent hosts
○ Genus and possibly species specific - Transmission
○ Aerosolization of rodent excreta (urine) -> occurred quite a lot in the war
