Virology Flashcards
Epidemiological virus classification
- Disease or syndrome they cause
- Physical properties of the virus- heat stability, pH stability, detergents/ ether
- Morphology of virion (EM)
- Sequence analysis of the viral genome
Enteroviruses, which virus families?
Acquired by ingestion (faecal-oral transmission) and replicate primarily in the rep tract
Parvoviridae, Reoviridae (genera rotavirus and reovirus), Coronaviridae (Alpha, Beta, etc.), and Adenoviridae (Canine Hepatitis)
Do cats get the flu?
Cats do not get the flu. Herpes, calicivirus, respiratory viruses
Respiratory viruses, which families?
Acquired by inhalation (resp transmission) or by fomites and replicate primarily in the respiratory tract. Examples_ Families Picornaviridae (genus Rhinovirus), Caliciviridae, Paramyxoviridae, Orthomyxoviridae, Adenoviridae
Arboviruses
Arthropod bourne virus. Replicate in their haematophagous arthropod hosts and transmissted to vertebrate host by biting. e.g. Families Togaviridae (equine encephal. EEE WEE VEE), Flaviridae (WNV), Rhabdoviridae, Bunyaviridae (Akabane virus- most imp. in Aus), Reoviridae
Examples of specific genera: African swine fever virus, Blue tongue another example
Akabane Virus
Curly calf disease. Imp. in Aus. An Arbovirus. Affects sheep and cattle. Fetus would have been infected- stops the brain from developing- fluid filled granules.
Oncogenic Viruses
Virus that induce neoplasia. Specific genes. Rely on host having specific genes as well. Target specific tissues, become persistent, and evoke host cellular transformation (neoplasia). I.e. Families: Retroviridae, Hepadnaviridae, Papovaviridae (Bovine Papillomavirus, Equine Papillomavirus, etc), Adenoviridae, Herpesviridae.
Virus taxonomy
Type of nucleic acid (RNA virus- little mutations occur more quickly, but otherwise that not important), strategy of viral replication, morphology of the virion (enveloped or not enveloped), sequence analysis of the viral genome
Morphology of virion
Enveloped or not enveloped?
Virus replication
- Attach to surface of host cell
- Penetration
- Uncoating
- Transcription
- Translation of early viral proteins
- Replication of viral nucleic acid
- Transcription of late mRNA
- Translation of late viral proteins
- Assembly of progeny virions
- Release
Attachment
- Attach to surface of host cell
- Attach to cell protein (not specialized virus receptor protein)
- Sialic acid, heparan sulfate, B2 ephrin
- Neutralizing Ab prevents attachment
Penetration
- Metabolically active process- 3 ways:
Translocation by endocytosis for example
Transcription of early mRNA
Shuts down host cell machinery, takes over machinery, and transcripts their own RNA or DNA
Translation of early viral proteins
Produce their own transcriptase in order to produce their own DNA and RNA
Double stranded DNA
Have quite large genomes, all the material they need to take over the host cell and replicate themselves all packed up in there. i.e. Herpes viruses
Parvo
has to rely on cell and cell has to be actively dividing in order for parvo to work.
Transcription of LATE mRNA
Code for structural proteins. Proteins that build new progeny virions that get released into the environment
Assembly of progeny virions
Capsids are formed and nucleic acid enclosed to form the progeny nucleocapsids. A little production line
Release
Enveloped viruses- acquire envelope by budding through the plasma membrane, the cytoplasmic membrane or the nuclear membrane
OR
Non-enveloped viruses- accumulate in cytoplasm and are released when cell lyses
Antiviral chemotherapy
Viruses depend on host enzymes and metabolic pathways of host cell to replicate. Therefore, to interfere with virus replication is to interfere with host cell function. Therefore there is not a lot you can do. (caveat: you might put an animal on antibiotics if they were then prone to a secondary bacterial infection)
Nucleoside analogues
Nucleosides (A, T, C, G) are incorporated into replicating strands of DNA. Nucleoside analogues, when phosphorylated, can be substituted for nucleosides, which blocks DNA synthesis by the viral DNA polymerase. “What the hells that, I better stop”
Early ones- topical quite toxic
Later ones- Acyclovir
Acyclovir
Herpes virus encode their own thymidine kinase. Inactive prodrug- requires phosphorylation by thymidine kinase to become active. Cellular TK relatively inactive compared to herpes virus TK.
Anti-influenza agents
- Amatadine and Rimantadine
- Zanamivir and Oseltamivir
(Stockpiles, resistance, inappropriate use)
Amatadine and Rimatadine
HAVE TO TAKE BEFORE INFECTED. Anti-influenza agents- inhibit uncoating of virus during entry into cells, inhibit release of virus from infected cells.
Zanamivir and Oseltamivir
*Sialic acid analogues- IMPORTANT- Neuraminidase binds to Sialic acid … last thing it does before it leaves the cell.
COMPETE WITH sialic acid with the host. So you don’t get RELEASE. Stops release, not the replication. Buys the immune system time to get on top of it.
- Neuraminidase cleaves sialic acid residues to enable influenza virus release from infected cells
- Competes to bind to neuraminidase, inhibits virus release
Anti-retoviral agents
Reverse transcriptase inhibitors:
- Act on the RNA dependent DNA polymerase- Thymidine analogues e.g. Zidovudine, Retrovir
- Non-nucleoside analogues (inhibitors- binds into a hydrophobic pocket in the RT)
* protease inhibitors
* * more for human medicine
Game changer for HIV
Anti-retroviral and protease inhibitors
Pox viruses *Family Poxviridae
Complex envelope. Large. Tough outer protein. Last for a long time in the environment. Single molecule of ds DNA coding for >200 proteins- codes for most of the proteins required for own replication. Has almost everything it needs for replication
Two sub families
Chordopoxvirinae and Entomopoxvirinae (insects)
Typical pox lesion
Raised, redenned macule. Progresses to form a papule. Becomes a fluid filled vesicle. Ruptures to form a crater (pock). Scarring. (THINK OF SMALL POX VACCINE)
- also think of Jenner noting that milkers didn’t get small pox after getting exposed to cowpox
- *Avipox viruses- form pock lesions as well- some are zoonotic.
- *Scabby mouth- Orf- zoonotic
Pathogensis
Clinical signs referrable to skin lesions in localized disease, or organ damage to generalized disease (such as sheeppox).
Transmission and epi of pox viruses
Very resistant in the environment.
Infectious viruses survives for years in infected material.
Sheep pox for example.
Surviving animals are NOT long term carriers- what’s bad about that???–>
Duration of immunity < life span of recovered animal
Reinfection possible- (think of small pox and you would need to get it redone in 10 years)
* not fragile, silken envelope (exception to the rule)
Poxvirus transmission between animals
- Via abraded skin.
- Respiratory route by droplets.
- Mechanical transmission.
Orthopox virus examples
Smallpox, vaccinia virus, cowpox virus, monkeypox
- small pox was a major cause of human mortality. Eradicated in 1977 following comprehensive global vaccination programme.
- highest mortality was in infants- people survived but with bad scarring.
Cowpox virus
Vesicles form and break- creating erosions. Though it is called coxpox, it is really a rodent pox. Endemic in Europe and Russia- not in AUS. Rodent reservoir. See it mostly in cows- on teats. Why do we see them? No hair and people milk them. People get them on their hands. Often spread through the heard by the hands of the people. Outbreaks in large cats and domestic cats.
Monkeypox
Forest rodent host in Africa. Transmitted to primates and to people. Introduced to USA in Gambian rats imported as pets. Spread to local Prairie dog population and then into people. Led to ban on import of African rodents into the US. Incidence on the increase- perhaps because fewer people have been infected or vaccinated for small pox.
OR perhaps because people deforesting- come in contact with these rodent carriers for the first time.
Capripox
Sheeppox, Lumpy skin disease, and goat pox (most important pox viruses for vets)– economically and trade issues most important of all pox viruses
- Closely related viruses
- Indistinguishable by serological assays
- Endemic in SE Europe, Middle East, Africa and Asia
- Virus shed from skin lesions and nasal/ocular discharge
- Infection via skin abrasions or inhalation of aerosols
- Endemic: Generalized disease and mortality uncommon (some level of background immunity to protect you)
- we don’t import ruminants from these areas/ most of these countries also have FMD… serious economic downside to people who live in these areas**
- Infection via skin
Pathogenesis sheep pox, goat pox, lumpy skin disease
Replicates locally in skin, replicates in lungs following inhalation, spread to regional lymph nodes
Clinical signs of sheep pox, goat pox, lumpy skin disease
Incubation period ~ 1 week
- Fever, oedema of eyelids, conjunctivitis, and nasal discharge
- skin lesions (lung consolidation and haemorrhage)
Mortality of sheeppox, goatpox, lumpy skin disease
Up to 50% in indigenous breeds. Up to 100% in European breeds.
Avipox viruses- why are they good vaccine viruses?
Fowlpox virus and other avian pox viruses. Spread through abraded skin. Great vector. Why? Large amounts of genetic material. Inserting foreign virus protein in there. Good vaccine viruses
Mechanical transmission by mosquitoes
Aerosol transmission
Parapox
- Orf virus (scabby mouth, contagious ecthyma) (one example)
Orf (Scabby Mouth) Transmission
Parapox. Occurs worldwide
Contagious pustular dermatitis or contagious ecthyma
Transmission: via direct or indirect contact, infectious in scab for months.
Orf Pathogenesis
Epitheliotropic virus, proliferative wart like lesions. replicates in epidermal keratinocytes. Papular lesions progress to vesicles, pustules and then scabs. Lesions heal within 4 weeks (if no secondary bacterial infection)
Not lethal but can kill lambs because they can be on mouths and teats. So Mom’s won’t let lambs suckle or lambs dont want to suckle
Epidemiology of Orf
Transmission via abrasions, primarily a disease in young sheep, maintained if flocks by chronic carriers
Lesions on lips and muzzle (feet, genitalia, and teats)
Control
Virulent vaccination (if this disease gets under your skin, causes lesions- as it is zoonotic)
Sacrification of axilla of ewe prior to lambing
Myxomatosis
Poxvirus disease of rabbits, causes of benign fibromas in wild rabbits in America, severe generalized disease in european rabbits.
Infected rabbits become listless and febrile.
Death often within 48 hours.
Survivors develop subcutaneous gelatinous swellings
Mortality rate- 99% of wild rabbits infected with virulent field strain
** highly host specific myxoma virus, high mortality rate
* endemic by mid-1960s in Australia- don’t get complete kill of target species, they become more resistant, virus adapts to live in host instead of killing host.
How is myxoma virus spread?
Fleas and mosquitos
Family Asfaviridae
Complex ds DNA virus
Enveloped
Stable in environment over wide range of temperatures (4-20C) and wide range of pH
May persist for months in meat of infected pigs
** pork meat can be a problem and if it is fed back to pigs, transmission starts back up again
* Respiratory spread
Family Asfarviridae
Only infects pigs, African Swine Fever Virus
Single molecule of DNA coding for about 200 proteins
Carry own genes for transcription and replication
Infect only Suidae and soft ticks
No disease in African Suidae, up to 100% mortality in European breeds (fever and haemorrhage)– endemic– so warthogs no viremia, virus in various lymphoid tissues. But in juvenile warhogs- significant viremia- how the virus has sustained itself.
Virus grows in RE system, circulates with leukocytes and erythrocytes
** Animals are viraemic
Tick to tick transmission where? What percentage?
Southern Africa. 20-25%. Explain how it lives with ticks, warthogs, and european pigs (no longer need the tick host in european pigs)
African Swine Fever Virus- consequences
Die of extensive haemorrhages due to platelet damage and complement activation- haemorrhage in all organs, lymph nodes, resemble blood clots
- survivors may be normally or chronically ill- all that survive are carriers
- No neutralizing antibody produced
- No vaccine
- Risks of international spread- live pigs, pig meat, food scraps
Where is African Swine Virus
Africa, Russia, Georgia, Kazakstan
Recommendations from WHO how to control outbreak of African Swine Fever
- Disease free zones
- prohibit free roaming pigs and to confine pigs
- restrict movement of pig products (fresh pork meat and products) in infected zones and intermediate zones
Herpesviruses common characteristics
Larged ds DNA viruses
Enveloped
Labile in environment (fragile envelope)
- easily inactiavted by heat, detergents, pH, drying
Close or mucosal contact for transmission (droplet)
Lifelong latent infection
** keys!
- recrudescent: recurs with stress (think of cold sores)
Herpes affects? Sub families called?
Herpesviridae: mammals, birds, and reptiles
Alloherpesviridae: fish and frogs
Mallacoherpesviridae: oysters and abalone
Three sub families: alpha beta and gamma
Alphaherpesvirinae
Replicate rapidly, can jump species a bit, variable host range, destroy host cells, latent in neural and lymphoid tissue (can affect nerves)
Betaherpesvirinae
Replicate slowly, very limited host range, cytomegaly, latent in secretory & lymphoreticular tissue
Gammaherpesvirinae
Lymphotropic, infect T or B lymphocytes, narrow host range, some oncogenic
Shingles
Recrudescent chicken pox
Bovine herpesvirus 1 (infectious bovine rhinotracheitis virus)
Causes a variety of clinical disease
* rhinotracheitis (nasal discharge, hyperaemic nasal mucosa, dyspnoea, coughing, recover within 5-10 (latency, reactivation, recrudescence)– sometimes younger animals will die)
Vulvovaginitis (pustules in bulls, pustules on mucosa, virus shed in semen)
Balanoposthitis
Conjunctivitis
Abortion
Enteritis
Generalized disease of newborn calves
** in intensive situations mobidity approaches 100%
* resp. infection by aerosol route
Transmission of Bovine herpesvirus 1
Resp route with dissemination to distance sites by cell associated viraemia
Lesions associated with focal areas of epithelial necrosis and inflammatory response
Occurred worldwide, although some European countries have recently eradicated BHV1
** Vaccines- used with reasonable success to prevent respiratory disease. Can manage repro disease by working it out of the bulls
Bovine herpesvirus 2
- Mammillitis- Vesicular lesions on the teats
2. Generalized skin lesions. Nodules & necrosis of the superficial epidermis.
Bovine encephalitis virus
Causes a fatal meningoencephalitis in valves thought to be direct neural spread from nasopharynx via trigeminal nerve
EHV1
Most important viral cause of abortion in horses worldwide
Endemic in all horse populations
Causes resp. disease, abortion,** and neurological disease** (then other horses exposed when aborted foal comes out)
Infection via respiratory tract
Rapidly establishes systemic infection and cell associated viraemia
Infects endothelium of the microvasculature of the endometrium and arterioles of the CNS
** EHV 1 becomes systemic whereas EHV4 will stop as a resp disease
** important in horse industry– paying stallion fee and 10 months later no foal
EHV1 abortions
No premonitory signs
Usually late gestation
Most commonly a single abortion
Outbreaks occur when index case is poorly managed
Recommendations to minimize risk of EHV1 abortions: Preg mares be kept separate from other horses, small groups based on foaling date
(when you see a mare that has aborted, keep the other mares away- how many animals have been exposed? vet should ask. Keep preg mares separate from other horses. Keep mares in small groups based on foaling date.)
When is mare infectious? When should you breed her again?
Ascitic oedema fluid and focal necrosis of foetal liver common. Aborting mare is infectious for 1-2 days from repro tract. Latent infection. Breed again on first oestrus after foal heat.
Adenoviridae
Non-enveloped, resp. and gasterointero disease- so an envelope is not a good career move. Relatively stable in the environment, narrow host ranges, persistent infection common, four distinct genera: mastadenovirus (canine hepatitis virus 1&2), aviadenovirus (inclusion body hepatitis), atadenovirus, siadenovirus
Canine hepatitis virus
part of C3 vaccination. Systemic disease affecting foxes, dogs, wolves, skunks, and other canids. Transmission via ingestion of urine, faeces, or saliva from an infected animal
Infection through nasopharyngeal, oral and conjunctival route of entry. Virus infects tonsillar crypts- spreads to regional lymph nodes then to blood stream via thoracic duct.
Viraemia results in spread to urine, faeces, and saliva (infect other animals)
Infection of endothelial and parenchymal cells of many organs leads to haemorrhage and necrosis of liver, kidneys, spleens and lungs
Clinical recovery coincides with production of neutralising antibody (about 10 days after infection)
Animals tend not to survive
Canine hepatitis virus- 3 overlapping syndromes
- Peracute disease: pup found dead, often with short lived (3-4 hours) or no apparent illness
- Acute disease: may be fatal. Fever, vomiting, bloody diarrhoea, pettechial haemorrhanges of gums, pale mucous membranes
- mild or inapparent disease
What is the incubation period of canine hepatitis virus?
Incubation period of 4-9 days
What in the dog’s history is suggestive?
Fever, sudden collapse, and abdominal pain in young dogs is suggestive
What does infection of kidney lead to?
Viuria, which leads to infection of further susceptible dogs.
How long can recovered dogs shed virus in their urine?
6 months
What is a characteristic of convalescent dogs and dogs vaccinated?
Corneal oedema (blue eye). Usually resolves quickly. Caused by virus- Ab compleses in the small blood vessels of the ciliary body affecting fluid exchange across the cornea. CAV2 used in vaccine antigen– to get away from this side effect
Canine Adenovirus 2
CAV2 causes localized resp disease (part of kennel cough complex)
Bronchitis and bronchiolitis
No systemic infection
CAV2 provides complete homologous protection and cross protection against disease caused by CAV 1 without side effects
Equine adenovirus 1 and 2
Isolated worldwide
Isolated from young horses with and without respiratory disease
Equine adenovirus 2 isolated from lymph nodes and faeces with resp disease and diarrhoes
Mostly asymptomatic or mild disease associated with these viruses
Main problem with Adenovirus 1?
Arabian foals with genetically based primary severe combined immunodeficiency- they tend to die (complete absence of T and B lymphocytes). They don’t affect an immunocompetent horse drastically.
Papillomavirus
Cause papillomas (warts) Non-enveloped double stranded circular DNA viruses Divided into 16 genera on basis of host range, DNA sequence homology, genome organisation and biological properties
Main characteristics of papillomavirus
Resistant in the environment and resist solvents, disinfectants, low pH and high temperature
Lead to replication linked to growth and differentiation of stratified squamous epithelium of skin and some mucous membranes
May give rise to carcinomas usually with appropriate co-factors (i.e. toxic chemical from a plant)
Who is most likely affected with papillomavirus?
Young animals, usually regress in weeks, lesions are typically finger like projections. Cattle are more likely affected than other species (bovine papillomavirus). Older animals brought into an environment with papillomavirus, they can pick it up as well.
How is papillomavirus transmitted?
Fomite transfer, sexual transmission of venereal warts is likely, more common if housed than at pasture, infection widespread, often without clinical signs (they are zoonotic)
Equine papillomaviruses cause? Occur in who? Behaviour?
Cause aural plaques and cutaneous papillomas
generally occur around the muzzle of young horses
Regress 1-9 months
Equine sarcoid
Most common skin tumour of horses, mules, and donkeys
More common yuonger than 4 yo
Occur singly or in groups
Head, ventral abdomen and limbs affected most commonly
Locally aggressive
Do not metastasize (often come back if taken out)
Superficial ulceration and secondary trauma are common
Bovine papillomavirus is associated but the relationship is still undefined
Parvovirus common characteristics
Small non-enveloped ss DNA viruses, replicate in nucleus, require rapidly dividing cells (S-phase), Very stable in the environment, very resistant to detergents, drying, heat, solvents, pH changes, disinfectants (formalin is effective but carcinogenic, sodium hypochlorite- bleach- in practical you cant get enough concentration to disinfect (because it is rapidly broken down by organic matter), beta propiolactone, oxidising agents)
Panleukopaenia virus (parvo)
- cats of all ages susceptible
- primarily see disease in kittens as maternal antibodies wane
- Many infections are subclinical
- seasonal disease pattern (kitten season)
- Trans-placental infection in susceptible queens (don’t vaccinate a potentially pregnant queen with live virus)
- virus excretion in faeces (several weeks after clinical recovery), also in saliva, urine, and vomit (acute stages)
Incubation period for feline panleukaemia virus
5 days
Feline panleukaemia virus onset of disease and characteristics
associated with profound panleukopaenia and fever, severe cases die in peracute stage, acute stages progress to vomiting, bloody diarrhoea, dehydration.
Strong, long lasting immunity
What clinical manifestations occur with perinatal or in utero infection? (feline panleukopaenia virus)
Cerebellar hypoplasia/ atrophy
Route of transmission for feline panleukopaenia virus
Virus enters via oropharynx replicates in pharyngeal lymphoid tissue, distributed by free and cell associated viraemia, mitotically active cells (s- phase- DNA synthesis)- intestinal crypt cells, lymphopoietic cells of bone marrow, foetal cells- cerebellum, retina, death)
Prevention and treatment of feline panleukopaenia virus?
No specific tx, supportive therapy: fluid, blood/ plasma transfusion, broad spectrum antibiotics, vaccination- inactivated and live- virus vaccines available. catteries: strict hygiene, quarantine and disinfection required
(acute disease, does not linger for months)
Canine parvovirus 2
first described in 1978. Spread rapidly worldwide. High morbitity and mortality in initial outbreak (all ages). Now genetic variation (3)
Route of exposure canine parvovirus 2
Faeco-oral route of infection following exposure to virus contaminated faeces, primarily disease of young dogs 6 weeks- 6 months old.
Very stable virus in environment.
Disease may be mild or sub-clinical if sufficient immunity.
Haemorrhagic gastroenteritis and vomiting.
Myocarditis (uncommon)
Pathogenesis canine parvovirus 2
Rapidly dividing cells in intestinal crypts are infected, crypt cells are progenitors to entire intestinal mucosa, so mucusoal collapse with contraction and fusion with villi of SI.
Maldigestion and malabsorption and often severe haemorrhage (foetid smell)
Severely affected animals die
Pathogenesis canine parvovirus 2
Myocarditis in pups infected late gestation or first 2 weeks of age due to rapid proliferation of myocytes in the perinatal period
Myocardial inflammation and necrosis
Diagnosis canine parvovirus 2
Presumptive diagnosis- sudden onset of foul smelling haemorrhagic diarrhoea- parvo until proven otherwise
Faecal immunoassays
Haemagglutination
PCR assays
Prevention and treatment canine parvovirus 2
Supportive treatment, possibly antibiotics due to secondary infections. Prevention is the best, vaccines are extremely effective
What is the C3 vaccine?
Canine Distemper Virus (CDV), Canine Parvovirus Type 2 (CPV-2), Canine Adenovirus Type 2 (CAV-2- also prevents CAV-1, ICH)
Why do we need a booster? Why do we give multiple doses of infectious vaccines to puppies?
Maternal antibodies.
What is the duration of maternal antibodies?
You cannot predict
Porcine parvovirus
Important cause of repro failure in swine worldwide
Endemic in many herds
Morbidity reduced by vaccination
Virus stable in environment for months
Most significant if virus introduced into seronegative herd
Repro problems in young gilts in their first pregnancy
Clinical signs of porcine parvovirus
Clinical signs referable to reproductive failure
First clinical sign is often increased number young sows returning to oestrus 3-8 weeks after breeding
Some sows remain “endocrinologically pregnant” and don’t come back into oestrus until expected farrowing date
Clinical signs in foetus depend on stage of gestation- apparent at farrowing
Family circoviridae
Non enveloped, ss DNA, very stable in environment (resistant to heating at 60C, 30 minutes, resistant to disinfectants, stable at pH3-9), require actively dividing cells, persistent infections, psittacine beak and feather disease, chicken anaemia virus, porcine circovirus
Epidemiology and clinical signs psittacine break and feather disease
Cockatoos, parrots, budgeriars
Birds under 5 yo
Feather loss, pin feathers constricted, stunted,blood in shaft
Broken beaks- overgrown and shiney beaks, delaminations, palatine necrosis (deformed palate)
pathogenesis psittacine beak and feather disease
Virus replicates in basal epithelial layer of feather follicles, beak and claws
Poor prognosis in the wild because they can’t get around and can’t eat
Basophillic intracytoplasmic inclusions in follicular epithelium
Lymphoid depletion
Progressive disease
In care, these birds can live for months/ years if fed
Prevention and control psittacine beak and feather disease
PCR assays for diagnosis
Strict hygiene and quarantine protocols needed to keep infection out of breeding aviaries
Resistance in environment- better to get rid of cages and everything
vaccine only experimental
Porcine circovirus 2
Widespread, variety of clinical disease: post-weaning, weight loss and wasting, large lymph nodes
Chicken anaemia virus
Young birds develop aplastic anaemia and generalized lymphoid atrophy, atrophy of thymus, aplastic anaemia, unable to mount immune response, horizontal and vertical transmission, virus shed in faeces and feather dander
Family Reoviridae
Non-enveloped, spherical outline, 80 nm diameter, icosahedral, linear segmented ds RNA genome
Orbivirus (arboviruses)
Bluetongue, African horse sickness, equine encephalosis
Are arboviruses contagious?
No, infectious
Bluetongue
Disease of sheep, cattle, and goats in tropical or sub-tropical conditons.
Hyperaemia of oral and buccal cavities (salivation/ frothy mouth), nasal discharge, cyanosis of the tongue associated with congestion, hyperaemia of the coronary bands, oedema (head and neck), conjunctivitis
Clinical signs of blue tongue
Course of disease is variable from sub-clinical to death, mild cases recover quickly, severe cases have a protracted recovery (may lose part of fleece). Outbreaks about 30% mortality rate, ewes affected during pregnancy either abort or produce lambs with congenital abnormalities
Pathogenesis of bluetongue
Incubation period about 1 week- get infected and show signs
Arbovirus so gets into the animals through bite of culicoides midge
Replicates in regional lymphoid tissue, otehr lymphoid tissue, and endothelial cells
Viraemia lasts 14-28 days (cows up to 10 weeks)- associated with RBCs and leukocytes (cows reinfect culicoides)
How is bluetongue transmitted?
Culicoides spp. (midges)
Host’s immune status is important
How many different serotypes of Bluetongue virus, different virulence? Why is this important?
> 25 (immunity is serotype specific). What vaccine are you going to use?
About the vector of bluetongue
Females have a blood meal every 3-4 days, live as long as 70 days, virus replicates in vector and is shed in saliva (replication cycle that occurs in the culicoides), no transovarial transmission (no “over-winter”)
Control of bluetongue
Vaccination programmes, monitoring schemes: vector and host surveillance, in AUS we have blue tongue virus but not bluetongue disease (blue tongue free is mainly in the north- from papua new guinea)- low virulent bluetongue strains
Diagnosis of bluetongue
Presumptive (clinical signs and post mortem), isolation, PCR test of choice
African horse sickness
Disease of equidae (horses, mules, donkeys, zebras), 3 forms of febrile illness, nasal discharge progressing to resp distress and often 100% mortality. Really high fever 41C, sudden onset of clinical signs: increasing dyspnoea, rapid abdominal breathing, paroxysmal coughing (dry progressing to frothy discharge from nostrils), pulmonary oedema obvious on ausculatation, saw-horse stance, clasic colic signs, collapse and die within 4-24 hours. (unable to expand lungs because they are compressed with the oedema fluid)
2nd) conjunctivitis, swelling in head and neck, abdominal pain, progressive dyspnoea, subcutaneous oedema
3rd) mild or subclinical- usually associated with donkeys or zebras
NOT A CONTAGIOUS DISEASE
Pathogenesis of african horse sickness
9 serotypes, need to be immune to all 9 to be protected, incubation pd 1 week, replicates in regional lymphoid tissue, with secondary replication in other lymphoid tissues, heart, brain, lungs and endothelial cells
How is African horse sickness spread?
Culicoides
How do we control AHS?
We know the nature of the virus, the mode of transmission, the incubation period. There are vaccinations.
Togaviridae
Enveloped, ss, positive sense RNA virus. 70 nm diameter. In the insect host or in mammalian host. Not in the environment. Replicate in cytoplasm. Arboviruses are what are important in veterinary science.
Endemic cycle
vertebrate host and invertebrate host, no dramas until spillover into incidental host (aka dead end host)
Arboviruses
Tend to be seasonal- climate favours maximum vector numbers. (Late summer after heavy rainfall).
Eastern and Western Equine encephalitis
Maintained in cycles involving mosquito vector and passerine birds (ornithophilic mosquito- likes to bite birds)
Eastern and Western Equine encephalitis (EE, VEE, WEE)
Maintained in cycles involving mosquito vector and passerine birds (ornithophilic mosquito- likes to bite birds). 2 incubation periods. Inside the bird and inside the mosquito.
Equine encephalitides Epi (Equine Eastern- EEE, Venezuelan Equine- VEE, and Equine- Western-WEE
Outbreaks of disease when sufficient infected vectors for virus to “spill over” into horse and human populations. Viraemia in horses with VEE is sufficiently high titre for horses to be a source of virus for vectors (amplifying host)
EEE
50-75% fatality (humans and horses are incidental hosts)- birds are natural reservoir host (discovered in Eastern United States)
Bridge vectors- passerine birds to zoophilic (will bite any mammal) mosquitoes that bite humans and horses
WEE
Less severe than EEE- CFR is 3-10% in humans. (Discovered in Western USA). Enzootic, spillover with bridging vector like EEE
VEE
Febrile illness with ~1% developing clinical encephalitis. With VEE- another sting in the tail. Enzootic cycle (possums, small mammals in central USA), mosquitos- no disease at first in either vertebrate or invertebrate. Then mutation in virus. And then goes into Large mammals and less pick mossies (zoophilic)
Other viruses in Togaviridaes
Ross River Virus, Sindbis, chikungunya, and o’nyong nyong
VEE
Febrile illness with ~1% developing clinical encephalitis. With VEE- another sting in the tail. Enzootic cycle (possums, small mammals in central USA), mosquitos- no disease at first in either vertebrate or invertebrate. Then mutation in virus. And then goes into Large mammals and less pick mossies (zoophilic).
**Large outbreaks in horses, large number of fatalities in horses and people– zoonotic concerns. Vaccinating horses especially. Early 70s it just stopped. So people assumed vaccines worked (association vs. causation). What was really happening? The virus from horses and humans were different to viruses getting from natural hosts- so mutation occurs.
Other viruses in Togaviridaes
Ross River Virus, Sindbis, chikungunya, and o’nyong nyong
Togaviridae- cause two main effects?
1)CNS disease and 2)polyarthritis and rash.
Togaviridae in our part of the world
Polyarthritis viruses- Ross River Virus, Sindbis, chikungunya, and o’nyong nyong
Equine encephalitis pathogenesis
Mosquito bite, replication in local cells- drain to regional lymph nodes, primary viraemia allows spread to muscle and connective tissues and reticuloendothelial system
Secondary replication in these tissues leads to secondary viraemia of high titre to allow CNS invasion
Neural necrosis, mononuclear infilration, perivascular cuffing and interstitial oedema (VEE also involve resp tract)
Clinical signs
Very similar with EEE, VEE, and WEE
Incubation up to 9 days
Range from mild fever and depression to fatal febrile encephalomyelitis
CNS signs: photophobia, head pressing, circling, ataxia, blindness, inability to swallow. Low carriage of head with wide base stance.
Terminal recumbency
Clinical signs
Very similar with EEE, VEE, and WEE
Incubation up to 9 days
Range from mild fever and depression to fatal febrile encephalomyelitis
CNS signs: photophobia, head pressing, circling, ataxia, blindness, inability to swallow. Low carriage of head with wide base stance.
Terminal recumbency (once horses become recumbent they tend not to get back up)
Clinical signs
Very similar with EEE, VEE, and WEE
Incubation up to 9 days
Range from mild fever and depression to fatal febrile encephalomyelitis
CNS signs: photophobia, head pressing, circling, ataxia, blindness, inability to swallow. Low carriage of head with wide base stance.
Terminal recumbency (once horses become recumbent they tend not to get back up)
Diagnosis of equine encephalitides
Difficult. Viraemia is transient- isolation from blood difficult. Lots of Ab out there in the populations. So lots of false pos. Serology IgM ELISA. If you have IgM then you have been RECENTLY infected.
Diagnosis of equine encephalitides
Difficult. Viraemia is transient- isolation from blood difficult. Lots of Ab out there in the populations. So lots of false pos. Serology IgM ELISA. If you have IgM then you have been RECENTLY infected.
Equine encephalitides control
Vaccination available in endemic areas, monovalent, bivalent and trivalent)
Live VEE, inactivated EEE and WEE (effective
Vector control: insecticides, repellent, insect proof stabling dusk and dawn especially (not very effective)
Equine encephalitides control
Vaccination available in endemic areas, monovalent, bivalent and trivalent)
Live VEE, inactivated EEE and WEE (effective
Vector control: insecticides, repellent, insect proof stabling dusk and dawn especially (not very effective)
AUS arbovirus outbreak in 2011
Late summer, early autumn. VIC, SA, NSW, QLD and WA. Seasonal patterns between different states.
Two distinct clinical syndromes: myalagia, arthralgia. Neurological signs and encephalitis.
Clinical signs: ataxia, depression, altered mental state, reluctace to walk, muscle tremors, hypermetria, lameness.
Geospatially clustered musculoskeletal disease- the type of syndrome you see. Widespread CNS disease. Often associated with premises along large waterways, however most farms are found along large waterways anyway.
AUS arbovirus outbreak in 2011
Late summer, early autumn. VIC, SA, NSW, QLD and WA. Seasonal patterns between different states.
Two distinct clinical syndromes: myalagia, arthralgia. Neurological signs and encephalitis.
Clinical signs: ataxia, depression, altered mental state, reluctace to walk, muscle tremors, hypermetria, lameness.
Geospatially clustered musculoskeletal disease- the type of syndrome you see. Widespread CNS disease. Often associated with premises along large waterways, however most farms are found along large waterways anyway.
Background: unusually wet summer, flooding in SE QLD, Cyclone Yasi in North QLD, Flooding in Southern NSW, Flooding Northern VIC (summer of people on sitting on the roofs of their cars)
AUS arbovirus outbreak in 2011
Late summer, early autumn. VIC, SA, NSW, QLD and WA. Seasonal patterns between different states.
Two distinct clinical syndromes: myalagia, arthralgia. Neurological signs and encephalitis.
Clinical signs: ataxia, depression, altered mental state, reluctace to walk, muscle tremors, hypermetria, lameness.
Geospatially clustered musculoskeletal disease- the type of syndrome you see. Widespread CNS disease. Often associated with premises along large waterways, however most farms are found along large waterways anyway.
Background: unusually wet summer, flooding in SE QLD, Cyclone Yasi in North QLD, Flooding in Southern NSW, Flooding Northern VIC (summer of people on sitting on the roofs of their cars)
AUS arbovirus outbreak in 2011
Late summer, early autumn. VIC, SA, NSW, QLD and WA. Seasonal patterns between different states.
Two distinct clinical syndromes: myalagia, arthralgia. Neurological signs and encephalitis.
Clinical signs: ataxia, depression, altered mental state, reluctace to walk, muscle tremors, hypermetria, lameness.
Geospatially clustered musculoskeletal disease- the type of syndrome you see. Widespread CNS disease. Often associated with premises along large waterways, however most farms are found along large waterways anyway.
Background: unusually wet summer, flooding in SE QLD, Cyclone Yasi in North QLD, Flooding in Southern NSW, Flooding Northern VIC (summer of people on sitting on the roofs of their cars)
What are the endemic arboviruses?
Ross river (togaviridae)- people horses Murray valley encephalitis virus (flaviviridae)- people horses Kunjin/ WNV (flaviviridae)- person horses dogs donkeys alpacas
Exotic arboviruses
Japanese encephalitis virus (flavaviridae)
Other arboviruses considered in outbreak of 2011
Hendra (hendra virus exclusion testing), orbiviruses
Other arboviruses considered in outbreak of 2011
Hendra (hendra virus exclusion testing), orbiviruses
What does the curve look like that you would see in a normal infectious outbreak scenario?
Increasing numbers of cases and the curve decreases as the susceptible population reduces (or as number of vectors in environment gets reduced– cold, less mosquito activity)
What does the curve look like that you would see in a normal infectious outbreak scenario?
Increasing numbers of cases and the curve decreases as the susceptible population reduces (or as number of vectors in environment gets reduced– cold, less mosquito activity)
Ross River Virus general
First isolated in Townsville
Aedes mosquitoes
fever, rash, and polyarthritis
Serological diagnosis (IgM or IgG seroconversion)
Virological diagnosis- RT PCR LOOKING FOR RNA
** Difficult to detect- so favor serological diagnosis
Ross River Virus reservoir, how it shows
Sub clinical infection in 60% of human cases, most common arboviral disease in AUS, horse may be amplifier
Flaviviridae
Replicate in cytoplasm, enveloped ss RNA
Two groups: Flavivirus- Japanese Encephalitis, West Nile, Louping Ill
Flaviviridae Pathogenesis
bite from infected arthropod, local virus replication, viraemia, dissemination to target organs (endothelium, liver, foetus, CNS)
Japanese Encephalitis
Endemic in SE Asia, Water birds are main reservoir host, pigs are important amplifying host, infection in humans and horses (dead end hosts) often cause severe and fatal encephalitis, inapparent infections in other species
In a dead end host or incidental host?
Insufficient viraemia to reinfect the mosquito
Sentinel chickens
Coups with chickens- seronegative chickens- mosquitoes bite chickens- chickens sero convert- if they are sero positive then you know the vector and virus is in the environment at the time.
Bad to use pigs because they are an amplifying host
Sentinel chickens
Coups with chickens- seronegative chickens- mosquitoes bite chickens- chickens sero convert- if they are sero positive then you know the vector and virus is in the environment at the time.
Measure of geographical range of mosquito species and whether they are infected. Can also put out traps.
Bad to use pigs because they are an amplifying host
Where is Japanese encephalistis maintained?
In a mosquito - pig cycle, reproductive failure in pigs (abortion, etc), Horses less important (declining numbers and vaccine)- fever, lethargy, and recovery or hyperexcitable and death
Where is Japanese encephalistis maintained?
In a mosquito - pig cycle, reproductive failure in pigs (abortion, etc), Horses less important (declining numbers and vaccine)- fever, lethargy, and recovery or hyperexcitable and death
Japanese encephalitis Diagnosis
Brain, tissue samples, and blood for serology
Virus isolation (intracerebral inoculation of suckling mice- old days), antigen from brain used in CF or HAI tests to ID sample as flavivirus, then serology to type to JE
* PCR
* Inactivated and live vaccines available- effective
West Nile Virus General
Occurs throughout Mediterranean, Asia, and Africa
Recent incursion in the US
Urban bird- mosquito cycle
Closely related to Kunjin virus
Can cause fatal encephalitis in horses and haemorrhagic fever in humans
West Nile Virus General
Occurs throughout Mediterranean, Asia, and Africa
Recent incursion in the US
Urban bird- mosquito cycle
Closely related to Kunjin virus
Can cause fatal encephalitis in horses and haemorrhagic fever in humans
Why would virus go so far west in the US?
Mosquitos infect birds and they migrate south for the winter and then go back north during summer- so it begins to spread everywhere.
Outbreak 1999-2003.
Why would virus go so far west in the US?
Mosquitos infect birds and they migrate south for the winter and then go back north during summer- so it begins to spread everywhere.
Outbreak 1999-2003.
What is the CFR in horses of WNV?
39%
WNV vaccine
Killed virus- more than 1 million doses distro in 2003. Not the most effective. New DNA and recombinant vaccines on the market now- more sophisticated, longer duration vaccines.
What is one reason why WNV widespread and fast?
Host adapted virus. No previous history. Completely susceptible population. Crows, jays, and cardinals- crows especially. Crows has HUGE viral titres in their blood- they would drop dead out of the sky. So then mosquitoes that bit the birds would easily spread the virus.
What is one reason why WNV widespread and fast?
Host adapted virus. No previous history. Completely susceptible population. Crows, jays, and cardinals- crows especially. Crows has HUGE viral titres in their blood- they would drop dead out of the sky. So then mosquitoes that bit the birds would easily spread the virus. Susceptible ecosystem, high levels of viraema, and mosq. species there in abundance as well. 10^10 titres- massive amount!!
Murray Valley Encephalitis Virus general
First isolated in 1951 from VIC/ SA Culex Herons, comorants, and darters Seven outbreaks since 1917 Often sub-clinical 1:800 cases have severe disease- some deaths Serological and virological tests
Murray Valley Encephalitis Virus general
First isolated in 1951 from VIC/ SA Culex Herons, comorants, and darters Seven outbreaks since 1917 Often sub-clinical 1:800 cases have severe disease- some deaths Serological and virological tests
Pestivirus- within Flaviviridae
NOT an arbovirus
Bovine Virus Diarrhoea- acute (diarrhoea) and chronic (mucosal disease)
Epi- non pregnant cattle- all ages susceptible- usually trivial disease (fever, leukopaenia, immunosuppression). Some cattle= diarrhoea, nasal/ocular discharge, ulcerative stomatitis and reduced milk production
BUT in pregnant animals- infection of susceptible adult cattle usually of little consequence unless pregnant (transplacental spread common), outcome of transplacental infection of foetus, stage of infection and strain)
BVD early infection
Abortion, mummification, early embroyonic death and resportion
BVD 80-125 days
Cytopathic strain- foetal lesions, weak or dead calves
Non-cytopathic strain= tolerance (don’t mount a response, and no disease- become persistent carriers)
BVD Infection late in gestation >125 days
Mount active immune response
Develop Ab and survive
+/- some pathology
Non- cytopathic strain
don’t mount a response, and no disease- become persistent carriers
BVD mucosal disease
Profuse watery diarrhoea, nasal discharge, salivation, ulcerative lesions- usually fatal within weeks
If a calf is initially infected with non-cytopathic and then exposed to cytopathic strain what happens?
They become massive amplifiers
BVD mucosal disease cytopathic strain infected calf
Profuse watery diarrhoea, nasal discharge, salivation, ulcerative lesions (hard palate picture)- usually fatal within weeks
If a calf is initially infected with non-cytopathic and then exposed to cytopathic strain what happens?
They become massive amplifiers
BVDV Diagnosis
Isolate virus, detect virus antigens- but some do not mount an Ab response
**Ear notching and looking for virus in calves that are persistently infected- try and isolate virus- serology is difficult because some of these calves recognize the virus as self so they do not mount an antibody response so they are serologically negative– biggest threat!!
What to do with BVDV
remove persistently infected animals – they they are ear notching
Classical Swine Fever
highly contagious, 2-10 day incubation Fever, hyperaemia, purpura Convulsions, sudden death Posterior paresis, paralysis, circling, tremors, and death within weeks Moderate strain- more chronic Low virulence- reduced fertility
Classical Swine Fever Transmission
Ingestion and inhalation
Replication in tonsils, spread to lymph, and endothelial cells
Haemorrhages, DIC, thrombosis of small vessels
Spread by direct contact with pigs
Family Picornaviridae
Lasts for long periods of time, non-enveloped, ss RNA, Poliovirus, shut down translation of cellular mRNA, very efficient, cytocidal replication (1 million viruses/cell- 3 hours)
Apthovirus genus (Family Picornaviridae)
FMD Disease, Equine Rhinitis A Virus
Enterovirus genus (Family Picornaviridae)
Procine enterovirus 1, Swine vesicular disease virus
Foot and Mouth Disease (Picornaviridae Family, Apthovirus genus) General facts
Highly contagious, high mobidity/low mortality, dramatic reduction in production (especially cattle), disease of economic importance (direct and trade) (for example: mastitis associated, 25% reduction in milk output for the rest of the animal’s life)
Foot and Mouth Disease- why is it so hard to control?
Multiple host species, multiple modes of transmission, multiple serotypes (antibodies to one group are not protection to the next group- work out what serotype is endemic in a certain area and make a vaccine for those), small infective dose, rapid replication (1 million viruses per cell in 3 hours!) therefore it can rapidly get out in the environment- shed and infect, virus shedding before clinical signs, highly contagious, carrier state
FMD affects who?
Cloven hooved animals- pigs, antelope, cattle (NOT HORSES)
What happens with FMD in dairy herds?
Lost milk production for remainder of lactation- 25% loss of milk production for the rest of the animal’s life
What happens with FMD in beef cattle and pigs?
Reduced growth rate
Clinical signs of FMD
Excessive salivation (vesicles develop tongue and oral mucosa) (vesicles are laden with viruses), Vesicles develop within 24 hours of when they start showing clinical signs and symptoms. Fever, inappetence, depression, reduced milk production, sore feet (think of pig with feet together), vesicles on interdigital region (eventually rupture), vesicles on coronary bands of cloven hooves, vesicles on teats, nasal mucosa, muzzle, Myocarditis- sudden death in young piglets and calves
Pathogenesis of FMD (routes of transmission)
- Main route of infection is via respiratory tract, inhalation of aerosolized droplets, low dose required: 10-25 TCID50 cattle and sheep (makes it more difficult to control)
- Oral transmission- pigs more susceptible than ruminants. Pigs: 8000 TCID50 while cattle are 600,000 TCID50 (THIS IS IMPORTANT TO KNOW IN EPIDEMICS)
- Broken skin, mucosa: low dose required to initiate infection
- Virus can remain infective in faeces, urine, and soil
- Virus can remain infective in uncooked, salted meats, improperly fermented salami, cheese, etc.
- FMDV is acid labile (pH 11)
Viraemia and virus excretion of FMD
Spread to other organs, mammary gland, LNs, epithelium, myocardium of young animals
Virus excretion: expired air (aerosols), secretions and excretions (including milk and semen), ruptured vesicles
Ruminants- excrete 120,000 TCID50
Pigs excrete- 4 million TCID50 from respiratory tract/day AMPLIFIER HOST
How long does the virus excretion go on before clinical signs?
4 days
When does virus excretion stop?
4-6 days after vesicle appearance (when circulating antibodies develop) (virus shed longer from hoof vesicles than oral)
What percentage of ruminants become persistently infected with FMD?
80%
What is still worrisome about vaccinated animals?
Vaccinated animals confers immunity to clinical disease, but can become carriers. They can still excrete virus.
How many serotypes of FMD? Protective immunity, is it effective on all serotypes?
- Protective immunity is serotype specific. (will work on the topotypes within a serotype endemic to a certain area though)
What are the vaccines?
Inactivated vaccines in endemic countries.
FMD Epi
Pigs are important in epidemics as amplifier hosts with respiratory spread- they are susceptible to infection (oral route). Sheep are important as inapparent carriers
What are outbreaks of FMD associated with?
Oral infection of pigs (swill feeding), direct contact with sub-clinical/ carrier animals or contaminated material, aerosol spread to a susceptible population (10 km over land and 250 km over water)
Diagnosis of FMD
Skin around the top of the vesicle (not the fibrin plug), pharyngeal/oesophageal fluid. It is clinically indistinguishable from other vesicular diseases of livestock. ELISA, virus culture, PCR (mostly PCR)
FMD control
Exportation of livestock or livestock products becomes difficult/impossible if FMD is endemic
Inactivated polyvalent vaccine (antigen bank- if you have an outbreak and need to access the vaccine)
Statuses of Countries regarding Trade/ Export with FMD
Endemic, FMD Free with vaccination (potential for circulating virus still just clinical signs hiding), or FMD free without vaccination
Vaccination vs. Slaughter
Slaughter- if you bury them it can get in the water. So you have to burn them.
Main facts about FMD control
- Excrete FMDV up to 4 days prior to clinical signs
2. Incubation period:
A good way to handle an outbreak- Netherlands & Uruguay- FMD. What is different about endemic FMD?
Use the vaccine to control the outbreak- all susceptible livestock (shedding less virus therefore reducing environmental contamination), then slaughter the vaccinated animals.
Now they can be “FMD Free without vaccination again”
** in an endemic situation- vaccinate and live
Retroviruses general facts
Oncogenic virus, fragile enveloped virus, reverse transcriptase (encode this enzyme and have enzyme sitting in the virion when they get transmitted- to kick off replication process, immunosuppression and neoplasia and degenerative disease, lifelong incubation, chronic diseases (most tend to be), ss RNA–> HIGH MUTATION RATE PLUS and RECOMBINATION (MEANS THEY CAN JUMP SPECIES MORE EASILY BY ADAPTED TO NEW CELLS MORE READILY)- can “recombine” with other viruses i.e. an endogenous retrovirus (provirus sitting in chromosome but not producing viruses released that are capable of transmission) and create a completely novel virus, vertical transmission for some (avian).
What does Reverse transcriptase of Retroviruses help the virus do? How many main genes?
Reverse transcriptase starts replicating once they attach- produces DNA copy which inserted in the host chromosome to form a pro virus- can sit there in acquiescent state for extended periods of time before getting initiated. Potentially transmitted to progeny- can even insert in multiple spots in host’s chromosome. This is one reason the virus can be neoplastic- it can induce changes in the host cell that lead to neoplastic changes.
Splicing of viral RNA but generally they have 3 main genes (one is resp. for replication, one for the nuclear capsid, for example)
Alpharetrovirus
avian tumour virus
Betaretrovirus
Tumours in primates and sheep (especially Jaagsiekte)
Gammaretrovirus
Feline leukaemia virus
Deltaretrovirus
Bovine leukaemia
Epsilonretrovirus
Tumours and leukaemia in fish
Lentivirus
Retrovirus- immunodeficiency viruses, slow virus disease
Lymphoid tumours, like leukaemia, or tumours in the skin, or tumours in the lung, caused by retroviruses, where for example?
Think of lymphosarcoma picture in the kidney Bovine leucosis (tumours on the skin) Ovine maedi- lung full of lymphoid cells= pneumonia
Diagnosis of Retroviruses (3)
- Detect antibody against the virus (ELISA, Gel diffusion)
- Detect viral antigen (ELISA)
- Use PCR (detect viral RNA (viral genome replicated, sitting in virions circulating in blood or tissue) OR detect viral DNA or proviral DNA)
** know what results you are expecting
Infection is more common than disease in this case. Meaning not just detecting prior infection (because infection is generally for life). Antibody commonly forms and persists.
* If genetic RNA is floating around in the system- then animal is probably currently infected*
THINK ABOUT CAT vs. HERD OF CATTLE- don’t want to use the antibody test on a cat but in a herd of cattle you might if you have the signs and symptoms. In an indiv. companion animal you could end up alarming an owner by getting a false positive with antibody test. So either antigen or PCR for RNA would be more useful
Alpharetroviruses
Avian neoplastic disease- horizontal transmission (in ovo or in the first few days of life- virus replicates unchecked- can cause neoplasia- accidents of what the virus does (inserting into the chromosome next to the gene it impacts), if they are infected after 5 days of age with more competent immune system then they generally will knock the virus on its head, vertical transmission (massive outbreak in 1990s of avian leucosis virus J- new recombinant- spread throughout the globe due to vertical transmission–> dominant company of meat chickens at the time- virus developed in great grandparents birds and distributed all over the world, even spread into other breeding companies because they were pinching genetic stock for faster growth genes), Germ line transmission, immunity and resistance, IMMUNOTOLERANCE (persistent infection with +++ viral shedding)
One way of controlling Alpharetroviruses
Eradicate it from stock (for production birds) or to select birds for resistance (some MHC types of chickens are more resistant than others for disease)
Jaagsiekte (ovine pulmonary adenomatosis) (Betaretrovirus)
Multiple lung tumours, long incubation (years), transformation of type II secretory epithelial cells, eradicate by removal of sick sheep and progeny
*NO EFFECTIVE DIAGNOSTIC TESTS
*INFECTED AND AFFECTED SHEEP DO NOT DEVELOP IMMUNE RESPONSE AGAINST THIS VIRUS
** because it is relatively slow virus- just removing affected sheep is enough of a control.
DIAGNOSIS- tipping sheep for fluid or post mortem
* PCR is not helpful because all sheep have endogenous retrovirus (so sitting in the chromosome not causing disease)
**notes: (if you tipped sheep up, you can pour lung fluid out- it is loaded with virus). Cannot grow virus in culture. Can grow some of the tumour cells in culture, but they don’t produce viable virus.
Feline Leukaemia (Gammaretrovirus)
- Lymphosarcomas and leukaemia
- Immune complex and immunodeficiency
- Two outcomes of infection:
- VN and FOCMA (feline onconovirus membrane antigen)- can detect formation of Ab against antigen- knocked it down to a pt. where unlikely to cause disease or transmit- but it IS in the pop. of cats
- Persistent viraemia IF THEY FAIL TO DEVELOP ANTIBODY (greatest risk to other cats as well)
- Diagnosis and control- this is where you have to be careful of false positives. LOW PREVALENCE IN CAT POP. 2% in Sydney for example. Occurs in high prevalence in some urban cat populations (50%). In AUS in general, low prevalence.
- Vaccines are available.
Enzootic Bovine Leukosis (Deltaretrovirus)
- Horizontal infection (but ineffective)– so you can remove infected animals from herd and get some control- relatively unusual in an infectious disease
- Most subclinical infection
- 30% lymphocytosis
*
Maedi/Visna) in Sheep (Lentivirus)
Virus replicating in the lungs- eventually fills the lungs up with lymphocytes and no longer any room for air. Long incubation (2+ years). can be spread from ewe to lamb- around birth-possibly via colostrum. Demyelination of the nerves becuase of the immune attack. Strong immune response but this drives the pathology, so not protection. Has been eradicated from Iceland- completely depopulate large areas of sheep for about 5 years. Exotic to AUS and NZ.
Caprine arthritis- encephalomyelitis (Lentivirus)
Host specific to goats. Leukoencephalomyelitis (central neurological signs, sometimes paralysis or wasting) in kids (under 2 months of age), arthritis in adults (immune attack is in the synovial tissue around the joints– big knees most commonly), lifelong infection, Ab present (not effective in eliminating virus probably because of mutation), transmission by colostrum
- Serological testing and culling infected goats. Feed them pasteurized colostrum- these are fragile viruses so will eliminate virus.
- High prevalence in goats in Australia.
Equine Infectious Anaemia (Lentivirus)
- 7-21 days > fever
- lifelong infection
- recurrent fever, jaundice, weakness, anaemia
- Ab present
- Vector and iatrogenic transmission (Vet/medical)** Unique to Lentiviruses- can be transmitted by mosquitoes
Feline Immunodeficiency Virus (Lentivirus)
- Worldwide
- Domestic and other cats
- Five subtypes A-E
- Initial acute disease- many months- years later wasting (decline in immune function), opportunistic infections, leukopenia, behavioural change
- lifelong infection
- Ab in serum
- Virus in saliva (not as much in semen)– probably transmitted when fighting!!
- Vaccine available but type specific
- Many cats that are infected never show clinical signs- usually live quite happily for most of their life- they do not usually come to an “AIDs-like” end. Contributing factor to predispose cats to a range of other diseases, however.
Bovine immunodeficiency (Lentivirus)
Virus persists but little indication of impact
Jembrana disease (Lentivirus)
Fatal disease, short incubation period, Balinese cattle
* Fever, panleukopenia, lymph node enlargement, haemorrhages throughout their body
- unusual virus- unique in causing rapidly fatal disease with short incubation period. Related to Bovine Immunodeficiency Virus- do not know the differences. Balinese cattle!! Indigenous cattle in Indonesia.
- If they survive, they will actually eliminate the virus
