Virology Summary Flashcards
Cowpox (4)
Poxviridae, Orthopox
* Exotic to Australia
* Rodent Reservoir
* Pock lesions on teats
* Can spread to cats
Poxviridae important general characteristics (5)
* Last for a long time in the environment
* Infectious virus survives in infected material (scabs) for years
* typical pock lesion
* generalized disease can occur with Capripox
* Surviving animals are NOT carriers- duration of immunity < life span of recovered animal: reinfection is possible
Monkeypox (3)
Poxviridae, Orthopoxvirus
* Forest rodent host in Africa
* Transmitted to primates
* Introduced in USA in Gambian rats imported as pets and spread to praire dogs and humans
Capripoxvirus
Poxviridae
* Sheeppox, goatpox, lumpy skin disease
* Geography: Most important pox virus in other parts of the world (SE Europe, Middle East, Africa and Asia)
* Transmission: Virus shed from ocular and nasal discharge OR via skin abrasions OR inhalation of aerosols
* Epi: Endemic: generalised disease and mortality uncommon- mortality in EU breeds: 100%
* Pathogenesis: replicates in skin AND lungs if inhaled–> spreads to LNs
* Clinical signs: incubation pd= 1 week. Fever, oedema of eyelids, conjunctivitis, nasal discharge, skin lesions (lung consolidation and haemorrhage)
Fowl pox (2)
Poxviridae, Avipox
* Mechanical transmission by mosquitoes OR aerosol transmission (lesions in respiratory tract)
* great viral vector for vaccines- large amount of genetic material (foreign virus protein)
* Looks similar to Gallid herpes 1 AKA Infectious Laryngeotracheitis virus
Orf
Poxviridae, Parapoxviruses
Geography: world wide
Transmission: Direct or indirect contact (infectious in scab)
Pathogenesis: epitheliotropic virus
Vaccines: yes
Important parts? * primarily young are ill
* mortality due to starvation due to not suckling from pain
* maintained in flocks by chronic carriers
* zoonosis
Myxomatosis
Poxviridae, Parapoxvirus
* Benign fibromas in wild rabbits, severe generalized disease in EU rabbits
* Clinical signs: listless and febrile, death often within 48 hours, subcutaneous gelatinous swellings
* it is not endemic, but mortality in virulent strain is 99%
African Swine Fever
Asfaviridae
* Stable in environment over a wide range of pH and temperatures
* may persist in meat of infected pigs for months
* warthogs, soft ticks, and EU breeds (100% mortality)
* Die of extensive haemorrhage due to complement activation
* All are carriers (survivors can be chronically ill)
* No vaccine
Herpesviruses general (3)
* Easily inactivated by heat, detergents, pH, and drying (labile)
* Close or mucosal contact for transmission (droplet)
* Lifelong latent infection (reactivation)
Bovine herpesvirus 1
Herpesvirus, Bovine rhinotracheitis virus (IBRV)
* Clinical signs: Rhinotracheitis, areas of epithelial necrosis, abortion, conjunctivitis, enteritis, generlized disease of newborn calves (can die)
* In intensive situations morbidity can approach 100%
* Respiratory infection by aerosol route, veneral route
Bovine Herpesvirus 2, 5
* Bovine herpes virus 2- Uncommon
* Bovine herpes virus 5- causes fatal meningoencephalitis in calves via neural spread from nasopharanynx via trigeminal nerve
Equine Herpes Virus 1
* Most important viral cause of abortion in horses worldwide
* Endemic in all horse populations (latent infection in many)
* Infects endothelium of the endometrium and arterioles of CNS. Causes respiratory disease, abortion, and neurological disease (systemic infection, viraemia)
* Abortions occur late gestation (can be a storm or single), no premonitory signs
* Pregnant mares should be kept separate from other horses and in small groups based on foaling date
* aborting mare is infectious for 1-2 days from reproductive tract and up to 2 weeks from the respiratory tract
Equine herpesvirus 4
aka Equine rhinopneumonitis
* acute respiratory disease with nasal discharge and lymphadenopathy
* foals infected early in life
* combined EHV1 and EHV4 vaccine available
Feline herpesvirus 1
Feline rhinotracheitis
* acute respiratory disease- nasal discharge, ocular discharge, sneezing, dyspnoea, and oral ulcers
* multi-cat households and catteries
* vaccines- yes
Gallid herpesvirus 1
aka Infectious laryngotracheitis
* most common in young chickens
* acute respiratory disease- nasal and ocular discharge, sneezing, dyspnoea, loud gasping, coughing
* haemorrhageic exudate occluding trachea
Arteriviridae
* Rapidly inactivated out in the environment
* Replicate in macrophages
Equine viral arteritis
* Geography: worldwide
* more common in SB population vs. TB population of horses
* Incubation 3-14 days
* Clinical signs: *rhinitis, *ventral oedema, fever, excessive lacrimation, conjunctivitis, stif gait
* Pathogenesis: Replicates in alveolar macrophages (aerosol transmission)- bronchial LNs- viraemia- PRIMARY TARGETS macrophages and endothelium
* More severe in very young/ old animals
** Abortion storms (mid-late gestation)
* Horses most susceptible> mules> donkeys
* Transmission: resp tract, genital tract, transplacental
* AUS has seropositive but no real outbreaks
** CARRIER STALLION (35% remain chronically infected)
* Mares infect each other through resp tract. Stallion infects mares via veneral transmission.
* Diagnosis: PCR
* Vaccines- yes
Porcine Respiratory and Reproductive Syndrome Virus
* Reproductive failure in sows (reduced conception, abortions, mummifications)
* Pneumonia in young pigs
* North America and Europe
* Vaccines- yes
Caliciviridae
* Relatively resistant to heat and detergent- few log reduction if at room temperature; no resistance to acid pH- inactivated at pH<3
* Released by cell lysis
What happens when you leave Herpes, Calicivirus, and Parvo sitting out for a week at room temperature?
Herpes- no infectivity left
Calicivirus- few log reduction in infectivity
Parvo- no change in infectivity
Vesicular exanthema of swine
Caliciviridae
* Clinically indistinguishable from FMD
* Stop feeding pigs animal waste products
Feline Calicivirus Infections
* URT tract pathogen of cats
* Seen as maternal antibody wanes (2-6 months)
* Vaccinate early and repeat vaccinations
* Excrete large amounts of virus- important because iatrogenic transmission and in catteries from handling cats
* Persistent infection after recovery (months to years)
* Transmission: aerosols OR direct contact OR oral nasal or ocular route
* Incubation route ~5 days
* Clinical signs: conjunctivitis, rhinitis, tracheitis, pneumonia, vesiculation and ulceration of tongue and oral mucosa
* Vaccines- F3
* Diagnosis- PCR
Do cats get influenza? What do they get?
No.
Feline herpesvirus, Feline Calicivirus, Chlamidophyla- which commonly cause URT disease
What are the three vaccines in F3?
Feline panleukopaenia, Feline herpesvirus, and Feline calicivirus
Rabbit Haemorrhage Disease
Caliciviridae
* Highly contagious and often fatal disease of European rabbits
* Endemic in Europe, Central America, and Africa
* Biological control agent in AUS and NZ
* Resistant in the environment
* Epi: virus shed in all secretions
* Transmission: faecal oral route, inhalation, conjunctiva, mechanical transmission (mosquitoes and fleas), fomites
* Clinical signs: SUDDEN DEATH, short incubation 3 day
* Pathogenesis:
Rotavirus
* Transmission: Contaminated food, water or fomites
* Fluid accumulation in gut lumen = secretory diarrhoea and osmostic diarrhoea because reduced ability to break down disaccharides
* Pathogenesis: very high concentrations are shed in faeces (survives in faeces for months), infectious dose is small- widespread disease
(MINIMAL CONTAMINATION = WIDESPREAD EFFECTS)
* SEVERE ENTERITIS: Affects intestinal epithelial cell destruction (APICAL CELLS- vs. parvo’s crypt cells). LIKE CORONAVIRUS.
* Resistant to BLEACH and CHLORINE
* Control: Ab in milk (LACTOGENIC IMMUNITY: neutralizes pathogen and just passes because it is in the small intestine lumen), dehydration and electrolyte balance major cause of death, IMPROVED HYGIENE (want a vaccine that will induce a mucosal response)
* Major cause of diarrhoea in many domestic species
* Short incubation period- 12-24 hours
* Clinical signs: profuse watery diarrhoea, may stop suckling, low mortality (associated with dehydration or secondary bacterial infection)
* Disease seen in animals 1-8 weeks old (not in first week due to colostrum)
Coronaviridae
* Enveloped
* Respiratory and/or GI epithelium
* Enteric disease, respiratory disease, immunopathological, and neurological
Bovine Coronavirus Diarrhoea
* Second most common cause of diarrhoes in calves (after rotavirus)
* Less than 2 weeks old (lasts 4-5 days)
* Replication in epithelium of mature villi
* similar to rotavirus!!
Porcine Coronaviruses- what are they (4)? Clinical signs?
Porcine Coronaviruses- Epi? Pathogenesis?
Porcine Coronaviruses- Animals affected? How badly?
Feline Infectious Peritonitis
Coronaviridae
* Epi- multi-cat households or catteries (15% of cats are persistently affected in affected households BUT infection does not always result in disease, EFFECTIVE CELL MEDIATED RESPONSE IN MOST KITTENS to eliminate)
* Cats of any age, but less than one year and older than 10 are most susceptible
* Transmission: faecal/ oral transmission OR respiratory
* FIPV exposure 3 possibilites (FIPV replicates in macrophages):
- Effective CMI
- Decreased CMI- Periodic FIPV replication and shedding (but subclinical)
- Defective CMI- Continuous FIPV = B cell activation = immune complexes= IMMUNE MEDIATED VASCULITIS which either becomes DRY (pyogranulomatous lesions- survives for months) or WET (marked vascular permeability- lives for weeks) but both are fatal.
Feline Coronaviruses- what are the 2? Simple pathogenesis?
Infectious Bronchitis
Coronaviridae
* Affects chickens- highly contagious- economically important disease worldwide
* Primary replication: Respiratory tract
* Viraemia within 1-2 days of exposure (= widespread distribution to oviducts, kidneys, and Bursa- severity of lesions depends on strain virulence)
* Transmission: Respiratory route (several weeks) OR faeces OR eggs of infected birds
* Clinical signs: most severe in young < 3 weeks- gasping, nasal exudate, mortality from occluded bronchi, REDUCED EGG PRODUCTION, 7 days in individuals, 10-14 days in flock
* Diagnosis: PCR
* Vaccines- yes
Togaviridae
* Replicate in cytoplasm to very high titres in mammalian cells with severe cytopathic effects
* Togaviruses of veterinary importance are arboviruses
* Do not have a survive in the environment phase, either in the insect host or in the mammalian host
Equine encephalitides
Togaviridae
* Epi- tend to be seasonal- late summer after heavy rainfall- due to mosquitoes
* Pathogenesis: mossie bite- replication in local cells- drains to local LNs- viraemia spreads to muscle and connective tissue and reticuloendothelial system –> SECONDARY replication in these tissues leads to secondary viraemia of high titre to allow CNS invasion THEREFORE neural necrosis, phagocyte infiltration and interstitial oedema (VEE also involves resp. tract)
* Clinical signs: CNS disease- incubation 9 days- range from mild fever and depression to fatal febrile encephalomyelitis- head pressing, circling, ataxia, blindness, inability to swallow
* EEE and WEE- Bird (passerine)- mosquito, bird (passerine) -mosquito- then into incidental host: consider two incubation periods- inside the bird and inside the mosquito (intrinsic and extrinsic incubation periods) (NOT sufficient viraemia in incidental hosts to continue the EEE or WEE)- HUMANS are IH (horses too)
* VEE - viraemia in horses with sufficiently high titre for horses to be a source of virus for vectors (HORSES ARE AMPLIFYING HOST)- HORSES are IH
* Diagnosis- viraemia is transient so difficult– also lots of infection BUT possibly not acute. Look for IgM!! therefore RECENT infection.
Control: vaccination available in endemic areas (BEFORE SUMMER or insect breeding season maybe boosting again)- live and inactivated. AND vector control- insecticides, repellent, insect proof stabling. EXAMPLE OF SENTINEL CHICKENS or insect traps.
Venezualan Equine Encephalitides
* Viraemia in horses is sufficiently high titre for horses to be a source of virus for vectors (amplifying host)
* Small mammals and mossies are the endemic cycle
* Bridge vectors- less selective mossies
* Mutation in the virus
* Less specific mossies= horses and humans
* Vaccinating horses
* Febrile illness with 1% developing clinical encephalitis (humans)
Eastern Equine Encephalitis Virus and WEE
* Endemic cycle- passerine birds and ornithophilic mossies
* Bridge vectors are zoophilic mossies
* mammals, humans, and horses are IH
* EEE- case fatality rate of 50-75% (humans, similar in horses)
* WEE- cast fatality rate 3-10% (humans, similar in horses)
Polyarthritis Viruses- what are they? Where are they found?
Australian arbovirus outbreak in 2011
* Ross River Virus & Flaviviruses (WNV, MV, RRV)
* widespread musculoskeletal (RRV) and neurological disease (encephalitis- Flaviviruses) reported in horses late summer and autumn (early February)
* Clinical signs- ataxia, headpressing, depression, hypermetria (funny walk)
* what was unique about 2011? Large weather events, unusually wet summer
What endemic arboviruses are in Australia? Who does each impact?
Ross River Virus (Togaviridae)- people, horses
Murray Valley Encephalitis Virus (Flaviviridae)- people and horses
Kunjin/ WNV (Flaviviridae)- people, horses, dogs, donkey, alpacas
Ross River Virus
Flavivirus, Polyarthritis virus
* Clinical signs: Fever, rash, and often polyarthritis
* Diagnosis- IgM or IgG seroconversion/ PCR
* Subclinical infection- 60% of human cases
* Most common arboviral disease reported in AUS
* reservoir hosts: grey kangaroo and maybe bats
Flavivirus
Flavivirus and Pestivirus (Flavivirus are arboviruses)
* Replicate in cytoplasm
* Do not tend to last outside the host (labile and sensitive)
* Stable in meat products for months
Japanese encephalitis virus
Flavivirus
* Exotic to Australia (we have had outbreaks in people and domestic animals)- SE Asia, India, Indonesia
* Pigs are important AMPLIFYING HOSTS (sufficient VIRAEMIA)- pigs tend to survive but with reproductive failure
* Endemic cycle- with birds and mossies- spillover into pigs- INCIDENTAL HOSTS: horse and humans (INSUFFIENT VIRAEMIA)
* OFTEN CAUSES FATAL ENCEPHALITIS but can have inapparent infections in other species
* Sentinel chickens- seronegative chickens- chickens seroconvert so if seropositive then you know it is in the envrionment at the moment
* Diagnosis: brain and tissue samples, blood for serology
* Vaccines: inactivated and live vaccines available EFFECTIVE
West Nile Virus
Flavivirus
* Mediterranean, Asia, and Africa, US (old world to new world- totally susceptible population)
* Bird and mossie cycle- closely related to Kunjin virus- essentially the same thing
* Follows bird migration routes
* DNA vaccines, recombinant vaccines now. At first killed. Better longer duration.
* One reason so fast and so widespread- COMPLETELY SUSCEPTIBLE- especially BIRDS, mosquitoes propagated the infection, people too. In Australia- would need unusual weather conditions- as we have some endemic already. Not completely susceptible population.
Murray Valley Encephalitis Virus
Flavivirus
* Mossies and birds– horses and people
Bovine Virus Diarrhoea
Flaviviridae, Pestivirus
* Acute disease- bovine virus diarrhoea (often undetected)
* Chronic disease- mucosal disease (persistent infection)
* Epi- non pregnant cattle- all ages susceptible, reduced production
* BUT IN PREGNANT animals: Infection of susceptible cattle- crosses the placenta- infects the foetus– depends on stage of gestation
* Early gestation < 80 days- SMEDI
* infection early in gestation 80-125 days- cytopathic strain of BVDV, foteal lesions, weak or dead calves. Non-cytopathic strain= tolerance (no response mounted)– GO ON TO BECOME PERSISTENT CARRIES SO IF EXPOSED TO CYTOPATHIC VIRUS THEN MASSIVE AMPLIFIERS!!!! (therefore poor reproductive outcomes of the other cows they infect)
* Infection late in gestation > 125- calf mounts own immune response. Develop Ab and survive.
** If mucosal disease–> fatal
* Diagnosis: difficult- persistently infected- serologically negative but they are the biggest risk
* Vaccines- yes BUT you can induce mucosal disease
REMOVE PERSISTENTLY INFECTED ANIMALS- however, how do you identify??
Classical Swine Fever
Flaviviridae
Exotic
* highly contagious
* 2-10 day incubation period
* fever, hyperaemia, purpura
* convulsions, SUDDEN DEATH
* Neurological- paralysis
* there are more moderate strains and more virulent strains (more moderate cause reduced fertility)
* Transmission: Ingestion and inhalation- replicates in tonsils–> LNs–> endothelial cells
* HAEMORRHAGE, DIC
Foot and Mouth Disease
Picornaviridae, Aphthovirus
* high morbidity, low mortality
* Disease of economic importance DIRECT AND WITH TRADE (outbreak in a dairy herd, lactation stops and reduction for the rest of the cow’s life AND reduced growth rate in pigs and cows)
* DISEASE OF CLOVEN HOOVED ANIMALS- DEER, ANTELOPE, PIGS, CALVES (NOT HORSES)
* FMD free (with vaccine or without vaccine) or FMD endemic
* If FMD free with vaccine- animals can still be infected and shed virus
* Clinical signs: 2-8 incubation, infects cloven hooves, vesicle develop less than 24 hours after first clinical signs, excessive salivation, fever, inappetance, MYOCARDITIS- SUDDEN DEATH
* Diagnosis: vesicles are laden with virus
* Transmission: Respiratory tract OR broken skin, low dose to initiate infection OR ORAL TRANSMISSION of pigs (fed infected meat)
* Pathogenesis: virus replicates in pharyngeal mucosa and draining LNs, viraemia- spread to other organs.
VIRUS EXCRETION respiratory route: Ruminants excrete 120,000 TCID50 from resp tract/ day. PIGS- 4 Million TCID50 resp tract/ day. PIGS ARE AMPLIFIER HOST
* VIRUS EXCRETION- up to 4 days BEFORE CLINICAL SIGNS and stop 4-6 days after VESICLES APPEAR
* SHED IN ALL SECRETIONS AND EXCRETIONS
* 80% of ruminants become persistently infected***
* Sample that is preferred is from the mouth- pharyngeal and uper oesophageal tissues. Pigs chewing on rope.
* Vaccines are SEROTYPE SPECIFIC… SEVEN different serotypes (only decreases clinical signs, does slightly cause less shedding)
* Control: FMD acid labile– so less than 4 pH or higher than 11
* Clinically indistinguishable from other vesicular disease from livestock- need to diagnose in lab (Swine vesicular disease (corona), Vesicular exanthema (calici), Vesicular stomatitis (rhabdo))
* SKIN AROUND THE TOP OF THE VESICLE- not the fibinr PLUG!!! epithelium or vesicular fluid
* PCR
* Think of Netherlands with control- cull the infected, blanket/ ring vaccine around the outbreaks and then cull the vaccinated so you can become FMD free without vaccine again for export purposes (Cheese!)
Why is FMD so difficult to control?
M3SRVHC
Equine Rhinitis A Virus
Picornaviridae
* URT disease in horses
* Virus excreted from resp tract
* Viraemia develops with excretion in urine
* PCR
Encephalomyocarditis
Picornaviridae, Cardiovirus, Genus: Enterovirus (aka Porcine enterovirus)
* Epi- rodents natural host (urine/ faeces excretion)–> pigs acquire infect, HIGHLY CONTAGIOUS, HIGH MORTALITY 90%, LONG EXCRETION TIME 7 weeks, survives up to 4 weeks in environment
* Pathogenesis: viraemia after ingestion, high virus titres in myocardium, spleen, mesenteric LNs… OR repro strains: SMEDI
* Important exotic disease of pigs
* Clinical signs: fever, depression, anorexia, tremors, ataxia, hind limbs show signs first- progressive paralysis, CONVULSIONS, COMA, DEATH
* Vaccinations available- quarantine, hygiene
* Diagnosis- culture, experimental infection
Swine Vesicular Disease
Picornaviridae, Genus: Enterovirus
* Mild vesicular disease of pigs
* Occurs sporadically in Europe and Asia
* CLINICALLY INDISTINGUISHABLE FROM FMD
* Presents as lameness due to vesicles around feelt
* Diagnosis: Antigen detection in vesicular epithelium
* Fed pigs sea lion meat that was contaminated with this the virus
Adenoviridae
Non-enveloped (relatively stable in the environment)
* GI virus- would not be a good career move to have an envelope
* Resp disease too
Canine Hepatitis Virus
* systemic disease affecting dogs, foxes, wolves, skunks, other canids
* Transmission: via ingestion of urine, faeces, or saliva from infected animal
* Infection through nasopharyngeal, oral and conjunctival route of infection– virus infects tonsillar crypts–> spreads to regional LNs–> bloodstream via thoracic duct–> infection of endothelial parenchymal cells and many organs = HAEMORRHAGE AND NECROSIS especially of liver, kidneys, spleen, lungs
* VIRAEMIA–> spreads to urine (infection of the kidney), faeces and saliva
* Clinical recovery about 10 days after infection if production of neutralizing antibody
3 Overlapping syndromes!!
* Incubation pd= 4-9 days
* History of sudden fever, collapse, and abdominal pain in young dogs is suggestive
* virus will continue to be shed for 6 months
* CAV 1 vaccine causes ocular oedema (immune complexes in the capillaries in the eye)- so use CAV 2 vaccine is used
What is Pseudotyping, Pseudodiploid, and Recombination?
Diploid genome- co infection by two different viruses in the same cell. What can happen:
* Pseudotyping- if one replicates more efficiently than the other- then you can have the genome of one virus coated with the capsid of the other virus (can result in changes in host cell range or host species range- retroviruses are therefore able to jump species easier than other viruses CAN ADAPT TO NEW CELL)
* Pseudodiploid- one copy of genome of one virus and one copy of the other. Two genomes transmitted at the same time therefore high likelihood of recombination. Can transmit the two viruses at the same time! HIGH LIKELIHOOD OF RECOMBINATION.
* Recombination- you can have proviruses already sitting in the chromosome- another one comes along and they can recombine with each other
** COMMON IN POULTRY
Retroviruses often cause lymphoid types of tumours e.g. Leukaemia. White cells in the blood stream or solid lymphoid tumours.
Picture: Lymphosarcoma
Alpharetroviruses
* Avian neoplastic diseases (avian tumour viruses).
CONTROL: Eradicate from BREEDING STOCK. SELECT BIRDS FOR RESISTANCE (Certain MHC Haplotypes)
3 categories:
- Replication incompetent
- Replication competent (less capable of causing tumours)
- Replication competent– rapidly transforming (reproduce themselves and can cause neoplasia in host cells)
* Horizontal and vertical transmission (think of worlds meat chickens carrying alpharetrovirus due to pinching genetic stock of best breeding company in the world)
* Germ line common- usually see in the first few days of life
*** If birds are infected after 5 days of age– they will generally eliminate these diseases (the birds that are infected early are of the most danger because the virus is replicating unchecked)
** Immunotolerance (persistent infection with ++++ viral shedding)
* LYMPHOID TUMOURS– ALL LYMPHOCYTES
Enzootic Bovine Leukosis
Deltaretrovirus
* CONTROL AND SPREAD: Horizonal infection (inefficient)- removal of affected animals can eradicate usually (because rate of infection relatively low)
* Most infections are subclinical- about 30% develop lymphocytosis and 10% of those develop lymphoid tumours after 4-8 years
* CAN AFFECT PRODUCTION
* Eradicate by tests for Ab and cull positives (for example, dairy cattle– effective eradication program in a number of countries)
* Iatrogenic spread (VET!!!)
Maedi/Visna
Lentivirus
* Long incubation (2+ years)
**RESPIRATORY SPREAD**
AND/OR
* Ewe to lamb transmission
* VISNA- immune attack of neural cells–paralysis and eventually muscles waste
* MAEDI- Chronic progressive pneumonia
* Strong immune response but this drives development of pathology, does not protect (Ab test is diagnostic)
** has been eradicated from some countries– ICELAND– completely depopulated large areas of sheep for 5 years**
* Exotic to AUS and NZ but present most everywhere else
Caprine Arthritis- Encephalomyelitis
Lentivirus
* Leukoencephalomyelitis in goat kids
* Sometimes wasting
* Arthritis in adults (BIG KNEES)
* Lifelong infection
* Antibody present (does not eliminate virus)
* TRANSMISSION by colostrum
* CONTROL: achieved by serologic testing and culling AND by PASTEURIZING COLOSTRUM before giving it to goats (fragile virus)
** high prevalence in goats in Australia**
Transmissible Spongiform Encephalopathies
* Long incubation period but subacute disease
because once they start showing signs they normally die fairly quickly
* Uniformly fatal
* Spongiform degenerative lesions (NO INFLAMMATORY response)
* Normal aging causes these type of lesions as well, so difficult to know if lesions are due to normal aging or disease
* Agent is about the same size of a virus, NO nucleic acid
* HIGHLY RESISTANT TO INACTIVATION
* LIPID ASSOCIATED (most viruses tend to be associated with the more aqeous parts of cells/ the brain)
* infectivity destroyed by protein disruption
What are the two types of Retroviruses? What is the structure in the genome? Furthermore, what are the two types within exogenous Retrovirus?
Exogenous (infect cell, go through lytic cycle, produce more virus that is then released) and Endogenous (DNA provirus in the chromosome of the host- never produce a virion- not all are a problem- can even be productive BUT can be capable of transforming cells- you would need a lot in order for them to end up going in the “wrong” cell- chance).
Within exogenous: Replication competent and replication incompetent.
Genes:
gag- structure of the virion
pol- replication (reverse transcriptase)
env- proteins on outer surface
What is the key for a virus to reliably cause cancer?
Either having the viral oncogene- nearly 100% of infected animals OR retroviruses sitting there for a long incubation period (proviruses) they usually do still cancer- just much later in life
Replication incompetent endogenous retroviruses- if their env gene is replaced by viral oncogene= CANCER
Koala Retrovirus
Myeloid Leukemia
Solid lymphoid tumours as well
DNA viruses and cancer
* Non-productive infection (need cell to survive infection).
* some contains analogues of oncogenes (genes that appear to be able to control cell growth- evolved these on their own)– adenoviruses and papillomaviruses (increase cellular expression)
* Poxvirus analogue of epidermal growth factor (benign. Why? because it creates more cells for them to infect.)
* Squirrel- tend to be benign but can occur in a bad place that does not allow the animal to live
* BUT EXCEPTION fowl pox vaccine strain- picked up retro viral proviral genome inside the poxvirus genome- retrovirus came with the vaccine- so high rate of leukaemia associated with fowl pox strains (can travel with other viral genomes)
Papillomaviruses
* Benign warts (which are a tumour) plus co-factors CAN lead to neoplasia and carcinoma
* Bovine type 4 papillomavirus plus bracken fern = GIT and bladder carcinoma as a result of virus and carcinogens in the bracken fern
* Bovine Occular papillomavirus, lack of pigment plus UV exposure
* Also, Equine Sarcoid- do not metastasize but proliferate locally (BOVINE PAPILLOMAVIRUS)
Herpesvirus (oncogenic)
* tumours affecting the nerves
* Rate of infection and mortality- 50% (high)
* See paralysis, tumours in feather follicles, bent necks, liver
* contains onco genes- do not appear to have origin in the host- developed by the virus (one induces increased transcription in the infected cell and a second onco gene which encodes a component of an enzyme that extends the telomeres)
* live virus vaccines- vaccines lack the v-onc gene (why they can induce protection)- used worldwide in poultry flocks- delivered by robots to get it in early enough to develop protection
Rabies Control (Urban)
* Don’t keep killing the strays- allows them to keep breeding because it opens up more room regarding resources
* Desexing, vaccine programs
** One vaccine is affective against all serotypes**
Sylvatic cycle in wildlife Control
* aerial baiting with attenuated vaccine (fox)- chicken heads
* more difficult when multiple species are involved (they eat different things!)
* Requires money!! (Vaccination)
* In South Africa, for example, there are a number of different cycles- Mongoose & Canid
** One vaccine is affective against all serotypes**
* Immune response- protective immunity involves both humoral and CMI– Immune host will clear virus from site of entry BEFORE virus enters the nervous system (post exposure vaccination and RIG)
* Vaccines: inactivated in injections– attenuated in chicken heads
Akabane
Bunyaviridae, Bunyavirus
* Cuilicoides brevitarsis- arbovirus of sheep and cattle
* Vertical transmission: foetal death, abortion, hydrancephaly, arthrogryposis
* Epi: tropical and sub-tropical regions in the Middle East, Asia, Australia, and Africa– sporadic epidemics correspond with movement of vectors– or movement susceptible animals into endemica area
* Disease in cattle, sheep, goats, and deer
* Previously unexposed dam is bitten by infected vector, virus crosses placenta from maternal circulation without producing clinical signs in the mother, severity of clinical sigsn in the foetus depend on stage of gestation when infected, primary foetal infection is an encephalomyelitis and polymyositis
* Pathogenesis: severely affected foetuses die and are aborted, survivors develop large cavitations in the cerebrum, hydrancephaly, and neurogenic arthrogryposis (kyphosis, scoliosis)
* Serological diagnosis- problem is everyone would be antibody positive but only the pregnant will have signs and symptoms, diagnosis is usually by gross pathological examination- virus is difficult to isolate from foetus/ newborn- caesarean
* GOOD immunity after infection
* Inactivated vaccines available in Japan and AUS
Hantaviruses
Bunyaviridae
* Shed in aerosolized urine and faeces of mice
Newcastle Disease
Paramyxoviridae, Rubulavirus
* Virulence is variable
* Resp, GI, Circulatory, NS
* Incubation
***the more cleavable the F protein is (proteases by cells) the more virulent the virus is***
- Velogenic = high virulence (mortality rates approaching 100% in viscerotropic)–> (haemorrhagic intestinal lesions and bright green diarrhoea–>viscerotropic velogenic isolates) AND Neurotropic–> mortality 10-20% resp signs, NS– tremor, paralysis, torticollis
- Mesogenic= intermediate (mild disease- mortality in young birds)–> 10% mortality– usually young- coughing, weight loss, reduced egg production
- Lentogenic (in Australia)= low virulence (mild dx or inapparent infection)
Pathogenesis: virus replication in epithelia of resp and GI– HAEMATOGENOUS SPREAD FROM THESE SITES– spleen and bone marrow. Secondary viraemia- infection of lung, intestinte, CNS
Epi- WIDE RANGE OF BIRD SPECIES (not called Newcastle disease in wild birds– Avian paramyxovirus 1)— because Neutropic is defined as Newcastle disease?? Easily transmissible to commercial birds for example– even if biosecurity is okay
Transmission- inhalation of aerosols or ingestion of contaminated food or water. Would have to get rid of bedding and clean out the carcasses. Excreted in faeces, from resp tract- survives in carcasses for weeks. Wild birds act as reservoir- mutation at cleavage site.
Diagnosis- virus isolation in embryonated eggs– pathogenicity tests- mean death time for eggs- RT PCR and sequencing of fusion protein. Antibody detection by HAI
Control: ND free countries: test and slaughter; ND endemic countries: attenuated live vaccines strains (V4 strain- endemic Australian strain, selected for temperature resistance, used to protect village poultry in Asia and Africa). Australia is a ND free disease WITH REGIONALIZATION. (ND is not an international trade barrier!!!)
* note diptheritic membrane on the inside of the trachea- which causes dyspnoea
Rinderpest
Paramyxoviridae, Genus: Morbillivirus
* Eradicated 2011
* acute fatal disease of domestic cattle, buffaloes, yaks
* high morbidity, high mortality (death within 12 days of dehydration and wasting, secondary infection)
* pyrexia, inflammation, and necrosis of mucous membranes (necrotic foci- become erosions), profuse haemorrhagic diarrhoea- lining of intestine comes out
* short incubation 3-5 days
How did it maintain itself in the population? NO RESERVOIR- cow to cow. Transmission by inhalation.
Epi- ONE SEROTYPE. Lots of strains but one vaccine ruled them all. One shot of the vaccine gave them lifelong protection. The vaccine covered any strain of Rinderpest that was out there. Virus is labile in the environment. No carrier state because they DIE.
Canine Distemper
Paramyxoviridae, Genus Morbillivirus
* highly contagious
* generalized infection affecting many organ systems
* there are cases in AUS but it is rare (it is worldwide)
Epi- outbreaks in dogs, foxes, skunks, racoons, ferrets, lions
Virus is labile in the env, Requires direct contact or close aerosol transmission, virus shed in expired air, faeces, urine, and other secretions
** urban dogs (young dogs as maternal Abs wane 3-6 months) vs. rural dogs (more susceptible because lower pop. pressure- if they are unvaccinated- fully susceptible- does not matter the age)
Clinical signs- pyrexia, ocunasal discharge, pharyngitis, tonsillar enlargement, skin rash and pustules, hyperkeratosis of nose and footpads, cough, vomiting, diarrhoea, NEURO SIGNS (OLD DOG ENCEPH)— GRAVE PROGNOSIS for dogs with neurological signs (even if they recover residual defecits)
** lifelong immunity if recover or vaccination.
Hendra Virus
Paramyxoviridae, Genus Henipavirus
(initially thought African Horse Sickness- but in September so no culicoides)
* horses were tachypnoeic, tachycardic, ataxic, frothy nasal discharge, congestion, fluid filled lungs, (7 deaths within 12 hours)
Nipah Virus
Paramyxoviridae, Genus Henipavirus
* outbreak of viral encephalitis in people in Malaysia Sept 98 and April 99
* Nipah closely related to Hendra
* Pteropid bats
* Hendravirus antibodies in each species of the Pteropid bat
Do not know how it goes from bat to bat. Some evidence of horse to horse. No evidence of bat to human.
