Virology Flashcards
Taxonomically classify the family Reoviridae ?
Describe the epidemiology of Orbivirus AHSV ?
African horse sickness virus genus Orbivirus
* Transmitted by biting midgess
* not a contagious disease
* Prevalent throughout Africa and there are some incursions up into Europe
* exotic disease to Australia
* 9 serotypes
* host horses, donkeys and zebras
Taxanomically classify and describe (6) the genus Orbivirus ?
Family Reoviridae genus Orbivirus
* non-enveloped virus
* triple capsid structure
* 10 segments of dsRNA
* replicate in the cytoplasm
* insect transmitted viruses, predominantly biting midgees (Culicoides)
* segmented genome - reasortment
* includes African horse sickness AHSV, Blue toungue virus (BTV) and Equine encephalosis (EEV)
Describe the transmission and host of African horse sickness (AHSV) ?
Pathogenesis AHSV
* host = horse, donkeys and zebras
* no clinical signs in donkeys and zebras
* transmitted by biting midgees
What are the clinical signs of AHSV in horses ?
There are three forms of AHSV
**Heart form (Dikkop)
* fever
* swellin of the head and eyes
* loss of ability to swallow + possible colic symptoms
* terminal signs include bleeding pin point membranes of the mouth and eyes
* slower onset of death (4 to 8 days) and reduced mortality (50%)
**Lung pulmonary form (Dunkop)
* very high fever (upto 41)
* difficulty in breathing, with mouth open + head down
* frothy discharge may pour from the nose
* sudden onset of death - very high mortality rate 90%
Mixed form
* symptoms of both lung + heart forms
* most commonly seen in outbreaks
* mortality rate 80%
How can we control for AHSV ?
Control methods for AHSV
* vaccine available - MLV attentuated 6/9 serotypes
* control vector
* animal management
* good management by stabling horses at night
Describe EEV genus Orbivirus ?
Describe the epidemiology of blue toungue virus ?
Blue toungue virus, genus Orbivirus
* 28 serotypes world wide
* introductions into Australia are believed to be wind blown dispersals from Indonesia
* note wild type virus were reasorting with live attentuated vaccines, adding substantially to the viruses evolution
Describe the clinical signs of BTV in sheep and cattle ?
Genus Orbivirus BTV clinical signs
**sheep
fever, excessive salivation, swelling of the face
* swelling of toungue and cyanos
* hyperaemia (increase in blood flow) of muzzle nose and coronet*
**cattle
* *conjunctivitis, rhinitis with nasal discharge
* ulceration of the nares
Describe the pathogenesis of BTV
BTV genus Orbivirus
Clinical presentation varies depending upon
* species, vector and environmental factors
* virulence of infecting strain
* expression of inflammatory mediators
Pathogenesis
* 6-8 day incubation period after the bite of insect vector
* tropism for phagocytic cells, dendritic cells and endothelial cells
* cell membrane invagination of erythrocytes and platelets during viraemia
* able to circulate for weeks in the presence of neutralising antibodies
* damage caused to endothelial cells in the walls of blood vessels
* vascular thrombosis, tissue infarction, necrosis, oedema
* in the foetus may result in abortion, growth retardation, viraemic off spring or no obvious signs all dependant on the gestational age of the offspring
How can we control for BTV ?
Genus Orbivirus BTV
* vaccination - 3 bottles of 5 serotypes each three weeks apart
* non endemic countries rather used inactivated vaccines during outbreaks
* recombination segmented virus
* vector control
* control for illegal movement of animals / biosecurity
Laboratory diagnostics and sampling for BTV ?
Genus Orbivirus BTV
Sampling
* blood (heparin, serum)
* PM biopsy: lung, spleen and heart
* Virus isolation 1. embryonated chicken eggs 2. cell cultures
Diagnosis
* SNT, RT-PCR
* ELISA
Describe Epizootic haemorragic disease Genus Orbivirus ?
Describe Rotavirus and its clinical signs ?
Family Reoviridae, genus Rotavirus
Rotavirus
significant cause of diarrhoea
* 11 segments
* 3 capsid layers resistant to dring out, chemicals
* often complicated by bacterial enteritis
* viral titres in faeces extremely high
* seven serotypes
* animals may be partially resistant and have subclinical infections
Describe the pathogenesis of rotavirus ?
Genus Rotavirus
* faecal oral route
* infects enterocytes on the tip of microvilli in the small intestine
* triple coat makes them resistant to the PH of the stomache
* enters host cell through receptor mediated endocytosis forming a vessical known as an endosome
Damage
* VP4 and VP7 makes holes in the membrane of the endosome allowing leakage of calcium into the cell
* with reduced calcium the trimers of the VP7 falls apart and the outer capsid is uncoated
* produces a virus encoded endotoxin NSP4
Rotavirus and the role of NSP4
Genus Rotavirus
* NSP4 is a virus encoded endotoxin
* non structural protein
* in affected cell associated with the assembly of a virion
* can attach to receptors on healthy enterocytes
* change Ca2+ concentration
* water and electrolytes leak from the infected cell into the lumen of the intestine
Describe the sampling / diagnosis of Rotavirus ?
Sampling and laboratory diagnosis
* specimens collected faeces and rectal sawbs
* ELISA
* RT-PCR
* EM not readily available
Describe family Reoviridae, genus Orthoreovirus and its clinical signs, diagnosis and treatment ?
Reovirus Tenosynovitis
* 10 segments RNA
* most commonly observed is infection of tendons and resulting rapture of the tendons and haemorrhage
* bruised muscle may affect carcass quality
* stunting and runting in chicks
* helicopter syndrome
Laboratory diagnosis and control
* ELISA + RT-PCR
* vaccine available
Describe the family Birnaviradae its clinical symptoms and pathogenesis ?
Family Birnaviradae
* Virus has two segments dsRNA
* the virus replicates in mature B cells causing necrosis of the bursa
* immunosuppression and consequent infection of host with other organisms
Describe how you would diagnose and control for the family Birnaviradae ?
Family Birnaviradae
Diagnosis
* histopathology of B cells in the bursa
* lesions may be observed on the spleen and caecal tonsils
* ELISA monitor antibodie titres
* RT-PCR
Control
* vaccination of breeders
* biosecurity
Describe the Taxonomy and characteristics of Poxviridae ?
Family Poxviridae
Avipoxvirus, Capripoxvirus, Leporipoxvirus and Parapoxvirus
* largest enveloped virus (30nm)
* complex structure and assembly
* replicate in cytoplasm, unlike most DNA viruses
* causes skin lesions, some cause systemic disease
* highly resistant in the environment
* readily diagnosed by clinical signs and EM (electron microscopy
The discovery of Edward Jenner and Pox viruses ?
Pox viruses and the first vaccine
* Edward Jenner
* tow observations
* reduced incidence of smallpox in dairy workers
* dairy workers were often inflected with cowpox lesions
* cowpox lesion on a milkmaid used to innoculate 8 year old boy which was later found to be resistant to infection with small pox
Describe the replication and taxonomy of Pox viruses ?
POX virus
* largest enveloped viruses
* complex structure and mode of assembly
* all cause skin lesions and some may cause serious systemic disease
Pox virus replication - assemble cytoplasm
* dsDNA encoding around 200 genes
* viral core has a RNA polmerase transcribes several viral genes nessary for replication and protein synthesis
* proteins translated prior to DNA transcription (early and late proteins)
* viral particles are constructed in the cytoplasm in vial factories (viral inclusion bodies)
* DNA is replicated as long concatemers, that are later joined together by endonuclease ( enzyme which repairs DNA)
Describe the pathogenesis of POX viruses ?
POX virus
Transmission = Infection of host through all possible routes - skin (mechanical), respiratory route and oral route
- generally acute symptoms with no strong evidence for latent or persistent infections
- may be systemic (with low mortality/morbidity or lethal within 10days)
- affect many species, however usually host specific
- initial replication usually at site of infection eg skin, respiratory tract
- virus taken to local lymph nodes and then by the thoracic duct to the blood
- immunity to most pox viruses strong and life long (excepts parapoxvirus orf).
- very resistant within the environment
What is the host immune reaction to a POX virus ?
Immune reaction to a POX virus ?
* progressive multifactoral
* early on interferons, inflammatory cells and natural killer cells may contribute to slowing the spread of infection
* most important is cell mediated cytotoxic T lymphocytes and delayed hypersensitivity for recovery
*B cell humoral has yet to be demonstrated in recovery, however is very important in preventing reinfection *
How do POX viruses evade the immune system ?
How POX viruses evade the immune system ?
* produce many gene products homologous to host genes
* these products damage the host immune response
* Epidermal growth factor and vascular growth factor which act to modulate the growth of genes
* complement proteins cytokines, interferon gamma proteins which enhance the viral environment for replication
How do we sample and diagnose a POX virus ?
POX virus sampling and diagnosis
Sampling
* clinical signs overt and typical
* if viremic - blood VI, PCR, EM
* scabs EM and VI
* serum, SNT and ELISA
* immunohistochemistry - immunoperoxidase
Describe the epidemiology and clinical signs of Avipoxvirus Fowlpox ?
Fowlpox
Occurance is worldwide
Two forms
Cutaneous form = nodular lesions of the wattle, comb and eyelids + other non feathered areas
* cutaneous form most common
Diphtheroid form = nodules on the mucosal membranes of pharynx, trachea and oesophagus
Special histological changes = cytoplasmic inclusion bodies*
Describe the diagnosis and control of Avipoxvirus ?
Diag / control Avipoxvirus Fowlpox
* skin lesions are relatively pathognomonic
* tracheal lesions (must be differentiated from larntracheitis infection)
* histopathology - lesions, proliferation, intracytoplasmic inclusion bodies
* PCR for specific sequencing of the genome
Control
* cell culture propagated vaccine for chicks one day old
* embryo origin vaccine chicks 8-10 weeks of age
* traditional vaccination via wing stab
Describe the epidemiology of Capripoxvirus and its general chracteristics ?
Capripoxvirus
Sheeppox virus, goat pox and lumpy skin disease
Transmision = oral, mechanical and respiratory
Occurance = Africa and Asia
* most important of mammalian poxvirus infections
* transboundary
* huge economic importance
* sheeppox and goatpox are distinct viruses, however recombination may occur between them
* may remain infectious for upto six months in sheep pens, or 3 months on wool and hair
* most isolates only infect sheep or goats, but some isolates may cause serious disease to both species
Describe the clinical signs of Capripoxvirus in sheep?
Clinical signs capripoxvirus sheep
* stable in the environment
* skin nodules - circumscribed firm
* lesions may develop in lungs and respiratory tract
* infections are generally acute with no strong evidence for latent or persistant infections
* occasionally fatal disease
* fever
* lymphadenopathy
* severe economic loss
Describe the pathology and clinical signs of LSD in cattle ?
LSD lumpy skin disease cattle (capripoxvirus)
* highly variable disease between indivduals - some are asymptomatic
* sudden onset of fever
* salivation
* occular and nasal discharge
* nodules on skin and internal organs
* pneumonia and death
* mortality 1% (upto 75% in outbreaks); this range is due to many factors including breed, virus isolate, prior animal health, type of insect vector, secondary infections
Describe the pathogenesis and diagnosis of lumpy skin disease in cattle ?
Capripoxvirus LSD
Transmission - cattle water buffalo
worldwide not Australia and NZ
* direct contact
* biting flies
* ticks
*semen
Diagnosis
* clinical signs - fever, enlarged lymph nodes, characteristic skin nodules
* note many animals are asymptomatic
*occasionally fatal disease
* lab test EM, PCR, Histopathology and ELISA
* requires a differential diagnosis
* vaccination is recomended in endemic countries
Why are POX viruses economically important and how can we control them ?
Discuss Leporipoxvirus - Myxoma
Myxoma
* Virus host coevolution - benign fibromas in American host but severe generalised disease in European rabbit
* most rabbits die 12 days
* surviving rabbits have subcutaneous swellings which appear all over the body (myxomatosis)
* when introduced to European rabbits in Australia mortality of 99%
* dvelopment of of resistance by the emergence of attentuated virus strains
Describe the clinical signs of Parapoxvirus ?
Clinical signs parapoxvirus - bovine papular stomatitis virus and Orf virus
Sheep and cattle
* contagious localised lesions in a range of animals
* scab formation around the mouth, nostrils and eyes
* lesions mammary gland vulva, infected lactating ewes may abandon lambs
* common in the commisure of the mouth
* capable of surviving for years in the environment
* common in sheep and goats / usually young animals
General characteristics
* easily distinguished from other pox viruses as as it is more narrow and oval shaped
How do we control for parapoxvirus ?
Parapoxvirus
* prevention by vaccination + disinfect equipment between animals
* live attenuated vaccine
* skin of inner thigh is scarified and a lesion will develop
* immunity achieved within two weeks
* vac pregnant ewes behind the elbow to prevent infection of the udder
Describe the general characteristics of the family Adenoviridae ?
Adenoviridae
Large dsDNA - replicate in the nucleus
* associated with infection respiratory tract, eye and GIT
* many infections with adenovirus are subclinical
* heavily dependant on the cell for transcription
* resist heat and many chemicals
Describe the clinical signs of canine adenovirus types 1 and two
Canine adenovirus
Cav-1
* once an important disease of dogs
* majority of infections are asymptomatic
* fever, hepatic necrosis, widespread haemmorrhage and vascular injury
* systemic paracute - pup found dead
* systemic acute - fatal, fever, loss of apetite, vomiting haemorrhages of the gums
* systemic mild - partial immunity
Cav-2
* respiratory disease (integral part of kennel cough complex)
How can we diagnose and control for Adenovirus in canines ?
What are the clinical signs of Fowl adenovirus (FAdV) ?
Fowl adenovirus
some causative agents of inclusion body hepatitis
transmission horizontal and vertical
Clinical signs
* hepatitis
* high mortality rate in young broilers
* hepatocyte viral inclusion bodies
* liver - pale, friable, swollen with focal to extensive necrosis
How do we control for Fowl adenovirus ?
Fowl Adenovirus
* control is via vaccination of breeding birds - broilers are protected by maternal antibody
* live attentuated vaccine for Australian outbreaks
* there is litle cross protection between different strains - which prevented the development of effective inactivated vaccines
* biosecurity to prevent horizontal spread
Please describe the characteristics and taxonomy of Flaviviridae ?
many mosquito borne viruses
ss + sense RNA enveloped
Describe and taxonomically classify Orthomyxoviridae ?
Orthomyxoviridae
* negative stranded, segmented RNA viruses
* enveloped viruses between 80-120nm
Describe the four types of influenza virus ?
Influenza A
* most common fastest mutating influenza virus
* birds, humans, pigs, horses and dogs
* currently circulating H3N2 and H1N1pdm9
Influenza B
* less common
* humans, seals
Influenza C
* humans, pigs
Influenza D
* cows, pigs
What are the natural host of influenza A viruses ?
Natural host influenza A viruses
* wild water birds Order Anseriformes (ducks, geese and swans)
* detected in 1-60% of migratory water birds depending upon season
* infected wild birds usually present asymptomatically
* replicate mainly in epithelial cells of the GIT (lesser extent respiratory) in wild birds
* large amount of virus excreted in faeces
Describe the two main mechanisms for AIV evolution ?
Two mechanisms for the rapid evolution for AIV evolution ?
Reassortment (antigenic shift)
* occurs when two influenza viruses concurrently infect the same person or host
* may result in a progeny virus with the genetic material from both parent viruses
* segmented virus
Mutation / adaptation (antigenic drift)
* occurs when an influenza virus accumulates mutations that enable more efficient infection and spreed within a new host
Influenza A virus is classified into two subtypes ?
Describe replication of the influenza virus ?
Why does the host eg human or avian affect the clinical signs of influenza ?
Influenza host affects symptoms
Influenza HA binds to salylated glycans on cell surface
Human
* bind to alpha2-6 sialic acid receptors
* epithelial cells upper respiratory tract
* usually a mild disease
Avian
* bind alpha2-3 sialic acid
* GIT and lower respiratory tract of birds
* severe pulmonary disease
* alpha2-3 sialic receptor are located deeper in the lungs causing a more severe disease
2-3 affinity will be less transmissable but causes deep lung disease
What determines LPAI and HPAI ?
What determines HPAI and LPAI ?
* where HPAI = high pathogenic avian influenza, and LPAI low pathogenic avian influenza
* In both LPAI and HPAI the hemagglutinin precursor molecule (HAO) must be cleaved by host proteases for HAI and HA2 to mediate fusion between the virus and host cells.
LPAI = The HAO from LP viruses can only be cleaved in the lungs and the GIT - resulting in mild localised infections
HPAI = The addition of multiple basic amino acids at the cleavage site results in HAO being cleaved by ubiquitos proteases in a wide range of organs - resulting in a lethal systemic infection.
What are the clinical signs of LPAI ?
The HAO from LP viruses can only be cleaved by proteases found within the intestinal and respiratory tract
* results in a mild localised infection
* respiratory and intestinal
* mild or asymptomatic
* sneezing, coughing, occular and nasal discharge / inflammation of the trachea and lungs
* may have reduced egg production or fertility
* morbidity / mortality are low
What are the symptoms of HPAI ?
High pathogenic avian influenza (HPAI)
The addition of multiple basic amino acids at the cleavage site results in HAO being cleaved by ubiquitous proteases in a wide range of organs.
* results in a lethal systemic infection
* high mortality
* in paracute cases death may occur before the onset of clinical signs
* cyanosis of the head wattle and cone
* petechial hemorrhages on visceral organs and muscles
* blood tinged oral and nasal discharge
* greenish diarrhoea
Compare AIV and Newcastle disease ?
Similar symptoms
How would we diagnose for AIV ?
Avian influenza of all subtypes is a notifiable disease
Diagnose
* oropharyngeal and cloacal swabs
* RT-PCR conserved regions of the matrix M gene
* Virus isolation best suited in mammalian viruses
* virus may also be isolated in the allantoic / amnitotic cavity of embryonated chicken eggs
How do we control for AIV ?
Control of AIV
* stamping out programs culling
* poultry vaccination
* destocking, cleaning and rest in live bird markets
* out right ban on live bird markets
Vaccination
* vaccination is now being used in some countries, however the live attentuated vaccine negatively affects export
* in addition the vaccine only acts to suppress symptoms it is still able to spread the virus
* costly to administer
* mostly used in Asia
Describe the characteristics, symptoms and clinical signs of swine influenza ?
Swine influenza
A number of genetically diverse genotypes are circulating in pigs worldwide - H1N1, H1N2 and H3N2
Clinical signs
* characterised by a largenumber of pigs being infected but low numbers dying as a result
* going off feed
* high fever
* discharge from eyes + nose sneezing
* breathing difficulties barking cough
* huddling and inactivity
With influenza viruses why are pigs the ideal mixing vessels ?
Influenza and the mixing vessel swine
*Several elements of pigs are important in the genesis of a pandemic virus
1. pigs can become naturally infected with both avian and mammalian viruses
2. tracheal epithelium in pigs contain both alpha 2-3 and alpha 2-6 receptors
3. avian virus replication in pigs gives rise to variants recognising human like receptors
4. reasortment in pigs resulted in the emergence of the 2009 H1N1 pandemic
Describe the symptoms and chracteristics of equine influenza ?
Describe the clinical signs of canine influenza ?
How could you act to isolate an influenza virus ?
How would we diagnose for AIV ?
Avian influenza of all subtypes is a notifiable disease
Diagnose
* oropharyngeal and cloacal swabs
* RT-PCR conserved regions of the matrix M gene
* Virus isolation best suited in mammalian viruses
* virus may also be isolated in the allantoic / amnitotic cavity of embryonated chicken eggs
Provide the taxanomy and characteristics of Paramyxoviridae ?
Paramyxoviridae
* negative stranded
* sphereical filamentous
* non-segmentaed
* pleomorhic
Genus Respirovirus
* Bovine influenza, Canine influenza, Menangle virus
Genus Morbillivirus
* Measles, Rinderpest, Peste-des-petits and canine distemper
Describe bovine parainfluenza ?
Describe the epidemiology and chracteristics of canine parainfluenza ?
Canine parainfluenza 5
infectious cofactor in canine respiratory disease (kennel cough, cird etc).
Frequently causes infections of the upper respiratory tract, along with Bordetella bronchiseptica
Epidemiology
* occurs world wide
* incubation 5-9 days after virus exposure
* usually restricted to the upper respiratory tract - occasionally recovered from the lungs
* most fequently seen in kennels
* more prevalent in younger dogs
What are the clinical signs of canine parainfluenza virus ?
Canine parainfluenza virus
* 3-14 days
* mucous nasal dischrage
* dry, harsh, hacking cough
* pharyngitis
* pyrexia (temp)
* tonsillitis
* commonly involves multiple pathogens making it difficult to atribute symptoms to CPIV alone
* studies of viral pathogenesis often asymptomatic
How do we diagnose and provide prophylaxis for canine parainfluenza virus ?
Canine parainfluenza virus
* virus genome RT-PCR
* virus will replicate in cell cultures forming a characteristic syncytia
* available in a vaccine usually in combination (reduces severeity)
* CPIV is a non core vaccine AVA
Provide the epidemiology and chracteristics of Menangle virus (MenV) ?
Menangle virus (MenV)
An outbreak of severe reproductive failure and congenital defects was observed in a large piggery in Menangle NSW
* first recognised 1997 (isolated to main piggery and 2 contract farms)
* zoonotic
Reservoir = native Australian fruit bats
Transmission - bat / pig = fecal oral
human = limited bat contact, however very close contact to contaminated pigs
What are the clinical signs of Menangle virus (MenV) ?
Menangle virus (MenV)
* reduced farrowing rate (82-38%)
* reduced liter size
* delivery at term of a large number of mummified and still born piglets
* foetuses severe skeletal + craniofacial defects + arthrogyposis (joint deformities)
* no disease in adult or young pigs
* not highly contagoius slow spread
* poor survival in the environment
* brachygnathia (recession of the jaw
* domed cranium
* MenV was consistently isolated from the brain and myocardium
Describe the characteristics of Rinderpest disease ?
Describe the general characteristics of Peste-des-petits ruminants virus (PPRV) ?
PPRV
Principally a disease of goats and sheep (Rinderpest of small ruminants)
* PPR global eradication program
* very similar antigenically - antibodies are cross protective
* genetically distinct
* cattle and pigs seroconvert but do not develop or transmit disease
* wild ungulates may be affected
Describe the epidemiology and transmission of PPRV ?
PPRV
Epidemiology
* more than one billion sheep and goats are vulnerable worldwide
* PRR recently observed in South and North Africa
* Lineages 1 and 2 found mainly in West Africa
* lineages 3 found East Africa
* Also present in Asia and Europe
Transmission
* is via close contact confinemant favours outbreaks
* inhalation
* can be shed during the incubation period, and has been found in nasal, ocular secretions, saliva, urine and faeces
What are the clinical signs of PRR, Peste-des-petits ?
Clinical signs PRR
* morbidity and mortality may reach 100% in anaive herd
* young animals most susceptable
* peracute cases when first introduced to a naive herd - fever, severe depression, death
Acute cases
* sudden fever, inappetence, depression and somnolence
* nasal and occular discharge (serous non purulent)
* painful lesions on gums, lips, palate, cheeks anf tongue
* profuse diarrhea, dehydration and emaciation
* pneumonia
What observations would we make in PRR post mortem ?
Provide a general description and epidemiology of canine distmeper virus ?
Canine distemper virus
Canine distemper virus is a highly contagoius, systemic viral disease of dogs seen worldwide (including sporadic cases in Australia)
* historically common infection of dogs
* in developed countries nearly eliminated through the use of vaccines
* epidemiology is complicated due to the wide number of species it affects
* Reservoir = domestic dogs (including feral dogs)
What are the clinical signs of canine distemper ?
Clinical signs
* infection may be mild or inapparent to severe disease
* transient fever observed 3-6 days after infection (leukopenia)
* fever will subside followed by a second fever which may be accompanied by nasal discharge, lethargy and anorexia
* gastrointestinal and respiratory disease
* typically accompanied by secondary infections
* encephlomelitis may occur (swelling of the brain and spinal cord)
How do we treat and diagnose canine distemper ?
Describe observations you would make of canine distemper post mortem, and neurological signs ?
Canine distemper
Neurological signs
* A longer course of illness is associated with neurological signs
* localised involuntary muscle twitching 9myoclonus, chorea, flexor spasm, hyperkinesia)
* convulsions
* increased salivation
* chewing movements of the jaw (chewing gum fits)
* this disease should be considered in the diagnosis of any febrile conditions in dogs with multisystemic infestations
Post mortem
* ncrosis of lymphatic tissues
* interstitual pneumonia
* cytoplasmic and intranuclear bodies
* thymic atrophy
* lesions within the CNS
Describe the epidemiology and transmission of Hendra virus ?
Hendra virus
* Respiratory and neurological disease in horses
* 62 equine out breaks, 7 human infections - zoonotic
Hendra virus reservoir = Australian fruit bats through QLD and NSW - found world wide
* there is no evidence of human bat transmission
* infection of horses through contact with bat urine, placenta and uterine fluids
* between horses not highly contagious
* the clinical response and pathological findings are similar in cats to horses
What are the clinical signs of Hendra in horses ?
Clinical signs of hendra
* incubation 8-16 days
* can be asymptomatic during incubation, but will still shed the virus
* depression
* pyrexia (fever)
* dyspnea
* initial nasal discharge
* infected mucous membranes
* dependant odema
* head pressing ataxia
* sudden death 1-3 days after onset
How do we prevent and control hendra virus in horses ?
What are the clinical symptoms of Nipah virus
Nipah virus
* zoonotic
* disease in pigs
* highly contagoius - incubation period 7-14 days
* may be asymptomatic
* severe respiratory disease
* acute fever (>40)
* characteristic harsh barking cough
* mortality 1-5% adults and 40% of piglets
Neurological signs = trembling, twitching, muscle spasms, rear leg weakness, possible lameness or spastic paresis
Describe the epidemiology and characteristic of New Castle disease ?
New Castle disease
* synonymous with avian paramyxovirus 1 (APMV-1)
* mortality rates are highly variable depending upon the viral strain
* Transmission = gastrointestinal or respiratory
New Castle disease graded according to their pathogenicity ?
NCD grading
Velogenic (90% mortality)
Viscerotropic velogenic = characterised by acute lethal infections, usually with haemorrhagic lesions in the intestine of dead birds
Neurotropic velogenic = characterised by high mortality following respiratory disease and neurological disease, but where gut lesions are usually absent
Mesogenic (10% mortality)
- respiratory disease and neurological signs but low mortality
Lentogenic (negligible mortality)
- respiratory infections and or asymptomatic viruses
- frequently used as vaccine viruses
What are the clinical signs of New Castle disease ?
Clinical signs New Castle disease
* sudden drop in egg production
* eggs that are produced are abnormal (no shell, misshappen, soft)
* loss of apetite, fever, weakness
* swelling and cyanosis of the comb and wattles
* distinctive bright green diarrhoea
* up RR, respiratory distress and coughing
* high pitched sneeze
Post mortem = brain lesions, thrombosis and oedema
Nervous signs = loss of balance, circling, twisting of head and neck or complete paralysis
Describe the virulence of Newcastle disease (NDV) virus ?
How do we detect NCD ?
Describe the characteristics of all viruses ?
Viruses
- smallest infectious agent size 20-300nm diameter
- filterable agents when compared to bacteria
- only have one type of nuceic acid either RNA or DNA
- surrounded by protective protein shell = capsid
- the capsid can not be hydrolysed by enzymes
- in some viruses the capsid is enclosed within an envelope = which contains both protein and lipid
What is a viral envelope, and what is its purpose ?
Viral envelope
- viruses may mature by budding through a membrane and acquiring a lipid envelope of host origin
- viral glycoproteins which are embedded in the envelope are important in virus/ host interactions
- large viral envelope glycoproteins may be referred to as spikes or peplomers (Coronaviridae
- the envelope is usually nessary for infectivity
What is positive and negative sense viral positive or negative sense ?
How is a viral protein structural or non structural ?
Viral proteins can be structural or non structural
- structural proteins are incorporated into the virions (eg capsid protect viral genome)
- most of the non-structural proteins are enzymes
- envelope proteins are frequently glycoproteins
Provide the characteristics and taxonomy of Rhabdoviridae ?
Family Rhabdoviridae
* bullet shape
* single molecule of -ve sense RNA
What is a maintenance and spillover host in rabies genus Lyssavirus ?
Maintenance host
* the species sustains the virus life cycle
* successful control of rabies virus in the maintenance host will lead to its eradication
* dog, fox, mongoose etc
Spillover host
* species which do not normally maintain the virus biotype
* no epidemiological significance in sustaining epidemics
* usually dead end hosts
* may transmit the virus but such events are relatively rare
* human, horse, cattle, sheep and pigs etc
Describe the clinical signs of rabies in dogs ?
Clinical signs of rabies - furious and paralytic rabies
Dogs are the most important host for rabies virus (cats second most important)
Furious rabies 20%
Paralytic rabies 80%
* cause acute encephalitis (flu) in almost all species eventually leading to death
* first signs are non specific lethargy, fever, vomiting and anorexia
* progresses through to cranial nerve dysfunction ataxia, paralysis, seisures, difficulty breathing, difficulty swallowing and excessive salivation
* abnormal behaviour aggresion and self mutilation
* following first clinical signs death within four days
Describe the pathogenesis in rabies virus ?
Describe the control of rabies virus
Rabies genus lyssavirus
* in humans 100% lethal
* preventable through the use of vaccine
* 60,000 rabies deaths occur each year mostly in Asia (India)
* present with hydrophobia, abdominal discomfort and convulsions
* most lethal virus known to science
How do we diagnose rabies virus ?
What are the clinical signs of lyssavirus in bats ?
Describe the general characteristics and epidemiology of Ephemerovirus ?
Ephemerovirus in cattle
* vector is mosquitos and biting midgees
* widespread through the tropical and subtropical world
* unusual out breaks have occured in Asia in the middle East with high mortality.
* endemic NA and epidemic QLD and further Soiuth
Describe how Ephemerovirus is spread through out Australia ?
One single point of entry
Describe the clinical signs of Ephemerovirus ?
Affects cattle
Why does Ephemerovirus cause such significant economic loss ?
What are the signs of BEF in a post mortem ?
Describe how we would diagnose and control for Ephemerovirus ?
Diagnose
* First via clinical signs muscle lamenes, muscular stiffness, pain, short fever and rapid spread through out the herd
* PCR test - most successful when samples are collected in the first few days of clinical disease
* alternatively two blood samples the first taken during the fever stage and the second 14 days later. This is used to detect the pressencer of antibodies to the virus
Control
* modified live vaccine
* good levels of protection and long lasting
* first vaccine 1-2, vaccinate before spring when insect populations emerge
* annual booster
Describe the epidemiology of Vesicular stomatitis virus ?
Vesicular Stomatitis virus
Host = cattle, horses and swine
Classified as two serotypes New Jersey VSNJV and Indiana VSNJ
* sporadic activity has benn reported in Northern Mexico and Western United States
* sporadic activity is not clearly understood
* VS produces severe economic losses especially in West America where the outbreaks display a pettern of epidemics once every ten years
* New Jersey causes the majority of out breaks 80%
* infection of horses is particularly significant in the United States
* primarily domesticated horses, cattle and swine
* infection is generally short lived and self limiting
*
What are the clinical signs of Vesicular stomatitis virus ?
Vesicular stomatitis virus
* horses, cattle and swine
* first manisfestation of disease is usually excessive salivation
* blanded raised and broken vesicles of various sizes in the mouth
* foot lesions observed in horses, cattle and pigs
* pigs may go lame
* teat lesions may occur in dairy cattle
* may be confused with blue toungue or swine vesicular disease
How is vesicular stomatitis transmitted between animals ?
Transmission of Vesicular stomatitis
During outbreaks VSV spreads quickly with animal herds
Direct contact
* infected animals salivate excessively, and their saliva contains high titres of virus
Fomites
* virus laden saliva and vesicular exudates easily spread within the environment - allowing a efficient animal to animal transmission
Vectors
* mechanical and biological vectors biting flies and non biting flies
How do we control and diagnose VSV Vesicular stomatitis virus ?
Diagnose
* vesicular fluid swabs of recently raptured vesicles
* mouth and feet
* PCR and ELISA
Control
* vaccination - may difficult in areas where disease is sporadic
* can be zoological humans present with influenza like disease for a few days rarely present with vesicles
Describe the general characteristics and epidemiology of Caliciviridae virus ?
Caliciviridae virus
* +ve sense
* not segmented
* single stranded RNA virus
* generally a gastrointestinal disease
* faecal oral route
* direct contact
* can not be grown in culture
Describe the clinical signs of Caliciviridae in humans ?
Describe the clinical signs of rabbit caliciviridae ?
Rabbit haemorrhagic disease virus (RHDV)
Released in Australia and NZ for the purposes of rabbit biol-control
Transmission = direct, mechanical (flies)
- extremely contagious and fatal viral hepatitis of adult domesticated and wild rabbits
- young rabbits (less than 8 weeks are sub-clinically infected)
- incubation period of 1-5 days
- symptoms fever, anorexia, apathy and prostration (lying stretched out on the ground)
- neurological = convulsion, ataxia, paralysis
- Respiratory = dyspnoea, frothy and bloody discharge
- cyanosis of mucous membranes
- death observed 12-36 hours after the onset of fever
- 80-90% mortality
What would we observe in a rabbit with caliciviridae post mortem ?
Rabbit haemorrhagic disease (RHDV)
Due to the rapid progress of disease animals are often found in good condition after death
- liver necrosis
- splenomegaly
- triggers a disseminated intravascular coagulation and death
How do we diagnose and control Vesicular exanthema of swine virus ?
Detection
* vesicular fluid
* RT PCR and ELISA
Control
* test and slaughter
* stop swill feeding
* classified as exotic in 1959 efforts were effective
What is the pathology, clinical signs and reservoir of Vesicular exanthema of swine virus (VESV) ?
Reservoir = fish offal Transmission = swill feeding
Pathology
Known for causing a highly infectious vesicular disease in febrile swine
Clinical signs
- vesicles in the mouth, tongue, lips, snout and feet
- lesions can occur on the coronary band and between the digits
- encephalitis
- myocarditis
- fever
- abortion
- diarrhea
- hepatitis
- pneumonia and haemorrhage
- failure of recovered animals to thrive
Describe the general characteristics and epidemiology of feline calicivirus ?
Feline calicivirus
* highly contagoius and distributed worldwide
* Transmission = virus is shed in nasal, oral secretions, and faeces (oral faecal route)
* infection through the oral, nasal or conjunctival routes
* many animals will recover but continue shedding the virus (>30days)
* there are many serological strains of calicivirus with different disease presentations
Describe the pathology and clinical signs of feline calicivirus ?
Feline Calcivirus
Pathology and clinical signs
Transient viremia occurs 3-4 days after infection and there is necrosis of epithelial tissue
* oral ulceration is consistent
* pulmonary involvement is rare but may progress to pneumonia
Transient lameness
* lesions in joints
* observed a few days or weeks post acute oral or respiratory signs
* acute synovitis - thickening of the synovial membrane and an increase in synovial fluid production
* viral antigens found within the macrophages of the synovial joint
Feline stomatitis
Feline lymphocyte-plasmocytic gingivitis and stomatitis
* serious condition but uncommon
* cats present with increasingly worse inflamation of the oral mucosa
VERY DIFFICULT TO TREAT REQUIRES PARTIAL REMOVAL OF THE JAW
Describe the clinical signs of Virulent systemic calcivirus (VS-FCV) ?
VS FCV
* high mortality 70% of infected cats
* pathogenesis not well understood
* widespread lesions
* subcutaneous ulcerations - particularly on the nose, ears and paw pads
* ulceration of the mouth
* bronchointerstitial pneumonia
* necrosis of the liver, spleen and pancreas
Mutations in the genome may be responsible for this highly virulent strain, however each out break has been distinct genetically
prolonged pharyngeal carrier state - survives a long time in the environment
How do we diagnose and control feline calicivirus ?
Diagnose
* conjunctival, oral swabs
* readily propagated in culture
* RT-PCR
Vaccination is a core vaccine by AVC
The continuing mutation of the virus and large variations between countries makes this difficult
Describe the characteristics and taxonomy of the family Astroviridae ?
Astroviridae
* small
* single stranded RNA
* +ve sense
* can not be grown in a lab easily
* contain the genus Mamastroviruses (gastrointestinal) and Avastroviruses (chickens and humans)
Describe the epidemiology, diagnosis and treatment of Avian nephritis virus family Astroviridae ?
Avian nephritis virus
Distribution = widely spread world wide
Transmission = direct or indirect transmission
Host = young chicks <7days, will develop immunity at a month
* virus is consistently detected in faeces for up-to ten days
* RT PCR
No effective treatment general hygienic precautions
Provide the clinical signs of Avian nephritis virus ?
Avian Nephritis virus
* diarrhoea
* growth retardation
* kidney damage
* gout
* moderate mortality 10%
* young chicks are most susceptible but develop immunity by about 1 month of age
* histological changes can be seen in the kidney
Describe the clinical signs of Astrovirus ?
RSS runting stunting syndrome
WCS white chick syndrome
Describe the general characteristics of Hepeviridae ?
small
non enveloped
ss RNA virus
genome is linear
Two genera
Orthohepevirus
Piscihepevirus
Describe the characteristics and epidemiology of Family Hepeviridae - hepatitis E virus ?
Hepatitis E virus
HEV the most common cause of enteric hepatitis infection (20mil a year in people)
* in humans most cases are from contaminated pork liver pate
* worldwide distribution
* zoonotic
What are the clnical signs of hepatitus in pigs ?
Hepatitius in pigs (HEV)
* ubiquitous most pigs are seropositive
* infections are usually subclinical
* some may present with mild multifocal hepatic lesions
* Transmission in pigs is by direct contact with faeces or contaminated water
Describe the transmission and clinical sympotoms of avian hepatitus ?
Avian hepatitus
Is distinct from mammalian hepatitis
* big liver and spleen
* hepatitus splenomegaly HSS syndrome in chickens
How do we diagnose and treat avian hepatitus ?
Describe the family Coronaviridae ?
Coronavirus
* enveloped
* single stranded
* RNA - largest RNA identified
Describe the epidemiology of canine coronavirus ?
CORONAVIRUS
Canine coronavirus worldwide, including Australia
Transmission = faecal oral route, with some evidence of aerosols
Susceptibility
- most susceptible puppies < 12 weeks of age
- A common infection of dogs, particularly those housed in large groups eg kennels, shelters and breeding facilities
- Two genotypes CCoV1 and CCoV2, closely related but have markedly different spike proteins.
- CCoV1 co-circulates extensively, CCoV2 often occurs as a co infection
Alphacoronavirus and Betacoronavirus
- geographical distribution highly dependant on bat populations
Describe the pathology and clinical signs canine Coronavirus ?
Canine Coronavirus
Pathology
* replicates in the epithelial cells of the intestines
* changes in intestinal morphology translate into a loss of normal absorptive and digestive properties resulting in diarrhea and dehydration in affected animals
* can be fatal in young dogs, particularly when coinfected with parvovirus
Clinical signs
* most susceptible animals pups <12 weeks of age
* mild gastro intestinal clinical signs
* diarrhoea
* vomiting
* dehydration
*can become fatal with secondary infections such as parvovirus
Describe the epidemiology and clinical signs of Feline coronavirus ?
Feline coronavirus
Clinical signs
* infection often subclinical
* transient mild gastrointestinal illness in kittens
* diarrhoea, occasionally vomiting
* death is uncommon
Epidemiology
* prevalent worldwide
* prolonged shedding
* transmitted by inhalation or ingestion of virus containing faeces or through contact with fomites
Treatment is usually symptomatic
What is positive or negative sense RNA ?
Positive sense RNA = is the same orientation as messenger RNA
A positive sence RNA may act as messenger RNA.
* produce a polymerase
* a full length negative strand is produced
* and then two mRNAs are produced
What are the six viral steps in replication ?
The five steps in viral replication
1. Attachment
2. Penetration
3. Uncoating
4. Eclipse phase - replication of viral proteins and nucleic acid
5. Assembly of the viral proteins and packaging of the nucleic acids (addition of envelope in some cases)
6. release of virions (budding, or lysis)
Describe the one step growth curve of viruses ?
- Eclipse phase - replication of nucleic acids
- Latent phase - from start of infection to first appearance of extracellular virus
- exponential phase
Describe attachment in virus replication ?
Viruses attachment
* Ligands, receptors on the surface of virions bind to receptors on the cell surface
* receptors immunoglobulin family
* bond may initially be reversable (electrostatic) or irreversable (temperature dependant)
* initial binding is by electrostatic forces (depends upon electrolyte balance)
* Attachment occurs at specific sites/ receptors distributed over the cell surface, corresponding to points of attachment by peplomers
* interaction of receptor and antireceptor depends on temperature, PH and ions
Tropism - is determined by the preseence or absence of sites which determines pathogenesis or which organ is affected
Describe the two different processes of virus penetration ?
Virus penetration
Endocytosis = the virus may enter the cell by receptor mediated endocytosis. The viruses are enclosed in vessicles within the cytoplasm.
Fusion - Enveloped viruses may fuse with the cell membrane, and the viral nucleocapsid enters the cytoplasm
Describe the process of virus uncoating ?
Viral uncoating
* different viruses uncoat in different ways
* this process is brought about by lysosomes by the host
* the protein coats if more than one is present are systematically removed
* some viruses may have their own uncoating enzymes
* nucleic acid is then set free in the cytoplasm
This is the begining of the eclipse phase
What is the eclipse phase and how does it progress ?
Describe the assembly of a virus (DNA, RNA) ?
How do negative sense RNA viruses reproduce ?
Negative sense
* paramyxoviridae, Filoviridae, Rhabdoviridae
* viral transcriptase is used to produce viral mRNAs
* a full length + strand is transcribed as a template for viral RNA
* assembly takes place via budding
Why are pigs an important host in Japanese encephalitus (JeV) ?
JeV and pigs
Pigs act as an amplifying host
* two viral amplification cycles in pigs
* 1= when pigs initially become infected by biting mosquitos leading to around a 20% infection rate
* the second round involves infection of mosquitos infected by viraemic pigs
* these mosquitos then infect other pigs leading to a 100% seroconversion amongst the pig population
* dense pig herds may increase transmission
* also can transfer virus by direct transfer through the oronasal route
Removal of pigs from areas of high human population have been shown to reduce JEV burden
Provide the general characteristics, and taxonomy of the family Flaviviridae ?
Family Flaviviridae
ss (+ve sense) RNA enveloped
mosquitos
Genus Flavivirus
* JEV Japanese encephalitis, Yellow fever virus, Dengue virus, Marry Valley encephalitis
Genus Pestivirus
* Classical swine fever virus, bovine diarrhea virus
Genus Hepacvirus
* Hep C virus in humans
What are the clinical signs of Japanese encephalitis virus ?
Japanese encephalitis
Reservoir mosquito, pig and wading birds
Humans
* humans are a dead end host
* primarily affects children < 14 years of age
* most humans have asymptomatic symptoms or flu like symptoms
* in rare cases encephalitis (inflammation of the brain)
* haemorrhagic lesions may develop in the brain
* those that recover may have lifelong mental impairment and physical ailments such as difficulty speaking and moving
Pigs
* generally asymptomatic or causes mild disease - making it difficult to detect
* may have reduced fertility in boars
* increase the rate of abortion and still birth in naive sows
* encephalitis has been observed in piglets following experimental infection
Describe the epidemiology of Japanese encephalitis ?
Japanese encephalitis
JEV circulates in a natural circle envovling a range of species including Culex mosquitos, wild wading birds and pigs
* Located throughout Asia and North QLD
* reservoir wading birds, but pigs often play an important role as a amplifying host
* often clinical signs present in children <14 years of age - most people have no symptoms
Problem
* many countries in Asia do not have surveilance
* may also lack the capabilities to diagnose JEV
What is a dead end host ?
Dead end host = develop low viraemia and incapable of transmitting the disease back to the reservoir eg mosquitos in JEV
How do we diagnose and treat for Japanese encephalitis ?
Treatment
* safe and effective vaccines available (live attentuated)
* remove pig populations from urban environments
* vacc pig populations difficult due to culling at 6 months of age
Diagnosis
* serological test paired serum samples 2-4 weeks apart (compared to related circulating Flaviviruses.)
* seroconversion between paired serum samples
* RT-PCR
* immunohistochemistry
* antibody in cell cultures
Describe the epidemiology of West Nile Virus - Kunjin (WNVkun) ?
West Nile virus Kunjin
* able to infect horses, humans and frogs
* emerging virus first discovered in US 19999
* endemic to parts of Australia + notifiable disease
Describe the clinical signs of West Nile virus - Kunjin ?
Humans
* dead end host
* usually asymptomatic or mild symptoms
* in rare cases develop into a life threatening illness involving inflammation of the brain and spinal cord
How do we control for and diagnose West Nile virus ?
Diagnose
Treatment
* able to vaccinate horses, not people
* vector control eg mosquitos
Describe the general characteristics of the Genus pestivirus ?
Genus Pestivirus
Describe the epidemiology of Pestivirus Bovine viral diarrhoea ?
Bovine viral diarrhoea
* 2 genotypes BVDV-1 and BVDV-2 (not present in Australia more pathogenic)
* Two biotypes cytopathic CP and non cytopathic NCP
* NCP is the most common biotype, but recombination may result in the more pathogenic BVDV CP
* important component of the shipping fever complex
Transfer
* may cross the placenta - infecting the foetus or placenta
* horizontel spread
Describe the clinical signs of Bovine viral diarrhoea ?
Pestivirus bovine viral diarrhoea
Foetus
* may cross placenta (infect foetus or placenta), outcome depends upon stage of placental development
* NCP BVDV depends upon stage of foetus
* virues which do not kill the foetus may present in T and B cells during development
Clinical affects
* <40 days abortion, congenital abnormalities and mummification
* 40-150 daysfoetus fails to recognise the virus as foreign persistant infection develops
* 120-180 days birth defects, retinal degeneration, cerebellar atrophy or hypoplasia)
* 180+ days normal calves with antibodies
* BVDV may cause abortions throughout gestation
If there is tolerance to viral antigens the offspring may be born persistently infected
What is mucosal disease, and what are the clinical signs ?
Bovine viral diarrhoea virus - mucosal disease
This occurs to animals in utero affected with non cytopathic BVDV - or with superinfection with cytopathic BVDV
* these animals become carriers
* carrier animal dose not recognise the virus as foreign and hence does not mount an immune reaction
* it develops the foetal condition known as mucosal disease
* the onset of mucosal disease occurs when the calf is between 6 months and two years of age but can be later
* death occurs quickly after the onset of symptoms
Clinical signs
* profuse watery diarrhea, unresponsive to drenching
* chronic weight loss
* erosions (ulcers) gums, dental pad and muzzle (sometimes covered in scabs)
* excessive salivation and nasal discharge
* ulcers may occur on the coronent and between the claws of the hoof causing lameness
* death quickly after onset of symptoms
How do we diagnose and treat for BVDV ?
Diagnose
* blood samples are usually taken from suspected animals
* cows who have aborted
* proportion of the herd
* blood is tested for antibodies to the virus
* RT-PCR ear notch or blood
Managment
* identified carriers are culled
* manage the herd to maximise infection of young heifers will before giving birth
* regular vaccination against Pesti virus
Describe the clinical signs of pestivirus, classical swine fever virus ?
Classical swine fever virus
* lesions which cause damage to blood vessels
* subsequent necrosis and haemorrhage
* haemorrhages may be observed in multiple organs on autopsy
The virus is able to cross the placenta and cause infection of the foetus - could result in a persistent infection or carrier
Describe the epidemiology of classical swine fever ?
Pestivirus classical swine fever
Endemic to most countries with significant economic harm
* last time it was observed in Australia 1962
This virus is able to cross the placenta causing infection of the foetus
* this can result in a persistent infection - which may continue to excrete the virus throughout their life
How do we diagnose and treat classical swine fever ?
Pestivirus Classical swine fever
* endemic to most countries - treatment with a attentuated live vaccine
* In epidemic countries (Australia and Europe) treatment is by detection and culling
* it is vital all carriers are detected and culled
Diagnosis
* persistently infected animals do not mount an immune response - persistent viraemia may not cause a cytopathic effect detect through the use of immunostaining
* RT-PCR
Describe the epidemiology and clinical signs of Asfarviridae ?
What is the taxonomy and general characteristics of Bunyaviruses ?
Bunyaviruses
* 3 segemnt large virus
* large, medium, small segments
* some +ve, some -ve sements
* RFVF - zoonotic haemorrhagic fever viruses
* large group of viruses > 100
Includes Phlebovirus Rift Valley virus, Orthobunyavirus Akubane and Schmallenberg
Provide the epidemiology of Rift Valley disease ?
Rift Valley disease
Affects cattle, sheep and goats usually
* can infect wild life = maintenance host
* outbreaks in Kenya, Egypt
Transmission to humans
* mosquito transmitted
* can also be spread through direct contact with tissues fluids of infected animals
* aerosol
* may also infect humans and wild life
Transmission to animals
* mosquito transmitted
What are the clinical signs of Rift Valley disease ?
Rift valley disease
Mostly infects cattle, sheep and goats, but may also infect humans and wild life
Vector = mosquito
Cattle (water buffalo, camels)
* high abortion rates
* death of young animals
Humans
* flu like symptoms and death
* inflammation of the brain and a bleeding disorder
Not specific - consistent symptoms between species
* anorexia, nasal discharge, fever
* lethargy, abortion and variable mortality rates
* young animals especially susceptible
Describe the epidemiology of Genus Orthobunyavirus, Akabane virus ?
Akabane virus
Spread by mosquitos (Culicoides biting midgees) down the coast during warmer months (favourable environmental conditions)
Endemic in Northern Australia
* immunity by sexual maturity
* seroprevalance 80%
Epidemics in Southern states
* naive susceptable animals
What are the clinical signs of Arkabane virus ?
Arkabane virus
adult sheep and cattle asymptomatic
pregnant ruminants = abortion and still birth
* premature births
* dystocia
* congenital defects - hydrocephalus, hypoplasia or spinal cord ageness, microencephally, hypoplastic skeletal muscles and lungs, fibrinous polyarticular synovitus
The clinical signs varie with the stage of gestation
- early behavioural = dummy calves / behavioural abnormality and skull deformity
- second trimester severe muscle atrophy, Arthrogyrosis - rigidly flexed joints, severe muscle atrophy, scoliosis (sideways spine curvature), kyphosis
last trimester bright and alert unable to stand ataxia, paralysed limbs, muscle atrophy
Describe the pathology and clinical signs of Schmallenberg virus ?
Clinical signs of Schmallenberg virus
Adult sheep and goats = generally asymptomatic
Adult cattle = reduced milk yield, fever, inappetence, loss of body condition and diarrhoea
The problem is the virus crosses the placenta to affect the growing foetus
* the most susceptible stages 60-180 days cattle, and 15-28 sheep
* damages foetal nerve tissue and results in brain and spinal cord abnormalities, with secondary problems in the muscle and skeleton caused by nerve damage
* at term may be born alive or dead
* abortion may occur following infection of the dam
* bent limbs, fixed joints
* brain deformities (hydraencephaly), and damage to the spinal cord
Describe the epidemiology of porcine respiratory and reproductive syndrome PRRS ?
Porcine respiratory and reproductive syndrome virus PRRS
Host = pigs
Vector = Culicoides midges and crosses the placenta to affect the foetus
- Currently a common disease in the USA, Asia and Europe
- In America 60% to 80% of pigs may be infected
- exotic to NZ and Australia
Out breaks of disease have lasted between 2-3 weeks, with individual affected animals only being afflicted for a few days.
Describe the clinical signs of Porcine respiratory and reproductive syndrom virus PRRS ?
PRRS
* associated with acute out breaks of reproductive failure in sows
Fertility
* anorexia, abortions, early farrowing’s *increased frequency of still borns
* mummies
* delayed return to oestrous
*weak born piglets
Respiratory
* respiratory distress, fever, pneumonia
* skin lesions and blue ears
* increased pre-weaning mortality in pigs
Problem may be exacerbated with secondary infections of Salmonella, Streptococcus and Haemophilus
Why are persistant infections a common problem of PRRS ?
PRRS
Persistance is a critical component of PRRSV pathogenesis
Subversion of innate and humoral immune response
Evasion of humoral response is through
* glycan shielding
* genetic variation
Can block the early induction of type one interferons
Describe the epidemiology of equine arteritis (EVA) ?
Equine arteritis virus EVA
Acute contagious vial disease
Host = horses predominately in standardbreds (other breeds usually seronegative)
- has been identified in Australia since 1975
- endemic in standardbred stallions and mares in Australia and NZ
Economic loss
Direct - abortion, pneumonia, febrile (fever) disease in performance horses
Indirect loss - losses are associated with National and International trade
Describe the epidemiology and transmission of foot and mouth disease ?
Picornaviridae foot and mouth disease
Highly contagious disease of even toed ungulates - cattle, sheep, goats and pigs
Transmission
* inhalation, fomites, contact with abraded skin
* highly contagious
* animal products meat, milk, offal, semen and embryos
Listed disease of major International importance - speed of spread and severe losses of production in infected animals
There are seven serotypes and infection with one dose not counter immunity against another
* Quasispecies strains are recognised in each serotype
* Africa and Asia
Describe the clinical signs of foot and mouth disease (6)?
Picornaviridae - foot and mouth disease
Characterised by fever and the formation of vessicles
- fever loss of appetite
- reduced milk production
- potential abortion due to fever
- profuse salivation as vessicles appear in the mouth and rapidly rapture leaving painful ulcer
- vessicles also appear on the coronary band and interdigital cleft - leading to weight shifting and lameness
- vessicle may appear on the teats of lactating cows
- calf deaths may occur due to myocarditis
In pigs the hoof lesions may be more pronounced leading to sloughing
Disease in sheep and goats is generally milder
The virus dose not cross the placenta
How do we control for foot and mouth disease ?
Control
Non-endemic country - detect and cull (burn carcasses and use acid)
* the virus is susceptible to low PH
* Premises are cleaned and treated with an acid solution to inactivate the virus
Endemic country
* vaccination
* must be of appropriate serotype and subtype
* immune response does not last longer than 12 months
* disease is intolerant to modern high production systems
* trade implications
How do we diagnose foot and mouth disease ?
Describe Apthovirus Equine rhinitus A, Erbovirus equine rhinitus B virus ?
Equine Rhinitus A virus
The virus produces a systemic infection with respiratory signs Rhinitus
* foals most susceptable to rhinitis
* worldwide distribution
* recently attributed to abortions in camels
* transfer via aerosol and nasal secretions
* Diagnosis = RT-PCR or ELISA
Equine rhinitus B virus
Upper and lower respiratory tract infections in young horses
* spread nasal secretions and aerosol
* Diagnosis RT-PCR and serology
* nasal and pharyngeal swabs collected during outbreaks
Describe Genus Cardiovirus ?
Describe the clinical signs of infectious peritonitus virus (FIPV) ?
Clinical signs of FIPV
The mortality is extremely high once clinical signs are present
* some cats may survive months to years after displaying clinical signs
* most common in young cats within a crowded environment
The signs
* abdominal distension with ascites
* dyspnoea with pleural effusion
* jaundice
* disernable masses on the kidneys or mysenteric lymph nodes
* eye inflammation
* neurological signs due to brain or spinal cord involvement
What is effusive and non effusive disease with relation to FIPV ?
Describe the epidemiology of Schmallenberg Virus ?
Epidemiology of Schmallenberg Virus
Host = sheep (most common), cattle and goats
Transmission = culicoides midges and crosses the placenta
New virus discovered in Germany spread from the middle East
- Germany, the Neverlands
- Orthobunyavirus common in Asia, Africa and Australia, but not previously in Europe
Describe the family Picornaviridae ?
Picornaviridae
- Linear ss (+) sense RNA viruses
- non enveloped
- spherical
- large family of viruses
Includes
* Apthovirus - Foot and mouth disease FMD and Equine rhinitus virus
* Enterovirus
Describe the pathology of foot and mouth disease (transmission, host, spread, cause of clinical signs) ?
FMD Pathology
Host = even toed ungulates cattle, sheep, goats, pigs and buffalo etc
Transmission
* direct contact
* inhalation
* ingestion, insemination, inoculation or contact with abraded skin
* animal products meat, offal, milk, semen and embryos
Spread
* incubation 2-8 days
*Viral replication occurs in the pharynx, followed by spread through the blood stream to predilected areas - mouth, muzzle, feet and teats.
Cause of clinical signs
* vesicle formation results from swelling and rapture of infected keratinocytes, in the stratified squamous epithelium
* profuse salivation due to vesicles in mouth
* vesicle on hoof = lameness
* vesicle teat udder
* abortion = fever
* calf mortality = myocarditis
Describe host immunity to foot and mouth disease FMD ?
FMD Immunity
There are seven serotypes and immunity against one dose not confer immunity against another
Quasispecies - strains are recognised in each strain
*Pigs - feet lesions are more pronounced and the hooves may slough
* sheep, and ruminants = disease is generally milder presenting as a rapidly spreading lameness accompanied by fever
Humans = fever, vesicles on the skin and mucous membranes
Important the virus can persist after recovery in the Pharyngeal region of animals that have recovered
* persistence, three years cattle, several months sheep, unknown in pigs
* transmission from a carrier to susceptible animal has only been demonstrated in wild buffalo
Describe Avian encephalomyelitis ?
Discuss Enterovirus Swine Vesicular disease ?
Swine Vesicular disease
Epidemiology
Host = pigs
Transmission = direct contact, not spread by aerosol
* resistant to PH change difficult to clean, and remove from faecal matter
Same symptoms as FMD
* produces vesicles around the feet and mouth
* many cases are subclinical may take a long time to identify
* damage to hooves observed progressing down the hoof
Describe papillomaviridae ?
Papillomaviridae
Circular DS DNA Icosahedral
replicates in the nucleus of cells
* genome frequently remains episomal and is not integrated into host chromosomses
* not enveloped
* difficult to culture
* all mRNAs are transcribed from only one DNA strand
* highly stable genomes
- infect nearly all animals
Describe the epidemiology of papilloma virus ?
Epidemiology Papilloma virus
Distribution - worldwide most species - highly species specific
Infection = occur where there is micro-injury to stratified squamous epithelium, allowing the virus to replicated in the basement membrane
Transmission = fomites, contact with infected surfaces, halters, nose leads
* venereal transmission/ sexual transmission in cattle is common
* papilloma virus is present in normal bovine skin
Describe Papillomavirus replication
Papillomavirus replication
Papillomavirus can only multiple in differentiating stratified squamous epithelium
* only 8 active genes in the virus - so heavily rely upon the host for replication
* as the cell matures the virus shiftsgear from maintaining its genome to full blown productive function
Persistance
* because basal stem cells are self renewing, infecting them allows HPV to establish a long term reservoir of infection
* HPV does not kill its target cells and most HPV infections are inapparent
Basal cells divide it own DNA, but HPV is “stay” or “go” within the daughter cell … eventually gone (approximately 6 months to regress.
Describe the genes expressed by Pappillomavirus’ and how these genes affect the host ?
Expression of genes by papilloma viruses
Effect
* inhibit apoptosis
* inhibit immune cell signalling
* increase cellular proliferation (formation of warts)
Viruses are shed from the body through desquamation - skin shedding.
E6, E7 and E2 and expressed by papilloma viruses
E6
- binds and inhibits p53 (host tumour suppression protein). P53 acts to suppress the cell cycle if DNA is damaged leading to apoptosis.
- also activates telomerase that allows cells to replicate continuously
E7
- bind pRB (tumor suppression gene) that is involved in DNA replication and cell division - break on proliferation
E2
- normally would act to supress the expression of E6 and E7
- the integrated viral genome fails to code for a functional E2 protein
- excessive expression of E6 and E7
Describe the genes expressed by Pappillomavirus’ and how these genes affect the host ?
Expression of genes by papilloma viruses
Effect
* inhibit apoptosis
* inhibit immune cell signalling
* increase cellular proliferation (formation of warts)
Viruses are shed from the body through desquamation - skin shedding.
E6, E7 and E2 and expressed by papilloma viruses
E6
- binds and inhibits p53 (host tumour suppression protein). P53 acts to suppress the cell cycle if DNA is damaged leading to apoptosis.
- also activates telomerase that allows cells to replicate continuously
E7
- bind pRB (tumor suppression gene) that is involved in DNA replication and cell division - break on proliferation
E2
- normally would act to supress the expression of E6 and E7
- the integrated viral genome fails to code for a functional E2 protein
- excessive expression of E6 and E7
Describe the pathogenesis and clinical signs of papilloma virus ?
Papilloma virus
Pathology
The virus enters through an abrasion of the skin or reactivation of already present infection of epithelial cells.
* causes hyperplasia
* subsequent degeneration
* hyperkeratinisation
Papilloma’s persist between 1-6 months before spontaneously regressing
* multiple warts regress spontaneously
Clinical signs
multiple papilloma - wart
Bovine - mucocutaneous papilloma’s that develop on haired skin, tongue, teats and penis
- upper ailamentary papillomas (oral cavity, oesophagus, rumen).
-usually confined to the neck and shoulders
What is a sarcoid, what is it caused by ?
Bovine papillomavirus infection of another species - sarcoid
Sarcoid
Persistent and progressive skin lumps that occur mainly around the head, in the axilla and the groin region, as well as developing from wounds
- locally invasive tumor (fibrosarcoma), but do not spread to other organs
- frequently recur after surgery
- not malignant do not metastasize
PCR and immunohistochemistry
- responsible for at least 85% of skin tumours in horses
- common in horses 1-3 years of age
- natural infection of horses with BPV exposure eg cattle, fomites
Describe the clinical signs of papilloma type 2 ?
How would you go about diagnosis and treatment of papillomavirus
Papillomavirus
Diagnosis
* Clinical signs benign lesions are characteristic
* PCR - not high risk as BPV is widespread, DNA may be detected in individuals not infected
Immunohistochemical staining - using appropriate antiserum useful in confirming the presence of a specific virus
Treatment
* warts will eventually disappear without treatment - self limiting
* vaccine but no protection between strains - too many virus isolates
* Bovine interferon alpha
* IMIQUIMED topical treatment not frequently used.
Describe the epidemiology and pathology of Parvovirus ?
Epidemiology of Parvovirus
Distribution = worldwide
Susceptible = young animals neonates and foetuses
Transmission =
- highly contagious
both feline and canine parvoviruses have a common ancestor
- highly resistant to desiccation in the environment
- prefer active dividing cells within the S phase - thus cause an age dependant susceptibility - more severe in foetuses and neonates
- considerable cell division may result in widespread infection and tissue damage that causes developmental defects
- tropism for rapidly dividing haemopoietic precursors and lymphocytes, and progenitor cells of the intestinal linning
- replication of these viruses is usually limited in older animals with already differentiated organs
Many parvoviruses cause acute immune infections where as others persist for long periods in the face of a robust host immune response - not well understood
Describe the parvovirus
ss DNA virus
small
replicate in the nucleus
intranuclear inclusion bodies - histopathology
virus extremely stable in the environment
replication is completed rolling, hair pin
Describe the epidemiology of canine parvovirus ?
Epidemiology
Distribution = worldwide
Transmission = saliva, mucous, cough
Susceptible = pups 6weeks to 6 months
-Two variants CPV-2 and CPV2a
-CPV-2 was rapidly spread worldwide, then quickly replaced by CPV-2a
- CPV-2 does not infect felids, where as CPV-2a can infect cats making them asymptomatic carriers
- a highly contagious cause of acute gastrointestinal disease in young dogs
Describe the pathogenesis of canine parvovirus ?
Pathogenesis canine parvovirus
Transmission = oropharyngeal entry of virus
Require cycling cells for virus replication - infects newborn
- Pathogenesis in dogs is distinguished by the absence of cerebellar hypoplasia/atrophy and the occurrence of myocarditis in pups
Myocarditis
- due to rapid proliferation of myocytes first week after birth
- myocardial necrosis and inflammation
- results in pulmonary oedema/ or hepatic congestion from acute heart failure
Intestinal lesions
- infection and destruction of enterocytes populating the intestinal crypts
- subsequent mucosal collapse, maldigestion, and malabsorption diarrhoea
- haemorrhages may also occur in other organs
Lymphoid tissue
- can become infected with subsequent destruction of lymphocytes
- results in immune suppression
What are the clinical signs of canine parvovirus ?
Clinical signs canine parvovirus
Parvovirus is characterised by a rapid onset of diarrhoea, vomiting, anorexia, fever, depression, lymphopenia and dehydration
- foul smelling bloody diarrhoea in young dogs
- high pup mortality
- infection of pregnant bitches can result in intrauterine infection and myocarditis in new born pups
How would you go about diagnosing canine parvovirus ?
Discuss immunity, prevention and control of canine parvovirus ?
Immunity after infection is life long
- maternal antibody is transferred in colostrum - titre is variable
- protection can be form a few weeks to 16 weeks
Prevention and control
- live attenuated vaccine
- cleaning of contaminated environments is crucial
- problems frequently occur in crowded spaces, kennels, shelters and colonies
Provide the epidemiology of feline panleukopenia virus ?
Panleukopenia virus
Host = all felids
Distribution = worldwide
Transmission = shed in faeces, vomitus, urine, saliva and is very stable within the environment
- highly contagious
The virus is most common in kittens around the time of weaning when maternal antibodies wane
- cats of all ages are susceptible
Clinical signs
- cerebellar hypoplasia / atrophy
frothy at mouth or vomiting
- diarrhoea
- fever
- lethargy, anorexia
Describe the pathogenesis and clinical signs of Panleukopenia virus ?
Pathogenesis
In foetuses infected in the last two weeks, or first two weeks of life, dramatic lesions are present in the external layer of granular layer of the cerebellum.
Virus enters oropharynx and initial replication occurs in the pharyngeal lymphoid tissue
- from there a cell associated viremia via blood to other organs
- incubation 5 days
- leukopenia involves all white blood cell elements including lymphocytes, neutrophils, monocytes and platelets are destroyed.
How would you go about diagnosing parvovirus in a kitten ?
Disscuss immunity, prevention and control of panleukopenia ?
Describe the epidemiology and immunity of Porcine parvovirus ?
Epidemiology Porcine parvovirus
Occurs worldwide
Transmission = direct contact / can cross the placenta
Infection disease of reproductive failure in swine
- losses are most extreme if the virus is introduced into a seronegative herd at a time when most sows are pregnant
- in most herd a large proportion of the gilts will be infected naturally before they conceive and are hence immune
- passive acquired antibodies persist for 6 months / interfare with vaccination
- there is reduced immunity during parturition which may lead to a decline in antibodies to unprotective levels - this makes the pregnancy high risk
Describe the clinic pathology and clinical signs of Porcine parvovirus ?
Porcine parvovirus
Pathology
The outcome of disease is dependant upon the stage of gestation
< 30 days = after conception early embryonic death
30-70 days = after conception can result in the death of the foetus and sometimes mummification - no development of immune response
> 70 days = after conception the foetus mounts an immune response, clears the virus and is healthy upon birth.
- not all foetuses are infected at the same time - and death at different stages of pregnancy is typical
- some foetuses survive and are born alive but are consistently infected, thus persistent shedding
Clinical signs = SMEDI
still birth, mummification, embryonic death and infertility
How would you go about diagnosing and treating Porcine Parvovirus ?
Porcine Parvovirus
Diagnosis
frozen section of aborted foetus immunofluoresence
Haemagglutination
PCR
Serolgy - antibodies
Treatment
Vaccination of gilts - inactivated and attenuated vaccines
Describe Circoviridae ?
Circoviridae
small circular DNA virus
non enveloped
icosahedral
replication in nucleus
Beak and feather disease
Porcine Circovirus 1 and 2
Describe beak and feather disease ?
Beak and feather disease Circiviridae
Host = parrots, principally cockatoos
Transmission = horizontal and vertical
Pathogenesis
- virus replicates in the basal epithelial layer of hair follicles, beak and claw
- intracytoplasmic inclusion bodies follicular epithelium, bursa, macrophage
- lymphoid depletion
- death - the disease is progressive
- infection result in persistent immunosuppression
Clinical signs
- permanent loss of feathers
- develop beak and claw deformities
- lesions - around the feathers or beak
- leukopenia
- non regenerative anemia
Diagnosis
- intracytoplasmic inclusion bodies
- histological examination of hair follicles
- PCR
Treatment
- test and cull
- no vaccination
- strict hygiene / quarantines in breeding colonies
Describe the epidemiology and pathology of porcine circovirus ?
Porcine circovirus
Transmission = direct contact, fomites, respiratory secretions and urine
PCV1 = not common considered apathogenic
PCV2 = antigenically distinct - isolated in most regions of the world
- porcine circovirus associated disease
- occurs commonly in piglets 7-15 weeks of age
- post weaning multisystemic wasting syndrome
- characterised by inflammation in lymphoid tissue, lungs, kidney and heart
- porcine dermatitis
- nephropathy syndrome - infarctive skin lesions particularly on the rear legs and kidney
Clinical signs
- post weaning multisystemic disease
- porcine dermatitis hind legs
- nephropathy syndrome
- granulomatous enteritis
- exudate epidermitis (greesy pig disease)
How would you go about diagnosing and controlling Porcine circovirus ?
Diagnosis
RT-PCR viral load
immunohistochemistry
Good nutrition and hygiene, disinfection transmission
inactivated and recombinant vaccines
How would you go about diagnosing and treating canine coronavirus ?
Canine coronavirus
Diagnose
* A definitive diagnosis is difficult to achieve - rarely done
* PCR
* genomes have a highly variable nature
* serological test
* can only confirm exposure , and can not distinguish between infecting CCoV serotypes or genotypes
Treatment
* There is alive attenuated vaccine, however this is not available in Australia
* no available antiviral drugs
* care is usually supportive eg fluids and electrolytes
Discuss Pantropic CCoV ?
Pantropic CCoV - Pantropic canine coronavirus
Increasing reports of lethal CCoV infections in dogs
Epidemiology
Increase in severity and the emergence of novel genes CCoVs can be attributed to the high level of recombination in the spike protein
* This can occur during infection by more than one CCoV type within the host
Pathology and clinical signs
*fatal systemic disease
* high fever
* haemorrhagic gastroenteritis, neurological signs and leukopenia
Discuss canine respiratory coronavirus CRCoV ?
Canine respiratory coronavirus CRCoV
Distribution = UK, Canada, USA - not in Australia
Transmission = inhalation, or contact with contaminated droplets on surfaces - highly contagious
- beleieved to have originated from bovine coronaviruses
CRCoV occurs in dogs of all ages
- causes mild respiratory disease often with coinfections
- may be involved in the canine respiratory disease complex
Describe the epidemiology and clinical signs of feline enteric coronavirus (Genus Alphcoronavirus) ?
Feline enteric coronavirus
Epidemiology
Distribution = worldwide, highly prevalent
Transmission = ingestion or inhalation of virus containing faeces, or through contact with contaminated fomites
* two genotypes exist type one is unique to cats, type two recombinant with canine coronavirus.
Faecal shedding begins within a week of infection and continues at high levels for up to two months. However lower shedding may continue for months or unto two years.
Clinical signs
Infection is often a subclinical or characterised by transient, mild gastrointestinal illness of kittens.
* diarrhoea
* occasionally vomiting may become acute or severe
* death is uncommon
Usually treated through symptoms eg fluid, electrolytes
Describe the epidemiology of infectious peritonitis virus (FIPV) ?
FIPV - Infectious peritonitis virus cats
There is a general consensus that FIPV arise by internal mutation from FECoVs
* the causative mutation occurs independently within each cat
* there are three mutations involved
* initially the mutations cause a switch from enterocyte to macrophage tropism
* this ultimately leads to infection, replication and survival in peritoneal macrophages
* only 1-5% of FECoV infected animals develop FIP, mainly kittens
Susceptability =
Although cats of any age can become infected it is more prevalent in kittens 4-16 months of age
- animals loaded in crowded places eg catteries, shelters and vets
Describe the clinical signs of feline infectious peritonitis virus (FIPV) ?
Clinical signs FIPV
The mortality is extremely high once clinical signs appear - although some cats survive for weeks, months or years
Clinical signs
* undulating antibiotic resistant fever
* abdominal distension with ascites (fluid build up)
* dyspnoea and pleural effusion
* disernable masses on the kidneys
* eye inflammation
* neurological signs due to brain and spinal involvement
Wet effusive FIP = Accumulation of fluid within the abdomen or chest, which can result in breathing difficulties
Dry non effusive FIP = similar clinical signs with out the accumulation of fluid
* cats with dry FIP are more likely to show ocular or neurological signs
Variable time to death
- shorter young cats
- shorter in cats with effusive disease
How would you go about diagnosing and treating feline enteritis coronavirus ?
Diagnose
* common in faeces from diarrhoeic or healthy shelter cats
* low intrinsic disease potential
* cats with FIP often shed FECoV, it is inconsistent and the virus is shed at lower levels than in healthy cats
* virus is usually of the enteric and not the FIP biotype
Treatment
Currently there is no effective treatment
no efficious vaccines for FECoV or FIPV
Describe the epidemiology pf porcine transmissible gastroenteritis virus ?
Porcine transmissible gastroenteritis virus (TGE)
Transmissible gastroenteritis virus (TGE) is a common viral disease of the small intestine that causes vomiting and profuse diarrhoea in pigs of all ages.
Distribution = most pig producing countries but not Australia
Transmission = easily spread during an epidemic, by animal contact and fomites (more prominent in water)
- appears to have originated from Canine coronavirus
Describe the pathology and clinical signs of Porcine transmissible gastroenteritis virus (TGE) ?
TGE
Pathology
* TGEV infects and destroys the villous epithelium cells of the jejunum, and ileum
* severe villous atrophy, malabsorption, osmotic diarrhoea and dehydration
* more prominent in winter
Clinical signs
* vomiting is the initial sign, followed by profuse watery diarrhoea
* dehydration and excessive thirst
* faeces of piglets often contain curds of undigested milk
* small intestine dilated with gas, thin walled
* mortality of piglets <1week old 100% usually through dehydration
How would you go about treatment and prevention of Porcine transmissible gastroenteritis virus ?
Treatment
* There is no specific treatment
* supportive care to prevent dehydration and heat loss
Vaccinate
* avoid vaccinating herds free of TGEV
Describe Retroviridae ?
Retroviridae
The only viruses which are diploid
- two single stranded RNA molecules are converted into a double stranded DNA molecule (reverse transcriptase)
- lacks the usual prrofreading of DNA, hence they mutate often
The DNA copy of the genome (provirus) is inserted into the DNA of the host cell that it invades - thus changing the genome of that cell.
This integration underlies the ability of retroviruses to cause persistent infections
What is an exogenous and endogenous retrovirus ?
Exogenous retrovirus =
Are transmitted horizontally among the host animals - not common
Endogenous retrovirus =
Are inherited vertically in the genomes of the host
- replication of a provirus in a host germ cell, the provirus may be inherited by the host’s progeny and down the generations as a ERV
-5-8% of human genome
- all vertebrate genomes examined so far contain ERV
Describe the epidemiology of Feline immunodeficiency virus (FIV) ?
Feline immunodeficiency virus
FIV decreases the function of the immune system of domestic and wild cats
Distribution = worldwide including Australia
Transmission = spread from cat to cat through saliva, primarily by biting
Susceptible animals =
- cats which roam outside
- once cats become infected they are infected for life, and most eventually have a deterioration of immune function and increased risk of other infections
Describe the pathology and clinical signs of feline immunodeficiency virus (FIV) ?
Feline immunodeficiency virus (FIV)
All animals become persistently infected
- a transient disease coincides with initial viremia thereafter, animals remain extensively healthy for many years
- increased viremia in later stages of disease is associated with opportunistic infections
- decrease CD4 + cells
Clinical signs
- increased likely-hood of acquiring other secondary infections
- increased risk of developing certain types of blood cancers: Lymphoma and leukamia
How would you go about preventing or treating feline immunodeficiency virus FIV ?
There is no effective treatment
Prevention
- provide supportive care
- prompt treatment of secondary infections
- balanced diet, control parasites and removing tumours
The best preventative measure is to spay/ neuter cats and keep them indoors to prevent exposure
A vaccination is available - but not all cats will be protected so it is better to prevent exposure (non-core)
How would you go about diagnosing FIV ?
Describe the epidemiology of Feline leukaemia virus (FeLV) ?
FELV epidemiology
Distribution = worldwide including Australia
Transmission = oronasal contact
* infections with saliva, urine represents the most likely mode of horizontal transmission
* the virus replicates in the oropharyngeal lymphoid tissue
* from there carried in the blood by mononuclear cells to the spleen, lymph nodes, epithelial cells of the intestine and bladder.
There are four FeLV subgroups of clinical importance
Almost all naturally affected cats are originally infected by FELV-A
Once a cat is infected with FeLV - A, a mutation of the virus can lead to new FeLV subgroups -
FeLV - B = increase neoplastic diseases
FeLV - C = erythroid hypoplasia and extreme anemia
FeLV - T = infect and destroy lymphocytes / immunodeficiency (rare)
Describe the pathology and clinical signs of FeLV (feline leukaemia) ?
Pathology and clinical signs
Immunosuppression is the single biggest cause of clinical signs in FeLV cats
* chronic and recurrent disease
* progressive deterioration over time
* extremely diverse clinical signs
* fever, lethargy, weight loss, persistent respiratory problems, skin and intestinal problems
* anaemia, neoplasia, reproductive problems, enteritis
* neurological dysfunction and stomatitis
How would you go about diagnosing, preventing or treating feline leukaemia virus (FeLV) ?
Prevention
* virus is unstable and susceptable to disinfection
* kittens most at risk
Treatment
* vaccination (non - core)
* avoid stress provide good husbandry
* some cats survive for years without serious complications (average 2.4 years)
Diagnosis
* PCR, rapid immunoassays and ELISA
* FeLV subtypes must be distinguished by sequence analysis
Discuss feline foamy virus ?
