Virology 2 Flashcards
Togaviridae what are the 2 genera within and the main diseases of veterinary importance
1) rubivirus -> Rubela
2) Alphavirus -> Equine encephalitides (EEE, VEE, WEE), Getah virus
Togaviridae features, transmission and where replicate
- Enveloped single stranded positive sense RNA viruses
- Replicate in cytoplasm to very high titres in mammalian cells with severe cytopathic effects (no CPE in insect cells)
- Arboviruses -> vector transmission
What are the following diseases
EEE, VEE, WEE
EEE = eastern equine encephalitides VEE = Venezuelan equine encephalitides WEE = western equine encephalitides
Equine encephalitides what type of virus, when maximum disease. when/what disease is horse an amplifying host and when human cases
Famile Togaviridae, Alphavirus
- Peak periods of disease when climate favours maximum vector numbers (Late Summer after heavy rainfall)
- Viraemia in horses with VEE (only this one) is sufficiently high titre for horses to be a source of virus for vectors (amplifying host)
Human Disease
- Cause CNS disease in humans
- EEE – case fatality rate 50-75%
- WEE less severe disease in humans (case-fatality 3-10%)
Explain the transmission cycle of Eastern equine encephalitis virus
maintained in cycles involving mosquito vector and passerine birds (generally)
- Outbreaks of disease when sufficient infected vectors for virus to “Spill over” into horse and human populations
○ Generally bite birds, some mosquitoes are less host specific so if too many and not enough birds then will bite mammals (dead-end host) -> act as bridge vectors
transmission cycle of
Venezuelan equine encephalitis virus
Can cycle within small mammals - enzootic - endemic (present in high amounts in normal population)
- Virus mutation within the small mammal cycle lead to spill over into epizootic cycle as can now infect other mosquitoes (bridging vectors) that result in large mammals being infected
- Horses can amplify the host therefore the virus can cycle within large mammals
- Still get outbreaks in horses and humans
Epizootic define
a disease that is temporarily present and widespread within a population
Equine encephalitis what are the stages wtihin the host
1) Primary viraemia allows spread to muscle and connective tissues and reticuloendothelial system
2) Secondary replication in these tissues leads to secondary viraemia of high titre to allow CNS invasion
○ Neural necrosis, mononuclear infiltration with perivascular cuffing and interstitial oedema (VEE also involves respiratory tract) - if recover never make a full recovery as neurologically damaged
What are the clinical signs of equine encephalitis
- Very similar EEE, VEE, WEE
- Incubation up to 9 days
- Range from mild fever and depression to fatal febrile encephalomyelitis
- CNS signs: photophobia, head pressing, circling, ataxia, blindness, inability to swallow
- Low carriage of head with wide base stance - heavy head
equine encephalitis diagnosis and what makes it hard
- Viraemia is transient – isolation from blood difficult
- Serology – IgM ELISA - harder to do with arboviruses, sensitivity and specificity not great
○ IgM need to take two tests to make sure IgM is increasing -> exposed recently
○ Neutralisation on paired sera
What are the two main control methods for equine encephalitis
1) Vaccination available in endemic areas
- depends on geographical area to whether include all or not, live VEE, inactivated EEE, WEE
2) vector control -> insecticides, repellent, insect proof stabling
What are 3 main arboviruses endemic to Australia and hosts
- Ross River virus - first found in ross river in Townsville (Family Togaviridae) people, horses
- Murray Valley encephalitis virus (Family Flaviviridae) people, horses
- WNV(west Nile virus) - same thing (Family Flaviviridae) person, horses ?dogs, donkey, alpacca?
Ross River virus what are the 3 main clinical signs, diagnosis, reservoir host
- Fever, rash (often) and polyarthritis (muscle soreness most common)
- Serological diagnosis (IgM, or IgG seroconversion) - better test for humans
- Grey kangaroo thought to be reservoir host (bats?)
Family Flaviviridae features, where replicate
- Enveloped single stranded positive sense
- RNA viruses
- Replicate in cytoplasm
- Mature virions quite labile:
○ sensitive to heat, detergents, common disinfectants
Family Flaviviridae what are the 3 genera and veterinary disease within
1) FLavivirus -> Japanese Encephalitis virus, west nile virus
2) Hepacivirus -> hepatitis C virus
3) Pestivirus -> bovine viral diarrhoea, classical swine fever
Genus Flavivirus how transmitted, what lead to and target organs
- Bite from infected arthropod - arbovirus
- Viraemia
Dissemination to target organs (endothelium, liver, foetus, CNS)
Japanese encephalitis what type of virus, what are the main hosts and what leads to
Family Flaviviridae, Flavivirus
1) Water birds are the main reservoir host
2) Pigs are important amplifying hosts - have a high enough titre of virus that allows vectors to become infected
○ Show reproductive loses no encephalitis
3) Infections in humans and horses (dead end hosts) often cause severe and fatal encephalitis
4) Inapparent infections in other species
Japanese encephalitis what type of virus, what general cycle and diagnosis techniques
Family Flaviviridae, Flavivirus
Generally maintain in mosquito - bird cycle but if go into pig population
Diagnosis:
- Brain, tissue samples and blood for serology
- Virus isolation (intracerebral inoculation of suckling mice)
- Inactivated and live vaccines available for humans and horses - quite affective
West Nile Virus what type of virus, where present, what is teh cycle maintained within and what can it cause
Family Flaviviridae, Flavivirus
- Occurs throughout the Mediterranean, Asia and Africa - Recent incursion into United States
- Urban bird – mosquito cycle
- Can cause (fatal) encephalitis in horses and haemorrhagic fever in humans
West Nile Virus how monitored and controlled in America
1) Monitored spread by testing dead birds
- American species of birds experience significant disease and death unlike Australian birds as hadn’t co-evolved with this virus
2) vaccine - killed virus product, needs 1 booster annually
Murray Valley encephalitis virus what type of virus, what vectors, result of disease
Family Flaviviridae, Flavivirus
- Culex species were the vectors
- Often subclinical but some severe disease - can result in death
Serological and virological tests to identify
Bovine viral Diarrhoea virus what type of virus, what are the 2 disease types and the two main populations infected
Family Flaviviridae, Pestivirus
1) Acute disease – bovine virus diarrhoea
2) Chronic disease – mucosal disease (persistent infection)
1) Non-pregnant cattle - usually trival
2) pregnant cattle -Outcome of transplacental infection of foetus depends on the age of the foetus and the virus strain
What is the critical stage with Bovine viral Diarrhoea virus foetal infection when tolerance occurs and outcome
Infection early in gestation (80-125 days)
- Tolerance - no antibody response as doesn’t recognise as foreign
Therefore when born shedding lots of disease through faecal oral route and infecting other cows
- Not an issue until the virus mutates and leads to the chronic disease - MUCOSAL DISEASE in the calf- FATAL
What is the result of Bovine viral Diarrhoea virus foetal infection
- Mucosal disease
- Profuse watery diarrhoea
- Nasal discharge, salivation
- Ulcerative lesions - Fatal
- Usually within weeks
Bovine viral Diarrhoea virus 3 diagnosis and 2 ways to control
- Isolate virus / detect virus antigens (3 cultures)
- Immunofluorescence on smears of tissue
- Serology (4 fold increase in neutralising titre)
How do you control Bovine Viral Diarrhoea?
1) Killed and live to vaccines
- Not fully protective, may induce MD (mucosal disease) in persistently infected animals (tolerant calves)
2) Remove persistently infected animals (source of virus)
- How do you identify seronegative animals?
- Identify the cases of disease?
Family Arteriviridae what are the two main genus features and viruses within
Genus Arterivirus
- Host specific (horses, pigs, mice, monkeys)
- Antigenically unrelated
- Macrophages are the target cell
Two viruses of interest in this Family
1) Equine Arteritis Virus (EAV)
2) Porcine Respiratory and Reproductive Syndrome Virus (PRRSV)
Order Nidovirales (nested)
- Enveloped, 40-60nm
- Replicate in the perinuclear cytoplasm - macrophages
- Relatively labile – sensitive to heat, low pH, detergents, disinfectants, UV irradiation,
Equine viral arteritis what type of virus, where occurs, clinical presentation, clinical signs
Family Arteriviridae, Arteivirus
- Occurs worldwide, have the virus in Australia but generally don’t see disease
- Most infections are asymptomatic
- Outbreaks of clinical disease are rare but large clinical signs
1. Infectious dose - shorter during outbreak as infectious dose is higher
2. Strains - high virulence vs low virulence strains - large variations within the population - Present with fever, excessive lacrimation, conjunctivitis, rhinitis and nasal discharge, stiff gait, ventral oedema
- More severe in very young / old animals
- Abortion (storms) - lots of mares together after rule out equine herpes virus-1
Equine viral arteritis what host most susceptible and why, how long does infection last, carriers? and what cause
- Horses > mules > donkeys are susceptible to infection
○ Standardbreds greater than Thoroughbreds - possible due to large amounts of AI - Virus is eliminated from mares and geldings
- Persistent infection of 35% stallions (doesn’t effect fertility)
- Asymptomatic carriage and shedding by stallions
Equine viral arteritis what are the 3 main ways of transmission
1) Transmission via respiratory tract:
- aerosol from respiratory tract, aborted conceptus
- Virus spread between the mares
- replicate in alveolar macrophages
2) Transmission via genital tract:
- 35% of stallions chronically shed EAV in semen - sexually transmitted
3) Transplacental transmission:
abortion storms (for this to occur mare will get transmission via respiratory tract from other mares, as cannot be sexually transmitted from stallions as stallion will not mate if the mare is pregnant)
Equine viral arteritis primary and secondary targets, diagnosis and control
- Primary targets- macrophages (viraemia) and endothelium - secondary signs
○ Secondary - most organs (kidneys, liver, seminiferous tubules) - at this sites able to chronically persist
Diagnosis: - RT-PCR (of foetus) or virus isolation from semen, respiratory samples
- Serology – neutralisation, CF, ELISA
Control: - Vaccinations available - potential males to breed should be vaccinated in areas with high disease
- Carrier stallion - ??future??
○ Decrease testosterone possible decrease shedding through semen
Porcine Respiratory and Reproductive Syndrome Virus what are the 2 main clinical signs, is it present in australia and host
1) reproductive failure in sows (reudced conception, farrowing rates
2) pneumonia in young pigs (respiratory distress and cyanosis of skin particularly around ears, vulva and abdomen)
○ Exacerbated by concurrent infection (Mycoplasma spp., Streptococcus suis)
- Exotic to Australia (North America and Europe)
Family Birnaviridae features and variation
- Non-enveloped - highly resistant in the environment
- Low and high virulence strains
Family Birnaviridae what is the main disease within, morbidity and mortality, transmission (replication), clinical signs and control
Infectious bursal disease of chickens
- Morbidity approaches 100%
- Mortality up to 90% - depending on the strain of the virus - can be very high or very low
- Oral route of transmission -> Preferential location in bursal lymphoid cells
- Depression, ruffled feathers, diarrhoea, dehydration
Control -
- No effective vaccine
- Extremely stable in environment
Cleaning and disinfection usually ineffective
Family Caliciviridae What are the 2 genera and important disease within
1) Genus vesivirus - Feline calcivirus infection
2) genus lagovirus - rabbit haemorrhagic disease virus
Family Caliciviridae features, where replicate and how released
- Non-enveloped
- Single strand positive sense RNA viruses
- Replicate in the cytoplasm of infected cells
- Released by cell lysis
- Relatively resistant to heat and detergent based disinfection
- No resistant to acid pH (99% inactivated pH<3)
Feline Calicivirus Infections what type of virus, what lead to, ages found in, how long last
Family Caliciviridae, vesivirus
- Significant upper respiratory tract pathogen of cats
- Cats of all ages susceptible
- Acute disease most common in kittens - 2 – 6 months as maternal antibody wanes
- Excrete large amounts of virus in oronasal secretions
- Persistent infection: after recovery, or after sub-clinical infection when protected by maternal antibody or vaccine
○ Small amount of cats
○ Shed virus for months – years from oropharynx
Feline Calicivirus Infections transmission, where replicates, incubation period, clinical signs and control
- Transmission by inhalation of aerosol or direct contact via oral nasal or ocular route
- Virus replication in oropharynx
- Incubation period ~ 5 days
- Conjunctivitis, rhinitis, tracheitis and pneumonia
- Vesiculation and ulceration of tongue and oral mucosa - hypersalivation
Shifting lameness
Control - vaccine F3 highly effective
Rabbit haemorrhagic disease what type of virus, what lead to, transmission, where replicate and control
Family Caliciviridae, lagovirus
- Highly contagious and often fatal disease of European rabbits -> sudden death
- faecal-oral route
- replicate in mononuclear phagocytic cells
control - inactivated vaccine in Aus
Family Paramyoviridae features where replicate and what are the 2 important molecules and their functions
- Enveloped
- Single strand negative sense
- RNA viruses
- Replicate in cytoplasm and bud through cell membrane
- Envelope covered in large peplomers
Two major glycoprotein peplomers:
1) HN: Haemagglutinin / Neuraminidase protein role in attachment neutralising antibodies are directed against HN
2) Fusion protein: cleavage of F protein essential for infectivity - determines virulence of virus
What molecule determines virulence and how
- More proteases present that can cleave F protein the higher the virulence of the strain - determined by the amino acid sequence of the F protein
Define velogeic, mesogenic and lentogenic strains
Velogenic = high virulence Mesogenic = intermediate Lentogenic = low virulence
Genus Rubulavirus what are the 3 main diseases
- Newcastle Disease
- Canine parainfluenza virus 2 (Kennel cough complex)
- Mumps
Newcastle disease what also called, how contagious, what characterised by and how vary
Avian paramyxovirus 1
- Important disease of poultry worldwide
- Highly contagious
- Spreads rapidly among susceptible birds
- Characterised by respiratory, gastrointestinal and nervous signs
- Virulence varies between strains - only called Newcastle disease if the highest virulence
Newcastle Disease what are the 4 characteristics that clinical presentation relates to
1) Age of chicken
2) Immune status
3) Tissue tropism - viscerotropic or neurotropic
4) Virulence
1. Velogenic strains are highly virulent
2. Lentogenic - mild disease or inapperant infection
3. medogenic - intermediate virulence -> mild disease and some mortality
Newcastle Disease (Avian paramyxovirus 1) where does replication occur, transmission and hosts
- Virus replication in epithelia of respiratory and gastrointestinal tracts
- Transmission by inhalation of aerosols or ingestion of contaminated food or water
- Virus is excreted in faeces, from respiratory tract and survives in environment and in carcasses for weeks
- Wide range of avian species are susceptible chickens (main), turkeys, ducks, geese, pheasants, pigeons…
Newcastle Disease (Avian paramyxovirus 1) Diagnosis and control
Diagnosis 1) virus isolation in embryonated eggs Control - ND free countries: test and slaughter - ND endemic countries: attenuated live vaccine strains
Rinderpest what type of virus, when eradicated, mortality and morbidity, how many serotypes and transmission
Family Paramyoviridae, Morbillivirus
- 2011, high morbidity and high mortality
- One serotype, but different strains recognised
- Infection requires close contact - Virus is labile in environment - doesn’t survive in environment
= No carrier state (young animals affected in endemic areas)
What are the 4 stages of clinical signs in rinderpest
1) mucosal phase: necrotic foci develop in nasal, oral and urogenital mucosa
2) necrotic -> erosions -> ulcers appear
3) profuse haemorrhagic diarrhoea
4) death within 12 days
How was rinderpest eradicated
○ Vaccination: attenuated vaccine (eradication planned by 2010, achieved 2011)
§ Lasting immunity to vaccine, no carriers, no animal reservoir, good diagnostic tests
Canine Distemper what type of virus, where found, transmission
Family Paramyoviridae, Morbillivirus
- Highly contagious disease of dogs and carnivores
- Worldwide distribution
- Generalised infection affecting many organ systems
- Requires direct contact or close aerosol transmission
- Virus shed in expired air, faeces, urine, other secretions
Canine Distemper how susceptible and disease within urban and rural dogs
Urban dogs: infection spreads rapidly among young dogs as maternal antibody wanes (3-6months)
Rural dogs: lower population pressure, more susceptible, unvaccinated dogs. Outbreaks in dogs of varying ages
Canine Distemper incubation period, and clinical signs
- Incubation 3- 6 days
1) hyperkeratosis of nose and footpads
2) acute disease is followed by recovery and life-long immunity, or progresses to CNS disease
○ Neurological signs include myoclonic contractions, ataxia, paresis, seizures and death
○ Grave prognosis for dogs with neurological signs
○ Old dog encephalitis: persistence in brain, motor and behavioural deterioration, invariably fatal
Canine Distemper pathogenesis, diagnosis and control
Pathogenesis:
- Initial replication in upper respiratory tract
- Cell associated viraemia (lymphocytes) carries virus to reticuloendothelial system
- Secondary viraemia spreads virus to mucosal epithelium of GIT and respiratory tract and to CNS
- Infects neurons and glial cells in CNS
Diagnosis:
- Presumptive
- Immunohistochemistry on smears from discharges
Control:
- Vaccination is very effective
- Maternal antibody
Hendra Virus what type of virus, what look like originally, reservoir and clinical signs
Family Paramyoviridae, henipavirus
African Horse Sickness
Reservoir - flying foxes (fruit bats)
Clinical signs
- Congested, firm, fluid filled lungs, with dilated lymphatics
- Thick, foamy, haemorrhagic exudate in airways
Nipah Virus what hosts, and what can it lead to
Pig Industry Costs
• 901,000 pigs culled on 896 farms in the outbreak areas
Orthomyxoviruses what are the main viruses within
Influenza virus
A,B and C
Influenza viruses features and the 2 main molecules
- Enveloped virus - susceptible
- RNA virus, dynamic viruses that change all the time
- Segmented genome - 8 segments
1) Haemagglutin molecule - responsible for getting virus into the cell
2) Neuraminidase molecules - responsible for getting out of the cell
Influenza A list 2 respiratory and 1 GI and respiratory and whether exotic or present
Respiratory - Equine influenza - EXOTIC - Swine influenza - EXOTIC GI and Respiratory - Avian influenza
Influenza what are subtypes based on and subdivided into
- Subtypes (serotypes) based on antigenicity and genome type of the Haemagglutin and neuraminidase molecules (HA and NA)
- All subtypes are present in the wild
- Subdivided into strains
○ At the strain level there is cross-reaction between antibodies for both HA and NA
Influenza A what are the 4 generall clinical signs, transmission
Clinical signs - Intestinal diarrhoea - Coughing sore throat - Lethargy - Lack of appetite Respiratory and faecal oral for brds
Swine influenza; H1N1 what is important about this
- Subclinical infections mask shedding
- High morbidity, low mortality (<1 – 4%)
- Common interspecies transmission – horse, humans, birds
- Closely monitored as a source of potential pandemic viruses
Equine Influenza - H3N8 (& H7N7) how long incubation period, clinical signs and vaccine
- 1 – 5 day incubation period in naïve horses
- Fever, nasal discharge
- Distinctive harsh dry cough that may persist for weeks
○ Vaccination with poor match to circulating strains
§ leads to clinical protection as doesn’t stop virus from replicating just stops clinical signs, in the perfect world want virological protection - Highly contagious
Avian Influenza where replicate what are the highly pathogenic strains and what molecule based on
- Respiratory and intestinal viral replication - different
- Highly pathogenic (HPAI) isolates usually H5 and H7 subtypes
- BASED ON HAEMAGLUTTIN PROTEIN
- Respiratory signs more obvious
- Coughing, sneezing, excess lacrimation and sinusitis
- Decreased food consumption
- Egg production drop up to 45%
- LPAI can mutate to HPAI (high pathogenic avian influenza virus) during LPAi outbreaks allowed to continue without adequate control or eradication
Highly pathogenic avian influenza (HPAI) what are the clinical signs
- Disease can occur suddenly without any premonitory signs
- Sudden death - 24 hours after 1st signs
- Watery diahorrea, excessive thirst
- Nervous signs
- Inappetence, staggering gate, ruffled feathers
- Laboured respiration, fever, halt in egg production
Cyanosis of combs, wattles and shanks, oedema of head
List 3 areas to get samples for Avian influenza and 4 diagnostic procedures
1) swabs in viral trasnport media -> nasal, tracheal
2) blood for serum or plasma
3) tissues
DIAGNOSTIC
1) quantitative RT-PCR
- As RNA virus need reverse transcriptase
2) Virus isolation
- embryonated hen eggs
- cell culture
3) ELISA eg. Directigen®
- (detects NP Ag)
4) HA; haemagglutination assays
Avian influenza what are some important control methods and what are the 3 things prevention relies on
- Asymptomatic wild waterbirds as reservoir
- Controlled by ‘all in - all out’ policy and segregation from wild birds
1) Early detection and warning
2) Biosecurity - movement control - effective in equine influenza outbreak
- natural/artificial boundaries
- management practices - generally all culled in avian influenza
3) Surveillance; Rapid confirmation of suspect cases
Influenza Immunity what are the antibodies targeted to and describe their structure and function
- Protective antibodies directed to HA (Haemagglutinin) and NA (Neuraminidase)
HA - homotrimer, used to attachment and fusion of virius into the cell (needs to be cleaved for fusion to occur)
NA - tetramer, assists exit from cell and promotes access to epithelial cells through mucous degradation
Why are influenzza viruses so successful
Long term success of influenza primarily due to genetic and antigenic variation in HA and NA
- Antigenic variation - results in
1. Reduced efficacy of pre-existing antibodies (from previous infection or vaccination)
2. Decreased immunity
3. Increased susceptibility to new strains/subtypes
What are the 2 process that lead to antigenic variation
1) ANTIGENIC DRIFT - new strains of the same subtype
2) ANTIGENIC SHIFT - new subtypes - results in pandemics and epidemics
Antigenic DRIFT what are the 5 steps and result
- Host has neutralising Ab to HA or NA
- Infecting virus has random mutations throughout genome, including HA or NA
- Some neutralising antibody no longer binds
○ mutants escape neutralisation -> survival advantage - Process repeats in successive hosts
- Amino acid mutations gradually accumulate
= NEW STRAINS (same subtype)
RESULT - Prexisting antibody becomes less effective -> continual reinfection with emerging strains of same subtype
- need frequent update of vaccine strains
Antigenic SHIFT list the 3 main steps and the result
- Genetic reassortment between subtypes - most common
- Direct transfer of a subtype from one species to another (due to segmented genome -> co-infection of same cell results in segment reshuffling)
- The re-emergence of a subtype in a species that has not been circulating for some time
Antibodies to one subtype do not protect against another subtype
- If the new subtype can be easily transmitted between individuals, antigenic shift results in epidemics or Pandemics
Influenza vaccines what correlates wtih protection and which species are vaccines commonly used and teh types
- Effective match between available vaccine strains necessary for best protection
- Levels of antibody to HA correlate with protection
- Human, equine; widely used
- Swine; less common
- Avian; historically less common
1) Inactivated - most common, annual updates but safe
2) live - increasingly useage as better protection
What are the 2 main properties of pandemic influenza and list possible threat
1) new virus. population with no/limited pre-existing immunity
2) easily transmitted
THREAT - HPAI H5N1
- poultry to human infection, no suspected human - human, high mortality in humans, proven ability to reassort
Family Picornaviridae list 5 main genera and the important one with disease
1) Apthovirus - Foot and mouth disease
2) Enterovirus
3) Cardiovirus
4) Rhinovirus
5) Erbovirus
Family Picornaviridae features and defining characteristic ,
• Non – enveloped ○ pH label • Icosahedral • Single stranded positive sense RNA • Very efficient, cytocidal replication (1 million viruses/cell – 3 hours) - highly contagious and rapid spread
Foot and mouth disease what type of virus, what is risk in australia and how trying to prevent
Family Picornaviridae, Apthovirus
- Considered Australia biggest biosecurity risk
- Reducing and eliminating FMD from South-East Asia is an important strategy○ Difficult to eradicate - MONEY
○ Free from FMD without vaccination is preferred status -> little restriction of trading with live export and other countries
○ If FMD endemic -> fierce competition for access to lucrative markets
§ Most countries just don’t trade with
Foot and Mouth Disease what type of disease, mortality and morbidity, what is the main concern with cattle and pigs
Family Picornaviridae, Apthovirus
- highly contagious
- very high morbidity / low mortality (generally)
- dramatic reduction in production (especially cattle
○ Dairy cows decrease milk production, lactation may stop
○ Pigs - weight loss and mortality
○ disease of economic importance (direct and trade)
§ in Australia if get outbreak would cost about $50 billion as would take over 10 years to get all exporting back
§ Estimated global impact 7-21 billion USD/year
List 7 reasosn why Foot and Mouth disease is difficult to control
1) Multiple host species - any cloven hoofed animals (not horse) -
2) Multiple modes of transmission
3) Multiple serotypes - 7 serotypes and NO CROSS PROTECTION - important with vaccines
4) Small infective dose
5) Rapid replication -> Virus shedding before clinical signs
6) Highly contagious - excretions and secretions - aerosols
7) Carrier state - some ruminants may become persistency infected
Foot and mouth disease list the clinical signs
- Vesicles develop (<24 hours): - VERY PAINFUL
○ Tongue and oral mucosa
§ Excessive salivation - just don’t want to swallow or drink
○ Interdigital region -> Coronary bands
○ Teats, nasal mucosa, muzzle
○ Vesicles coalesce and rupture leaving large ulcerative lesions - Myocarditis – sudden death in young piglets and calves
○ In large outbreaks, not common in endemic areas
Foot and mouth disease what are the 2 routes of infection, where virus replicate and excrete from
Respiratory and oral transmission
- Virus replication in pharyngeal mucosa and draining lymph nodes
- Viraemia: spread to other organs
- Virus excretion:
○ Expired air (aerosols)
○ Secretions and excretions (including milk (23 days) and semen (56 days))
○ Ruptured vesicles -> longer than oral
Foot and mouth disease what are 3 important features that are important in epidemics
1) Oral transmission: Pigs more susceptible than ruminants -> act as amplifier host and generally how transferred trans-boundary
2) Virus excretion begins up to 4 days before clinical signs - IMPORTANT IN EPIDEMICS
3) 80% of ruminants become persistently infected (pharyngeal and upper oesophageal tissues) - IMPORTANT IN EPIDEMICS
Foot and mouth disease how many serotypes and name them, also what occurs with vaccinated individuals
Seven serotypes: O, A, C ,SAT 1, SAT 2, SAT 3 Asia 1
Vaccinated -> confers immunity to clinical disease, can still excrete virus and become carrier animals (sheep are important as in apparent carrier)
What is Foot and Mouth disease susceptible to how diagnose and preferred sample
FMDV is acid labile (pH < 4 or > 11) - not a difficult virus to kill
- Urgent laboratory
diagnosis required
1. Antigen detection by ELISA from tissue or fluid - can be infected for many day before detect antibody
2. Virus culture
3. Polymerase Chain Reaction (PCR)
- Preferred sample:
○ epithelium from unruptured or freshly ruptured vesicles
○ pharyngeal / oesophageal fluid (collect by probang in ruminants, or swab in pigs) - goes down oesophagus then back up with epithelium sample
§ SAMPLE OF CHOICE
What are the 3 other diseases FMD is clinically indistinguishable from and which present
1) Swine vesicular disease
2) Vesicular exanthema
3) Vesicular stomatitis - only one circulating around the world
Vaccination vs slaughter for Foot and Mouth disease
1) FMD free with vaccination (will not trade with) or FMD free without vaccination
○ International livestock trade regulations
2) Lots of ways to transmit -> Foot baths, clothes, trucks
3) Vaccinate? -> how far has it spread, can you make a blockage of vaccinated animals to prevent further spread or has it spread everywhere
4) Need to vaccinate all carriers, need sufficient time to mount an immune response, clinically not biologically protected so will still be infected -> will that just lead to endemic FDM
TO BE FREE WITHOUT VACCINATION - serological test and slaughter
