Picornavirus Flashcards
Foot and Mouth disease
Species affected
- Cloven-hooved species (ruminants, pigs), Guinea pig, Hedgehog,
- Dog and Human can also be affected —> Zoonotic!
Foot and Mouth disease
Most susceptible
Cattle and buffalo are the main hosts.
Domestic pigs are very effective in propagating the disease —> pigs are amplifiers and multipliers of the disease, they shed the virus 1000-3000x more than cattle in a short time.
Sheep and goat have mild symptoms
All age groups
Foot and Mouth disease
Occurrence
Endemic in Turkey, MiddleEast, Arabic
Peninsula, Africa, Asia and South America
Sporadic in Europe (O strain
was pandemic in 2001-2002)
Free in North and Central America, Australia, New Zealand and Japan
Foot and Mouth disease
Spread
Extremely contagious, spreads quickly, shedding starts at 9 hours post infection
Live animal (direct contact, saliva, body fluids, milk)
Environment and air (airborne)
Contaminated feed and water
Vehicles and people
Frozen or raw meat, skin, fur and milk
Horses may act as mechanical vectors!
Foot and Mouth disease
Pathogenesis
PO/Air Infection —>laryngeal and
pharyngeal mucosa —> viraemia
(blood and lymphatic tissue) —> vesicles in predilection sites:
• Mouth and Tongue
• Muzzle
• Feet
• Teats
Virus is shed with all body fluids
(including milk and semen) and is airborne. Virus is also shed through the vesicular fluid and wall.
Virus is shed from 9 hours post infection up to 11 days post infection
It may be present in milk and semen for up to 4 days before the onset of clinical signs.
Long term carriage in the tonsills, lymphatic tissue and hoof
• Sheep, Goat and Cattle: 0.5-3 years of carriage
• Swine and other species: few weeks of carriage
Foot and Mouth disease
Primary Replication
Laryngeal and Pharyngeal mucosa
Incubation period of 2-6 days
Foot and Mouth disease
Target Organs
Epitheliotropic virus!
Epithelium of mouth and tongue, muzzle, feet (coronary bands), teats
Foot and Mouth disease
Clinical Signs
Fever, depression
Salivation of viscous and frothy saliva (because of the vesicle formation in the oral
cavity) —> foaming around mouth Reddened mucosa
Vesicles/Blisters formation after 2-3 days post infection:
• They form on the oral mucosa, coronary band (blanching of coronary band) and interdigital cleft. Vesicles may appear on the teats and udder especially in lactatin animals
• In the mouth, the vesicles are with a red based and a tattered edge
• Rupture of vesicles within 1-2 days and healing within a few days —> heal with
fibrin layer
• Healing only after immune response, older animals heal within 2-3 weeks
• Secondary bacterial infections possible —> bacterial superinfection
Young animals (calves, lambs, piglets): myocardial lesions (virus induced myocardial
damage) —> myocarditis and Zenker’s
necrosis —> death due to heart failure
Cattle:
• Most susceptible to disease with most severe clinical signs
• If milking: virus present in milk —> humans
and calves infected this way
• Atypical form (without vesicles) is rare
• Lameness
Sheep:
• Like cattle but milder lesions, mainly on legs —> lameness
Goats:
• Lesions localised in nasal and oral mucosa
Pigs:
• Like cattle
• Loss of hoof (keratin layer)
Wild animals:
• Mild symptoms
Human:
• Moderately susceptible, rare
• Infected by milk from cows, secretions and
excretions of infected animals (example
fluid from vesicles)
• Usually seroconversion without clinical
signs
• Fever, sore throat, vesicles on feet and
mouth
• Myocardial lesions on babies
Foot and Mouth disease
Pathology / Histopathology
Vesicles in mouth, coronary band and in internal organs (ex rumen, GI tract)
Muscle degeneration —> diffuse (acute cases), nodular (prolonged cases) —> tiger heart
In young animals —> pale heart
Foot and Mouth disease
Diagnosis
Clinical signs and PM lesions —> suspicion of Foot and Mouth Disease
• Collection of samples for
analysis from vesicles, vesicle fluid and saliva
Virus antigen: ELISA —> to differentiate the 7 serotypes
Virus isolation on cattle and pig cells or on guinea pig foot scarification RNA detection by RT-PCR
Antibody detection: VN, ELISA
Notifiable disease!
Foot and Mouth disease
Treatment
In Europe and FMD free regions: no effective treatment In Endemic regions: • Hyperimmune serum • Clean environment • Soft litter and feed • Gentle milking • Treatment of the lesions
Foot and Mouth disease
Prevention and Immunity
FMD free countries:
• Aim is to maintain freedom from the disease
• Control measures —> slaughter of all affected and in contact animals, with strict movement restrictions on both animals and vehicles
• Stamping out: carcasses are either burned or buried on the premises and all buildings, equipment etc are
thoroughly disinfected; all live animals and raw products of animal origin from infected countries are banned
• Protection zone of 3km and surveillance zone of 10km radiuses
• No vaccines in FMD free countries! (vaccine reserves in case of an outbreak)
FMD endemic countries:
• Combination of vaccination,
movement restriction and prevention of FMDV entering the premises
• Vaccine:
• In cattle:
• Inactivated, aluminium gel absorbed, mono/bi/tri valent
• Twice in 1 year —> then every year after the first year
• Protection for 6-12 months
• In pigs:
• Inactivated, oil adjuvant vaccines
• Protection for 3-6 months
• Vaccine is subtype specific
Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease
Species affected
Pigs
Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease
Most susceptible
Teschen: All age groups susceptible
Talfan: Suckling piglets of < 4 months (usually before weaning, 1-3 weeks)
Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease
Occurrence
Teschen (1930) - Endemic in central EU and Madagascar
Talfan (1957) - EU, America, Australia
Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease
Spread
Spread by live infected animals, infected faeces, infected brain and spinal cord tissue
Also in the environment and pig swill (food)
Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease
Pathogenesis
Nerves —> Central Nervous System PO Infection: • Enteric phase: • Primary replication in the gastrointestinal epithelium • Asymptomatic, seroconversion, shedding of the virus • Local immunity, virus shedding stops • Viraemic Phase: • Accompanied by fever • Neural Phase: • Secondary replication in the CNS • Encephalomyelitis and clinical signs Virus is shed in the faeces
Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease
Primary Replication
If PO infection —> Gut epithelium
Teschen:
Incubation period of 1-3 weeks, virus will be shed at that time!
Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease
Target Organs
CNS
Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease
Clinical Signs
Teschen:
• Mild fever, anorexis
• Piglet, grower:
• Signs of brain and spinal cord inflammation
• Vomiting, ataxia, convulsions, flaccid paralysis (first hindlimbs, then forelimbs), respiratory paralysis, hyperaesthesia
• Older animals:
• Flaccid paralysis of the hindlimbs
• Some animals may recover
Talfan:
• Ataxia, anorexia, fever, hindlimb paralysis
(transient), opisthotonus
• Usually transient and animals recover but
ataxia may remain
• Coma and death after 3-4 days in some
cases
Virulent serotype 1 strain results in high morbidity and mortality in pigs of all ages
Serotype 2 causes crumbling movements
Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease
Pathology / Histopathology
No gross pathological lesions
Lymphocytic infiltration, necrosis (Teschen) and degeneration of the:
• Grey matter of the brain (serotype 2 also the white
matter)
• Brain Stem
• Cerebellum
• Ventral horns of the Spinal cord
Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease
Diagnosis
Clinical Signs and Histopathology —> presumptive diagnosis, however laboratory confirmation needed since disease is notifiable in Hungary Detection of virus: RT-PCR, IF, IP Virus isolation from CNS Detection of antibodies: VN
Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease
Treatment
No effective treatment
Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease
Prevention and Immunity
Teschen: • Movement restriction • Stamping out Talfan: • Seroconveriosn No vaccine available!
Swine Vesicular
Disease (SVD)
Species Affected
Pigs
Newborn mice
(Humans: some cases were identified however virus is not regarded as zoonotic anymore )
Swine Vesicular
Disease (SVD)
Most susceptible
Pigs: All age groups
Swine Vesicular
Disease (SVD)
Occurrence
Europe basically SVD-free: • First seen in Northern Italy (1966) • Last seen in Portugal (2007-2008) • Endemic in Southern Italy (asymptomatic)
Swine Vesicular
Disease (SVD)
Spread
Spread by direct contact of
swine, raw pork, swill (feed)
Swine Vesicular
Disease (SVD)
Pathogenesis
PO/Skin abrasion Infection —> Throat and Gut —> Viraemia —> Other organs:
• Epithelial cells of mouth, snout, teats and legs —> vesicle formation
• Central Nervous System —> asymptomatic or rare clinical signs
• Foetus —> rare
Shedding of the virus by faeces and vesicles.
Shedding of the virus lasts for 4 months. Asymptomatic carriers also shed the virus.
Placental crossing (rare)
Swine Vesicular
Disease (SVD)
Primary Replication
Throat and Gastrointestinal tract
Pigs: Incubation period
of 2-7 days
Humans: Incubation period of 1-2 weeks
Swine Vesicular
Disease (SVD)
Target Organs
Epitheliotropic:
Epithelial cells
CNS
Swine Vesicular
Disease (SVD)
Clinical Signs
Pigs: • Fever of 41℃ for 1-2 days • Primary sign: Vesicle formation: • On nose and snout • In mouth and on oral mucous membrane • On legs • Coronary band, interdigital cleft —> malformation of the hoof • Damaged horn production • On teats • Quick healing: vesicles rupture after 1-2 days releasing a large amount of the virus • Lack of appetite, anorexia, shivering • Limping, unsteady gate • Fast recovery (Humans: • Mild flu-like symptoms • Abdominal and muscle pain • No vesicles • Complete recovery)
