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Picornavirus Flashcards

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1
Q

Foot and Mouth disease

Species affected

A
  • Cloven-hooved species (ruminants, pigs), Guinea pig, Hedgehog,
  • Dog and Human can also be affected —> Zoonotic!
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2
Q

Foot and Mouth disease

Most susceptible

A

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

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3
Q

Foot and Mouth disease

Occurrence

A

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

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4
Q

Foot and Mouth disease

Spread

A

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!

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5
Q

Foot and Mouth disease

Pathogenesis

A

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

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6
Q

Foot and Mouth disease

Primary Replication

A

Laryngeal and Pharyngeal mucosa

Incubation period of 2-6 days

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7
Q

Foot and Mouth disease

Target Organs

A

Epitheliotropic virus!

Epithelium of mouth and tongue, muzzle, feet (coronary bands), teats

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8
Q

Foot and Mouth disease

Clinical Signs

A

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

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9
Q

Foot and Mouth disease

Pathology / Histopathology

A

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

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10
Q

Foot and Mouth disease

Diagnosis

A

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!

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11
Q

Foot and Mouth disease

Treatment

A 
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
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12
Q

Foot and Mouth disease

Prevention and Immunity

A

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

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13
Q

Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease

Species affected

A

Pigs

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14
Q

Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease

Most susceptible

A

Teschen: All age groups susceptible
Talfan: Suckling piglets of < 4 months (usually before weaning, 1-3 weeks)

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15
Q

Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease

Occurrence

A

Teschen (1930) - Endemic in central EU and Madagascar

Talfan (1957) - EU, America, Australia

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16
Q

Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease

Spread

A

Spread by live infected animals, infected faeces, infected brain and spinal cord tissue
Also in the environment and pig swill (food)

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17
Q

Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease

Pathogenesis

A 
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
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18
Q

Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease

Primary Replication

A

If PO infection —> Gut epithelium
Teschen:
Incubation period of 1-3 weeks, virus will be shed at that time!

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19
Q

Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease

Target Organs

A

CNS

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20
Q

Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease

Clinical Signs

A

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

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21
Q

Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease

Pathology / Histopathology

A

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

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22
Q

Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease

Diagnosis

A 
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
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23
Q

Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease

Treatment

A

No effective treatment

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24
Q

Porcine Enteroviral
Encephalomyelitis /
Teschen Disease /
Talfan Disease

Prevention and Immunity

A 
Teschen:
• Movement restriction
• Stamping out
Talfan:
• Seroconveriosn
No vaccine available!
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25
Swine Vesicular Disease (SVD) Species Affected
Pigs Newborn mice (Humans: some cases were identified however virus is not regarded as zoonotic anymore )
26
Swine Vesicular Disease (SVD) Most susceptible
Pigs: All age groups
27
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) ```
28
Swine Vesicular Disease (SVD) Spread
Spread by direct contact of | swine, raw pork, swill (feed)
29
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)
30
Swine Vesicular Disease (SVD) Primary Replication
Throat and Gastrointestinal tract Pigs: Incubation period of 2-7 days Humans: Incubation period of 1-2 weeks
31
Swine Vesicular Disease (SVD) Target Organs
Epitheliotropic: Epithelial cells CNS
32
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) ```
33
Swine Vesicular Disease (SVD) Pathology / Histopathology
No gross lesions
34
Swine Vesicular Disease (SVD) Diagnosis
``` Clinical signs Detection of the virus: RT-PCR, CFT, ELISA Virus isolation from lesions Detection of antibodies: VN, ELISA Notifiable disease ```
35
Swine Vesicular Disease (SVD) Treatment
No effective treatment
36
Swine Vesicular Disease (SVD) Prevention and Immunity
``` Maintenance of SVD free countries by: • Control if traffic of pugs and pork products • Ban of feeding with swill In case of introduction: • Stamping out of infected herds —> isolate and slaughter infected animals • Movement restrictions No vaccine available! ```
37
Encephalomyocarditis Species Affected
``` It is a rodent virus that affects: • Rodents —> asymptomatic • Swine • Elephant —> Encephalomyocarditis • Chimpanzee • Hippopotamus • Lions • Humans —> Zoonotic! • Other mammals and birds ```
38
Encephalomyocarditis Most susceptible
All age groups
39
Encephalomyocarditis Occurrence
``` EMCV-1: • Widespread • Europe, North America, Australia • In Hungary it has not been identified yet EMCV-2: • Germany, 2012 ```
40
Encephalomyocarditis Spread
Virus is spread by faeces and urine of infected rodents, which may contaminate food and water supplies of large mammals Ingestion of dead or dying infected rodents may also cause infection (carnivores) Slow spread among swine —> pigs shed the virus for about 3 days in nasal secretions and faeces, which may infect other pigs but this mode of transmission is insufficient
41
Encephalomyocarditis Pathogenesis
``` PO Infection —> Tonsils —> Viraemia —> Other organs: • Heart —> necrosis in heart muscle • Small intestine —> shedding • Liver, kidney, spleen, lungs • CNS —> encephalomyelitis • Foetus —> abortion, weak piglets Virus is shed for about 3 days in nasal secretions and faeces Placental crossing! (in swine) ```
42
Encephalomyocarditis Primary Replication
Tonsils
43
Encephalomyocarditis Target Organs
Predilection sites: Cardiovascular system CNS
44
Encephalomyocarditis Clinical Signs
``` Type A: Cardiac muscle failure —> death due to heart insufficiency, acute myocarditis Anorexia, depression, fever (41℃) Shaking and paralysis, Dyspnoea Type B: Reproduction problems —> reproductive failure, abortion, SMEDI Mortality: • Newborn animals: 1—% • Growers, Fattening: 5-25% Humans: • From rodents and swine • Clinical signs are rare • Asymptomatic infection —> myocardial necrosis, damage of the cornea ```
45
Encephalomyocarditis Pathology / Histopathology
``` Heart: • Enlarged, soft, pale necrotic foci • Hydropericardium, hydrothorax, pulmonary oedema • If death because of acute myocarditis —> some epicardial haemorrhages Brain: • Congestion Foetus: • No gross lesions • Sometimes oedema and haemorrhages Severe myocarditis characterised by interstitial infiltration of lymphocytes Immuno-positive myocardial cells when using immunohistochemistry Non-purulent encephalitis ```
46
Encephalomyocarditis Diagnosis
Clinical signs, PM lesions and histopathology Detection of virus: PCR, IF Isolation of virus (cell culture, embryonated egg) Detection of antibodies in foetuses: HA, ELISA, VN
47
Encephalomyocarditis Treatment
No effective treatment
48
Encephalomyocarditis Prevention and Immunity
General epidemiological rules Seroconversion Rodent control Proper disposal of animals that have died of disease Inactivated vaccines are available in some countries
49
Avian Encephalomyelitis Species Affected
Chicken, Pheasant, Turkey, Quail, Guinea Fow
50
Avian Encephalomyelitis Most susceptible
All age groups Clinical signs at 1-2 weeks, up to 4-5 weeks of age After 5 weeks chicken are resistant to disease but not to infection —> asymptomatic carriers
51
Avian Encephalomyelitis Occurrence
Worldwide | Clinical from is not that common
52
Avian Encephalomyelitis Spread
Spreading by faeces —> horizontal infection Vertical transmission: • If breeder is infected during egg production, the virus is transmitted to offspring and major outbreak occurs • Germinative infection —> infected eggs for up to 3 weeks
53
Avian Encephalomyelitis Pathogenesis
``` PO Infection —> Mucous membrane of gut —> Viraemia —> Other organs: • Pancreas, liver, spleen • Ovary —> does not kill the embryo • Central nervous systems —> neurological signs Virus is shed in faeces for several weeks ```
54
Avian Encephalomyelitis Primary Replication
Intestinal mucous membranes Incubation period of 1-11 days
55
Avian Encephalomyelitis Target Organs
Enteroptropic: | pancreas, liver, spleen
56
Avian Encephalomyelitis Clinical Signs
Younger chickens at 0-2 weeks: • Vertically infected chicks commonly show clinical signs during the first week after hatching • Horizontally infected hatch mates (feacooral route) will have clinical signs later • Neurological symptoms: • Depression, Ataxia • Fine tremor of head, neck and limbs —> Epidemic tremors • Unsteadiness • Paresis, inability to move, paralysis and recumbency • No drinking and eating —> death Older animals: • Subclinical • Drop in egg production by 5-10% • Usually lasts under 2 weeks followed by a return in normal egg production • No change in egg shell quality • Long-lasting immunity, yolk-immunity Morbidity 50-60%, Lethality: high
57
Avian Encephalomyelitis Pathology / Histopathology
No gross lesions Lymphocytic infiltration of CNS, muscles of gizzard, proventriculus and myocardium Degeneration and necrosis of neurons
58
Avian Encephalomyelitis Diagnosis
Clinical signs and histopathology Detection of virus: PCR, IF Isolation of virus Detection of antibodies: AGID, VN, ELISA
59
Avian Encephalomyelitis Treatment
No effective treatment
60
Avian Encephalomyelitis Prevention and Immunity
Good immunity and maternal protection of animals who survived infection Vaccine: • Vaccination of breeder pullets at 10-15 weeks (1 month before laying) with a live vaccine in drinking water—> prevent vertical transmission and provide progeny with maternal immunity • Usually combined with Fowlpox +/- Infectious Laryngotracheitis vaccine • Virus is shed in 5-10% of the animals vaccinated in a flock! Affected chicks and poults are destroyed as they do not usually recover
61
Duck Viral Hepatitis Type 1 Species Affected
Ducks experimentally in geese, turkeys, pheasants and quails Rats are possible reservoirs
62
Duck Viral Hepatitis Type 1 Most susceptible
Ducklings up to 6 weeks of age
63
Duck Viral Hepatitis Type 1 Occurrence
Worldwide
64
Duck Viral Hepatitis Type 1 Spread
Spread by faeces and tracheal discharge (respiratory secretions) No germinative infection
65
Duck Viral Hepatitis Type 1 Pathogenesis
``` PO Infection —> Gastrointestinal tract —> Viraemia —> Other organs: • Liver, Spleen, Kidney —> Replication • Liver dystrophy, necrosis of hepatocytes —> death Secondary bacterial infection can happen —> especially salmonellosis Virus is shed in faeces and respiratory secretions for several weeks ```
66
Duck Viral Hepatitis Type 1 Primary Replication
Gastrointestinal Tract | Incubation period of 18-48 hours
67
Duck Viral Hepatitis Type 1 Target Organs
Liver, Spleen, Kidney
68
Duck Viral Hepatitis Type 1 Clinical Signs
Day old ducklings: • Explosive, 90% mortality • If there is yolk immunity —> slower (till the age of 2-3 weeks) —> 50% mortality Clinical signs in young ducklings (0-4 weeks): • Peracute —> large scale death within a few hours (en masse) • Acute —> death within a few days • Depression, lethargic, loose balance • Spasmodical paddling with opisthotonus and a hunched back up to 95% mortality within 1 week of infection Long-lasting immunity, yolk-immunity for those who survive
69
Duck Viral Hepatitis Type 1 Pathology / Histopathology
``` Liver: • Enlarged and yellow —> Hepatomegaly • Liver dystrophy • Haemorrhages with sharp edge Spleen: • Enlarged, mottled —> Splenomegaly Kidney: • Swollen, plethoric, nephrosis ```
70
Duck Viral Hepatitis Type 1 Diagnosis
Clinical signs and PM lesions —> presumptive diagnosis Detection of virus: PCR, IF Virus isolation Detection of antibodies: VN, ELISA
71
Duck Viral Hepatitis Type 1 Treatment
No effective treatment
72
Duck Viral Hepatitis Type 1 Prevention and Immunity
Epidemiological rules: • Strict isolation in the first 5 weeks of life • Isolation from wild ducks, rats (possible reservoirs) Vaccine: • Inactivated: • Vaccination of layers, boosters • Attenuated: • Layers and day-old ducklings, aerosol, drinking, subcutaneous injection • Vaccination at the age of 7 weeks and 2-3 weeks before laying • Attenuated and inactivated: • 7-12 weeks old: attenuated • 18 weeks old: inactivated
73
Duck Viral Hepatitis Type 2 Species Affected
Ducks
74
Duck Viral Hepatitis Type 2 Most susceptible
Ducklings up to 6 | weeks of age
75
Duck Viral Hepatitis Type 2 Occurrence
UK
76
Duck Viral Hepatitis Type 3 Species Affected
Ducks
77
Duck Viral Hepatitis Type 3 Most susceptible
Embryos
78
Duck Viral Hepatitis Type 3 Clinical Signs
30% mortality
79
Duck Viral Hepatitis Type B Species Affected
Ducks and Geese
80
Duck Viral Hepatitis Type B Most susceptible
Older animals
81
Duck Viral Hepatitis Type B Occurrence
China
82
General characteristics of Picornavirus
+ssRNA virus with an icosahedral shape and which has no envelope Has 4-5 structural proteins, VP1-5 Its antigens are group and type specific has no vectors! Eneterovirus, Hepatovirus, Avihepatovirus, Teshcovirus, Tremovirus —> narrow host spectrum; good resistance: pH3-9 stable; asymptomatic replication in gut after po infection and then viraemia Erbovirus and other rhinoviruses —> inactivated below pH6, 33℃ Darciovirus, Aphtovirus —> not species specific, inactivated below pH6 FMDV: • Eputheliotropic virus! • Good resistance (56℃, pH6.5); can survive in shadowed wet cool sites of the pasture and in a dirty stall for weeks, in manure for 40 days, in frozen meat and milk powder for months. Highly acidic or alkaline disinfectants needed for inactivation • 4 structural proteins (VP1: neutralising antibodies) • 7 serotypes: • FMDV type O, FMDV type A: worldwide • FMDV type C: rare, extinct • FMDV type SAT-1, FMDV type SAT-2, FMDV type SAT-3: Africa • FMDV type Asia1: Asia, Turkey, Middle East • Several subtypes but no cross protection! • Highly variable virus —> Point mutations, recombinations etc • Differentiate by ELISA, VN PTV: • Causes either Teschen or Talfan Disease • Serotype 1 is of the most clinical importance (but sometimes the other serotypes cause disease as well) • Resistant in the environment: can survive up to 3 weeks • Virulence variants EMCV: • Types 1 or 2 according to their occurrence • Types A and B according to their clinical signs • Type A strains causes reproduction problems • Type B strains cause myocarditis • Some strains cause both • Slight difference in the strains isolated from rodents and swine • Wide host range: rodent virus that affects at least 30 other species • Good resistance —> survives in environment for several weeks SVD: • Strains of Coxsakie B5 virus adapted to swine • Good resistance: survives in the environment for 3-4 months and in meat DHAV: • DHAV Type 1 is the most pathogenic and widespread • No haemagglutination • Highly resistant: In environment for weeks

Epidemiology (16 decks)

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