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Picornaviridae. Foot and mouth disease – oral mucus discharge Genera – major difference between the various genera is the stability at low pH Apthovirus – unstable below pH 7 Rhinovirus – unstable at pH 5 and below

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picornaviridae
Picornaviridae
  • Foot and mouth disease – oral mucus discharge
  • Genera – major difference between the various genera is the stability at low pH
  • Apthovirus – unstable below pH 7
  • Rhinovirus – unstable at pH 5 and below
  • Enterovirus,Cardiovirus, Hepatovirus that includes Simian hepatitis A are stable at pH 3
  • Parechovirus – stable at pH 3 that includes Human echovirus 22 and 23 – aseptic meningitis
picornaviridae1
Picornaviridae
  • Stability – important in the epidemiology of the disease
  • VERY STABLE
  • If protected by mucus or feces, and shielded from direct sunlight, they are relatively heat stable at normal temps
  • Apthoviruses and rhinoviruses are less stable, but high humidity can sustain droplets for several hours
  • Apthoviruses –
  • Food and mouth disease – Ruminants and swine
  • Equine rhinovirus 1 – horses – systemic dz.
picornaviridae2
Picornaviridae
  • Enterovirus –
  • Bovine enteroviruses 1-7 bovine subclinical infections
  • Porcine enterovirus 1 swine polioencephalomyelitis
  • Porcine enteroviruses 2-11 Swine SMEDI, diarrhea, pericarditis
  • Swine vesicular disease Swine Swine vesicular disease
  • Avian enteroviruses Chicken Avian encephalomyelitis
  • Avian enteroviruses Ducks and turkeys Hepatitis
  • Rhinovirus-
  • Bovine rhinovirus 1-3 Cattle Mild rhinitis
  • Human rhinovirus >100 Humans Common Cold
  • Cardiovirus -
  • Encephalomyocarditis swine etc. Encephalomyocarditis
  • Unclassified virus -
  • Equine rhinovirus 2 Horses Rhinitis
foot and mouth disease apthous fever epidemic aphthae
Foot and Mouth Disease – Apthous fever, Epidemic aphthae
  • Foot and mouth disease – oral lesions
  • Aphtha – Gr. Small ulcer
  • Distribution – currently, North and Central America, Oceania, and the Caribbean – DISEASE FREE
  • Endemic areas –
  • Asia, Africa, Middle East and most of South America
  • Hosts – cloven hooved domestic and wild animals
    • Cattle, sheep, goats, swine, buffalo
    • NOT HORSES
foot and mouth disease
Foot and Mouth Disease
  • Lesions of the hard palate and gingiva
  • Etiologic agent – Aphthovirus – 7 serotypes A,O,C,SAT-1, SAT-2 and SAT-3 (S.African territories), and ASIA-1 and 80 subtypes
  • NO CROSS PROTECTION AMONG SEROTYPES
  • Virus has been shown to survive for 14 days in a stall and for as long as 20 weeks on sacks and hay
  • Virus in muscle is inactivated in 48 hours of slaughter but survives for longer periods in bone marrow, viscera, blood clots
foot and mouth disease1
Foot and Mouth Disease
  • Foot and mouth disease – lesions of the hock region
  • Infectivity is destroyed by high temps and UV light
  • Virus is sensitive to acid and alkaline pH, stable at pH between 6-9, basic disinfectants work well
    • NaOH, Na carbonate, citric acid, acetic acid
  • Transmission – inhalation, infected animals generate large volumes of aerosols
  • Direct contact between infected and susceptible animals by contaminated animal products – meat, milk, semen etc.
foot and mouth disease2
Foot and Mouth Disease
  • Foot and mouth – sloughing of the hoof epidermis
  • Transmission cont. -
  • Garbage with uncooked meat and bones from infected animals has been a high source of infection in pigs
  • Virus can be spread over long distances, country to country, by asymptomatic carriers or animals incubating the disease – virus shedding begins 24 hours prior to observance of clinical signs
  • Birds, rodents and arthropods have been implicated in the spread of the disease
pathogenesis foot and mouth
Pathogenesis – Foot and Mouth
  • After inhalation – virus replicates in pharynx, viremic spread to the organs follows, REPLICATION OCCURS IN THE EPITHELIAL CELLS OF MUCOSA and skin, causing characteristic lesions
  • Initial hyperemic areas develop into vesicles, some of which may coalesce to form large blisters. The vesicles are filled with clear, yellow fluid
  • Myocardial lesions – small gray foci and streaks of irregular size and shape in the myocardium, giving the MYOCARDIUM A STRIPED APPEARANCE, the so-called TIGER HEART are the most common cause of FATAL FMD in young calves, lambs, goats, pigs and buffaloes.
  • Carrier state – can persist in the pharynx for up to 2 years in cattle and up to 6 months in sheep. There is no carrier state in swine.
clinical features foot and mouth disease cattle
Clinical Features – Foot and Mouth Disease – Cattle
  • Clinical Features – Most severe in cattle and swine ; Sheep and goats develop subclinical infections
  • Cattle –
  • IP – 2-8 days; Course 2-3 weeks.
  • Morbidity high, Mortality less than 5%
  • Fever, anorexia and depression within 24 hours
  • Infection causes profuse salivation, lip smacking and are lame
  • Vesicles are present on the tongue, lips, gums and palate, teats, rumen pillars, coronary band, and interdigital areas.
  • Ulceration leads to secondary bacterial infection
  • Abortion – pregnant animals and mastitis with about 25% drop in milk production
clinical features swine and ruminants
Clinical Features – Swine and Ruminants
  • Swine Clinical Features
  • Aerosols contain high levels of virus
  • Vesicles and erosions of snout, lips, and tongue, coronary band
  • Sheep, goats, and other wild ruminants Clinical Features
  • Mostly asymptomatic
  • Disease is usually mild and is characterized by foot lesions and lameness
  • Diagnosis –
  • Differentials – vesicular stomatitis, swine vesicular disease, vesicular exanthema, bluetongue, rinderpest, bovine viral diarrhea-mucosal disease
  • Virus isolation – Vesicular fluid, blood, esophageal and pharyngeal fluid
  • Cell cultures of bovine origin
  • ELISA – vesicular fluid or tissues; antibody detection
  • Virus identification – Virus neutralization, AGID, and complement fixation test
foot and mouth disease immunity control
Foot and Mouth Disease Immunity, Control
  • Cattle recovering from FMD are usually immune to reinfection with the same virus type for a year or longer, but immunity is NOT lifelong
  • Immunity – type specific, recovered animals can be infected immediately with any of the other serotypes and develop disease
  • Control – FMD is notifiable disease
  • Endemic countries –
  • Vaccination using inactivated and modified live virus vaccines. Quarantine if outbreak
  • Disease free countries –
  • Quarantine and slaughter; disposal of carcasses- burning/deep burial,decontamination of premises
  • Federal law prohibits the importation of animals or products from infected countries unless they are cooked or dried
  • Zoonosis – Most infections subclinical – fever, anorexia, vesicular lesions on skin and/or mucous membranes followed by recovery
porcine polioencephalomyelitis teschen talfan disease
Porcine Polioencephalomyelitis Teschen/Talfan Disease
  • Severe devastating, neurologic disease of pigs in the Teschen district of Czech Republic
  • Milder form, Talfan disease is more common and occurs worldwide
  • Hosts – Swine of all ages are susceptible, however, clinical disease is usually limited to pigs less than 12 weeks of age
  • Etiologic agent – Porcine enterovirus 1 – Variation in virulence among different strains
  • Transmission – Ingestion of virus
  • Virus can survive for months in the environment
teschen talfan disease
Teschen/Talfan Disease
  • Pathogenesis –
  • Following ingestion, virus replicates in the GIT and associated lymphoid tissues
  • There is NO DESTRUCTION OF GUT EPITHELIUM, however, virus is shed into the feces for several weeks
  • In pigs infected with virulent strains, viremia occurs and results in spread of infection to the CNS
  • Clinical Features –
  • IP – 1-4 weeks, course 2 weeks
  • Tremors, incoordination beginning with hindlimbs, paralysis, prostration, convulsions, coma, death
  • Mortality may reach 75%
  • Mild form – Ataxia associated with hind limb paresis followed by recovery
teschen talfan disease vaccine
Teschen/Talfan Disease - Vaccine
  • Diagnosis –
  • Virus isolation. Brain. Inoculation into porcine cell cultures
    • FAT staining of infected cell culture for rapid diagnosis
  • Identification of virus using virus neutralization assay
  • Pathology – NO SIGNIFICANT GROSS LESIONS ARE OBSERVED AT NECROPSY
  • Paired serum samples – 4 fold increase in antibody titer
  • Control –
  • inactivated and attenuated vaccines are available commercially
  • Vaccination not practiced in the US
  • Quarantine and hygiene used primarily
porcine enteroviruses 2 11
Porcine Enteroviruses 2-11
  • Porcine Enteroviruses 2-11
  • Frequently isolated from the feces of NORMAL swine and also from sine with diarrhea and pericarditis
  • There have been isolated from cases of stillbirth, mummification, embryonic death and infertility – SMEDI
avian encephalomyelitis epidemic tremor
Avian Encephalomyelitis “Epidemic Tremor”
  • Worldwide
  • Mostly chickens 1-3 weeks of age
  • Mild encephalomyelitis is seen in turkey poults, quail and pheasants
  • Etiologic agent – Avian enterovirus
  • One serotype. Strains may vary in virulence
  • Transmission – mainly fecal-oral route
  • Through eggs during a short viremic phase – 1 week – in infected breeder hens – no disease in adults
avian encephalomyelitis avian enterovirus
Avian Encephalomyelitis – Avian enterovirus
  • Clinical Features –
  • Main signs are unsteadiness, sitting on hocks, tremors especially of the head and neck, prostration, blindness, paralysis, coma and death
  • Recovered birds may have CNS deficiencies – may have to be destroyed
  • Mortality rate may exceed 50%
  • Diagnosis – viral antigen immunofluorescent stain
  • Virus isolation – brain. Yolk sac of embryonated eggs/ cell culture
  • Pathology – No gross lesions seen at necropsy
  • Control – Either depopulation or vaccination
  • An attenuated live-virus vaccine administered in the drinking water to breeding hens ensures passively immune progeny.
  • Maternal antibodies protect chicks for the first few weeks of life
encephalomyocarditis rodent spread
Encephalomyocarditis – rodent spread
  • Etiologic agent –
  • Cardiovirus. One serotype.
  • RODENTS ARE THE NATURAL HOSTS OF THE VIRUS.
  • The virus infects humans, swine, monkeys, cattle and horses
  • MOST SEVERE IN YOUNG PIGLETS
  • Transmission –
  • Swine are infected by eating rodent urine and feces
  • Clinical features –
  • Subclinical in weaned pigs and adults
  • Sudden death – myocardial failure, encephalomyelitis in young pigs
  • Anorexia, depression, difficulty breathing
  • Mortality approaches 100% in very young pigs
  • In utero – fetal death
encephalomyocarditis
Encephalomyocarditis
  • Diagnosis –
  • Pathognomonic cardiac lesions – myocardial infarcts esp. in the right ventricle
  • FAT staining of the affected tissues
  • Virus isolation – heart and brain
  • Prevention and Control –
  • Rodent control.
  • Outbreaks usually run short courses with immunity occurring in surviving animals
  • An inactivated vaccine aids in the prevention of reproductive failures in swine