ASFV and CSFV Flashcards

1
Q

What is Classical Swine Fever Virus (CSFV)?

A
  • Flaviviridae
    • Flavi = yellow
  • ssRNA: 12.3kb
  • Single-stranded, positive-sense RNA virus, enveloped
  • Genus Pestivirus:
    • BVDV, BDV, CSFV
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2
Q

What is the history of CSFV?

A
  • 1833 - 1st reported in US “Hog cholera”
  • 1960 - cost %50mil / year
  • 1978 - US declared “hog cholera” free
    • 17 year Federal-state eradication program
  • 1997- Netherlands outbreak 12mill pigs dead
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3
Q

What is the epidemiologic information for CSFV?

A
  • Natural host - swine
  • Highly contagious - high morbidity and mortality
  • 3 genotype (1, 2, 3) and subgenotypes
    • high, moderate, and low virulence strains
  • Severity of illness varies with viral isolate, age of pig, immune status, dose, health status
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4
Q

How is CSFV transmitted?

A
  • Primarily oronasal transmission (direct or indirect contact)
    • virus shed in oronasal and ocular seretions, urine, feces, blood
    • genital and transplacental transmission also possible
    • Spread readily by feeding uncooked swill from infected pigs
    • transmissible through contaminated fomites
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5
Q

how does the virulence of CSFV differ?

A
  • Acute and severe disease in naive herds
    • highly virulent strains
    • high mortality - can approach 100%
      • death typically within 1-3 weeks
    • Rapid recognition/diagnosis
  • Subacute
    • clinical signs less severe, prolonged time course, lower mortality
  • Chronic disease:
    • Seen with moderate or low virulence strains
    • May be difficult to recognize/diagnose
    • May only affect a few animals
    • Clinical sings wax and wane for weeks to months
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6
Q

What are the clinical signs of Acute CSFV in a naive herd?

A
  • High fever
  • huddling
  • weakness
  • lethargy
  • decreased appetite
  • conjunctivitis
  • constipation or diarrhea
  • incoordination
  • posterior paresis
  • convulsions
  • vomiting
  • respiratory signs
  • skin hyperemia, hemorrhage or cyanosis
  • sever leukopenia
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7
Q

What are the clinical signs of Chronic CSFV?

A
  • Decreased appetite
  • depression
  • fever
  • leukopenia
  • constipation or diarrhea
  • wasting or poor growth
  • skin lesions
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8
Q

What are the overall Clinical signs of CSFV?

A
  • Poor reproductive performance
    • may be only sign in herds infected with less virulent strains
    • Abortion, stillbirths, mummified, malformed, weak piglets
    • Piglets may be born with congenital tremor
    • Piglets may be born persistently infected
      • Nonclinical at birth
      • late-onset C/S - inappetence, depression, poor growth, dermatitis, diarrhea, conjunctivitis, ataxia, posterior paresis
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9
Q

What lesions are associated with CSFV?

A
  • Highly variable
  • Acute disease:
    • Hemorrhage most common
    • skin discolored purple, cyanosis of extremities
    • lymph nodes swollen and hemorrhagic
    • Petechial or ecchymotic hemorrhages on serosal and mucosal surface
  • GI- hemorrhage, enteritis, button ulcers
  • Fluid in peritoneum, thorax or pericardial sac
  • Tonsilitis (+/- necrotic foci)
  • Splenic infarcts
  • Lungs - congestion and hemorrhage
  • Encephalitis
  • Kidney - Cortical petechiae and pale infarcts surrounded by hemorrhage
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10
Q

How is CSFV diagnosed?

A
  • Virus detection
    • PCR, sequencing, FA, ELISA, VI
    • blood, tonsil or nasal swabs (live)
    • Tonsils, lymph nodes, brain, spleen, kidneys, ileum (necropsy)
  • Serology: FAVN, ELISA
    • Ab develop 2-3 weeks post-infection, usually lifelong
    • persistently infected piglets with be negative fo Ab
  • Consider Cross-reactivity with ruminant pestiviruses
    • BVDV and BDV occasionally infect pigs
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11
Q

What are some differentials for suspected CSFV?

A
  • PDNS
  • ASFV
  • septicemic bacterial diseases (Salmonellosis, Erysipelas, acute Pasteurella
  • Severe PRRSV
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12
Q

How is CSFV controlled?

A
  • MLV vaccines
    • reduce clinical signs, limit transmission
    • Employed to reduce infections during eradication program
    • Widely used in CSF-endemic countries
    • Prohibited in CSF-free areas
    • Not DIVA
  • Biosecurity, movement restrictions, quarantine, surveillance
  • CSFV generally labile in environment
    • inactivated by disinfectants, drying, heat, UV
      • remains infectious for months in meat
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13
Q

What are the characteristics of the African Swine Fever Virus (ASFV)?

A
  • Asfarviridae
  • Genus Asfivirus (only member)
    • Large complex dsDNA virus, enveloped
      • 170-190 kb, >150 proteins
    • Environmentally stable - resistant to pH and temperature
      • can survive at room temp and in meat for months
  • Soft ticks of the genus Ornithodoros can be involved n the infection cycle
    • Only DNA virus classified as arthropod borne virus
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14
Q

What is the history of ASFV?

A
  • Never been documented in the US
    • Economically important
    • Trade restrictions
    • Reportable
  • Since 2007- outbreaks in Caucus region, russia, and eastern Europe
    • increased risk of spread
  • August 2018 -
    • China +12 Asian Countries
    • Belgium, Slovakia, Serbia
  • Sept 2020 - Germany
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15
Q

What is ASFV?

A
  • Contagious hemorrhagic disease
  • clinically indistinguishable from CSFV
  • Occurs in domestic pigs and European wild boar
    • all ages susceptible
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16
Q

How is ASFV transmitted?

A
  • Oronasal route by direct or indirect contact
  • Bite of an infected soft tick
  • Ingestion of uncooked pork in food waste
  • Ingestion of contaminated feed
17
Q

What is the Pathogenesis of ASFV?

A
  • Primary route of infection is oral or upper respiratory tract
  • Virus replicates in the tonsil and regional lymph nodes
    • predominately in monocytes and macrophages
  • Generalized infection follows rapidly via the blood stream
    • high concentration of virus found in the spleen
18
Q

What is the cellular pathogenesis of ASFV?

A
  • Causes severe disruption to blood clotting mechanism
  • Destruction of macrophages
    • impaired hemostasis
    • release of cytokines nd complement
  • Thrombocytopenia
  • Lymphopenia
19
Q

what is the incubation period of ASFV?

A
  • Incubation period: 4-19 days
  • Peracute, acute, subacute, chronic, and subclinical forms
20
Q

What are the clinical signs of ASFV?

A
  • Sudden death
  • high fever
  • skin hyperemia or cyanosis (ears abdomen legs)
  • depression
  • decreased appetite
  • recumbency
  • conjunctivitis
  • vomiting
  • watery to bloody diarrhea
  • tachypnea
  • tachycardia
  • abortion
  • incoordination
21
Q

What are additional clinical signs in the Acute and lethal forms of ASFV?

A
  • Hemorrhagic lesions (petechiae, epistaxis, hematochezia)
  • DIC
  • Thrombocytopenia
  • increased vascular permeability
  • death within 5-10 days
22
Q

What are additional clinical signs of the less acute form of ASFV?

A
  • Respiratory signs
    • coughing
    • sneezing
    • dyspnea
  • GI signs
    • diarrhea
    • constipation
23
Q

What are the additional clinical signs of the chronic form of ASFV?

A
  • emaciation
  • swollen joints
  • respiratory disease
24
Q

What is the mortality rate of ASFV?

A
  • ranges from 0-100%
    • depends on strain virulence
25
Q

What lesions are associated with ASFV?

A
  • Hyperemia and hemorrhage on skin
  • Extensive hemorrhages in: LN, kidneys, heart, other organs
  • Straw-colored or blood-stained fluid in pleural, pericardial, or peritoneal cavities
  • Lung hemorrhages
  • pulmonary edema
  • splenic enlargement
26
Q

How is ASFV diagnosed?

A
  • Reportable to federal authorities
  • Differentials same as A+CSFV
  • Virus detection:
    • Whole blood, spleen, tonsil, LN
    • VI, PCR, ELISA, FA, ISH
  • Serology:
    • ELISA, IFA
27
Q

How is ASFV controlled?

A
  • No treatment NO VACCINE
  • Eliminate risk factors for viral introduction
    • prevent infected live pigs, contaminated pig meat or feed from being introduced
    • Reduce exposure to soft tick vector
    • Biosecurity of personnel and farm supplies
  • Eradication - depends on rapid diagnosis, slaughter, and disposal of infected animals
    • Controlled or stopped pig movement
    • Treatment of food waste or ban of swell feeding
    • Biosecurity and reducing exposure to wild suids