African Swine Fever

Timeline of pathogen movement

1. Originally (restricted) in Africa

2. Outbreak in Portugal twice (1957, 1960)

3. Then spread to other EU countries

4. Contributing factors

   1. Infected swill is the likely culprit

   2. Movement of infected individuals across borders

Etiology

1. African swine fever virus (family asfarviridae)

2. Large virus

3. Capsid contains genetic material (dsDNA) for immune system

4. Evasion, cell process modulation and virulence

5. 23 genotype

   1. All 23 are present in Africa

   2. I and II are present in other parts of the world

   3. Cytoplasmic virus

Transmission

1. Direct contact with infected individual

   1. Virus can be found in all fluids

   2. Persistence in blood and lymph

   3. Persistent in tissues after death

2. Indirect contact with contaminated fomites

   1. Highly stable in proteinaceous resources

   2. Can persist stably on surfaces

3. Infected tick bite (Omithodoros spp.)

   1. Competent vectors of ASFV can be found globally

   2. Ticks can maintain the virus transstadially, transovarially, and sexually

Vector role – ornithodoros ticks

1. Nidicolous

2. Feed often and frequently

3. Maintain virus across generations

Host – family suidae

1. Warthog

   1. Young develop significant viremia and show no clinical disease

   2. Adults show no clinical signs and are infected/ive for life

   3. Only ticks contribute to transmission

2. Bush pig

   1. Resistant to clinical disease despite high viremia for extended time

   2. Transmissible to other pigs

3. Javelina

   1. Resistant to infection

   2. Peccary macrophages are not compatible to the virus

4. Wild boar - develop harsh clinical sign

5. Domestic pig - develop harsh clinical sign

Clinical disease

1. Acute hemorrhagic fever

   1. Caused by highly virulent strains

   2. Almost always 100% mortality

   3. Signs: high fever, lethargy, weakness, diarrhea, hemorrhagic signs

   4. Death occurs 1-4 days post sign

   5. Most common in disease free regions

2. Chronic infection

   1. Caused by less virulent strains

   2. Low mortality

   3. Signs: intermittent fever, loss of appetite, depression

   4. Domestic pigs are MOST infectious during incubation period and can shed virus up to one month after clearing signs

   5. Prolonged infection = disease persistence

Diagnosis

1. RT-PCR

2. Immunofluorescence Assay

3. Cell culturing and serology

4. Best tissues: spleen, kidney, and lymph nodes

Vaccine

1. No vaccine available

   1. Too much diversity of viral strain

   2. Inadequate understanding of virus-host-cell interaction

   3. Genetic diversity of the host

   4. Inadequate understanding of protective antigens

Housing domestic swine in the US

1. Maintenance is a highly regulated closed system

2. Housed indoors

3. High biosecurity measures from birth to slaughter 

4. Frequent sanitation of slaughter materials, feed, and transportation devices

Contributing factors to geographic spread

1. Legal

   1. Movement of domestic swine from neighboring countries

   2. Imported stuff needs permit

2. Illegal

   1. Improper border security

   2. Bioterrorism

      1. Pathogen is stable in frozen products

3. Major consequences? Crippling economic loss!

Complications if introduced to the US

1. Role of soft ticks species is generally unknown in the US

2. Virus can persist in a range of climates

3. Backyard and feral swine could contribute to short term outbreaks

The problem with feral hogs

1. Feral hogs are free roaming

2. Reproductive females live in small communities (sounders)

3. Sounder interaction is reduced by at least 2km which reduced transmission