by PA Suum — i7228e.pdf. Accessed 18 Jun 2019. Blome S, Gabriel C, Beer M. Pathogenesis of African swine fever in domestic pigs and European wild boar. Virus Res. 2013
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www.cfsph.iastate.ed u Email: firstname.lastname@example.org © 2003 – 2019 page 1 of 9 African Swine Fever P este Porcine Africaine, Fiebre Porcina Africana, Pestis Africana Suum, Maladie de Montgomery, Warthog Disease, Afrikaanse Varkpes, Afrikanische Schweinepest Last Updated: June 2019 Importance African swine fever is a n important viral disease of pigs that has become a serious threat to worldwide pork production since 2007 . African swine fever virus (ASFV) usually circulates in sub – Saharan Africa , where it is thought to have originated in wild warthogs but has become a common virus in domesticated pigs . ASF viruses range from highly pathogenic strains that may kill near ly the entire herd to less virulent isolates that cause a milder, nonspecific illness difficult to recognize as African swine fever . There is no vaccine and no effective treatment, and severely affected pigs usually die. The spread of ASFV is facilitated by a number of factors, including its persist ence for long periods in uncooked pork pr oducts , which may be fed to pigs in food scraps (pig swill) , and its ability to become established in wild or feral suids . In some areas, c ontrol is complicated by the establishment of the virus in Ornithodoros ticks , which occurs in addition to direct tra nsmission between animals . One tick vector hindered eradication efforts during a previous outbreak in Spain and Portugal, where complete elimination of the virus took more than 30 years. In 2007, ASFV was accidentally introduced into the Caucasus region o f Eurasia , most likely in pig swill from Africa . This highly virulent virus caused outbreaks on pig farms, but it also bec a me established in wild boar , and has been spreading slowly and steadily in these animals , with occasional larger jumps attributed to transmission by people or the transport of domesticated pigs . As of June 2019, i nfected wild boar have been found as far west as the Baltic region, parts of C entral Europe (e.g., Poland, Hungary ) and Belgium . While outbreaks in domesticated herds have been eradicated, it is still un certain whether the virus can be eliminated from wild boar. In 2018, the same virus was detected in China , where it appears to have spread widely before the outbreak was recognized . African swine fever has since been reported in domesticated pigs in several other southern Asian countries , as well as in w ild boar , and the virus appears to be spreading quickly in some parts of Asia . There are fears that it could be transported from Eurasia to other locations, including the Americas, as at least one virus was in the past. One report from 2010 described finding ASFV in wild boar in Iran, though there are no other reports indicating its presence in the Middle East . Etiology African swine fever results from infection by African swine fev er virus (ASFV) , an enveloped virus in the genus Asfivirus and family Asfarviridae. More than 20 genotypes of ASFV have been identified, many from wildlife cycles in Africa. Some of these viruses also occur in domesticated pigs . The virus introduced in 2007 into the Caucasus belongs to genotype II, while a virus that has been endemic in Sardinia (Italy) since the 1960s is of genotype I. ASFV isolates differ greatly in virulence, from highly pathogenic viruses that kill most pigs to strains that resul t only in seroconversion. The genotype II virus currently circulating in Eurasia is highly virulent and remains the predominant strain , though less virulent viruses have been reported sporadically during this outbreak . Species Affected African swine fever affects members of the pig family (Suidae). Species known to be susceptible to infection include domesticated swine and wild boar ( both subspecies of Sus scrofa ), warthogs ( Phacochoerus spp.), bush pigs ( Potamochoerus larvatus and Potamochoerus porcus ) and giant forest hogs ( Hylochoerus spp.). Most of these animals can develop clinical signs, although infections in warthogs seem to be subclinical or mild. Some older reviews and textbooks suggest that peccaries ( Tayassu spp.) may also become infected without clinical signs, although one attempt to infect collared peccaries ( Tayassu tajacu ) in 1969 was unsuccessful. Recent reviews state that that peccaries are not susceptible. Warthogs are thought to be the primary wildlife reservoirs for the virus in Africa, although other wild suids might a lso play a role. Domesticated pigs also maintain ASFV. Zoonotic potential There is no evidence that ASFV infects humans.
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African Swine Fever © 2003 – 2019 www.cfsph.iastate.ed u Email: email@example.com page 2 of 9 Geographic Distribution African swine fever is endemic in much of sub – Saharan Africa including the island of Madagascar. Outbreaks have been seen occasionally outside Africa , but t he virus was almost always eradicated . It has , however, persisted on the Mediterranean island of Sardinia (Italy), where free – range product ion systems, uncontrolled pig movements and socioeconomic factors complicate control efforts. In 2007, ASFV was introduced into the Caucasus region of Eurasia, via the Republic of Georgia, and it has spread to domesticated swine and/or wild boars in a numb er of countries in this area . As of June 2019, infections had been reported as far west as the Baltic states, Romania, Bulgaria, Poland, Hungary and Belgium. In most cases, the virus appears to be spreading in wild boar, but domesticated pigs were also aff ected in some nations. Viruses that apparently originated from this outbreak were found in wild boar in Iran in 2010, but there have been no reports of ASFV in the Middle East since then. In 2018, a virus from Eurasia was detected in domesticated pigs in C hina . Since then, it has spread to pigs in other Asian countries including Vietnam, Mongolia, Cambodia , Lao and North Korea. Infected wild boar have also been detected in this region . Transmission African swine fever can be transmitted either with or without tick vectors as intermediaries. Domesticated pigs can shed ASFV in all secretions and excretions including oronasal fluid , urine and feces . Significant virus shedding can begin 2 days before the onset of clinical signs. Blood contains large amounts of the virus, and m assive environmental contamination may result if blood is shed during necropsies or pig fights, or if a pig develops bloody diarrhea. I nformation about virus shedding in other suids is more limited; however , virus replication appear s to be much lower in adult warthogs than pigs, and they are not thought to transmit the virus by direct contact. ASFV can most likely enter the body through various mucous membranes after direct (non – tick borne) contact with infected pigs or the environment , but most animals are thought to be infected by inhalation or ingestion . Higher doses of the virus are generally required to infect a pig in solid feed, compared to inhalation, but ingestion of virus in liquids also seems to be efficient. A erosolized viruses may contribute to transmission within a building or farm, but current evidence suggests that this only occurs over relatively short distances. Because ASFV can persist in tissues after death, it can be spread by feeding uncooked or undercooked pig swill that contains tissues from infected animals. C annibalism of dead pigs m ight be important in some outbreaks . Vector – mediated transmission occurs through the bites of some members of the soft tick genus Ornithodoros . In some part s of Africa, ASFV cycle s between juvenile common warthogs ( Phacochoerus africanus ) and soft ticks of the Ornithodoros moubata complex, which live in their burrows. Transstadial, transovarial and sexual transmission have been demonstrated in these ticks. A similar cycle is thought to exist between domesti cated pigs in Africa and the Ornithodoros moubata complex ticks that colonize their pens. Ornithodoros erraticus acted as a biological vector on the Iberian Peninsula during ou tbreaks in Europe, and additional species of Ornithodoros have been infected in the laboratory. Ornithodoros spp. ticks are long – lived, and colonies have been demonstrated to maintain ASFV for several years (e.g., 5 years in O. erraticus ). However, the y ca n eventually clear the virus if they are not reinfected. There is no evidence that hard ticks act as biological vectors for ASFV. Other bloodsucking insects such as mosquitoes and biting flies might be able to transmit ASFV mechanically. ASFV was found in swine lice ( Haematopinus suis ) collected from experimentally infected pigs. Stable flies ( Stomoxys calcitrans ) can carry high levels of the virus for 2 days. Under experimental conditions, these flies could transmit ASFV 24 hours after feeding on infected pigs. Pigs also bec a me infected when they were fed stable flies that had been been fed on infected blood . Fairly l arge number s of flies were used to infect pig s in both of these experiments , but it is possible that transmission by other blood – sucking flies is more efficient. How long pigs can remain infected with ASFV is uncertain. S ome studies have found this virus in the tissues of domesticated pigs for as long as 2 – 6 months after experimental inoculation, and there are reports of virus shedding and transmission for at least 70 days . In other reports, pigs transmit ted ASFV for less than a month . L onger transmission seem s to be associated with less virulent viruses , which can cause chronic infections and persistent viremia . R ecent studies that used highly virulent or moderately virulent ASFV circulating in Europe found that recovered pigs did not infect naive pigs via prolonged close contact after live virus could no longer be isolated from their blood. Some of these pigs were stil l PCR – positive at the time . Currently, there is no evidence that ASFV persists long – term in a latent state. ASFV can spread on fomites, includin g vehicles, feed and equipment. It is reported to survive for several days in feces or urine at room temperature, and in feces for at least 11 days in one study where the sample was stored in the dark. One study estimated the infectious period for urine, based on the half – life of ASFV and the estimated dose required for infection, as 3 days at 37ºC (99ºF) and 15 days at 4ºC (39ºF) . Feces was estimated to remain infectious at these temperatures for 4 and 8 days, respectively. ASFV is also reported to persist for a year and a half in blood or approximately 5 months in boned meat , both stored at 4ºC , and 140 days in salted dried hams, A recent study, which used pork products made from experimentally infected animals, isolated virus from dry cured salami at 18 days but not 26 days after processing , from dry cured pork belly at
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African Swine Fever © 2003 – 2019 www.cfsph.iastate.ed u Email: firstname.lastname@example.org page 3 of 9 60 but not 137 days and from dry c ured loin at 83 but not 137 days. Pigs fed salami held for 26 days and pork belly or loin at 137 days , respectively, did not become infected . One source suggests that it may persist for several years in frozen carcasses , and unpublished findings from a report in the 1960s indicated that at least small amounts of infectious virus might persist in forest soil for nearly 4 months, in fresh water for up to 7 weeks in summer and approximately 6 months in winter , and on wooden boards or bricks buried in dirt for 2 – 3 months . However, this study injected pigs with virus, which may not be applicable to natural exposure. M ore recent investigations det ected nucleic acids for several days to weeks in the soil where wild boar carcasses had been removed , but infectious virus could not be found . Few studies have examined virus transmission to pigs from fomites or other environmental sources, but in one recent report, pigs became infected when they were placed in pens that had housed animals with African swine fever, but not when the pens were left empty of pigs for 3 days or longer. These pens contained feces and urine, but visible blood had been washed away and bloodstained areas decontaminated. The length of virus persistence is likely to be influenced by the level of virus contamination. Disinf ection Many common disinfectants are ineffective against ASFV; care should be taken to use a disinfectant specifically approved for this virus. Sodium hypochlorite, citric acid and some iodine and quaternary ammonium compounds are reported to destroy ASFV on some nonporous surfaces. In one experiment, either 2% citric acid or higher concentrations of sodium hypochlorite (e.g., 2000 ppm) could disinfect the virus on wood; however, citric acid was more effective. Unprocessed meat must be heated to at least 7 0ºC (158ºF) for 30 minutes to inactivate ASFV; 30 minutes at 60ºC (140ºF) is sufficient for serum and body fluids. V irus in serum – free medium can also be inactivated by pH < 3.9 or > 11.5. Incubation Period The incubation period is reported to be 4 to 19 d ays in naturally – acquired cases . Clinical Signs African swine fever can present as a peracute, acute, subacute or chronic disease , and s ome animals may seroconvert without becoming ill. The course of the disease is generally correlated with the virulence of the virus, although a given virus can cause more than one form. Even in herds infected with highly virulent isolates, severely ill pigs are sometimes uncommon until the later stages of an outbre ak, with most affected animals initially having mild , nonspecific clinical signs. Sudden deaths with few lesions (peracute cases) may be the first sign of an infection in some herd s . Acute cases are characterized by a high fever, anorexia, lethargy, weakn ess and recumbency. Erythema can be seen, and is most apparent in white pigs. Some pigs develop cyanotic skin blotching, especially on the ears, tail, lower legs or hams. Pigs may also experience diarrhea, constipation or vomiting and/or display signs of a bdominal pain; the diarrhea is initially mucoid and may later become bloody. There may also be other hemorrhagic signs , including epistaxis and hemorrhages in the skin. Respiratory signs ( including dyspnea ) , nasal and conjunctival discharges, and neurological signs have been reported. Pregnant animals frequently abort. Leukopenia and thrombocytopenia of varying severity may be detected in laboratory tests. Death often occurs within 7 – 10 days. Subacute African swine fever is similar , but with less severe clinical signs. Fever, thrombocytopenia and leukopenia may be transient; however, hemorrhages can occur during the period of thrombocytopenia. Abortions are sometimes the first sign of an outbreak in this form. Affected pigs usually die or recover w ithin 3 to 4 weeks. Petechiae and cyanotic lesions have been reported in some recovering animals. Pigs with the chronic form have nonspecific signs such as an intermittent low fever, appetite loss and depression. Other signs may be limited to emaciation an d stunting , but some pigs develop respiratory problems and swollen joints. Coughing is common, and diarrhea and occasional vomiting have been reported. Ulcers and reddened or raised necrotic skin foci may appear over body protrusions and other areas subjec t to trauma. Chronic African swine fever can be fatal. Signs in wild boar inoculated with a highly virulent isolate were similar to those in domesticated pigs; however, some runted animals infected with very low viral doses had few or no clinical signs, i ncluding fever, before death. Warthogs and bush pigs usually become infected asymptomatically or have mild cases . Post Mortem Lesions Click to view images The gross lesio n s are highly variable, and are influenced by the virulence of the isolate and the course of the disease. Numerous organs may be affected, to varying extent, in animals with acute or subacute African swine fever. The carcass is often in good condition in animals that die acutely. There may be bluish – purple discoloration and/or hemorrhages in the skin, and signs of bloody diarrhea or other internal hemorrhages. The major internal lesions are hemorrhagic, and occur most consistently in the spleen, lymph node s, kidneys and heart. In animals infected with highly virulent isolates, the spleen can be very large, friable, and dark red to black. In other cases, the spleen may be enlarged but not friable, and the color may be closer to normal. The lymph nodes are of ten swollen and hemorrhagic, and may look like blood clots . T he gastrohepatic and renal lymph nodes are affected most often. Petechiae are common on the cortical and cut surfaces of the kidneys, and sometimes in the renal pelvis.
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African Swine Fever © 2003 – 2019 www.cfsph.iastate.ed u Email: email@example.com page 4 of 9 Perirenal edema may be pre sent. Hemorrhages, petechiae and/or ecchymoses are sometimes detected in other organs including the urinary bladder, lungs, stomach and intestines. Pulmonary edema and congestion can be prominent in some pigs. There may also be congestion of the liver and edema in the wall of the gall bladder and bile duct, and the pleural, pericardial and/or peritoneal cavities may contain straw – colored or blood – stained fluid. The brain and meninges can be congested, edematous or hemorrhagic. Animals that die peracutely ma y have few or poorly developed lesions. In animals with chronic African swine fever, the carcass may be emaciated. Other possible post mortem lesions include focal areas of skin necrosis, skin ulcers, consolidated lobules in the lung, caseous pneumonia, n onseptic fibrinous pericarditis, pleural adhesions, generalized lymphadenopathy and swollen joints. Some of these lesions may result from secondary infections. Aborted fetuses can be anasarcous and have a mottled liver. They may have petechiae or ecchymose s in the skin and myocardium. Petechiae may also be found in the placenta. Diagnostic Tests Clinical samples generally include blood from live animals and tissues (especially spleen, kidney, tonsils , lymph nodes , liver, heart and lung ) collected at necropsy. The spleen and lymph nodes usually contain the highest concentrations of virus , and viral DNA may persist longer in the spleen than other internal organs after death. Nucleic acids may also be detected in the bone marrow, which can be useful when other tissues from carcasses are not available or usable , and the intra – articular tissues of joints are sometimes tested in chronic cases. ASFV does not occur in aborted fetuses; in cases of abortion, a blood sample should be collected from the dam. ASFV is usually isolated in primary porcine cells, includ ing pig leukocyte or bone marrow cultures, porcine alveolar macrophages or blood monocyte cultures. ASFV – infected cells in the culture may be identified by their ability to induce hemadsorp tion of pig erythrocytes to their surfaces. However, a few non – hemadsorbing isolates can be missed with this test . M ost of the latter viruses are avirulent, but some do produce illnesses, including chronic disease . Other methods to detect virus – infected ce lls include PCR and immunofluorescence, and PCR can be used to confirm identity. PCR can also detect nucleic acids directly in clinical samples . A wide variety of PCR tests have been described, with some real time assays reported to be mo re sen sitive than others . L oop – mediated isothermal amplification assays (LAMPs) have been published. A SFV a ntigens may be found in tissue smears or cryostat sections, as well as in buffy coat samples, using ELISAs or immunofluorescence. Antigens are easiest to detect in acute cases; the tests are less sensitive in subacutely or chronically infected animals. They are best employed as herd tests, and in conjunction with other assays. to detect ASFV directly in peripheral blood leukocytes; however, this test has mostly been replaced by PCR, which is easier to evaluate. Rapid penside l ateral flow devices for antigen detection have been published. Pigs with acute disease often die before developing ant ibodies; however, antibodies to ASFV persist for long periods in animals that survive. Many serological tests have been developed for the diagnosis of African swine fever, but only a few have been standardized for routine use in diagnostic laboratories. Cu rrently used assays include ELISAs, immunoblotting , indirect fluorescent antibody (IFA) and indirect immunoperoxidase (IPT) tests. The ELISA is prescribed for international trade, and is generally confirmed by immunoblotting , but IFA or IPT can also be use d for confirmation . Treatment There is no treatment for African swine fever, other than supportive care. Control Disease reporting A quick response is vital for containing outbreaks in ASFV – free regions. Veterinarians who encounter or suspect African swin e fever should follow their national and/or local guidelines for disease reporting. In the U.S., state or federal veterinary authorities should be informed immediately. Prevention Biosecurity measures (e.g., fences, restricted visitor access, good hygiene, disinfection of footwear or the use of dedicated footwear, closed herds, quarantines of new animals) help prevent virus introduction onto farms. Separation of the herd from wild suids, their environments and carcasses, as well as measures to prevent accid ental human transport of ASFV, must be considered. In the past, many ASFV – free countries used heat treatment to inactivate viruses in pig swill and prevent the entry of ASFV. Due to the risk that this and other viruses may not be completely inactivated (fo r example, if parts of the swill do not reach the target temperature), some nations have completely forbidden feeding swill to pigs. In areas w here this is not feasible, some sources recommend b oiling the swill for at least 30 minutes, with frequent or con tinuous stirring. Solid walls without cracks are considered the optimal building material to discourage the establishment of Ornithodoros ticks and facilitate control. Acaricides are generally ineffective where wooden, stone, earth or overlapping metal walls/ fences provide hiding places for these ticks. Some areas have successfully eradicated African swine fever outbreaks by standard stamping out measures (e.g., slaugh ter of infected and in contact animals, sanitation,
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African Swine Fever © 2003 – 2019 www.cfsph.iastate.ed u Email: firstname.lastname@example.org page 5 of 9 disinfection, movement controls and quarantines ) , but more complex measures were needed in some regions . On the Iberian Peninsula , ASFV became established in wild boar and Ornithodoros erraticus ticks in the 1960s , and complete eradication took decades. Pigpens with infected ticks were destroyed or isolated as part of this campaign. Current regulations in the EU allow pig farms to be restocked as soon as 40 days after cleaning and disinfection, if an Afric an swine fever outbreak occurs in the absence of vectors , but the minimum quarantine is 6 years if vectors are thought to be involved in transmission. Current control measures in wild boar mainly focus on reducing the ir numbers, as higher population densi t ies are thought to facilitate maintenance of the virus, and attempting to discourage the movement s of infected animals . Authorities in the Czech Republic apparently controlled a single focus of infection in wild boar with intensive measures that included fencing , trapping and targeted hunting. Biosecurity measures to reduce the risk of transporting ASFV during hunting (e.g., the use of leak – proof vessels to remove carcasses and store offal, limits on vehicles in infected areas, precautions for cleaning and disinfect ing tools ) have been recommended . Eradication of ASFV from some wild reservoirs in Africa, such as warthogs, appears unlikely. However, c ompartments where African swine fever is controlled and barriers (double fenc ing ) prevent contact with wild r eservoirs have been established in some parts of Africa where warthog – mediated introduction is a concern . No vaccine is currently available. Morbidity and Mortality T he morbidity rate for African swine fever can approach 100% in naïve herds of domesticated pigs . C umulative mortality depends on the virulence of the isolate, and can range from < 5% to 100% . It is usually 30 - 70% in subacute cases . H owever, viruses can sometimes take days to weeks to spread through a herd, and initial herd morta lity rates may be low even when the case fatality rate is high . Less virulent isolates are more likely to kill pigs with concurrent disease s , pregnant or nursing sows, and young animals. Mor bidity and mor tality rates also tend to be high er when ASFV is int roduced into new regions, with an increased incidence of subacute and subclinical cases once it becomes endemic. Chronic African swine fever was first described during outbreaks on the Iberian Peninsula, and some authors speculated that the viruses that ca use this form might have originated from live attenuated vaccine strains tested at the time. However, chronic disease has since been reported in pigs that were experimentally infected with recent European strains, and it has also been seen in Angola. Some populations of pigs in Africa are reported to be more resistant to African swine fever than others, but the basis for this resistance is not known. The role of wild suids in spreading African swine fever differ s betwe e n regions. Warthogs cause some outbrea ks in Africa, but, at present, domesticated pigs seems to be driv ing virus spread in many African countries . In the current outbreaks in Europe , ASFV appears to persist in wild boar populations independent ly of outbreaks among domesticated pigs. Although previous experiences suggested that the virus would eventually die out in these animals if it was not reintroduced, neither explosive outbreaks nor self - extinction has been reported to date. Instead, the viru s has been spreading slowly and steadily across Europe in wild boar . Why this is occurring is unclear. The high density of animals in many areas probably play s a role, but virus spread has also occurred in areas where wild boar density is low. Other factor s likely to influence ASFV transmission rates include wild boars social structure , where family groups are prominent, and exposure to infectious carcasses. In 2019 , one study found that the incidence of ASFV had decreased for the first time in wild boar i n Estonia . The density of wild boar is relatively low in this area , and decreased further after virus introduction, possibly due to the effects of the disease as well as deliberate measures to decrease animal numbers. Whether this will eventually lead to t he extinction of ASFV in Estonia is still uncertain . There is currently no evidence that Ornithodoros ticks play any role in the current European outbreak, but some authors note that there is relatively little in formation on their distribution, and member s of the O. erraticus complex were known to occur in the Caucasus at one time. Recent studies of exposure to Ornithodoros have reported strong positives among backyard pigs in the southern parts of the Russian Federation . There is little or no information about whether wild boar or ticks play any role in the outbreaks in southern Asia, but the virus is spreading rapidly in some domestic herds. Internet Resources CIRAD Pigtrop (Pig Production in Developing Countries) http://pigtrop.cirad.fr/home Food and Agriculture Organization of the United Nations (FAO) . Recognizing African Swine Fever. A Field Manual. ht tp://www.fao.org/docrep/004/X8060E/X8060E00.HT M FAO. Up dates on the ASF S ituation W orldwide (with links to African swine fever information ) http://www.fao.org/ag/ againfo/programmes/en/e mpres/ ASF/situation_update.html FAO: African S wine F ever: D etection and D iagnosis A M anual for V eterinarians (English version) http://www.fao.org/3/a - i7228e.pdf The Merck Veterinary Manual http://www.merckvetmanual.com/ PAGE - 6 ============ African Swine Fever © 2003 - 2019 www.cfsph.iastate.ed u Email: email@example.com page 6 of 9 United States Animal Health Association. Foreign Animal Diseases http://www.aphis.usda.gov/emergency_response/downl oads/nahems/fad.pdf World Organization for Animal Health (OIE) http://www.oie.int OIE Manual of Diagnostic Tests and Vaccines for Terrestrial Animals http://www.oie.int/international - standard - setting/terrestrial - manual/access - online/ OIE Terrestrial Animal Health Code http://www.oie.int/international - standard - setting/terrestrial - code/access - online/ Acknowledgements This factsheet was written by Anna Rovid Spickler, DVM, PhD, Veterinary Specialist from the Center for Food Security and Public Health. The U.S. Department of Agriculture Animal and Plant Health Inspection Service (USDA APHIS) provided funding for this factsheet through a series of cooperative agreements related to the development of resources for initial a ccreditation training. The f ollowing format can be used to cite this factsheet. Spickler, Anna Rovid. 2019 . African Swine Fever . Retrieved from http://www.cfsph.iastate.edu/DiseaseInfo/ factsheets.php . References Animal Health Australia. The National Animal Health Information System (NAHIS). African swine fever [online]. Available at: http://www.brs.gov.au/usr bin/aphb/ahsq?dislist=alpha.* Accessed 18 Oct 2001. Arias M , Jurado C , Gallardo C , Fernández - Pinero J , Sánchez - Vizcaíno JM . Gaps in African swine fever: Analysis and priorities. Transbound Emerg Dis. 2018 ; 65 Suppl 1:235 - 47. Ayoade GO; Adeyemi IG. African swine fever: an overview. Revue Élev Méd vét Pays Trop. 2003;56:129 - 34. Bellini S , Rutili D , Guberti V . Preventive measures aimed at minimizing the risk of African swine fever virus spread in pig farming systems. Acta Vet Scand. 2016;58(1):82. Beltrán - Alcrudo D, Arias M, Gallardo C, Kramer S , Penrith ML. African swine fever: detection and diagnosis A manual for veterinarians. FAO Animal Production and Health Manual No. 19. Rome : Food and Agriculture Organization of the United Nations (FAO) ; 2017. Available at: http://www.fao.org/3/a - i7228e.pdf . Accessed 18 Jun 2019. Blome S, Gabriel C, Beer M. Pathogenesis of African swine fever in domestic pigs and European wild boar. Virus Res. 2013;173(1):122 - 30. Boinas FS, Wilson AJ, Hutchings GH, Martins C, Dixon LJ. The persistence of African swine fever virus in field - infected Ornithodoros erraticus during the ASF endemic period in Portugal. PLoS One. 2011;6(5):e20383. Chenais E , Depner K , Guberti V , Dietze K , Viltrop A , Ståhl K . Epidemiological cons iderations on African swine fever in Europe 2014 - 2018. Porcine Health Manag. 2019;5:6. Costard S, Mur L, Lubroth J, Sanchez - Vizcaino JM, Pfeiffer DU. Epidemiology of African swine fever virus. Virus Res. 2013;173(1):191 - 7. Costard S, Wieland B, de Glanvi lle W, Jori F, Rowlands R, Vosloo W, Roger F, Pfeiffer DU, Dixon LK. African swine fever: how can global spread be prevented? Philos Trans R Soc Lond B Biol Sci. 2009;364(1530):2683 - 96. Cubillos C, Gómez - Sebastian S, Moreno N, Nuñez MC, Mulumba - Mfumu LK, Q uembo CJ, Heath L, Etter EM, Jori F, Escribano JM, Blanco E. African swine fever virus serodiagnosis: a general review with a focus on the analyses of African serum samples. Virus Res. 2013;173(1):159 - 67. Dardiri AH, Yedloutschnig RJ, Taylor WD. Clinical a nd serologic response of American white - collared peccaries to African swine fever, foot - and - mouth disease, vesicular stomatitis, vesicular exanthema of swine, hog cholera, and rinderpest viruses. Proc Annu Meet U S Anim Health Assoc. 1969;73:437 - 52. Davie s K, Goatley LC, Guinat C, Netherton CL, Gubbins S, Dixon LK, Reis AL. Survival of African swine fever virus in excretions from pigs experimentally infected with the Georgia 2007/1 isolate. Transbound Emerg Dis. 2017 ;64(2):425 - 31. de Carvalho Ferreira HC, Tudela Zúquete S, Wijnveld M, Weesendorp E, Jongejan F, Stegeman A, Loeffen WL. No evidence of African swine fever virus replication in hard ticks. Ticks Tick Borne Dis. 2014;5(5):582 - 9. de Carvalho Ferreira HC, Weesendorp E, Quak S, Stegeman JA, Loeffen WL. Quantification of airborne African swine fever virus after experimental infection.Vet Microbiol. 2013;165(3 - 4):243 - 51. de Carvalho Ferreira HC, Weesendorp E, Quak S, Stegeman JA, Loeffen WL. Suitability of faeces and tissue samples as a basis for non - i nvasive sampling for African swine fever in wild boar. Vet Microbiol. 2014;172(3 - 4):449 - 54. Diaz AV, Netherton CL, Dixon LK, Wilson AJ. African swine fever virus strain Georgia 2007/1 in Ornithodoros erraticus ticks. Emerg Infect Dis. 2012 ; 18(6):1026 - 8. D ixon LK , Sun H , Roberts H . African swine fever. Ant iviral Res. 2019 ; 165:34 - 41. Endris RG, Hess WR. Experimental transmission of African swine fever virus by the soft tick Ornithodoros (Pavlovskyella) marocanus (Acari: Ixodoidea: Argasidae). J Med Entomol. 1992;29:652 - 6. Food and Agriculture Organization of the United Nations ( [FAO ). ASF situation in Asia. Update 14 June 2019, 11:00 hours; Rome. Available at: http://www.fao.org/ag/againfo/programmes/en/empres/ASF/sit uation_update.html. Accessed 13 Jun 2019. Food and Agriculture Organization of the United Nations ( FAO ). Recognizing African swine fever. A field manual [online]. FAO Animal Health Manual No. 9. Rome: FAO; 2000. Available at: http: //www.fao.org/docrep/004/X8060E/ X8060E00.HTM . Accessed 4 Dec 2006. 215 KB – 9 Pages