Ghosh P
Pallabi Ghosh
3rd Year, B.V.Sc. & A.H.
Ranchi Veterinary College, Ranchi
INTRODUCTION
Classical Swine Fever (CSF) and African Swine Fever (ASF) both are listed in the OIE World Organisation for Animal Health (OIE) Terrestrial Animal Health Code and must be reported to the OIE (OIE Terrestrial Animal Health Code) that is both are notifiable disease. CSF and ASF have the same natural host that is Suidae family. The clinical signs that are manifested in both the disease are quiet similar and distribution also overlap in some places so differential diagnosis is very important to take up specific preventive or control measures. In the global scenario both of them are important as they lead to huge economic losses because of mortality of pigs or decrease in their production and fertility.
ETIOLOGY
CLASSICAL SWINE FEVER (CSF)
The CSF virus belongs to the genus Pestivirus within the Flaviviridae family. CSFV strains can be assigned to three distinct genotypes with three to four subtypes ( Paton DJ et al.) (Postel A. et al.)
AFRICAN SWINE FEVER (ASF)
The ASF virus belongs to the genus Asfivirus within the Asfarviridae family. It is the only DNA arbovirus (arthropod borne ) among all the viruses known so far.
MORPHOLOGY OF THE VIRUS
CSF
The virus causing CSF is a small, positive single stranded RNA virus. The viron constitutes of the core (C) protein along with three enveloped glycoproteins (E1, E2 and Erns) and Npro, p7, NS2-3, NS4A, NS4B, NS5A ans NS5B are NS proteins. (Elbers K et al.) (Lattwein E et al.)
ASF
The ASF virus is a large DNA virus. The virion is icosahedral in morphology (L K Dixon, 1986.) The virus particles consist of a nucleoprotein core surrounded by a lipid membrane covered by a capsid. The external envelope doesnot seem to be essential for infectivity (Moura Nunes et al, 1977.) It consists of hexagonal arrangement of capsomeres which appear as hexagonal prisms.
TRANSMISSION
CSF
The principal means of viral transmission is direct contact between infected and susceptible pigs.Chronically infected pigs shed the CSFV in oronasal and lacrimal secretions, urine and faeces continuously or intermittently until death. The virus may be mechanically transmitted by birds, pets and arthropods. CSFV survives in frozen meat. Clinical outbreaks of CSF disease has also resulted from garbage feeding by pigs ( Torremorrell M. ) CSFV can cross placental barrier and consequently to infect fetuses in the uterus.
ASF
Here also the principal means of viral transmission is direct contact with infected domestic or wild pigs. Indirect transmission happens through ingestion of contaminated feed or garbage or from contaminated fomites. Mechanical transmission by biological vectors like soft ticks of the genus Ornithodoros. (OIE.int)
Basically three types of cycles occurs. One is the sylvatic cycle and the other is the tick-pig cycle and the third is the domestic cycle. In the sylvatic cycle circulation happens between the African wild suid population and soft ticks. This cycle can be seen in African countries where ASF and ticks of the genus Ornithodoros are endemic. The tick- pig cycle played a role on the Iberian Peninsula, where ticks infested pig pens and shelters. The domestic cycle involves the direct or indirect transmission between domestic pigs.(Costard L et al, 2013) (Guinat C et al, 2016)
EPIDEMIOLOGY AND DISTRBUTION
CSF
CSF virus was first reported from Ohio, USA in 1833. In 1978, CSF was eradicated in North America (Br Vet Journal 1991.) However, it is known that CSF has been endemic in parts of Asia as well as in areas of Central and South America since many years (Postel A et al. 2013) There were devastating outbreaks in the Netherlands and in Germany in the late 1990s and sporadic outbreaks occurred thereafter.
ASF
ASF virus mostly occurred in Africa. Even when occasional incursions had been there in Europe or America (except that of the endemic situation of Sardinia ) always had been controlled successfully. Except for Sardinia, ASF was eradicated in Europe in the late 1990s, which led to a research focus on CSF. But following an introduction of the virus in 2007, it has now expanded its geographical distribution into Caucasus and Eastern Europe where it was difficult to control. (Costard et al, 2013). The ASFV strains causing the outbreaks in Eastern Europe are highly virulent and the clinical courses are usually acute and lethal (Gallardo C, 2014) (Blome S, 2012.)
As per the report of OIE on ASF 30 April to May 14, 2020, a total of 11,247 animals were notified as losses and 23 countries or territories notified new or outgoing outbreaks.
CLINICAL SIGNS
CSF
The natural hosts are domestic and wild pigs. This virus causes one of the most serious diseases in pigs with grave economic losses. Depending on factors like viral virulence, age of the affected animal and its habitat the clinical signs may differ.
Three different courses of infection are known namely acute, sub acute and chronic form. The acute form is caused by highly virulent strains that usually have an incubation period of 3 to 7 days and death happens within 10 days of infection. Fever >41°C (105.8 °F) is usually seen and persists until terminal stages of the disease when temperature drops. Vomiting and constipation followed by diarrhea is common (MSD Vet manual.) Respiratory and gastro- intestinal signs, lethargy and inappetence is seen often. The acute lethal form can be accompanied by severe hemorrhagic or neurological signs. Mortality in piglets can be very high, whereas older animals can withstand an infection and develop a life-long immunity ( OIE.int).
Moderate to low virulence strains cause sub-acute and chronic forms of the disease. It is characterized by high fever, staggering gait, cough, diarrhea and purple discoloration of the skin notably at the ears, lower abdomen and extremities. Low virulence strains can be difficult to detect, the only clinical expression may be poor reproductive performance of sows and the birth of piglets with neurologic defects (eg. Congenital tremor.)
In chronic forms of CSF there is an initial acute febrile phase, infected animals may show an apparent recovery but then relapse, withsigns like anorexia, depression, fever and progressive loss of condition (marked weight loss.) Then the animal succumb and die. During the whole time the animal shed large amounts of virus. (Moennig V et al 2003) (OIE.int)
The outcome of transplacental infection depends on the stage of gestation. In early pregnancy, CSF virus infection usually causes abortion, still birth, mummification or malformation (Moennig V et al, 2003.) However, infections in the 2nd and 3rd month of pregnancy may lead to immunotolerant piglets towards the causative virus strain and may be born healthy. However, they usually runt and develop the so-called late onset form of CSF. Also, these animals constantly shed virus until they eventually die (Artois M et al, 2002.)
ASF
The clinical signs may differ according to virulence of the virus, breed and health status of the pig, the route of infection and dose. The incubation period is usually 2 to 7 days (Blome S, 2013). Peracute, acute, subacute and chronic forms are seen.
The peracute forms are caused by virus of high virulence. Clinical signs include high fever, appetite loss, lethargy, hyperpnoea. Mortality is very high upto 90-100 %. The acute form is characterized by fever, depression, anorexia and loss of appetite, haemorrhages in the skin, abortion in pregnant sows, cyanosis, vomiting, diarrhea and death within 6-13 days (or upto 20 days.)
The subacute and chronic forms is caused by moderate and low virulence strains respectively. In subacute forms clinical signs are similar to acute form but less pronounced, mortality rates range from 30-70 % (OIE.int). In chronic form respiratory signs and lameness is seen and fever is irregular or absent (Schultz K, 2017.)
PATHOLOGY
CSF
A very important pathological sign of classical swine fever is “button” ulcers in the intestine, particularly near the ileo-caecal junction. Another principal lesion is geneneralised vasculitis. Vasculitis in the CNS leads to incoordination (staggering gait) or may even cause convulsions. Clinical vasculitis is manifested as hemorrhages and cyanosis of the skin, there may also be a generalized erythema of the skin.
Microscopically, non- suppurative encephalitis with a characteristic vascular cuffing is common. In acute forms lymph nodes, spleen and kidneys as well as other organs may be oedematous and hemorrhagic. In chronic forms, atrophy of the thymus and depletion of lymphoid follicles in lymph nodes are seen. In animals dying due to the chronic form of CSF, the typcal hemorrhages are usually missing, while necrotic lesions in the GIT are more common (Moennig V et al., 2003.)
The principal PM findings are widespread petechial and ecchymotic haemorrhages, especially in lymph nodes (eg, mandibular and retropharyngeal), tonsils, larynx, kidneys, spleen, urinary bladder and ileum. In the periphery of the spleen infarctions may be seen.
ASF
Skin erythema is usually seen and in chronic cases it becomes necrosed. In acute cases gastro-hepatic and renal lymph node have marbled aspect Hyperaemic spleenomegaly is seen with petechial haemorrhages. Severe alveolar oedema is seen in the lungs. Haemorrhages are also seen in epicardium, pericardium and gall bladder. In subacute cases thrombocytopenia is transient. Most lymph nodes resemble a blood clot. There is partial hyperaemic spleenomegaly or focal infarction in the spleen. There is petechial haemorrhages in cortex, medulla and pelvis; peri – renal oedema in the kidney and oedema in the wall of gall bladder. Haemorrhages in epicardium and endocardium are seen, also hydropericardium may be seen. Abortion may also occur. Swollen lymph nodes and enlarged spleen with normal colour, Pleuritis and pneumonia may occur along with fibrinous pericarditis. Tonsils may have necrotic foci. Abortion is the reproductive alteration that may be seen.( Sanchez- Vizcaino et al., 2015)
DIAGNOSIS
CSF
A presumptive diagnosis is done by the veterinarian in the field by seeing the clinical signs and knowing the history of the herd. But confirmation is done only by laboratory tests because clinical signs of CSF are also seen in other diseases of pig. Differential diagnosis is especially needed from African swine fever.
For sample collection suitable tissues are tonsils, spleen, kidney, ileum, lymph nodes especially mandibular, retropharyngeal, gastrohepatic and mesenteric.
Virus detection is done from whole blood collection with EDTA as anticoagulant. Nasal swabs and tonsil scrapings are also used to detect the virus or the viral RNA. For detection of CSFV antibodies, clotted blood samples (serum) are taken. Antigen detection may be done by direct immunofluorescence on frozen tissue sections especially from the tonsil samples. It can also be done by ELISA but sensitivity is less.
For rapid detection of CSFV RNA in tissues, blood, serum, or oro-nasal fluids RT-PCR or RT-qPCR are broadly used. Antibodies against CSFV are detected later during the infection (2–3 weeks post-infection.)
New generations of CSFV marker vaccines have also been developed to make emergency vaccination compatible with control of CSF. The application of a marker vaccine is possible if tests such as ELISA can distinguish between antibodies produced in response to a natural infection and those produced by vaccination.
ASF
Presumptive diagnosis is done on the basis of history and clinical signs but confirmation is important which is done by laboratory diagnostic tests.
Laboratory diagnostic procedures fall into 2 categories: one is detection of the virus and the other is serology. Isolation of virus for detection is done by inoculation of pig leukocyte or bone marrow cultures. The detection of antigens in cryostat sections of tissues or smears may be done by fluorescent antibody test. PCR or real-time PCR may also be used for the detection of genomic DNA, these are excellent and highly sensitive and rapid techniques for ASFV detection.
Serological tests may also be done. Places where the disease is endemic or where a primary outbreak is caused by a strain of low or moderate virulence, the investigation of new outbreaks should include the detection of specific antibodies. Enzyme-linked immunosorbent assay (ELISA), the Indirect Fluorescent Antibody Test (IFAT), the indirect immunoperoxidase test (IPT), and the immunoblotting test (IBT) are some of the tests available for antibody detection.
DIFFERENTIAL DIAGNOSIS BASED ON CLINICAL SIGNS
Although the symptoms and post-mortem lesions of ASF in general resemble those of CSF, differences might be observed especially in acute and per-acute fatal infections. Such outbreaks of ASF are characterized by high body temperatures while the animals behave normally for 1-3 days, followed by inappetance, a reddish and later cyanotic discoloration of the snout, ears, legs and/or abdomen, respiratory distress, vomiting and blood-tinged stools (Jover, F. P. et al. 1961) (Steyn, 1928) (Montgomery, 1921) (Jover P, 1961.) The reddish discoloration of the skin and labored breathing are less frequently observed in CSF. Also, discharge of blood with the faeces is not recorded in CSF (Dunne,1964) (Fuchs, 1968.) Signs of the central nervous system and coma are more common in the terminal stage of ASF than in CSF. Haemostasis is severely impaired in ASF, resulting in secondary hemorrhages and protracted bleeding from intramuscular inoculation sites, and from the vulva in case of abortion (Biront, 1985.) Continued bleeding is rare in CSF (Terpestra C, 1987.)
Since the “carrier sow syndrome” is typical for infections with moderate or low virulent strains of CSFV its consequences in the form of the birth of piglets with congenital tremor, hemorrhages, malformation and/or oedema do not apply to ASF infections.
CONTROL
CSF
Live-attenuated vaccines are highly effective and are widely used in endemic areas to control the spread of the CSF virus. Emergency ring vaccination around the outbreak can be done to prevent further spread of CSFV. CSF live-attenuated vaccines are safe and highly efficient, being able to induce protection shortly after vaccination (within 3 days). More recently, subunit CSFV vaccines containing only the major viral surface glycoprotein of the virus have been licensed. Although these vaccines allow differentiation of infected from vaccinated animals (DIVA capabilities), they lack the efficiency of live-attenuated vaccines. No treatment is available. Since CSF is a notifiable disease special care is to be taken. Control is usually strictly regulated by local laws. Elimination of exposed herds is done to prevent expansion during outbreaks in non endemic countries. Restriction of movement is applied to contain spread of the infection within a well-defined radius from the outbreak.
ASF
Currently, no vaccination for ASF is available. To prevent the introduction of ASF, movement restrictions regarding pigs and other products from pigs kept in affected areas as well as potentially contaminated material, vehicles etc. are in place and not allowed to move. Following European Commission, necessary biosecurity measures are defined, e.g. swill feeding, in commercial pig farms as well as in wild boars, must be prohibited, especially in high risk areas. Direct or indirect contact to wild boar or to any by products has to be avoided. When an outbreak of ASF in a farm has been confirmed, elimination of the exposed herd is done to prevent its spread. In addition, further measures like the safe disposal of all potentially contaminated material, restriction (minimum radius of 3 km) and surveillance (minimum radius of 10 km) zones with movement restrictions for pigs and products of porcine origin have to be set up (Schultz K et al., 2017.) Specific regulations have been defined for both zones in European Commission.
CONCLUSION
Both CSF and ASF are notifiable disease and cause great economic losses in outbreaks. There etiology is different but clinical signs are difficult to differentiate. The reddish discoloration of the skin and labored breathing are less frequently observed in CSF. Also, discharge of blood with the faeces is not recorded in CSF (Dunne, 1964) (Fuchs, 1968.) Continued bleeding is rare in CSF (Terpestra C, 1987.)Some other small differences like these may be seen. Since the outbreaks are difficult to control so strict preventive measures are to be taken. Vaccination for CSF is available in the form of live attenuated vaccines but vaccine against ASF is not available. Special care is to be taken in the endemic areas and transportation of pig and its products should be done with strict regulation of local laws.
REFERANCES
Costard S, Mur L, Lubroth J, Sanchez-Viscaino JM, Pfeffer DU. Epidemiology of African swine fever virus. Virus Res. 2013;173:191–197. doi: 10.1016/j.virusres.2012.10.030
Guinat C, Gogin A, Blome S, Keil G, Pollin R, Pfeiffer DU, Dixon L. Transmission routes of African swine fever virus to domestic pigs: current knowledge and future research directions. Vet Rec. 2016;178(262):267
Artois M, Depner KR, Guberti V, Hars J, Rossi S, Rutili D. Classical swine fever (hog cholera) in wild boar in Europe. Rev Sci Tech. 2002;21:287–303. doi: 10.20506/rst.21.2.1332
Torremorrell M, Current Therapy in Large Animal Theriogenology (Second Edition), 2007
Dewulf J, Laevens H, Koenen F, Mintiens K, De Kruif A. An experimental infection with classical swine fever virus in pregnant sows: transmission of the virus, course of the disease, antibody response and effect on gestation. J Vet Med B Infect Dis Vet Public Health. 2001;48:583–591. doi: 10.1046/j.1439-0450.2001.00467.x.ss
Schulz, K., Staubach, C., & Blome, S. (2017). African and classical swine fever: similarities, differences and epidemiological consequences. Veterinary research, 48(1), 84.
Elbers K, Tautz N, Becher P, Stoll D, Rumenapf T, Thiel HJ. Processing in the pestivirus E2-NS2 region: identification of proteins p7 and E2p7. J Virol. 1996;70:4131–4135
Montgomery, R. E. (1921). On a form of swine fever occurring in British East Africa (Kenya Colony). Journal of comparative pathology and therapeutics, 34, 159-191.
De Kock, G. Robinson, E.M. and Keppel, J.J.G. Onderstepoort J. vet. Sci. Anim. Ind. 14: 31–93, 1940
Steyn, D.G. (quoted by Maurer et al.) Rep. Direct, vet. Educ. and Res. Onderstepoort 13: 415–428, 1928.
Jover, F. P., & Botija, C. S. (1961). African swine fever virus in Spain. Bull. Off. Int. Epiz., 55, 107-147.
Lattwein E, Klemens O, Schwindt S, Becher P, Tautz N. Pestivirus virion morphogenesis in the absence of uncleaved nonstructural protein 2-3. J Virol. 2012;86:427–437. doi: 10.1128/JVI.06133-11
Moura Nunes J.F. , Vigario J.D. & Terrinha A.M (1975). — Ultrastructural study of African swine fever virus replication in cultures of swine bone marrow cells. Arch. Virol
Costard S, Mur L, Lubroth J, Sanchez-Vizcaino JM, Pfeiffer DU. Epidemiology of African swine fever virus. Virus Res. 2013;173(1):191‐197. doi:10.1016/j.virusres.2012.10.030
Dixon L K, “The structure and function of the African swine fever virus genome”,Rev. sci. tech. Off. Int. Epiz., 1986
World Organisation for Animal Health (2009) Classical swine fever (hog cholera). In: Manual of diagnostic tests and vaccines for terrestrial animals. OIE Biological Standards Commission, Paris
Moennig V, Floegel-Niesmann G, Greiser-Wilke I, “Clinical signs and epidemiology of classical swine fever: a review of new knowledge”, “Vet J. 2003 Jan; 165(1):11-20”
“Blome S, Gabriel C, Dietze K, Breithaupt A, Beer M”, “High virulence of African swine fever virus caucasus isolate in European wild boars of all ages”, “Emerg Infect Dis. 2012 Apr; 18(4):708.”
Gallardo C, Fernández-Pinero J, Pelayo V, Gazaev I, Markowska-Daniel I, Pridotkas G, Nieto R, Fernández-Pacheco P, Bokhan S, Nevolko O, Drozhzhe Z, Pérez C, Soler A, Kolvasov D, Arias M, “Genetic variation among African swine fever genotype II viruses, eastern and central Europe.”Emerg Infect Dis. 2014 Sep; 20(9):1544-7
Terpstra C, “ Differential diagnosis between African Swine Fever and Hog Cholera” Developments in Veterinary Virology.
Dunne, H.W . In: “Diseases of Swine”, 2nd. edition, Ed. H.W. Dunne. Iowa State Univ. Press, Ames, Iowa, pp. 140–186, 1964
Fuchs, F. In: “Handbuch der Virusinfektionen bei Tieren”. Ed. H. Röhrer. Gustav Fischer Verlag, Jena, Band III/l, pp. 15–250, 1968.
Terpstra, C. (1987). Differential diagnosis between African swine fever and hog cholera. In African Swine Fever (pp. 73-80). Springer, Boston, MA.
Commission European. Council directive 2002/60/EC of 27 June 2002 laying down specific provisions for the control of African swine fever and amending Directive 92/119/EEC as regards Teschen disease and African swine fever. Off J Eur Communities L. 2002;192:27–46.
https://www.oie.int/en/animal-health-in-the-world/animal-diseases/african-swine-fever/
https://www.msdvetmanual.com/generalized-conditions/classical-swine-fever/classical-swine-fever#v3274907
