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African horse sickness in Spain: Epizootiological and regulatory consideretions
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woRLo EOUln__gEWrER nAR'/ASSOClArIO_nn PRESENTEDAT THE WORLDVETERINARYCONGRESS,RIO DE JANEIRO,BRA2]L, AUGUSTlg91.
AFRICANHORSESICKNESSIN SPAIN: EPIZOOTIOLOGICALAND REGULATORYCONSIDERATIONS M. Rodriguez;1 J. L Ladero;z M. Castafio 1 and H. Hooghuisa
INTRODUCTION
African Horse Sickness (AHS) is a highly fatal noncontagious viral disease of Equidae, transmitted by arthropod vectors of the genus Culicoides, 4,14,1s with a seasonal incidence and a mortality rate related with the vector population present .7
ETIOPATHOGENESlS
AHS is caused by a double-stranded RNA, icosahedral viscerotropic virus of the Reoviridae family, genus Orbivirus. is Nine different serotypes of the virus have been identified,r The pathogenesis of AHA and Bluetongue seems to be similar, with primary viral replication occurring in the lymph nodes closet to the site where the animal is bitten by the vector. The dissemination of the virus to other tissues and organs of the reticuloendothelial system follows, until a secondary viraemia develops. The origin of the respiratory and circulatory disorders typical of the disease is an inflammatory response which affects small and middle-sized vessels,s,ll
CLINICAL
FINDINGS
Three forms of the disease have been described: an acute (pulmonary) form; a subaeute (cardiac) form; and a febrile Authom' address: IDepartamento de Patologia Animal II, faeultad de Vaterinaria, UniversidadComplutense28040, Madrid,Spain; 2Subdirecci6n General de Sanidad Animal Ministedode Agricultura,Pesa y Alimantaci6n, 28014 Madrid, Spain; 3Laboratoriode Sanidad y ProduccionAnimal Ministerio de Agriculture,Pesca y Alimentaci6n,28110 Algete, Madrid, Spain.
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form ("horse sickness fever),5,z although they are not always easy to differentiate since the clinical signs may overlap. According to our experience, the pulmonary form of AHS begins with sudden fever lasting 2-4 days, followed by respiratory signs including taehypnoea, labored respiration with coughing and frothy nasal discharge. Oedema of the supraorbital fossae is seen and death occurs due to severe pulmonary edema with cardiac failure.17 The clinical course of the cardiac form of the disease is longer, starting also with fever. The clinical signs are mainly due to functional circulatory disorders, and increase progressively, with development of edemas involving the head, neck and sternal region. A notable prominence of the supraorbital fossae is found (Fig.l), together with hemorrhagic and edematous conjunctivitis and blepharitis. Oedema of the frontal region and of the lips is common, as are petechiae on the ventral surface of the tongue. Death is caused by cardiac insufficiency with progressive pulmonary edema, lr Lesions The dominant gross lesions in cases of the pulmonary form are congestive-cyanotic mucous membranes, peteehiae on the underside of the tongue and, almost invariably, whitish or yellow-reddish foam in the nostrils (Figure2), and edema of the supraorbital fossae. The carcass is usually in good condition. A notable necropsy finding is a yellowish and gelatinous edema of the subcutaneous connective tissue, especially in the intercostal muscles. Upon opening the abdominal cavity, a slight ascites, focal subcapsular petechiae and slightly hypertrophic mesenteric lymph nodes can be observed, together with marked submucosal congestion of the fundus of the stomach, subserous and submucous petechiae in certain areas of the small intestine and, in some eases, diffuse congestion of the mucous membrane of the large intestine.
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WORLD EQUINE VETERINARY ASSOCIATION PRESENTEDM THEWORLDVETERINARYCONGRESS,RIODEJANEIRO,BRAZIL,AUGUST1901.
Figure 2. Frothy fluid which has oozed out of the nostrils (AHS).
Diagnosis
Figure 1. Edema of the supraorbital fossae (AHS). Upon opening the thoracic cavity a small accumulation of fluid is found, with interstitial and alveolar edema and frothy fluid in the trachea. Hydropericardium and petechiae of the coronary sulcus and subendocardial hemorrhage occur frequently. 16 In the subacute form on external inspection the animals also present a good general condition, congestive-cyanotic mucous membranes and edema of the supraorbital fossae. Blepharitis and edema of the palpebral conjunctiva is seen, often together with chemosis. A yellowish, gelatinous edema of the subcutaneous connective tissue is found, mainly located in the frontal, cervical and sternal regions, and in the ventral portion of the abdomen. As in the pulmonary form, ascites and hydrothorax are seen, but in a more severe degree, and hydropericardium is a constant findinglr (Figure3).
396
The clinical picture, the pathological changes and the epizootic nature of the disease in non-endemic areas provide sufficient evidence for a clinical diagnosis, but laboratory confirmationis required due to similarities with other diseases such as equine viral arteritis, piroplasmosis, equine infectious anemia, anthrax and certain intoxications (eg. Crotalaria). 7'12 The diagnosis of the disease cannot be based on serological tests because usually there is not time enough for an immune response to develop before death occurs. For this reason, various methods of virus isolation are employed, using heparinized blood samples obtained from febrile equidae or post mortem spleen samples.8 Two biological methods are generally used: inoculation of cell culture monolayers (VERO or MS) in order to assess the cytopathic effect of the inoculum, and intracerebral inoculation of suckling mice, which present nervous clinical signs in positive cases. The next diagnostic step involves viral identification by means of an indirect complement fixation test, 7 or typing by means of a serum neutralization test. Nowadays an indirect, group specific ELISA sandwich test has been developed, which permits the detection of the causative agent directly from blood samples obtained from febrile horses or spleen homogenates.13 This diagnostic method has the significant advantage of its speed. Immunity and control
A satisfactory attenuated vaccine is available for all 9
JOURNAL OF EQUINE VETERINARY SCIENCE
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EQU,NE VETER,NARYASSOC,AT,ON ~ PRESENTEDATTHEWORLDVETERINARYCONGRESS,RIODEJANEIRO,BRAZIL,AUGUST1991.
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Figure3. Hydropericardium(cardiacformofAHS). serotypes of AHS virus, and can be used in monovalent or polyvalent form for immunization of susceptible Equidae. Recently an inactivated vaccine has been developed, with adequate preliminary results. Strict prophylactic measures must be taken in order to control the spread of the disease in outbreak areas, including: • Total ban on the movement of Equidae; • Immediate slaughter or isolation of sick animals which may act as sources of the virus; • Destruction of arthropod vectors using insecticides, improved drainage of possible vector breeding sites, nocturnal stabling of susceptible animals, use of insect repellents, etc; and • Immediate and mandatory vaccination of all Equidae, with permanent identification of vaccinated animals, preferably by means of branding.
Epizootiology of AHS in Spain AHS is enzootic in southern Africa, but the disease has
Volume12, Number6,1992
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occasionally been detected in the Middle East and in northern Africa. In 1965, AHS appeared in the Maghreb countries (Tunisia, Algeria and Morocco), causing the death of more than 300,000 homes, mules and donkeys.11 In 1966, an outbreak of the disease occurred in Spain, and 21 years later, in 1987, the disease was detected in central Spain, with further outbreaks taking place in the southern region of the country during 1988, 1989 and 1990. The 1966 AHS outbreak in Spain took place in the Gibraltar area, and was due to Type 9 AHS virus. 8 This outbreak was almost certainly caused by the arrival of infected arthropod vectors from North Africa, since simultaneously a serious outbreak caused by the same serotype was taking place in the Maghreb countries, including Morocco. In 1987, AHS was detected near Madrid and affected the area along two local river basins. During this outbreak, 146 Equidae died or were slaughtered, and more than 38,000 animals received a dose of attenuated polyvalent AHS vaccine. This outbreak could be related to the entry of several zebra from the southeastern coast of Africa into a Safari Park on the outskirts of Madrid during the month of June. The first deaths of Equidae were attributed to an intoxication due to Crotalaria, but when horses began to die outside the initial area in September the animal health authorities were alerted and a diagnosis o fAHS was established. Type 4 AHS virus was isolated and identified. The last animal died in October of 1987.16 One year later, in October of 1988, the death of horses due to AHS in a holding in southern Spain, over 600 km away from the Madrid area, was confirmed. This outbreak was also due to Type 4 AHS virus and caused the death of 156 animals. Since it is accepted that Equidae are not carriers6 and thatAHS virus cannot pass from one generation of arthropod vectors to the next, l° various theories concerning the origin of this new outbreak were taken into consideration, including the arrival of sick Equidae from enzootic areas of Africa, or the arrival of infected insect vectors. These theories are not plausible since AHS did not exist at the time in northern Africa. The possible recursion of the vaccine virus to a virulent form was also considered, but this theory is also improbable, since the strains employed are stable and 12 months had elapsed after vaccination. Another possibility is that no real interruption of the disease had occurred, with a relative epizootic silence during which mules and donkeys acted as viral reservoirs. When the weather turns cooler the vector population is reduced, but the vector arthropods present a longer life-span, dying only when the temperature drops below freezing. Nevertheless, it is highly unlikely that the disease would go unnoticed during this period between outbreaks, at least in some susceptible horses.
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of the arthropod vectors does not take place. Also, Andalusia has a very large marshy wildlife park with groups of wild horses which are difficult to control. Finally, it is possible that in some cases, due to the lack of cooperation of individual horse owners, animals were not vaccinated. Considering these factors, it could be likely that no true epizootic silence existed between these three outbreaks, with unvaccinated mules and donkeys acting as possible sources of virus, since these Equidae present milder clinical signs and a lower mortality rate than horses. ! During 1991 no new cases of AHS have been detected in the Iberian peninsula, but nevertheless strict control measures are still being enforced. C u r r e n t r e g u l a t o r y situation
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Figure4. Geographical Ioalization of the 1990AHS outbreak in Spain. The most worrisome theory would be that the 1988 outbreak represented a recrudescence of the disease, which would imply the existence of carders, the persistence of the virus in the vector population, or the presence of an unidentified viral reservoir. The first two theories have been ruled out, and the third one is highly unlikely. In fact, AHS has never persisted indefinitely outside the African continent, where a possible unknown reservoir of the virus is believed to exist. 1° In July 1989, another horse died due to AHS in the same holding in which the disease had appeared the year before. This was the beginning of the worst outbreak yet to occur in Spain, affecting five provinces and causing the death of more than 1,000 Equidae. More than 242,000 animals in 12 provinces of the country received the monovalent type 4 attenuated vaccine.At the same time, two neighboring countries, namely Portugal and Morocco, also diagnosed AHS due to the type 4 virus.2,a New cases of AHS began to be seen in September 1990 in the Spanish province of Malaga, more than 1,000 km away from the Barcelona area, in which the 1992 Olympic Games will be held (Figure 4). This outbreak involved 66 Equidae, and the last positive case was diagnosed in November 1990, after mandatory vaccination of all Equidae in Andalusia had begun. When considering the three Andalusian AHS outbreaks (1988, 1989 and 1990), again no logical explanation as to the reappearance of the disease exists, although several factors have to be taken into account. First of all, the Andalusian winter is milk, so maybe a total interruption of the life cycle
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Due to the outbreaks of AHS which have occurred lately in Spain, the regulations concerning the control of this disease, including the movement of Equidae, have been reevaluated. In this sense, the chapter which deals with AHS in the International Zoosanitary Code (a compendium of nonbinding recommendations which deal particularly with the international movement of animals) published by the Office International des Epizooties, was revised. The main modification is the inclusion of the regionalization concept, ie., the possibility of considering not only countries, but also areas within countries, to be infected or free from the disease. A country considered to be free from epizootiological nor clinical evidence of the disease during the previous 24 months, and in which at least 12 months have elapsed without vaccinating against the disease. An area within a country is considered to be free if, as well as satisfying the above-mentioned conditions, it is also clearly delimited by geographical barriers. Factors such as the seasonal absence or presence of vectors, the existence of add or mountainous zones which prevent the movement of arthropod vectors, etc., must also be taken into account. The country in question must also have published regulations which prevent the transit of Equidae from the infected area to the free area. An "infected" area presents two parts: a protection zone in which all Equidae have been vaccinated and identified, and a surveillance area in which the animals are not vaccinated. No Equidae can leave the "infected" area unless a series of conditions are met. These include the absence of clinical signs of AHS at the time of shipment, a previous 40-day quarantine period, AHS vaccination at least two months before, and permanent identification, or, in the case of non-vaccinated animals, a negative complement fixation result 10 days before shipment, protection against vectors during the quarantine period and shipment, and departure during the period in which vector activity is the lowest.
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WORLD EQUINE VETERINARY ASSOCIATION PRESENTEDAT THE WORLDVETERINARYCONGRESS,RIO DE JANEIRO,BRAWL, AUGUST1991.
In Spain, the regulations concerning the prevention, eradication and control of AHS are found in the royal Decree 1,604, published in the 30,12,1989 Official Gazette. This Decree establishes that in case of suspected AHS, animal health officials must be notified at once, and samples must be sent immediately to the reference laboratory. At the same time, preventive measures should be taken, such as the isolation of the holding and the separation of sick and healthy animals, a ban on the movement of animals into or out of the holding, and vector control measures, as well as the immobilization of all Equidae in a certain radius. This regulation has been partially modified after the Commission of the European Economic Community (EEC) issued the 90/426, EEC directive, which refers to the movement of Equidae within EEC as well as imported from nonmember countries. IfAHS would appear in Spain, a minimum protection zone of 100 km around the outbreak area would be immediately established together with a surveillance area of an additional 50 km. During 1989, as a safety measure, the Spanish animal health officers decided to vaccinate the total equine census of the areas of Andalusia, Extremadura and two provinces of the Castilla-La Mancha area. In 1990, the total equine census of Andalusia was revaccinated and permanently branded, amply surpassing the mandatory 100 km around the outbreak area. According to the stated EEC regulation, the protection and surveillance zones have the same sanitary status, namely, they are considered "infected", so Spain is divided in two areas concerning the movement of Equidae: the first one formed by the protection and surveillance zones, inside which movements are allowed under veterinary control, and the second one formed by the free zone, in which movements are not restricted (Figure5). The movement of horses from the protection and surveillance zone to the free zone is prohibited, and only in the periods of low vector activity would horses from this area be able to enter the free zone after an adequate quarantine period and laboratory testing. The entrance of horses from the free zone into the protection and surveillance one is allowed, but mandatory vaccination of the animal is carried out in isolation facilities located in this zone. This way, vaccination in the free zone is avoided. The stated EEC regulation has been enforced since January 1, 1992. In case of intra-community movement, the horse must be registered, identified and possess a sanitary certificate issued by an official veterinarian declaring freedom of signs of disease. If a severe equine infectious disease appears in a Member State, this country must present a detailed control and eradication program to the EEC Commis-
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Figure 5. Protection and surveillance zones forAHS control in Spain.
sion, which in turn may establish complementary measures to protect the intra-community health status. In cases of AHS, Equidae may only leave the infected area after enforcement of the conditions set forth in the International Zoosanitary Code. In October 1990, in face of the last AHS outbreak in Spain, the EEC Commission accepted regionalization, delimiting an area from which any movement of Equidae is prohibited, including all the vaccinated areas in Spain and all of Portugal, since in this country the entire equine census was vaccinated. Only during the period of lowest vector activity, which will be approved by the EEC Commission, will movement of Equidae be authorized, according to the previously described conditions. Strict enforcement of these regulations has resulted in the control of the disease during 1991 in Spain, since no new outbreaks have been detected since 1990. Nevertheless, for the final success of the eradication program, the active collaboration of the equine sector will continue to be necessary, and only in this case will the Andalusian horse industry develop again to its full potential.
REFERENCES 1. BloodDC, Radositis OM, Henderson JA (1989): Veterinary Medicine. A textbook of the diseases of cattle, sheep, pigs goats and horses. VII ed., Bailliere-Tindall:London. 2. Bulletin de I'Office International des Epizooties (1989) 101-9:496. 3. Bulletin de I'Office International des Epizooties (1989) 101-10:550.
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WORLDEEQUINEVETERINARYASSOCIATION 4. BuxtonA, Fraser G (1977): Animal Microbiology, Vol. 2, Blackwell Scientific Publications Ltd:Oxford. 5. Wilder FW (1982): Illustratedmanual for the recognition and diagnosis of certain animal diseases. Mexico-United States Commission for the prevention of foot and mouth disease. 6. DardiriAH (1984): African Horse Sickness, in: Foreign Animal Diseases Reference Manual, Vol. 1, USDA, APHIS, NVSL, Ames, Iowa. 7. Dardiri AH (1986): Paste Equina Africana, in: Enfermedades ex6ticas de los animales. Su prevencibn, diagn6stico y control. Comit(~ de enfermedades ex6ticas de la Asociacibn de SanidadAnimal de los Estados Unidos. Comisi6n Mexico-Americana para la prevencibn de la fiebre aftosa. Mexico, DF. 8. Diaz-Montilla R, ParSes P (1967): Epizootiologia de la Paste Equina en EspaSa. Bulletin de roffice International des Epizooties, 68:704-705. 9. Diaz-Yubero MA (1987): Informe Paste Equina en EspaSa. Informaci6nEpizootiolbgicaN6 Esp. 87/5/142, OfficeInternational des Epizooties. 10. ErasmusBJ (1988): Personal communication. 11. FennerF, Bachmann PA, Gibbs EPJ, Murphy FA, Studdert MJ, White DO (1987): Veterinary Virology. Academic Press:Orlando.
12. French A, Geering WA (1978): Exotic diseases of Animals. A manual for diagnosis. Australian Government Publishing Service:Canberra. 13. Harnblin C, Graham SD, Anderson EC, Crowther JC (1991): Aserogroup specific Enzyme-linkedimmunosorbentassay for the detection and identificationof African Horse SicknessViruses. Journal of Virological Methods, 32:285-292. 14. Mohanty SB, Dutta SK (1981): Veterinary Virology, Lea and Febiger:Philadelphia. 15. OellermanRA, EIs HJ, ErasmusBJ (1970):Characterization of African Horse Sickness viruses. Archiv f~r die gesamte Virusforschung, 29:163-174. 16. Rodriguez M, Castafio M, Escolar E, Floras J, Toni P, Gonzalez M, Jimenez F, Gonzalez JL, Montoya JA (1987): Peste EquinaAfricana: descripcibn del brote en Espar~a.MedicinaVeterinaria, 4:537-557. 17. RodriguezM, Castar~oM, Garcia I (1989): Peste Equina Africana en Espar~a:Feces de 1987, 1988 y 1989. Proceedings III Jornadas T~cnicas sobre el Caballo, Expoaviga 89. 18. Wetzel H, Nevill EM, Erasmus BJ (1970): Studies on the transmission of African Horse Sickness. Onderstepoort J Vet Res 37:165-168.
IMPRINT TRAINING OF T H E N E W B O R N F O A L By Robert M. Miller, DVM This new book describes, in words and photos, how imprint training of the newborn foal works. Dr. Miller is a popular lecturer at veterinary and horsemen meetings. Imprinting has been a favorite topic. He says in the introduction that most of the techniques described in the book involve learning processes other than imprinting. He is certain that the imprinting phenomenon is involved in the immediate postpartum procedures, and that the imprinting phenomenon greatly facilitates the subsequent procedures employed. Miller covers what is imprinting?; bonding; habituation; sensitization; dominance; the mare; immediate postpartum procedure, the second session; the third session; teaching the foal to tie; more halter training; advanced halter training; teaching performance basics; reinforcing responses; preventing problems; the race horse; mules; and effects of imprint training on mares. In a nutshell, Miller's technique of foal imprinting involves 10 sessions: at the time of birth; when the foal is standing; when the foal is moving about in a coordinated manner; the day'after birth; the third day; at one week of age; at eight days of age; at nine days of age; 10 days of age; and at two weeks of age. "Imprint training works," Miller says, "and it works consistently and very, very effectively." (144 pages; 81/2x 11) $13.95; (overseas, $18.95. Available from Veterinary Data, PO Box 1209, Wildomar, CA 92595 Phone (714) 678-1889 • FAX (714) 678-1885
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AFRICANHORSESICKNESSIN SPAIN: EPIZOOTIOLOGICALAND REGULATORYCONSIDERATIONS M. Rodriguez;1 J. L Ladero;z M. Castafio 1 and H. Hooghuisa
INTRODUCTION
African Horse Sickness (AHS) is a highly fatal noncontagious viral disease of Equidae, transmitted by arthropod vectors of the genus Culicoides, 4,14,1s with a seasonal incidence and a mortality rate related with the vector population present .7
ETIOPATHOGENESlS
AHS is caused by a double-stranded RNA, icosahedral viscerotropic virus of the Reoviridae family, genus Orbivirus. is Nine different serotypes of the virus have been identified,r The pathogenesis of AHA and Bluetongue seems to be similar, with primary viral replication occurring in the lymph nodes closet to the site where the animal is bitten by the vector. The dissemination of the virus to other tissues and organs of the reticuloendothelial system follows, until a secondary viraemia develops. The origin of the respiratory and circulatory disorders typical of the disease is an inflammatory response which affects small and middle-sized vessels,s,ll
CLINICAL
FINDINGS
Three forms of the disease have been described: an acute (pulmonary) form; a subaeute (cardiac) form; and a febrile Authom' address: IDepartamento de Patologia Animal II, faeultad de Vaterinaria, UniversidadComplutense28040, Madrid,Spain; 2Subdirecci6n General de Sanidad Animal Ministedode Agricultura,Pesa y Alimantaci6n, 28014 Madrid, Spain; 3Laboratoriode Sanidad y ProduccionAnimal Ministerio de Agriculture,Pesca y Alimentaci6n,28110 Algete, Madrid, Spain.
Volume12, Number 6,1992
form ("horse sickness fever),5,z although they are not always easy to differentiate since the clinical signs may overlap. According to our experience, the pulmonary form of AHS begins with sudden fever lasting 2-4 days, followed by respiratory signs including taehypnoea, labored respiration with coughing and frothy nasal discharge. Oedema of the supraorbital fossae is seen and death occurs due to severe pulmonary edema with cardiac failure.17 The clinical course of the cardiac form of the disease is longer, starting also with fever. The clinical signs are mainly due to functional circulatory disorders, and increase progressively, with development of edemas involving the head, neck and sternal region. A notable prominence of the supraorbital fossae is found (Fig.l), together with hemorrhagic and edematous conjunctivitis and blepharitis. Oedema of the frontal region and of the lips is common, as are petechiae on the ventral surface of the tongue. Death is caused by cardiac insufficiency with progressive pulmonary edema, lr Lesions The dominant gross lesions in cases of the pulmonary form are congestive-cyanotic mucous membranes, peteehiae on the underside of the tongue and, almost invariably, whitish or yellow-reddish foam in the nostrils (Figure2), and edema of the supraorbital fossae. The carcass is usually in good condition. A notable necropsy finding is a yellowish and gelatinous edema of the subcutaneous connective tissue, especially in the intercostal muscles. Upon opening the abdominal cavity, a slight ascites, focal subcapsular petechiae and slightly hypertrophic mesenteric lymph nodes can be observed, together with marked submucosal congestion of the fundus of the stomach, subserous and submucous petechiae in certain areas of the small intestine and, in some eases, diffuse congestion of the mucous membrane of the large intestine.
395
WORLD EQUINE VETERINARY ASSOCIATION PRESENTEDM THEWORLDVETERINARYCONGRESS,RIODEJANEIRO,BRAZIL,AUGUST1901.
Figure 2. Frothy fluid which has oozed out of the nostrils (AHS).
Diagnosis
Figure 1. Edema of the supraorbital fossae (AHS). Upon opening the thoracic cavity a small accumulation of fluid is found, with interstitial and alveolar edema and frothy fluid in the trachea. Hydropericardium and petechiae of the coronary sulcus and subendocardial hemorrhage occur frequently. 16 In the subacute form on external inspection the animals also present a good general condition, congestive-cyanotic mucous membranes and edema of the supraorbital fossae. Blepharitis and edema of the palpebral conjunctiva is seen, often together with chemosis. A yellowish, gelatinous edema of the subcutaneous connective tissue is found, mainly located in the frontal, cervical and sternal regions, and in the ventral portion of the abdomen. As in the pulmonary form, ascites and hydrothorax are seen, but in a more severe degree, and hydropericardium is a constant findinglr (Figure3).
396
The clinical picture, the pathological changes and the epizootic nature of the disease in non-endemic areas provide sufficient evidence for a clinical diagnosis, but laboratory confirmationis required due to similarities with other diseases such as equine viral arteritis, piroplasmosis, equine infectious anemia, anthrax and certain intoxications (eg. Crotalaria). 7'12 The diagnosis of the disease cannot be based on serological tests because usually there is not time enough for an immune response to develop before death occurs. For this reason, various methods of virus isolation are employed, using heparinized blood samples obtained from febrile equidae or post mortem spleen samples.8 Two biological methods are generally used: inoculation of cell culture monolayers (VERO or MS) in order to assess the cytopathic effect of the inoculum, and intracerebral inoculation of suckling mice, which present nervous clinical signs in positive cases. The next diagnostic step involves viral identification by means of an indirect complement fixation test, 7 or typing by means of a serum neutralization test. Nowadays an indirect, group specific ELISA sandwich test has been developed, which permits the detection of the causative agent directly from blood samples obtained from febrile horses or spleen homogenates.13 This diagnostic method has the significant advantage of its speed. Immunity and control
A satisfactory attenuated vaccine is available for all 9
JOURNAL OF EQUINE VETERINARY SCIENCE
~ WORLD
EQU,NE VETER,NARYASSOC,AT,ON ~ PRESENTEDATTHEWORLDVETERINARYCONGRESS,RIODEJANEIRO,BRAZIL,AUGUST1991.
J
Figure3. Hydropericardium(cardiacformofAHS). serotypes of AHS virus, and can be used in monovalent or polyvalent form for immunization of susceptible Equidae. Recently an inactivated vaccine has been developed, with adequate preliminary results. Strict prophylactic measures must be taken in order to control the spread of the disease in outbreak areas, including: • Total ban on the movement of Equidae; • Immediate slaughter or isolation of sick animals which may act as sources of the virus; • Destruction of arthropod vectors using insecticides, improved drainage of possible vector breeding sites, nocturnal stabling of susceptible animals, use of insect repellents, etc; and • Immediate and mandatory vaccination of all Equidae, with permanent identification of vaccinated animals, preferably by means of branding.
Epizootiology of AHS in Spain AHS is enzootic in southern Africa, but the disease has
Volume12, Number6,1992
~~ . . . . l
.
y
.
I
"'
~
occasionally been detected in the Middle East and in northern Africa. In 1965, AHS appeared in the Maghreb countries (Tunisia, Algeria and Morocco), causing the death of more than 300,000 homes, mules and donkeys.11 In 1966, an outbreak of the disease occurred in Spain, and 21 years later, in 1987, the disease was detected in central Spain, with further outbreaks taking place in the southern region of the country during 1988, 1989 and 1990. The 1966 AHS outbreak in Spain took place in the Gibraltar area, and was due to Type 9 AHS virus. 8 This outbreak was almost certainly caused by the arrival of infected arthropod vectors from North Africa, since simultaneously a serious outbreak caused by the same serotype was taking place in the Maghreb countries, including Morocco. In 1987, AHS was detected near Madrid and affected the area along two local river basins. During this outbreak, 146 Equidae died or were slaughtered, and more than 38,000 animals received a dose of attenuated polyvalent AHS vaccine. This outbreak could be related to the entry of several zebra from the southeastern coast of Africa into a Safari Park on the outskirts of Madrid during the month of June. The first deaths of Equidae were attributed to an intoxication due to Crotalaria, but when horses began to die outside the initial area in September the animal health authorities were alerted and a diagnosis o fAHS was established. Type 4 AHS virus was isolated and identified. The last animal died in October of 1987.16 One year later, in October of 1988, the death of horses due to AHS in a holding in southern Spain, over 600 km away from the Madrid area, was confirmed. This outbreak was also due to Type 4 AHS virus and caused the death of 156 animals. Since it is accepted that Equidae are not carriers6 and thatAHS virus cannot pass from one generation of arthropod vectors to the next, l° various theories concerning the origin of this new outbreak were taken into consideration, including the arrival of sick Equidae from enzootic areas of Africa, or the arrival of infected insect vectors. These theories are not plausible since AHS did not exist at the time in northern Africa. The possible recursion of the vaccine virus to a virulent form was also considered, but this theory is also improbable, since the strains employed are stable and 12 months had elapsed after vaccination. Another possibility is that no real interruption of the disease had occurred, with a relative epizootic silence during which mules and donkeys acted as viral reservoirs. When the weather turns cooler the vector population is reduced, but the vector arthropods present a longer life-span, dying only when the temperature drops below freezing. Nevertheless, it is highly unlikely that the disease would go unnoticed during this period between outbreaks, at least in some susceptible horses.
397
J
I W O R L D EQUINE V E T E R I N A R Y ASSOCIATION PRESENTEDATTHE WORLDVETERINARYCONGRESS,RIO DE JANEIRO,BRAZIL,AUGUST1~1.
F~nce
SPAIN Portugal
of the arthropod vectors does not take place. Also, Andalusia has a very large marshy wildlife park with groups of wild horses which are difficult to control. Finally, it is possible that in some cases, due to the lack of cooperation of individual horse owners, animals were not vaccinated. Considering these factors, it could be likely that no true epizootic silence existed between these three outbreaks, with unvaccinated mules and donkeys acting as possible sources of virus, since these Equidae present milder clinical signs and a lower mortality rate than horses. ! During 1991 no new cases of AHS have been detected in the Iberian peninsula, but nevertheless strict control measures are still being enforced. C u r r e n t r e g u l a t o r y situation
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Figure4. Geographical Ioalization of the 1990AHS outbreak in Spain. The most worrisome theory would be that the 1988 outbreak represented a recrudescence of the disease, which would imply the existence of carders, the persistence of the virus in the vector population, or the presence of an unidentified viral reservoir. The first two theories have been ruled out, and the third one is highly unlikely. In fact, AHS has never persisted indefinitely outside the African continent, where a possible unknown reservoir of the virus is believed to exist. 1° In July 1989, another horse died due to AHS in the same holding in which the disease had appeared the year before. This was the beginning of the worst outbreak yet to occur in Spain, affecting five provinces and causing the death of more than 1,000 Equidae. More than 242,000 animals in 12 provinces of the country received the monovalent type 4 attenuated vaccine.At the same time, two neighboring countries, namely Portugal and Morocco, also diagnosed AHS due to the type 4 virus.2,a New cases of AHS began to be seen in September 1990 in the Spanish province of Malaga, more than 1,000 km away from the Barcelona area, in which the 1992 Olympic Games will be held (Figure 4). This outbreak involved 66 Equidae, and the last positive case was diagnosed in November 1990, after mandatory vaccination of all Equidae in Andalusia had begun. When considering the three Andalusian AHS outbreaks (1988, 1989 and 1990), again no logical explanation as to the reappearance of the disease exists, although several factors have to be taken into account. First of all, the Andalusian winter is milk, so maybe a total interruption of the life cycle
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Due to the outbreaks of AHS which have occurred lately in Spain, the regulations concerning the control of this disease, including the movement of Equidae, have been reevaluated. In this sense, the chapter which deals with AHS in the International Zoosanitary Code (a compendium of nonbinding recommendations which deal particularly with the international movement of animals) published by the Office International des Epizooties, was revised. The main modification is the inclusion of the regionalization concept, ie., the possibility of considering not only countries, but also areas within countries, to be infected or free from the disease. A country considered to be free from epizootiological nor clinical evidence of the disease during the previous 24 months, and in which at least 12 months have elapsed without vaccinating against the disease. An area within a country is considered to be free if, as well as satisfying the above-mentioned conditions, it is also clearly delimited by geographical barriers. Factors such as the seasonal absence or presence of vectors, the existence of add or mountainous zones which prevent the movement of arthropod vectors, etc., must also be taken into account. The country in question must also have published regulations which prevent the transit of Equidae from the infected area to the free area. An "infected" area presents two parts: a protection zone in which all Equidae have been vaccinated and identified, and a surveillance area in which the animals are not vaccinated. No Equidae can leave the "infected" area unless a series of conditions are met. These include the absence of clinical signs of AHS at the time of shipment, a previous 40-day quarantine period, AHS vaccination at least two months before, and permanent identification, or, in the case of non-vaccinated animals, a negative complement fixation result 10 days before shipment, protection against vectors during the quarantine period and shipment, and departure during the period in which vector activity is the lowest.
JOURNAL OF EQUINE VETERINARY SCIENCE
WORLD EQUINE VETERINARY ASSOCIATION PRESENTEDAT THE WORLDVETERINARYCONGRESS,RIO DE JANEIRO,BRAWL, AUGUST1991.
In Spain, the regulations concerning the prevention, eradication and control of AHS are found in the royal Decree 1,604, published in the 30,12,1989 Official Gazette. This Decree establishes that in case of suspected AHS, animal health officials must be notified at once, and samples must be sent immediately to the reference laboratory. At the same time, preventive measures should be taken, such as the isolation of the holding and the separation of sick and healthy animals, a ban on the movement of animals into or out of the holding, and vector control measures, as well as the immobilization of all Equidae in a certain radius. This regulation has been partially modified after the Commission of the European Economic Community (EEC) issued the 90/426, EEC directive, which refers to the movement of Equidae within EEC as well as imported from nonmember countries. IfAHS would appear in Spain, a minimum protection zone of 100 km around the outbreak area would be immediately established together with a surveillance area of an additional 50 km. During 1989, as a safety measure, the Spanish animal health officers decided to vaccinate the total equine census of the areas of Andalusia, Extremadura and two provinces of the Castilla-La Mancha area. In 1990, the total equine census of Andalusia was revaccinated and permanently branded, amply surpassing the mandatory 100 km around the outbreak area. According to the stated EEC regulation, the protection and surveillance zones have the same sanitary status, namely, they are considered "infected", so Spain is divided in two areas concerning the movement of Equidae: the first one formed by the protection and surveillance zones, inside which movements are allowed under veterinary control, and the second one formed by the free zone, in which movements are not restricted (Figure5). The movement of horses from the protection and surveillance zone to the free zone is prohibited, and only in the periods of low vector activity would horses from this area be able to enter the free zone after an adequate quarantine period and laboratory testing. The entrance of horses from the free zone into the protection and surveillance one is allowed, but mandatory vaccination of the animal is carried out in isolation facilities located in this zone. This way, vaccination in the free zone is avoided. The stated EEC regulation has been enforced since January 1, 1992. In case of intra-community movement, the horse must be registered, identified and possess a sanitary certificate issued by an official veterinarian declaring freedom of signs of disease. If a severe equine infectious disease appears in a Member State, this country must present a detailed control and eradication program to the EEC Commis-
Volume12, Number 6,1992
Figure 5. Protection and surveillance zones forAHS control in Spain.
sion, which in turn may establish complementary measures to protect the intra-community health status. In cases of AHS, Equidae may only leave the infected area after enforcement of the conditions set forth in the International Zoosanitary Code. In October 1990, in face of the last AHS outbreak in Spain, the EEC Commission accepted regionalization, delimiting an area from which any movement of Equidae is prohibited, including all the vaccinated areas in Spain and all of Portugal, since in this country the entire equine census was vaccinated. Only during the period of lowest vector activity, which will be approved by the EEC Commission, will movement of Equidae be authorized, according to the previously described conditions. Strict enforcement of these regulations has resulted in the control of the disease during 1991 in Spain, since no new outbreaks have been detected since 1990. Nevertheless, for the final success of the eradication program, the active collaboration of the equine sector will continue to be necessary, and only in this case will the Andalusian horse industry develop again to its full potential.
REFERENCES 1. BloodDC, Radositis OM, Henderson JA (1989): Veterinary Medicine. A textbook of the diseases of cattle, sheep, pigs goats and horses. VII ed., Bailliere-Tindall:London. 2. Bulletin de I'Office International des Epizooties (1989) 101-9:496. 3. Bulletin de I'Office International des Epizooties (1989) 101-10:550.
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WORLDEEQUINEVETERINARYASSOCIATION 4. BuxtonA, Fraser G (1977): Animal Microbiology, Vol. 2, Blackwell Scientific Publications Ltd:Oxford. 5. Wilder FW (1982): Illustratedmanual for the recognition and diagnosis of certain animal diseases. Mexico-United States Commission for the prevention of foot and mouth disease. 6. DardiriAH (1984): African Horse Sickness, in: Foreign Animal Diseases Reference Manual, Vol. 1, USDA, APHIS, NVSL, Ames, Iowa. 7. Dardiri AH (1986): Paste Equina Africana, in: Enfermedades ex6ticas de los animales. Su prevencibn, diagn6stico y control. Comit(~ de enfermedades ex6ticas de la Asociacibn de SanidadAnimal de los Estados Unidos. Comisi6n Mexico-Americana para la prevencibn de la fiebre aftosa. Mexico, DF. 8. Diaz-Montilla R, ParSes P (1967): Epizootiologia de la Paste Equina en EspaSa. Bulletin de roffice International des Epizooties, 68:704-705. 9. Diaz-Yubero MA (1987): Informe Paste Equina en EspaSa. Informaci6nEpizootiolbgicaN6 Esp. 87/5/142, OfficeInternational des Epizooties. 10. ErasmusBJ (1988): Personal communication. 11. FennerF, Bachmann PA, Gibbs EPJ, Murphy FA, Studdert MJ, White DO (1987): Veterinary Virology. Academic Press:Orlando.
12. French A, Geering WA (1978): Exotic diseases of Animals. A manual for diagnosis. Australian Government Publishing Service:Canberra. 13. Harnblin C, Graham SD, Anderson EC, Crowther JC (1991): Aserogroup specific Enzyme-linkedimmunosorbentassay for the detection and identificationof African Horse SicknessViruses. Journal of Virological Methods, 32:285-292. 14. Mohanty SB, Dutta SK (1981): Veterinary Virology, Lea and Febiger:Philadelphia. 15. OellermanRA, EIs HJ, ErasmusBJ (1970):Characterization of African Horse Sickness viruses. Archiv f~r die gesamte Virusforschung, 29:163-174. 16. Rodriguez M, Castafio M, Escolar E, Floras J, Toni P, Gonzalez M, Jimenez F, Gonzalez JL, Montoya JA (1987): Peste EquinaAfricana: descripcibn del brote en Espar~a.MedicinaVeterinaria, 4:537-557. 17. RodriguezM, Castar~oM, Garcia I (1989): Peste Equina Africana en Espar~a:Feces de 1987, 1988 y 1989. Proceedings III Jornadas T~cnicas sobre el Caballo, Expoaviga 89. 18. Wetzel H, Nevill EM, Erasmus BJ (1970): Studies on the transmission of African Horse Sickness. Onderstepoort J Vet Res 37:165-168.
IMPRINT TRAINING OF T H E N E W B O R N F O A L By Robert M. Miller, DVM This new book describes, in words and photos, how imprint training of the newborn foal works. Dr. Miller is a popular lecturer at veterinary and horsemen meetings. Imprinting has been a favorite topic. He says in the introduction that most of the techniques described in the book involve learning processes other than imprinting. He is certain that the imprinting phenomenon is involved in the immediate postpartum procedures, and that the imprinting phenomenon greatly facilitates the subsequent procedures employed. Miller covers what is imprinting?; bonding; habituation; sensitization; dominance; the mare; immediate postpartum procedure, the second session; the third session; teaching the foal to tie; more halter training; advanced halter training; teaching performance basics; reinforcing responses; preventing problems; the race horse; mules; and effects of imprint training on mares. In a nutshell, Miller's technique of foal imprinting involves 10 sessions: at the time of birth; when the foal is standing; when the foal is moving about in a coordinated manner; the day'after birth; the third day; at one week of age; at eight days of age; at nine days of age; 10 days of age; and at two weeks of age. "Imprint training works," Miller says, "and it works consistently and very, very effectively." (144 pages; 81/2x 11) $13.95; (overseas, $18.95. Available from Veterinary Data, PO Box 1209, Wildomar, CA 92595 Phone (714) 678-1889 • FAX (714) 678-1885
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