Embedded Scribd iPaper - Requires Javascript and Flash Player
REVIEW
MANAGEMENT OF 21 EMERGING LIVESTOCK DISEASES BY THE ISRAEL VETERINARY SERVICES
B R E N N E R J., E L A D D . and M A L K I N S O N M . Kimron Veterinary Institute, Israel Veterinary Services, 50250, Bet Dagan, Israel.
ABSTRACT
The threat of terrorism is ever present in Israeli daily life since its establishment in 1948. The possibility of epidemics occurring as a consequence of agro-(bio)-terrorism is a real threat to Israel and therefore discriminating between deliberately introduced and naturally occurring infectious or non-infectious diseases becomes a real concern. In this review we present twenty-one outbreaks of disease that occurred over the last 30 years and for which epidemiological data were available.
Outbreak RSF-Reproductive Failure of swine and Exudative Skin Disease in piglets TGE- Transmissible Gastroenteritis RHD - Rabbit Hemorrhagic Disease WCS - Weak Calf Syndrome; neonatal calf adenovirosis Calf intestinal atresia AHS-Arthrogryposis/Hydranencephaly Syndrome RP - Rinderpest LSD- Lumpy Skin Disease L H A - Lamb Hemolytic Anemia PPR - Peste des Petits Ruminants JHS - Jejunal Hemorrhagic Syndrome B N W - Bovine Necrotic Vulvo-Vaginitis BSE- Bovine Spongiform Encephalopathy HPAI - Highly Pathogenic Avian Influenza (H5N1) GNPS - Geese Neuro-Paralytic Syndrome; West Nile Virus infection in domestic geese; EHDV-7 - Epizootic Hemorrhagic Disease Virus -7; S A-MCF, Sheep Associated Malignant Catarrhal Fever BTV-15; Bluetongue Virus -15
Year of the outbreak 1994 1990 and 2004 1990 2003 1999 1969-70 and 2001-03 1983 1989,2006 1991 1993 2001 2000 2002
INTRODUCTION
The Israeli livestock industry has experienced many outbreaks of infectious and non-infectious diseases in the last half-century. Located in the Middle East, therefore, discrimination between deliberately introduced and naturally occurring infectious and non-infectious diseases (1) becomes a real concern. Moreover, Israel is located geographically at the meeting point o f three continents, and might be considered as a portal o f entry for many "exotic" pathogens introduced by more than 500,000,000 birds that migrate across Israel from north to south, and west to east and vice versa according to the season. In addition, smuggling and illegal transportation of animals that might originate from "exotic" endemic regions, from Africa (Sinai Peninsula) to Asia (Jordan) and back are widespread. This problem is further confounded by the nomadic way o f life of the Bedouin who still coexist alongside the industrialized farming system in many areas within Israel, thus creating an epidemiological entity which is often difficult to control. In this review we present twenty-one outbreaks o f disease that occurred over the last 30 years, and for which veterinary epidemiological data are available. The authors also eye-witnessed most o f the outbreaks and had participated personally in their investigation. Zoonotic disease and malicious biocontamination o f food (2) are not included in this review. The following diseases are included (Table 1): Brief descriptions of outbreaks
2006 1997 2006 2001 2006 Reproductive failure i n swine and exudative skin disease i n piglets Swine reproductive failure (RSF) and exudative skin disease in piglets are both clinical manifestations related to porcine parvovirus (PPV) infection in unvaccinated swine populations (3). N o clinical cases related to P P V were noted in Israel prior to September 1994. Brief description o f outbreak In August 1994, 10 pregnant sows, twice vaccinated against P P V with an inactivated vaccine were imported from Cyprus by a closed pig farm located in a semiarid zone. O n arrival in Israel, quarantine was imposed for 14 days. After release from quarantine in midSeptember, the imported sows were placed in a yard at the farm
Table 1- The twenty-one selected outbreaks and at which year they were recorded
102
website: www.isrvma.org
V o l u m e 63 (4) 2008
ISRAEL JOURNAL OF VETERINARY MEDICINE that was separated from the adjacent local pregnant sows only by a barbed wire fence. The litters born to the imported sows during September/October were normal, while the reproductive problems initially occurred in the group adjacent to the imported one. In October, local sows farrowed litters of reduced size, and cases o f stillbirths, neonatal deaths and mummifications were observed. In total, 60 local sows delivered defective litters through the end o f January 1995 (4). The I V S were notified about this unprecedented malady only at the beginning of February 1995. Due to the clinical manifestations and the pathological findings, P P V was taken as the most probable infectious agent responsible for the outbreak. Preparedness and response o f the diagnostic laboratories and the IVS The veterinary community in Israel until that time had not experienced any epidemic diseases in the swine industry or had to cope with any kind o f outbreak o f such a magnitude. Moreover and in parallel, diagnostic laboratories did not possess specific diagnostic tools to confirm the clinical suspicion. For the detection of specific P P V antibodies and P P V antigen, E L I S A double antibody sandwich (DAS) and D A S - E L I S A (Hispanet, 28230 Las Rozas, Madrid, Spain) commercial kits were purchased by K V I at the end of January 1995. The definitive laboratory diagnosis was delivered to the breeder two days after the arrival o f the kits, and the total time had taken approximately 2 weeks. Diagnosis and confirmation of the etiological agent A l l the pathological samples and sera from the affected farm were positive for P P V antibodies and antigens while all pathological materials from control farms were negative (4). components was negligible due to Jewish and M u s l i m religious customs. On M a y 24*, investigators from the K V I visited the affected farms in order to collect pathological and epidemiological data from the suspected T G E outbreak. Although the investigators and the laboratory personnel started from zero, positive laboratory results (using a commercial E L I S A k i t for the detection of intestinal enteropathogens in calves) confirming coronavirus intestinal infection in piglets was given after one day. Ten days later, the definitive confirmation of swine intestinal coronavirus was made by the Istituto Zooprofilatico di Brecsia (IZS) where pathological specimens had been sent (7). Diagnosis and confirmation of the etiological agent Due to the absence o f species specific diagnostic tools but assuming that porcine and bovine coronaviruses share common antigenic epitopes, the B i o - X Combined Digestive E L I S A K i t (B-6900 Marche-en-Famenne, Belgium), for antigenic detection of rotavirus, coronavirus and F5 in bovine feces was employed (7,8). Another set of diagnostic procedures was carried out at IZS, using immuno-fluorescence (IFA) on intestinal sections, electronmicroscopy ( E M ) and immuno-EM (IEM) with specific antiT G E V and the polymerase chain reaction (PCR). This approach was later adopted as a routine diagnostic procedure at the K V I . The typical findings o f villous atrophy and lymphopenia pointed at a probable viral etiology (9). The clinical manifestations and especially the age distribution o f the diseased animals, the rapid spread o f the disease among the piggeries, its high mortality rate, the antigenic E L I S A positive reaction in 63% of the fecal samples submitted to K V I , and the confirmations of serological and antigenic tests from the IZS, lead us to conclude that T G E V was responsible for the outbreak.
Transmissible gastroenteritis in pigs (TGE^ Transmissible gastroenteritis (TGE) is a contagious disease of pigs that occurs as explosive epizootics. T G E is caused by the T G E virus ( T G E V ) , a member of the family c o r o n a v i r i d a e . T G E V is a common cause of diarrhea in pigs, affecting all ages but significant deaths occur only i n suckling pigs and the severity is related to the age o f the infected animals. Almost all susceptible piglets under 10 days o f age die within a few days o f exposure. When T G E V spreads within a fully susceptible herd with no previous history o f infection, up to 100% mortality is expected among newborn pigs, and marked diarrhea and dehydration in weaned pigs. Partial or total agalactia o f sows is common (5,6). Brief description o f outbreak The Israeli pig industry benefits from a unique epidemiological status. Due to religious customs in the Middle East where the Jewish and M u s l i m religions prevail, the pig industry is largely isolated, and located far from any area with an intensive pig industry. Consequently, very few epidemics were recorded among Israeli pig herds. The first cases o f diarrhea followed by dehydration and death o f piglets, 1 to 7 days old were noted i n piggeries on M a y 7 2004 where 13 pig herds were raised in northern Israel in a restricted zone of about 1.5 k m by 1.5 km. This episode gained epidemic proportions, with mortality as high as 70 to 80% during the first week o f life. Two piglets aged 2 days old were brought to the K V I for post-mortem examination on 14 May. Routine histological examination of the small intestine revealed villous atrophy, suggesting the presence of an enteric virus infection. Preparedness and response of the diagnostic laboratories and I V S The know-how regarding the pig industry and its various
th th
Rabbit Hemorrhagic Disease (RHD) Rabbit Hemorrhagic Disease ( R H D ) is an acute viral disease in rabbits with high morbidity and mortality, caused by a virus belonging to the C a l i c i v i r i d a e family. Although R H D was classified as a notifable disease by the OIE (10), it was not included in the list o f notifiable diseases by the IVS. Brief descriptions of the outbreaks The first outbreak o f R H D occurred in 1990 in an experimental unit for laboratory animals in the Israel Institute for Biological Research with an unprecedented fulminating mortality. More than 43% (12/28) o f the rabbits in the unit succumbed within a very short time. The rapidity o f the malady and its spread among the caged rabbits, together with and histopathological findings raised the possibility o f a viral infection and R H D was suspected. The rabbits had been imported from France (11). The second outbreak occurred in a pets' corner at a school, 17 year later when histopathological findings led the investigators to suspect R H D V infection (12). Preparedness and response o f the diagnostic laboratories and the IVS The time that elapsed between the observation o f the disease and the definitive diagnosis o f the 1990 outbreak had taken about 6 months. To the authors' knowledge, no specific reference reagents have been prepared or purchased by the I V S following the first R H D outbreak. The second R H D outbreak was suspected by a junior pathologist employed at the K V I in July 2006. Remarkably, the pathologist to whom this case was assigned was unaware of previous publication o f the R H D V outbreak (11), so that the 103
V o l u m e 63 (4) 2008
website: www.isrvma.org
REVIEW definitive diagnosis was made only two months later when it was confirmed by a senior pathologist. Diagnosis and confirmation of the etiological agent The confirmation of the first Israeli outbreak o f R H D V was made by a laboratory experienced with R H D V infections (University o f Vienna (13)). The Israeli isolate was confirmed later as belonging to the European group o f strains (French) o f R H D V (13, 14, 15). The investigators who had suspected R H D infection in July 2006, were not aware about the 1990 outbreak, and wrote erroneously, that the 2006 outbreak "is the first case o f R H D in rabbits in Israel". Definitive confirmation came from a laboratory (University o f Utrecht) that diagnosed c a l i c i v i m s e s routinely (personal communication). Q U I C K rotavirus/adenovirus- combi commercial kit (R-Biopharm, A G , Darmstadt, H R B 8321, Gemany) designed for rapid diagnosis of these two human enteric pathogens was applied. The positive results confirmation o f our results took an additional 12 months. Diagnosis and confirmation of the etiological agent By using the commercial kit RIDA® Q U I C K rotavirus/adenoviruscombi test we were able to demonstrate the presence of adenovirus in calf feces, synovial fluid and aqueous humor, while fecal samples from healthy calf neonates were negative (19). In order to confirm the suitability o f the kit for bovine Adenovirus antigen in calf pathological secretions, the assay was repeated with feces that was seeded with bovine adenoviruses (serotypes 3 and 5) provided by Palfi, Hungary (19).
Neonatal calf adenovirosis - weak calf syndrome W C S A particular polyarthritis (PA) syndrome was observed twice in Israel. It was suggested as one of the multiple features of the weak calf syndrome ( W C S ) by some American investigators (16, 17). This syndrome is characterized by the appearance of joint swelling, and blood-tinged faeces in very young calves. K o c h postulates confirmed that an adenovirus isolated from affected animals that were in a controlled clinical trial was the causative agent o f W C S (16). Brief outbreaks descriptions The first clinical cases suggested that neonatal calf adenovirosis appeared i n Israel in 1995, although no confirmation o f the causative agent o f this episode was available (18). The first outbreak o f PA in newborn calves was brought to our attention in 1995. Its rather rapid mode of spread from farm to farm suggested a viral infection most probably o f intrauterine origin. Initially, the affected epicenter comprised 7 large dairy farms and all o f them were located around Jerusalem or in the adjacent foothills. The affected calves were usually weak at birth, unable to rise without assistance and when forced to move, walked stiffly suggestive of pain joints. Clinical signs included intra-articular blood-tinged synoviae and the presence o f fibrin strands, fresh blood in the feces and eventually massive sub-corneal hemorrhages. The second similar outbreak o f W C S was reported in M a y 2003, when the local veterinary practitioner noticed that from the first colostral meal immediately after birth, the newborn calves were reluctant to suckle. Clinically, the neonates were unusually weak, unable to rise without assistance and when forced to move, walked stiffly, suggestive o f painful joints. Five out o f 40 calves died during this episode. O n clinical examination the stifle, hock, carpal and tarsal joints were enlarged and on palpation o f the adjacent tissues, sub-cutaneous edema and crepitation sounds were felt. From each enlarged joint, about 10 ml o f blood-tinged synovial fluid was easily aspirated and fibrin clots appeared shortly after withdrawal. Ecchymotic hemorrhages were noted on the sclera. In several cases a fluid-filled swelling distal to the carpal joint denoted seepage of synovium from the joint cavity. The fresh feces visible on the ground were dotted with drops o f fresh blood (19). Preparedness and response o f the diagnostic laboratories and the IVS The first episode o f W C S disappeared spontaneously and no causative agent was identified. With the occurrence o f the second similar outbreak, a possible diagnosis was reached. A rapid diagnostic procedure for the identification o f bovine adenovirus was unavailable in veterinary laboratories. Therefore, the RIDA®
Intestinal atresia in calves Intestinal a t r e s i a ( c o l i or/or i l e i ) denoted that an intestinal "culde-sac" is formed by two adjacent normally developed intestinal segments. There have been several reports associating the birth o f calves with intestinal a t r e s i a with palpation of the amniotic vesicle during pregnancy before 42 days o f gestation (20, 21). These publications had appeared prior to its occurring in Israeli dairy herds in 1999. Brief outbreak description In mid-April 1999, a t r e s i a c o l i was diagnosed in a newborn calf on post-mortem examination at the K V I . It was then reported that other calves at two adjacent dairy herds located 1 k m away did not defecate and had died at the age of 3-4 days [22, 23]. The herds were attended by the same veterinarian. Preparedness and response o f the diagnostic laboratories and I V S The post-mortem examination, an immediate visit to the affected herds, and especially a search o f the literature by the investigators yielded an immediate diagnosis. Moreover, the information provided by the investigators on the iatrogenic nature o f this outbreak, avoided the I V S making an unnecessary intervention, such as an imposed quarantine due an unknown etiological agent. The field investigation, the information gathered and the published data were completed i n about 2 weeks. Diagnosis and confirmation o f the etiological agent At necropsy, stasis of the intestinal contents was observed in parts of the intestine. The intestinal "cu-de-sac" segment appeared as a massive swelling anteriorally; while caudally a thin transparent cord without content was identified. A n epidemiological investigation of this outbreak showed a linkage with rectal palpation for early pregnancy diagnosis, performed less than 42 days after insemination. It was calculated that the odds of an affected calf, i.e., one born to a dam that was diagnosed by early palpation as having intestinal a t r e s i a was 119.7 times higher that one born in normal control herds. A total o f 47 calves were born with intestinal a t r e s i a through mid-2000, out of a total o f 682 calves at-risk (22). The possibilities o f genetic involvement (24), infectious agent(s) and/or toxicosis were ruled out. The similarity o f this outbreak with the other incidents (20, 21), the characteristic pathological case and the absence of new cases after cessation of early palpation (22), could be considered as a definitive diagnosis.
104
website: www.isrvma.org
V o l u m e 63 (4) 2008
ISRAEL JOURNAL OF VETERINARY MEDICINE Congenital abnormalities associated with teratogenic Simbu serogroup virus infections of ruminants The Israeli ruminants were affected by two defined episodes o f neonatal malformation following two arboviral Simbu serogroup infections occurring 35 years apart, in 1969-70 and in 2002-3, respectively (25,26). Members of the Simbu serogroup of viruses, such as Akabane virus ( A K A V ) , and A i n o virus ( A I N O V ) cause epidemics of abnormal parturitions in domestic ruminants, including abortion, stillbirth and birth o f deformed calves [27, 28]. The complex is known as the congenital arthrogryposishydranencephaly (and hydrocephalus) syndrome (AHS) affecting the musculoskeletal and nervous systems, respectively (29, 30, 31). Brief outbreaks descriptions The firstrecorded outbreak of congenital malformations was in Israeli dairy calves, lambs and kids in 1969/70, and was characterized by the appearance o f arthrogryposis and hydranencephaly syndrome (AHS) (25, 32, 33). Based on serological (34), epidemiological [25], clinico-pathological and histopathological findings (32), A H S has been strongly connected with the activity o f Akabane virus, and probably also with its principal insect vector in our region, C u l i c o i d e s i m i c o l a (30, 35). The second episode commenced in February 2002, when the first cases of "blind newborn calves" ( B N C ) appeared in two large neighboring dairy herds in the northern Israel valleys (36). In the following four months, dozens of farms were affected. A t necropsy of the calves, the cerebellum appeared normal, while severe microhydranencephaly was also observed but arthrogryposis was rarely encountered. Unlike the 1969-70 A H S outbreak, in 2002 outbreak no parallel findings were recorded in sheep or goats. A l l the clinical cases were confined to the northern valleys of Israel and the 3 TOO' latitude was the southernmost line of the 2002 epidemic. The same distribution was also noted during the 1969-70 epizootic (25, 36). The 2002 outbreak persisted until the end of A p r i l 2002 suggesting that the circulation of A K A V began in August 2001 and ended prior to November 2001 (36). But, in February 2003, B N C reappeared south of the 3 TOO' latitude reaching the Arava Rift Valley 400 k m south of the 2002 epicenter. Moreover, the 2003 outbreak appeared in areas where it was never recorded previously and that were beyond the southernmost point recorded in the 1969-70 epidemic (25, 36). B N C was found on dairy farms located very close to the Red S e a a t 2 9 ° 3 0 ' ( 3 6 ) . Preparedness and response o f the diagnostic laboratories and the IVS The first A H S outbreak in Israel coincided with the similar outbreaks reported in Australia and the Far East (28, 29, 30, 31, 37). So practically the I V S and the K V I laboratories reacted as expected i n face o f the emerging syndromes (38). Only through collaboration with an expert arbovirus diagnostic laboratory combined with other epidemiological studies and other laboratory assistances, did it become possible to associate A H S with Akabane virus infection. The definitive confirmation o f the identity of the causative agent i n Israel had taken about 4 years. There were some clinical features o f the second episode that resembled the first one and enabled investigators to suspect a possible arboviral infection, but there were three major differences: The first appearance of blind of calves in the semi-arid and arid zones, the almost complete absence of arthrogryposis in cattle (the predominance o f the C N S pathology), and the observation that sheep and goats were almost completely spared during the 2002-3 epizootic. The two waves o f the outbreak, met with different states o f V o l u m e 63 (4) 2008 awareness and therefore preparedness that could be considered as being between an "enzootic disease" and a "(re)-emerging disease" status (38). The main reason for the notification delay which lasted over one month was related to the unfamiliarity of young veterinary clinicians with the clinical manifestations o f teratogenic arboviral infections in both cases. This was also true for the diagnostic laboratory personnel. The reestablishment of the diagnostic chain from the farm to diagnostic laboratory based on such experiences took some time. The identification of the causative agent in the latter outbreak was based on serological assays (after their internal and external evaluation). In consequence, confirmation o f the causative agent o f first episode took about 3 months, while the second one took only less than 2 weeks to confirm. Diagnosis and confirmation of the etiological agent The laboratory and epidemiological tools adopted by the Israeli teams to demonstrate the association between congenital malformations in domestic ruminants and A K A V infection during and after the first episode consisted o f collecting demographic and seasonal data and investigating the spatial distribution o f the affected zones as well the clinical features, description o f the macro- and micro-pathology of congenital malformation, the adoption of A K A V SNT in the investigation of the seroreactivity o f affected and non-affected farms (zones), to analyze sera of animals that were alive during the epidemics (in the affected zones), and of animals born 3 years after the end of the epizootic (25, 26, 32, 33, 34, 36). Furthermore, it was demonstrated that a bovine fetus of 150 days can amount a specific antibody immune response on antigenic stimulation and that specific antibodies in pre-colostral calf serum have a definitive diagnostic value in identifying the causative agent (39,40,41,42). The causal agent o f the 2002-03 episode was confirmed by findings of A K A V seroreactivity in cattle located in the affected zone, in contrast to none in animals from unaffected farms during the second outbreak (87% and 3.7%, respectively) (36), and by further demonstration and characterization of the Israeli A K A V in C. imicola and in material from aborted fetuses (43,44). Lumpy Skin Disease (LSD) Lumpy skin disease ( L S D ) presents as an acute, sub-acute or inapparent infectious disease o f cattle caused by a single strain of capripox virus known as Neethling virus. L S D is characterized by the rapid eruption o f multiple circumscribed skin nodules, generalized lymphadenitis and fever. Other lesions visible at necropsy include necrotic plaques in the membranes, chiefly of the upper respiratory tract, the oral cavity and rumen, and infection may result in mastitis and orchitis (45, 46). Although the field experience and circumstantial evidence suggested that transmission o f L S D V occurred primarily by biting insects the mode o f field transmission is not fully understood. The results of controlled studies suggested that L S D V transmission between animals by contagion is extremely inefficient, and that parenteral inoculation o f virus is required to establish infection (47). L S D V probably circulates the Middle East, and the first case outside Africa was described in Kuwait in 1986 (48). Since then cases have been confirmed or suspected in the United Arab Emirates, Arab Republic of Yemen, Democratic People's Republic of Yemen (49), and Israel in 1989. The Israeli L S D episode was probably an extension o f the Egyptian outbreak (50, 51, 52) while L S D V was also reported in Saudi Arabia in 1992 (53). In 2005-06 an epizootic o f L S D V affected 16 provinces in Egypt (54). Brief description o f outbreaks The first clinical cases in the 1989 outbreak appeared on August 105
website: www.isrvma.org
REVIEW 19. The clinical signs spread to additional herds and to two farms in a neighboring village where a local veterinarian had probably transported the secondary outbreak. N o clinical description of this outbreak was provided by the authors. Although all the affected herds were slaughtered, only 10% of the animals at risk developed clinical signs (50, 51). The second occasion on which the I V S intervened in an L S D outbreak began on the evening o f 19 June 2006, when a phone call announced the appearance o f lumpy urticaria-like lesions in 7 to 10 lactating cows in a large dairy herd. The reappearance o f L S D was immediately suspected. The most significant clinical features were the presence o f the characteristic bumps that covered the entire skin o f the affected cows. A l l the developmental stages of the lumps were noted from the initial miliary scattered form, namely, the presence o f small-localized intradermal lesions, or small intradermal swellings, well developed nodules, very hard on touch, and ensuing sloughing off lesions. Generalized lymphadenopathy could be demonstrated and edematous swelling o f the lower gluteal muscles was also noted. The rectal temperature was 40°-41°C (55). One third o f the affected dairy herd was affected and therefore was destroyed. One additional confirmed case o f L S D occurred in an adult lactating cow on an adjacent dairy farm located within the restricted zone imposed by the IVS. Preparedness and response o f the diagnostic laboratories and the IVS The clinical diagnosis o f the first L S D outbreak was made in 1989 was based on the characteristic clinical signs. The rational given by the authors o f this work for the delay in announcing the clinical diagnosis o f L S D was related to gross similarity o f the lesions with delayed-type anaphylaxis following foot-andmouth disease vaccination (?), and to the rarity o f the disease (45). In contrast, the I V S responded to the second outbreak by establishing a team of veterinary officers and virologists that were ready for an early morning visit to the affected herd. O n 20 June 2006 a clinical diagnosis was confirmed one day after the disease was notified to IVS. This happened because two members o f the visiting team had been involved both in the diagnosis o f the 1989 outbreak (50, 55), and in a controlled clinical trial to assess the efficacy o f a sheep-pox vaccine (56). The definitive laboratory confirmation was given by the virology and molecular virology diagnostic laboratories o f the K V I within 24 hours o f the visit to the affected site. Diagnosis and confirmation of the etiological agent The first clinical cases of the 1989 outbreak appeared on August 19 and a clinical diagnosis was made on September 19. The laboratory confirmation was made by E M as no other diagnostic means existed at that time (57). In 2006 while the local practitioner did not suspect the infectious nature of the outbreak for 2-3 weeks, the K V I and IVS experts gave a clinical confirmation of this outbreak immediately, and the definitive antigen o f L S D V was confirmed on the following day by the laboratory o f molecular virology. on the juvenile erythrocytes. Anti-sheep toxic factors are also present in the colostrum o f some cows. This haemolytic anaemia can be easily differentiated form other anemias by finding unique pathognomonic findings o f a "pale white bone marrow" in the affected small ruminants (58, 60, 61, 62). Brief outbreaks descriptions During the 1991 lambing season, in a flock of A s a f ewes heavily infected with maedi/visna virus, the newborn lambs were immediately separated from their dams and given bovine colostrum. A l l the lambs given the colostrum died at the age o f 8 to 12 days with clinical signs of marked anemia. Lambs were sent to K V I where the pathological diagnosis and hematological results confirmed the clinical findings (63). Preparedness and response o f the diagnostic laboratories and the IVS When the clinician understood that the intensive medical assistance given to the newborn lambs had failed he attended the necropsy at K V I in person. A n expert who acted as the head o f a team dealing with the prevention of neonatal ruminant diseases also interviewed the practitioner and raised the suspicion about anemia caused by feeding lambs with bovine colostrum. The marrow o f a long bone was then examined and a diagnosis was made. When the instructions given to the farmer were adopted the outbreak immediately ceased. Diagnosis and confirmation of the etiological agent The anamnesis and the "pale bone marrow" together with other similar published cases ( 5 8 , 5 9 , 6 0 , 6 1 , 6 2 , 63) provided sufficient evidence on which to base conclusions about its etiology. Peste des petits ruminants (PPR) PPR is an acute or subacute disease of small ruminants characterized by necrotising stomatitis, enteritis and bronchopneumonia caused by a M o r b i l l i v i r u s of the paramyxoviridae family (64). The lesions in the mucosal and lymphoid tissues resemble rinderpest in cattle (65). Evidence o f clinical P P R in the Middle East and Egypt suggested that the virus has been circulating in these regions from 1986 onwards (66). Brief outbreak description The first clinical signs were observed in an isolated flock of sheep kept in December 1993 and persisted till February 1994. The main clinical features were high fever (41-42°C), waterybloodstained diarrhea, necrotic lesions on the oral mucosa, and profuse salivation. The mode o f transmission of the virus and establishment o f the primary infectious site remained unclear as the nearest international borders were at least 100 k m to the north and east-north (67). Preparedness and response o f the diagnostic laboratories and the IVS Faced with the probable entry of P P R V into Israel from neighboring countries, a specific serological test using reference R P V hyperimmune serum was developed in 1984 (68). The clinical acumen o f the head o f the small ruminant diseases division of the IVS led him to suspect an outbreak o f PPR on his first visit to the affected flock, a few days after the appearance of the first signs. Laboratory confirmation o f PPV was secured six weeks later. Diagnosis and confirmation of the etiological agent As mentioned above, the serological results (67, 68, 69), clinical manifestations (70), and pathological findings were sufficient to confirm the first P P R outbreak in Israel. In addition, P P R antigens were detected in tissues and buffy coat from affected animals and
Bovine-colostrum induced anaemia in lambs This particular form o f anaemia of lambs and kids appeared on farms where bovine colostrum was fed in order to increase fecundity and break the transmission cycle of retroviral infection transferred by sheep and goat colostrum to their offspring [58,59]. The anaemia is caused by the formation of immune complexes
106
website: www.isrvma.org
V o l u m e 63 (4) 2008
ISRAEL JOURNAL OF VETERINARY MEDICINE aborted fetuses (69). northeast Israel, several months after the introduction of new stock. Heifers and transferred cows were affected more frequently than multiparous and local cows, respectively. Towards the end of2001, two similar outbreaks of B N W were reported, one in a previously unaffected herd. The heifers o f these herds were transferred as calves to another farm and returned before calving. B N V V was not observed on the host farm. A third outbreak began in January 2002 on a farm that had been affected in the winter of the previous year. After B N V V was described and its putative etiologic agent identified, several sporadic cases were diagnosed on other farms, indicating that it might be under-diagnosed (78,79). Preparedness and response of the diagnostic laboratories and I V S After a delay of several months during which the local veterinarian tried to cope with the episode by himself, the K V I investigators initiated a vast ongoing investigation to clarify the origin o f this new syndrome and to differentiate it from being an "exotic" malady. The putative microorganism has been identified, and it seems that the main risk factors associated with B N W have been identified (78, 79, 80). The estimated time to reach these conclusions took from 4 to 6 months. Diagnosis and confirmation of the etiological agent Samples were examined for C h l a m y d i a and C o x i e l l a b u r n e t i i . The only microorganisms cultured consistently from affected cows but not from healthy ones were pigmented, gram-negative, non-sporogenic, anaerobic rods. Autosatellitism was observed in several instances. Identification o f the pigmented isolates as P. levii was done according to the Manual of Clinical Microbiology (81). Other potentially pathogenic bacteria have been isolated on occasion, but they could not be correlated with the clinical signs. Isolates o f B o H V - 4 were also identified by P C R however; subsequent surveys showed that B o H V - 4 is not necessary to induce B N V V (77).
Adult bovine jejunal hemorrhage syndrome (JHS) The pathognomic clinical features o f adult bovine jejunal hemorrhage syndrome (JHS) are defined as acute hemorrhagic enteritis of the small intestine or the hemorrhagic bowel syndrome of adult cattle. The affected cows are often found dead or death ensued within 24 to 36 hours from the onset o f clinical signs (85% case fatality rate) (71, 72, 73, 74). The diagnosis is based on the unique post-mortem findings where a section o f the jejunum is distended by large amounts of blood or a blood clot that obstructs the intestinal lumen. I n t r a - v i t e m , non-specific clinical manifestations are observed such as a severe drop in milk production, colic, and abdominal distension. Brief description o f the outbreaks Three adult dairy cows from three separate farms were necropsied at K V I 2001 because o f "sudden death". N o specific clinical details were provided, and the owners reported no signs prior to finding the dead cows. O n post-mortem examination, extensive hemorrhage and blood clots in the lumen of the small intestine were found. The small intestine of one cow appeared as if the blood "was held" in the upper part since blood was not observed caudally in the colon. The macroscopic and histological examinations of the internal organs as well as routine laboratory examinations revealed no specific disease or pathogens. The cause o f death thus appeared to be anemia due to massive intestinal hemorrhage. A n additional five cases o f "bloody profuse diarrhea" were encountered on three large dairy farms in the south o f Israel during January 2002. N o other signs were noted other than a marked drop of milk production on the same or previous day to the appearance of the diarrhea. The cows had a normal body temperature. Abdominal colic was the only clinical manifestation and the cows resisted strongly to the penetration of the practitioner's hand during rectal palpation (75). Preparedness and response o f the diagnostic laboratories and I V S There were only very few publications dealing with this emerging syndrome, and only electronic-library evidence, accessible to K V I personnel, contributed to solve these unknown outbreaks. "Preparedness" was based on professional training alone but there was zero information o f such a syndrome. Diagnosis and confirmation of the etiological agent The clinical cases examined (and one similar clinical and pathological case in January 1999 that was examined by the K V I ) could be considered as probable cases of JHS only retrospectively. No etiological agent(s) has been found so far. The diagnosis was made by comparison o f the preliminary findings with those of American investigators who described a newly emerging syndrome, which they tentatively defined as "jejunal hemorrhage syndrome" (JHS) in adult cattle [71,74].
Bovine necrotic vulvovaginitis (BNVV) Bovine necrotic vulvovaginitis ( B N W ) is characterized primarily by erythema that progresses to hemorrhagic necrosis o f the vulvovaginal mucosa. The chronic phase consists of a mucopurulent vaginal discharge. If not treated topically, some cows may develop metritis and/or peritonitis. Systemic treatment has no clinical or bacteriostatic effect on the vulvovaginal lesions (76,77). Brief description of the outbreaks A t the end of2000 and the beginning of2001, outbreaks of B N V V lasting about 4 months, were observed in three dairy herds in V o l u m e 63 (4) 2008
Bovine spongiform encephalopathy (BSE): ("Mad cow disease") Bovine spongiform encepholopathy (BSE) belongs to the transmissible spongiform encephalopathy (TSE) group and affects humans and animals (82). Epidemiological studies in the U K have shown that B S E was caused by contamination o f cattle feed with a scrapie-like agent that was found in meat and bone meal ( M B M ) used as a protein additive in cattle feed (83). B S E became extremely important as a zoonosis because of its apparent link with a new variant o f C J D (nvCJD), o f which the first 10 cases were reported in 1996 (84). Brief description of the outbreak A 1 0 year old dairy cow from a Kibbutz herd located on the Golan, died on M a y 20, 2002 following a two-day illness, characterized by a drop in milk yield and nervous symptoms including ataxia, teeth grinding and involuntary chewing movements. The cow had calved twins on M a y 15, 2002. Because rabies is endemic in this region and i n view o f the presented nervous signs, a rabies F A test was performed. Samples from the medulla in the obex region were taken for immunoblotting, histopathology and immunohistochemistry (mandatory, see below) (85, 86). Preparedness and response of the diagnostic laboratories and I V S The I V S had prepared itself well in advance o f the possible introduction o f B S E prion into Israel and had therefore, taken some procedural and veterinary precautions: A ban on the importation of ruminant meat and bone meal ( M B M ) from the U K since December 1988 (in fact no ruminant M B M 107
website: www.isrvma.org
REVIEW from the U K had been imported to Israel for at least 5 years prior to the ban), a ban on the importation o f M B M o f mammalian origin from all countries since July 1990. Moreover, a State regulation that bans feeding M B M to (all) farm animals since August 1996 was in place. Consequently, recycling of local mammalian material was discontinued in 1996 (85, 86, 87). A specialist veterinary pathologist and highly skilled laboratory technicians were sent to reference laboratories for training in diagnosing T S E diseases, and B S E i n particular. The chief IVS veterinarian issued a decree where it was obligatory to submit any case o f ruminant nervous disease for the histopathological diagnosis o f T S E . Personnel from the K V I departments of pathology and immunology, was trained in specialized appropriated laboratory courses on the epidemiology, pathology, and immune techniques o f T S E . Diagnosis and confirmation of the etiological agent Diagnosis was confirmed by all the diagnostic means available at that time. A s the rabies tests were negative, histopathology was performed on the paraffin section o f the medulla oblongata o f the obex region. Marked spongiform changes in the neuropil of the nucleus o f the solitary tact were seen as well as vacuolation in the vagal and olivary nuclei. Immunoblotting using the Prionicscheck test was positive for PrPsc and immunohistochemistry for PrPsc using the monoclonal antibody F89/160.1.5 showed marked accumulation o f PrPsc in the vagus nuclear complex, the nucleus of the solitary tract and other nuclei of the medulla oblongata. O I E reference laboratories, the University o f Bern (Switzerland) and the Veterinary Laboratories Agency, Weybridge ( U K ) confirmed the K V I results (85). There is no clear explanation for the first and the only B S E case in Israel; and it was therefore, classified as "sporadic". The probable source o f contamination (not proved) may have been tallow o f European origin that was present in imported calf- milk substitutes. 02/08/2005-Emergency Committee o f the Minister o f Health organizes a meeting on " A I " . 23/8/2005 - I V S assesses the system(s) preparedness (diagnostic ability, monitory status, and links to other governmental systems). 06/09/2005 - IVS establishes an " A I task force". 07/09/2005 - I V S issues an " A I fact sheet" that was mailed to every veterinarian in Israel. 19/09/2005 - The Ministry of Agriculture and Ministry o f Health, organizes an open meeting to discuss topics related to A I , in the agriculture sectors and the general public for all those who might be involved in the A I crisis. 27/09/2005 - Ministerial " A I task force" established by the Ministry of Agriculture. 30/10/2005 - I V S makes its own preliminary risk assessment, before the first case diagnosis, and suggestions of how to minimize A I spread from the first infected site. 03/11/2005 - The I V S and the Poultry Marketing Board notified the policymakers about the logistic problems related to "mass poultry destruction". 06/11/2005 - The Government Secretary issues its first decree regarding the possible entry of A I into Israel. 15/11/2005 - Experts from the diagnostic laboratories o f the K V I revised all instrumental diagnostic processes and means to face A I diagnosis. 17/11/2005 - The first meeting of the I V S A I task force takes place. 20/11/2005 - Middle East Consortium on Infectious Diseases Surveillance (MECIDS) Regional Pandemic Influenza preparedness meeting convenes. 18/12/2005 - The Israeli Ministry of Defense issues its program to face an A I pandemic episode in Israel. 29/01/2006 - The Civilian Authority of the Samaria-Yehuda-Gaza strip holds a meeting to discuss A I strategy with the Palestinian Authority. Two Israeli tasks forces (Agriculture and Health) presented the Israeli position and the Palestinian authority is presented by its own specialists (Tasks Forces?). 16/03/2006 - In two settlements' (Kibbutzim) poultry farm, near the border with the Gaza Strip an outbreak with clinical signs and mortality probably related with A I V infection was noted. Immediate action started including animal destruction. 19/03/2006 - The poultry diagnostic laboratories o f K V I communicated to the head o f IVS on the diagnosis of A I H 5 N 1 . In a summary of the March 2006 outbreak, there were 4 infectious sites in the first wave on 16-17/3 and additional 2 infectious sites on 19-20/3 making it a cluster of 6 farms. Then on 23,26 and 31 o f March additional farms were affected, respectively. The laboratory o f (avian) influenza in the K V I possessed almost all the necessary reference reagents for many years, and conducted daily "routine" work with A I viruses (90,91). Diagnosis and confirmation of the etiological agent The ultimate confirmation o f the most dangerous scenario, with HPAI H5N1 type came less than 72 hours from of the outbreak.
Highly pathogenic avian influenza (HPAI) It is not within the scope of this article to discuss the typical signs o f H P A I , but for didactic purposes we present the most characteristic features o f A I infections that w i l l vary according the virulence o f the infecting virus, age and species affected, concurrent diseases, and husbandry at the farm. The disease appears suddenly, many birds die either without clinical signs or with minimal signs o f depression, inappetence, ruffling o f feathers and fever. Sick birds sit or stand in a comatose state (head bent downward); the combs and wattles are cyanotic, with edema and or ecchymotic hemorrhages at their tips. Clear respiratory signs are noted and sometimes heard (88). Brief description o f H P A I (H5N11 outbreaks A t two Kibbutz poultry farm located near the border with the Gaza Strip clinical signs and mortality probably related with A I V infections (see above) were noted. Immediate action was taken including animal destruction (89). Preparedness and response of the diagnostic laboratories and the IVS This topic is better understood i f the chronological events are followed and the more significant milestones in the preparatory process to face the avian influenza (AI) outbreak (H5N1) are highlighted: 7-8/04/2005 - O I E Symposium on H 5 N 1 , "global situation and warning". The head of Division of Poultry diseases ( K V I ) presents Israel.
Sheep associated malignant catarrhal fever (SA-MCF) Sheep associated malignant catarrhal fever ( S A - M C F ) is an invariably fatal communicable disease o f cattle, caused by the ovine herpes virus-2 (OvHV-2) a gamma-herpes virus (92, 93). Sheep, and probably goats, are asymptomatic carriers o f O v H V - 2 . Other wild ruminant species might also become infected (94).
108
website: www.isrvma.org
V o l u m e 63 (4) 2008
ISRAEL JOURNAL OF VETERINARY MEDICINE M C F appears sporadically, affecting a small number o f animals, but O v H V - 2 infections can cause epidemics. The most prominent clinical manifestations o f M C F are high temperature ( 4 1 ^ 2 ° C), abundant and repugnant nasal and/or ocular secretions, hyperventilation and death. However, M C F may appear in many clinical forms, none o f which by itself is pathognomic (94). The manifestations vary from a mild, almost unnoticed, form to the multi-organ lesion form accompanied by central nervous system (cerebral) involvement (94). Other forms include the intestinal form o f bloody profuse diarrhea, the classical form 'head and eye' (exophthalmus, blindness, photophobia, nystagmus and lacrimation), the respiratory form that comprises lesions o f varying degrees i n the mouth, larynx, and nose; (intensive redness, ulcerative-necrotic lesions a soft cough, abdominal respiration, head extension, and dyspnoea) [95, 96]. A new rare form o f S A - M C F , the cutaneous form, has been recently described [97] in addition to a variety of the intestinal form characterized by a prolapsed rectum (personal observation). The sole definitive diagnosis of M C F virus is to confirm its presence in organs, secretions or blood o f the diseased animal (98). Brief description of the outbreak Four calves, between 4 and 7 months old, originating from a feedlot farm located at the coastal plain in Israel, were brought for necropsy in M a y 2001. The farm housed one hundred Israeli Holstein-Friesian calves ranging from 4 to 8 months old that were kept in five adjacent covered yards, according to age groups, and about 20 calves, were allocated to each yard. In an adjacent yard a flock o f 50 Awassi sheep, and in another yard a flock o f 20 mixed-breed milk goats, was kept under the same roof. One roof covered all the yards, and simple iron grids that did not prevent close physical contact between the different animal species were in place. One o f the yards for cattle shared the same drinking and food troughs with the sheep while the other group o f cattle shared drinking and food troughs with the goats. Lambs and kids, between 2 and 8 weeks o f age were held together with their dams. The attending veterinarian reported that the initial clinical signs consisted only o f one case of profuse diarrhea and some cases o f ocular lacrimation, with a high temperature of 42'C. The sick calves died within 3-7 days within the appearance o f the initial clinical signs. Necropsy o f the four calves revealed no specific gross lesions, while one showed mild abomasal hemorrhages. Four cases o f the head and eye form were observed 1 week later. One calf, otherwise without additional signs, showed incoordination and neck stiffness, suggestive of the nervous form. These were the first clinical signs suggestive o f M C F . A t the same time the first histopathological examination showed obliterative arteriopathy in the brain. A tentative diagnosis o f M C F was advanced. During the next 3 months, 30 additional calves became ill at the rate o f one to four calves per week, and all of them died. Most of the initial cases were the head and eye form, but some of them progressed to other forms, so as the epidemic progressed, typical manifestations of the respiratory, intestinal and nervous forms were all encountered (99, 100). Preparedness and response o f the diagnostic laboratories and the interim period. Moreover, seventeen cases of M C F were diagnosed in the first 6 months following the 2001 outbreak. Most o f these cases were sent to the K V I for diagnosis of C N S symptoms such as rabies and listeriosis (100). The classical diagnostics procedures, based on the characteristic histopathological pictures was used. The newer P C R methods was adopted in this case and the heminested P C R for the detection of O v H V - 2 sequences was conducted by the two-step amplification reaction cycle. It is documented that P C R was in use elsewhere from 1993 onwards (98). Diagnosis and confirmation of the etiological agent Organs were fixed in 10% neutral buffer formalin and prepared for histopathological examination. As mentioned above, the histopathological findings were suggestive of M C F . But a definitive diagnosis was conducted, and the reagents were externally evaluated by two experts. This process lasted more than one year.
rvs
Although, theoretically M C F was known to our professional stuff, the possibility that S A - M C F diagnosis was probably underestimated in Israel and elsewhere, could be deduced from the IVS epidemiological bulletins reporting communicable diseases. The last S A - M C F case reported by the IVS before this episode was in 1991, and it seems unlikely that Israel was free of S A - M C F in the V o l u m e 63 (4) 2008
Bluetongue virus 15 infection Brief description o f outbreak Typical bluetongue symptoms were observed in November 2006 in an Assaf and mixed flock o f 450 sheep located on the fringe o f the Negev Desert. The animals presented the typical edematous head, ulcerative lesions in the oral cavity and interdigital tegument. The typical "dancing sheep" and the "kisses" left no doubt about the etiology. The mortality was very high, and 64 deaths were recorded in less than 7 days. The exact number of diseased animals was estimated to be between 50% and 60%. This episode was very unusual in our region; the outbreak erupted in one flock and none of the many other flocks around was affected in the vicinity. The B T V affected a rather resistant breed with clinical manifestations of the B T V endemic strains. Moreover, for at least 15 years all the recorded clinical signs, i f presented, were very sporadic. We attributed the lack o f B T outbreaks to the fact that Israeli sheep breeds are relatively resistant to all five endemic serotypes B T V - 2 , 4 , 6 , 1 0 and 16. We therefore suspected the emergence of an exotic strain, and the suspicion was confirmed within a few days, because all the B T V seroassays available at the K V I reacted negatively. Additional unusual signs were also noted; the cattle herd, on the same farm, located only a few meters from the sheep pens, was unaffected. Also, the distribution o f affected animals within the flock was very unusual. In one pen most o f the deaths and symptoms occurred, while in the next pen, separated by a simple fence, there were few deaths, there were pens with no mortality and in one pen all the animals were apparently healthy. Surprisingly, no age-related attack pattern could be discerned. Diagnosis and confirmation o f the etiological agent The virus was identified as B T V serotype 15 (BTV-15) from infected eggs cultivated at the K V I diagnostic laboratory by the U K reference laboratory at Pirbright. This was confirmed antigenically (PCR) and serologically (SNT) with sera provided from the K V I (101). Preparedness and response o f the diagnostic laboratories and the IVS K V I and I V S monitor B T V presence in Israel on a regular basis, by conducting serological surveys passively and actively. Most of the field veterinary officers are familiar with the classical B T symptoms and recognize them from time to time- 2 to 4 cases each year. For this reason an exotic strain was immediately suspected although no specific reference reagents were available. The appropriate laboratory assays initiated by the K V I aided the rapid 109
website: www.isrvma.org
REVIEW definition by the B T reference laboratory. cases recumbency. Several animals appeared with red to purple discoloration o f the udder and hoof edema with echymotic hemorrhages. Not all o f the above mentioned clinical signs were seen on the same farm. Throughout, the following weeks, the disease outbreaks extended northwards and southwards in the Jordan Valley into the Upper Galilee and the Dead Sea area, while from the beginning o f October the disease spread westward to dairy farms in the Jezre'el Valley and the Golan heights. Several foci appeared in the Mediterranean coast plain. A total o f 105 cattle herds were involved, 80 of the affected were dairy, 21 beef and 4 feedlots. Morbidity rate within herd was from 5% to 80% o f milking cows with varied involvement of replacement heifers. The mortality rate was very low. The duration of the disease in affected animals was reported to range between 3 to 30 days. There were no reports of a distinctive disease syndrome in sheep or goats in these areas (101,107). Hemorrhagic diseases that are caused by Orbiviruses are seasonal since their vector might be some blood suckling insects, as is the case o f B T V which is transported in our region by C u l i c o i d e s i m i c o l a (109). However, the source and the vector of the E H D V is still unknown. Preparedness and response of the diagnostic laboratories and the IVS Laboratory investigations: the first samples were tested for B E F and B T by P C R and virus isolation in embryonated chicken eggs. Since E H D was never seen in Israel nor in the region, no diagnostic procedures were readily available therefore, samples were sent to the B T reference laboratory at Pirbright, U K . Not only were the specific reagents unavailable at the diagnostic laboratories o f the K V I but this outbreak found the personnel in total initial confusion. Diagnosis and confirmation of the etiological agent Of the total 31 samples sent, 11 were confirmed positive for E H D virus- type 7 by PCR while all samples were B T V negative. These results were from 15 farms o f which 10 were positive for E H D V , and in addition, results were confirmed by the detection of specific E H D V (107) antibodies by E L I S A . Although all the systems were unprepared, the definitive causative agent was confirmed after approximately one month by using external help and intellectual agility. Rinderpest Rinderpest (RP) is caused by a negative-strand R N A virus of the M o r b i l l i n i r u s genus, family P a r a m y x o v i r i d a e . The classical description o f R P refers to it as a highly fatal disease of domestic cattle, buffalo and yaks. Also the virus affects small domestic ruminants and a variety of wildlife species within the order A r t i o d a c t y l a . The disease is characterized by pyrexia, the progressive development of mucopurulent ocular and nasal discharges and high morbidity and mortality. Digestive tract involvement is marked by the development o f diarrhea and dysentery. If rinderpest is suspected, particular attention should be paid on post-mortem examination to the abomasums, which may be engorged, and the Peyer's patches which lymphoid necrosis. Reports o f R P in the Palestine Mandate go back to 1927, and when it appeared in the Middle East in 1970-71, the entire cattle population in Israel was vaccinated against RP. Vaccination was repeated in February-March 1982 only in the northern regions o f Israel due to its reappearance in the Middle East. Brief descriptions o f outbreaks
West Nile disease of domestic geese (Goose neuroparalytic syndrome GNPS) West Nile virus is transmitted by mosquitoes o f the C u l e x spp and is the casual agent of West Nile fever (102). A variant isolate Isr98/ N Y 9 9 was able to infect flocks of young domestic geese between 3 and 10 weeks old (102). Many species of wild and captive birds are also affected, while geese are the only domestic avian species that succumb to W N V infection. Israeli goose farms were decimated by the disease between 1997 and 2001 (103, 104,105). Brief description o f outbreaks The fist outbreak in geese was notified in the fall of 1997 as a characteristic neuroparalytic syndrome o f flocks between 5 and 9 weeks of age. Goslings as old as 11 weeks also were affected, and virus neutralizing antibodies were found (106). Preparedness and response of the diagnostic laboratories and I V S Three distinct K V I laboratories had their specific reference reagents prepared in advance as the " W N epidemic" was an ongoing fact at these times (105). Diagnosis and confirmation o f the etiological agent The definitive diagnosis was made available in less than 2 weeks from the date that IVS was notified and suspected materials reached the K V I laboratories. W N V was isolated from the brains of sick geese by inoculating the yolk sacs o f embryonated chicken eggs at day 7 o f inoculation with a goose brain homogenate. A l l the procedure including immunofluorescence and P C R confirmation lasted approximately 3 months. Epizootic hemorrhagic virus infection in cattle The hemorrhagic syndrome caused by epizootic hemorrhagic virus ( E H D V ) infection o f cattle was first described as follows: 10-20% reduction in milk production, partial anorexia, reduced rumination, short-term low fever (101, 107). Additional signs included a marked serous to purulent nasal discharge, excessive salivation, nasal and lip redness, with scaling and tongue swelling, cyanosis and erosions, petechia on the tips o f the lingual and buccal papillae similar to those noted in several other hemorrhagic syndromes in ruminants (108). Ocular lesions might be noted and they appear as epiphora, conjunctival hyperemia and palpebral edema. Some cases of stiff gait, muscle tremors of the appendages and recumbency were also noted. Several animals exhibited red to purple discoloration of the udder and hoof edema with echymotic hemorrhages (101,107). Brief description of the outbreak The I V S was notified of a novel disease syndrome, on September 5, 2006. However, the first clinical signs were seen toward the end of August 2006. The outbreak was first reported from several dairy farms located in the southern Jordan River Valley in Israel (part of the Rift Valley). This first reports described decreased milk production o f 10-20% and partial anorexia, followed by clinical signs o f reduced rumination, low rise of fever of short duration, weakness and stiff gait. In addition, prominent serous to purulent nasal discharge, excessive salivation, and nasal and lip redness with scaling and tongue swelling cyanosis and erosions were observed, petechia on the tips of the lingual and buccal papillae were similar to those noted in several ruminant hemorrhagic syndromes (108). Ocular lesions appeared in some animals as epiphora, conjunctival hyperemia and palpebral edema. Also evident in some animals were a stiff gait, muscle tremors o f the appendages and in some
110
website: www.isrvma.org
V o l u m e 63 (4) 2008
ISRAEL JOURNAL OF VETERINARY MEDICINE In early 1982, a R P outbreak was reported in a small herd o f local beef cattle near the northern border o f Israel. Subsequently 3 additional foci were reported at the same time in herds of beef cattle. A l l these herds were either partially or totally unvaccinated (114). Dairy cattle and small ruminants were not affected in this outbreak. In six partially vaccinated beef herds the mortality rate reached 70 to 90% whereas in 3 completely vaccinated beef cattle herds it was between 6 and 16%. Anorexia, an elevated body temperature o f 40-42°C, excessive salivation with fetid odors, diarrhea and dysentery were the major visible clinical signs o f the affected animals. A mucosal disease was noted. Mortality ensued within 24-48 hours of the onset of the clinical signs in some peracute cases. Preparedness and response of the diagnostic laboratories and the IVS In 1970-71 due to the presence o f R P in the Middle East, a general vaccination was carried out in Israel as a precautionary measure. Information regarding the appearance o f R P in countries surrounding Israel reached the I V S through O I E alerts, publications in February-March 1982 and information provided directly to the I V S by the breeders along the Lebanese border about an unusual disease presence in Lebanon. In consequence, the cattle in the northern sector o f Israel and its northern borders were vaccinated against R P and movement o f cattle and small ruminants in these regions was completely prohibited. The unusual mortality in beef cattle herds near the Lebanese border was recognized promptly and relevant samples were shipped immediately to K V I . Statutory regulations, such as the disposal of affected herds, and confiscation and destruction of livestock transported without special permission. In February 1984, 7 months after the last outbreak o f RP, Israel was declared free of RP. Diagnosis and confirmation of the etiological agent The first diagnosis was based on the characteristic clinical signs, gross pathological changes, and the geographical appearance o f the first focus of disease. The virological assays carried out in the diagnostic viral laboratory where isolation of the virus corroborated the clinical diagnosis (114). cost on the reference diagnostic laboratory and probably would lead to incorrect conclusions. It was interesting to compare the examples of reemerging diseases that have appeared twice. The A K A V infection appeared in 1969-70 and in 2001-02. The causative agent was elucidated in the first episode by a foreign diagnostic laboratory approximately 4 years after the clinical features o f the epidemic were described. The second episode was confirmed also by the same laboratory, because the local laboratory raised the possibility of a Simbo serogroup infection. The partial dependence on external help might be the reason for a shorter elapsed time between the second outbreak and the confirmation o f the same causative agent. Knowledge o f arthrogryposis/hydran/microencephaly is a good example why professional preparedness is a favorable factor although it is not reflected in this work. The same but more significantly concerns the two separate outbreaks of L S D . Because one of the authors was involved in the diagnosis o f the first episode o f 1989, the second outbreak was clinically diagnosed on the spot and confirmed by P C R in less than 24 hours. The reemergence o f L S D , that to date (August 2007), affects many settlements along the Gaza Strip, is an example o f the difficulty o f the I V S to control an epidemic due to the lack o f veterinary infrastructure across the border, and the complete separation between the two neighboring veterinary services, therefore, could be considered a form of agro-terrorism. The R H D outbreak is a good example o f what happened when the system learnt nothing from an emerging situation and why it is important to transmit intellectual property between generations. Although, the fist outbreak was published and one of the pathologist stuff was employed at the times at the K V I , a new stuff member failed to suspect the second case although death rabbits were submitted for post- mortem examination. This happened because no records of the first R H D outbreak were kept. There are few syndromes with a strict local connection. The B N V V disease was extensively and exclusively described in Israel. Can this outbreak bear a massage for others, indicating an epidemic elsewhere? Does environmental destabilization might be a cause of such health consequences on animals that suffered stressful movement and mixing with other populations. We think that this work might also serve as a lever for the policy makers placed "in the high windows" responsible for the allocation of necessary resources, and provides also an umbrella under which the process of preparedness transpires. In Israel the same vision is also shared by investigators dealing with zoonotic diseases in thee human medicine field, and considering that most agents with bioterrorism potential are zoonotic (111). Field Epidemiology training Program (FETPs) sponsored by the U.S. Center for disease Control Prevention (CDC) have provided training for (local) epidemiologist as the Organization's World Health Report (112). Lescano et al., [113] have reported that graduates from these C D C courses, participated in more outbreaks investigation after training (0.2 vs. 0.9 investigations per traineeyear P O . 0 0 1 ) . This seems to be a powerful tool for ameliorating what we define as "professional preparedness": Veterinary Medicine needs such
DISCUSSION
When a mass outbreak o f a disease or an unusual event affecting animal health occurs, it is extremely important to determine whether an infectious (or contagious), transmissible agent is involved. Mass toxicosis or/and iatrogenic (deliberate or not) causes must be included. Some authors have used markers to help discern between deliberate, malicious and natural (infectious) causes (1). In this paper we have presented various epidemics o f different natures, fortunately none of them were deliberate, but which could potentially become terrorist acts. Most o f the presented outbreaks are of an infectious origin, some pose an immediate global concern such as are the H P A I (N5H1) and W N V diseases. Few pose a regional risk and are represented by the vector-born infections such as the L S D V , B T V and E H D V infections (Rift Valley Fever virus and Bovine Ephemeral virus were not included in this paper). There are outbreaks triggered by field veterinarians or by the animal breeders. These are represented by the calf intestinal a t r e s i a and hemolytic anemia in lambs. In these two last two syndromes an immediate process o f investigation must be carried out because they might resemble infectious disease, and i f not promptly diagnosed as such, could carry a heavy unnecessary burden and V o l u m e 63 (4) 2008
website: www.isrvma.org
111
REVIEW
REFERENCES
17. 1. Dembek Z F , Kortepeter, M G , Pavalin J A . Discernment between deliberate and natural infectious. E p i d e m i o l o g y a n d I n f e c t i o n 135: 335-371, 2006 E l a d D . R i s k assessment of malicious biocontamination o f food. J o u r n a l of F o o d P r o t e c t i o n 68: 1302-1305,2005 Joo H S , Johnson R H . Porcine parvovirus: A review. V e t e r i n a r y B u l l e t i n 46: 653-660, 1976 Brenner J, D , et a l . A n outbreak o f porcine parvovirus infection in a farm in Israel. I s r a e l J o u r n a l o f V e t e r i n a r y M e d i c i n e 51: 79-82, 1996 O . I. E . M a n u a l o f D i a g n o s t i c Tests a n d Vaccines f o r T e r r e s t r i a l A n i m a l s Fifth Edition, Transmissible gastroenteritis, pp 792-801, 2004 S a i f L J, Wesley R . D . Transmissible gastroenteritis and porcine respiratory coronavirus. In: Diseases of Swine, 8 Edition: Straw B E , D'allairte S, M e n g e l i n g W L , Taylor D J , eds. Iowa State University Press/ A m e s , Iowa U S A , pp. 295-325, 1999
th
1975 M c C l u r k i n A W , C o r i a M F . Infectivity of bovine adenovirus type 5 recovered from a polyarthritic c a l f with weak c a l f syndrome. J o u r n a l o f A m e r i c a n V e t e r i n a r y M e d i c a l A s s o c i a t i o n 167 139-141, 1975 Brenner J , et a l . Description o f an episode o f multifocal polyarthritis o f unknown aetiology i n newborn calves. I s r a e l J o u r n a l o f ' V e t e r i n a r y M e d i c i n e 58: 102-104, 1998 Brenner J, et a l . The detection o f an unidentified type o f adenovirus i n the stools of calves with weak c a l f syndrome by use o f a commercial kit designed for the detection o f human adenoviruses. J o u r n a l o f V e t e r i n a r y M e d i c i n e B , 52:98-101,2005 Benda A , et a l . Occurrence o f a t r e s i a c o l i in calf, (in German). M o n a t s h e f t e f u r V e t e r i n d r m e i z i n 33: 683-687, 1978 Ness H , L e o p o l d G . M u l l e r W. Genesis o f congenital i l e u s in c a l f (in German). M o n a t s h e f t e f u r V e t e r i n d r m e i z i n 37: 89-92, 1982 Brenner J. Orgad U . Epidemiological investigations o f an outbreak o f intestinal a t r e s i a i n two Israeli dairy herds. J o u r n a l o f V e t e r i n a r y M e d i c i n e Science 65:141-143, 2003 Brenner, J. and Orgad, U . A n outbreak o f intestinal atresia in dairy cattle. I s r a e l J o u r n a l o f V e t e r i n a r y M e d i c i n e 59: 54: 93, 1999 Rosenberger G . 1970. Krankheiten des rindes. Pp. 338. Verlag Paul Parey, Berlin. Markusfeld-Nir O . M a y e r E . A n arthrogryposids/ hydranencephaly syndrome i n calves i n Israel 1969/70 epidemiological and clinical aspects. Refuah Veterinarit 28: 144-151, 1971 B r e n n e r J , et a l . Serological and clinical evidence for reactivity o f arboviral teratogenic S i m b u sero-group infection i n Israel; 2001/2003 episode(s). V e t e r i n a r i a I t a l i a n a 40: 1 1 3 - 1 2 3 , 2 0 0 4 Parsonson I M , M c P h e e D A . Bunyavirus pathogenesis. In: Maramorosch, K . Murphy, F.A. Shatkin, A . J . eds. A d v a n c e i n V i r u s Research 30: pp279. N e w York, A c d e m i c Press, 1985 Inaba Y, K u r o g i H , O m o r i T. Akabane disease: epizootic abortion, premature birth, stillbirth and congenital arthrogryposis-hydranencephaly i n cattle, sheep and goats caused by Akabane virus. A u s t r a l i a n V e t e r i n a r y J o u r n a l 51: 584-585, 1975 K u r o g i H , et a l . Serologic evidence for etiologic role of Akabane virus in epizootic abortion-arthrogryposishydranencephaly i n cattle i n Japan, 1972-1974. A r c h i v e o f V i r o l o g y A l : 71-83, 1975 K u r o g i H , et a l . Epizootic congenital malformation arthrogryposis-hydranencephaly syndrome in cattle: Isolation of Akabane virus from affected fetuses. A r c h i v e o f V i r o l o g y 51: 67-74, 1976 K u r o g i H , et a l . Congenital abnormalities i n newborn calves after inoculation o f pregnant cows with Akabane
2. 3. 4.
18.
19.
5.
20.
6.
21.
22.
7.
P o z z i S, et a l . C l i n i c a l , epidemiological, diagnostic, productive investigations i n course of a T . G . E . outbreak i n Israel, (in Italian). A t t i d e l l a S o c i e t d I t a l i a n a d i P a t h o l o g i a d e g l i A l l e v a m e n t i d e i S u i n i . 26: 263-272, 2005 Brenner J , et a l . Investigation o f the first transmissible gastro-enteritis ( T G E ) epidemic in pigs i n Israel. I s r a e l J o u r n a l o f V e t e r i n a r y M e d i c i n e 59: 39-42, 2004 C o o p e r V L . Diagnosis of neonatal pig diarrhea. V e t e r i n a r y Clinic o f North America, Food Animal Practice 16: 117-133,2000 O . I. E . M a n u a l o f D i a g n o s t i c Tests a n d V a c c i n e s f o r T e r r e s t r i a l A n i m a l s Fifth Edition, Rabbit haemorrhagic disease, pp. 950-962,2004 K u t t i n E S, et a l . Rabbit heamorrhagic disease - first outbreak i n Israel and review o f the literature. Israel Journal o f Veterinary M e d i c i n e 146: 119-126, 1999 L o u v e , E . Rabbit hemorrhagic disease i n a school pet corner. Oral presentation i n the 3 annual Meeting o f the Israeli Veterinary M i c r o b i o l o g y and Immunology Association, December 2006 Bet Dagan
rd
23.
8.
24. 25.
9.
10.
26.
11.
12.
27.
13.
14.
N o v o t n y N , et a l . European brown hare syndrome ( E B H S ) , Experimentelle untersuchungen. Wiener Tierdrztiche M o n a t s s c h r i f t 78: 370-378, 1991 W i r b l i c h , C , et a l . European brown hare syndrome, virus: relationship to rabbit hemorrhagic virus and other calciviruses. J o u r n a l o f V i r o l o g y 68: 5164-5173, 1994 Bascunana C R , N o w o t n y N , Belak S. Detection and differentiation of rabbit hemorrhagic disease and European brown hare syndrome biruses by amplification o f V P 6 0 genomic sequences from fresh and fixed tissue specimens. J o u r n a l o f C l i n i c a l M i c r o b i o l o g y 35:2492-2495, 1997 Cutlip R C , M c C l u r k i n A W . Lesions and pathogenesis o f disease i n young calves experimentally induced by bovine adenovirus type 5 isolated from weak c a l f syndrome. A m e r i c a n J o u r n a l o f V e t e r i n a r y Research 36: 1095-1098,
28.
29.
15.
30.
16.
31.
112
website: www.isrvma.org
V o l u m e 63 (4) 2008
ISRAEL JOURNAL OF VETERINARY MEDICINE virus. I n f e c t i o n a n d I m m u n i t y 17: 338-343, 1977 N o b e l T A , Klopfer-Orgad U , Neumann F. Pathology o f an arthrogryposids-hydranencephaly syndrome i n domestic ruminants i n Israel- Refuah V e t e r i n a r i t 1971; 28: 144-151, 1969/70. Shimshony A . A n epizootic Akabane disease i n bovines, ovines and caprines i n Israel, 1969-70: Epidemiological assessment. A c t a M o r p h o l o g i c a A c a d e m i a e Scientiarum H u n g a r i c a e 28: 197-199,1980 49. 50. 51. Office International Des Epizooties (O.I.E.), W o r l d A n i m a l H e a l t h ; 5: 703, 1990 Yeruham I, et a l . Spread o f lumpy skin disease i n Israel dairy herds. V e t e r i n a r y R e c o r d ; 137: 91-93, 1995 Shimshony A . L u m p y skin disease. I s r a e l i Veterinary Services E p i d e m i o l o g i c a l Q u a r t e r l y 1989; (3) pp. 5-7. (in Hebrew). A l i A A , Esmat M , Attia H . et a l . C l i n i c a l and pathological studies on lumpy skin disease i n Egypt. V e t e r i n a r y R e c o r d ; 127: 549-550, 1990 Greth A , et a l . Capripoxvirus disease i n an A r a b i a n O r y x (Oryx leucoryx) from Saudi Arabia. J o u r n a l o f W i l d l i f e Diseases; 28: 295-300,1992
32.
33.
52.
34. K a l m a r E , Peleg B - A , Savir D . ArthrogryposisHydranencephaly syndrome in newborn cattle, sheep and goat - serological survey for antibodies against the Akabane virus. Refuah V e t e r i n a r i t 32:47-54, 1975 35. Della-Porta A J , et a l . Akabane disease: Isolation o f the virus from naturally infection ovine fetuses. A u s t r a l i a n V e t e r i n a r y J o u r n a l 53: 51-52, 1977 Brenner J, et a l . Serological evidence for reactivity o f Akabane virus in the northern valleys o f Israel in 2001. J o u r n a l o f V e t e r i n a r y M e d i c i n e Science 66:441-443, 2004 Haughey K J , et a l . Akabane disease i n ovine fetuses. A u s t r a l i a n V e t e r i n a r y J o u r n a l 65: 136-140, 1988 Brenner J , M a l k i n s o n M , Y a d i n H . Application o f various diagnostic procedures to epidemiological situations encountered during arboviral infection. Veterinaria I t a l i a n a 40: 567-571, 2004 Trainin Z . A c t i v e production o f immunoglobulins in c a l f embryos. Refuah V e t e r i n a r i t 7: 627-628, 1971 Trainin Z , M e i r o m R . C a l f congenital malformation. Research 15: 1-7, 1973 immunoglobulins and in Veterinary Science;
53.
54. http://www.oie.int/eng/info/hebdo/a_csum.htm. 55. Brenner J, et a l . L u m p y skin disease (LSD) in a large dairy herd in Israel, July 2006. I s r a e l J o u r n a l o f V e t e r i n a r y M e d i c i n e ; 61: 73-77, 2006 56. Brenner J , et a l . Experimental infection with local lumpy skin disease virus in cattle vaccinated with sheep pox vaccine. I s r a e l J o u r n a l o f V e t e r i n a r y M e d i c i n e ; 47: 17-21, 1992 A b r a h a m A , Zissman A . Isolation o f lumpy skin disease virus Israel. I s r a e l J o u r n a l o f V e t e r i n a r y M e d i c i n e ; 46: 20-23, 1991 Inglis D M , G r a y D . Feeding cow's colostrum to newborn lambs. V e t e r i n a r y R e c o r d ; 112: 181-182, 1983 D e B o e r GF, et a l . Studies i n epidemiology of maedi/visna in sheep. Research i n V e t e r i n a r y Science 26: 202-208, 1979 Winter A C , Clarkson M J . F a r m investigation o f anaemia in lambs caused by feeding cow colostrum. V e t e r i n a r y R e c o r d 131:213-216, 1992 Winter A C , Clarkson M J . A n a e m i a i n lambs and kids caused by feeding c o w colostrum. I n P r a c t i c e 14: 283-287, 1992 Perrim G , Polack B . B o v i n e colostrum warning. V e t e r i n a r y R e c o r d 122: 240, 1988 Perl S, et a l . A n a e m i a i n lambs caused by feeding bovine colostrum: C l i n i c a l and pathological findings. A field outbreak. I s r a e l J o u r n a l o f V e t e r i n a r y M e d i c i n e 50: 61-63, 1995
36.
37. 38.
57.
58. 59.
39. 40.
60.
41.
42.
M c C l u r e S, et a l . Maturation o f immunological reactivity in the fetal lamb infected w i t h Akabane virus. J o u r n a l o f C o m p a r a t i v e P a t h o l o g y 99: 133-143, 1988 M i u r a Y , et a l . Neutralizing antibody against Akabane virus i n precolostral sera from calves with congenital arthrogryposis-hydranencephaly syndrome. A r c h i v fuer die Gesamte Virusforschung 46: 377-380, 1974
61.
62. 63.
43.
Stram Y , et a l . Akabane virus in Israel: A new Virus lineage. V i r u s Research 115:93-97,2004 44. Stram Y, et a l . Detection and quantitation of Akabane and A i n o viruses by multiplex real-time reverse-transcriptase PCR. J o u r n a l o f V i r o l o g i c a l M e t h o d s 116: 147-154, 2004 Coetzer JAW. L u m p y skin disease. In: Infectious Diseases of Livestock. 2nd Edition. Coetzer JAW, Tustin R C . eds. Oxford University Press, pp. 1268-1276, 2004 H a i g D A . L u m p y skin disease. Bulletin o f Epizootic Diseases of A f r i c a 5: 421-430,1957 C a m V M , K i t c h i n g RP. A n investigation of possible routes of transmission o f lumpy skin disease virus (Neethling). E p i d e m i o l o g y a n d I n f e c t i o n 114: 219-226, 1995 Ordner G . Lefervre P C . L a dermatose nodulaire contagieuse des bovines. Etudes et sytheses de I ' I n s t i t u t d ' E l e v a g e et de M e d i c i n e V e t e r i n a r i e T r o p i c a l e , M a i s o n A l f o r t , Paris, pp. 92. 1978.
64. Gibbs EPJ, e t a l . Classification of peste des petits ruminants virus as the fourth member o f the genus M o r b i l l i v i r u s . Intervirology II. 268-274, 1979 65. H a m d y F M , Dardiri A H . Response of white-tailed deer to infection with peste des petits ruminants virus. J o u r n a l o f W i l d l i f e Diseases 12: 516-522, 1976 Leferve P C , D i a l l o A . Peste des petits ruminants. Revue Scientifique et T e c h c h n i q u e Office I n t e r n a t i o n a l des E p i z o o t i e s 9: 951-965, 1990 Rapaport E , et a l . Peste des petitis ruminant ( P P R ) i n Israel - first report. P r o c e e d i n g o f t h e 3 I n t e r n a t i o n a l Symposium o n Sheep Diseases. Edinburgh. Sheep Veterinary Society, Edinburgh. 1993.
rd
45.
46. 47.
66.
67.
48.
68.
A b r a h a m A , Lebel E , Davidson M . V i r o l o g i c a l and serological investigations on rinderpest i n Israel. Refuah
Volume 63 (4) 2008
website: www.isrvma.org
113
REVIEW Veterinarit 41: 112-121, 1984 Abraham A , E l i g u s h v i l l i R , D a v i d s o n M . P P R virus diagnosis, i n the virology laboratory in the K V I . E p i d e m i o l o g i c a l Q u a r t e r l y 2/93 (in Hebrew), 1993 Perl S, et a l . Peste des petitis ruminant ( P P R ) o f sheep i n Israel: case report. I s r a e l J o u r n a l o f V e t e r i n a r y M e d i c i n e 49: 59-62, 1994; Kirkpatrick M A , T i m m s L L , Kersting K W . Case reportjejunal hemorrhage syndrome o f dairy cattle, B o v i n e P r a c t i t i o n e r 35: 104-116,2001 Dennison A C , et a l . Hemorrhagic bowel syndrome in dairy cattle: 22 cases (1997-2000). J o u r n a l o f A m e r i c a n V e t e r i n a r y M e d i c a l A s s o c i a t i o n 221: 686-689, 2002 Berghaus R D , M c C l u s k e y B J , C a l l a n R J . R i s k factors associated w i t h hemorrhagic bowel syndrome i n dairy cattle. J o u r n a l o f A m e r i c a n V e t e r i n a r y M e d i c a l A s s o c i a t i o n , 226: 1700-1706, 2005 Godden S, R o d F, Trevor A . Survey o f Minnesota dairy veterinarians on the occurrence o f and potential risk factors for jejunal hemorrhage syndrome i n adult dairy cows. B o v i n e P r a c t i t i o n e r 35: 97-103, 2001 Brenner J, et a l . A d u l t bovine jejunal hemorrhage syndrome - an emerging dairy cows disease? Israel J o u r n a l o f V e t e r i n a r y M e d i c i n e 57: 4 1 , 2002 E l a d D , et a l . B o v i n e vulvovaginitis associated with P o r p h y r o m o n a s levii. E m e r g i n g I n f e c t i o u s Diseases 10: 505-506, 2004 B l u m S, et a l . Sample-based assessment o f the microbial etiology of bovine necrotic vulvovaginitis. T h e r i o g e n o l o g y 68: 290-293, 2007 B l u m S, et a l . Effect o f bovine necrotic vulvovaginitis on productivity in a dairy herd in Israel. V e t e r i n a r y J o u r n a l 2007 (accepted). B l u m S, et a l . Porphyromonas levii in B o v i n e Necrotic Vulvovaginitis negative dairy herds. V e t e r i n a r y R e c o r d 2007 (accepted). Yeruham I, et a l . Bovine necrotic vulvovaginatis in dairy herds. V e t e r i n a r y R e c o r d 160: 164-166,2007 Jousimies-Somer H , Summanen P H , Finegold S M . Bacteriodes, Porphyromnas, Prevotella, Fusobacterium, and other anaerobic gram-negative rods and cocci. In: Murray, P.R. eds. M a n u a l o f clinical microbiology. Washington: A S M Press;, pp 690-711, 1999 Gavier-Widen D , et a l . Diagnosis o f transmissible spongiform encepahalpathies i n animals: a review. J o u r n a l o f Veterinary Diagnostic Investigation 17: 509-527, 2005 Wells, G . A . H . , Scott, A . C . , Johnson, C.T., G u n n i n g , R.F., Hancock, R . D . , Jeffery, M . , D a w s o n , M . , and Bradley, R . 1987. A novel progressive spongiform encephalopathy i n cattle. V e t e r i n a r y Record121: 419-420. Bruce M E , et a l . Transmissions to mice indicate that "new variant" C J D is caused by the B S E agent. N a t u r e 389: 498-501, 1997 Perl S, et a l . B S E - first documented case i n Israel and current status i n other countries. I s r a e l V e t e r i n a r y M e d i c i n e 58:62-67, 2002 Journal o f
69.
70.
8 6 . E p i d e m i o l o g i c a l B u l l e t i n o f I V S 2002 87. Perl S, et a l . B S E survey i n Israel and current status in Europe. I s r a e l J o u r n a l o f V e t e r i n a r y M e d i c i n e 55: 55-58, 2000 O . I . E http://www.oie.int/eng/normes/ M M A N U A L / A _ 0 0 0 3 7 . h t m ) 2005. 8 9 . I s r a e l V e t e r i n a r y Services (IVS) A r c h i v e 2 0 0 6 90. Banet-Noach C , et a l . Genetic analysis o f nonstructural genes (NS1 and N S 2 ) o f H 9 N 2 and H5N1 viruses recently isolated i n Israel. V i r u s Genes 34: 157-168,2007 Perk S, et a l . E c o l o g y and molecular epidemiology o f H 9 N 2 avian influenza viruses isolated i n Israel during 2000-2004 epizootic. Developments i n B i o l i o l o g i c a l s (Basel) 124: 201-209, 2006 Office International des Epizooties (OIE), 2000: Malignant catarrhal fever. In: M a n u a l o f S t a n d a r d s f o r D i a g n o s t i c Tests a n d V a c c i n e s , pp.813-821. Radostits O M , G a y C C , . B l o o d D C , H i n c h c l i f f K W . eds. Malignant catarrhal fever. In: Veterinary M e d i c i n e , pp. 1081-1134. W . B . Saunders C o m p a n y L t d . , L o n d o n , 2000 Selman I E . The epidemiology o f malignant catarrhal fever. Veterinary A n n u a l 27: 98-102, 1987 O ' T o o l e , D , et a l . Chronic generalized obliterative arteriopathy i n cattle: a sequel to sheep-associated malignant catarrhal fever. J o u r n a l o f V e t e r i n a r y D i a g n o s t i c I n v e s t i g a t i o n 7:108-121, 1995 O ' T o o l e , D , et a l . Chronic and recovered cases o f sheepassociated malignant catarrhal fever i n cattle. V e t e r i n a r y R e c o r d 1 4 0 : 5 1 9 - 5 2 4 , 1997 D a v i d D , et a l . T w o cases o f the sheep-associated malignant catarrhal fever in cattle. V e t e r i n a r y R e c o r d 56:118-120, 2005 Baxter SIF, P o w I, B r i d g e n A , et a l . P C R detection o f the sheep-associated agent o f malignant catarrhal fever. Archive in Virology 99. 132, 145-159,1993 88.
71.
72.
91.
73.
92.
74.
93.
75.
94. 95.
76.
77.
96.
78.
97.
79.
98.
80. 81.
82.
Brenner J, e t a l . A n unusual outbreak of malignant catarrhal fever in a beef herd i n Israel. J o u r n a l o f V e t e r i n a r y M e d i c i n e B , 46: 304-307, 2002 100. Brenner J. D a v i d D . Sheep-associated malignant catarrhal fever i n cattle ( S A - M C F ) : Recent clinical and epidemiological aspects i n Israel. I s r a e l J o u r n a l o f V e t e r i n a r y M e d i c i n e 60: 19-22,2005 101. Yadin H . , et a l . Epizootic Hemorrhagic Disease Virus type 7 infection i n cattle in Israel, August-October 2006. V e t e r i n a r y R e c o r d 2007 (accepted). 102. Guy J S, M a l k i n s o n M . Arbovirus infection. In Saif, Y . M . , editor. Disease o f Poultry. 11 eds. A m e s , I A : Iowa State University Press; pp 388-398, 2003 103. Banet-Noach C , Simanov L , M a s l k i s o n M . Direct (nonvector) transmission o f West N i l e virus in geese. A v i a n P a t h o l o g y 32: 489-494, 2003
th
83.
84.
85.
104. M a s l k i s o n M , B a n e t C , Machany S. Virus encephalomyelitis
114
website: www.isrvma.org
V o l u m e 63 (4) 2008
ISRAEL JOURNAL OF VETERINARY MEDICINE of geese: some properties o f the viral isolate. I s r a e l J o u r n a l o f V e t e r i n a r y M e d i c i n e 53: 44-45, 1998 105.Maslkison M , et a l . Use o f live and inactivate vaccines i n the control o f West N i l e fever i n domestic geese. A n a l o f New Y o r k Academy o f Science 951: 255-261, 2001 106.Samina I, K h i n i c h Y , Simanov M , et a l . A n inactivated West N i l e virus vaccine for domestic geese-efficacy study and a summary of 4 years o f field application. V a c c i n e 23: 4955-4958, 2005 107. Y a d i n , H , et a l . A large-scale outbreak o f bovine hemorrhagic disease i n Israel. I s r a e l J o u r n a l o f V e t e r i n a r y M e d i c i n e E . 62: 28-29,2007 108. Radostits O M , G a y C C , B l o o d D C , H i n c h c l i f f K W . Hemorrhagic diseases. In: Veterinary Medicine 9 eds. W.S. Saunders C o . L t d . L o n d o n , N e w York, Philadelphia, San, Francisco, St L o u i s , Sydney,, pp 1134, 2000
th
109.Osborn B I , M i l l e r J . Report of the Bluetongue and B o v i n e Leucosis Committee. P r o c e e d i n g s o f t h e U.S. A n i m a l H e a l t h A s s o c i a t i o n 87: 111, 1983 110.O.I.E, Office International des Epizooties 2007 http:// www.oie.int/eng/normes/mcode/en_partie_4.htm 111. Pitlik S. Vets, M e d s , and Zoonotic Threats. E m e r g i n g I n f e c t i o u s Diseases 10: 760-761, 2004 112. W o r l d Health Organization, W o r l d H e a l t h R e p o r t Geneva, 2007). (WHO,
113. Lescano A G , et a l . . Outbreak Investigation and response training. Science 318: 574-575, 2007
Cover image - Rock hyrax
The hyrax is 30 to 70 cm long and weighs between 2 and 4.5kg, Male hyraxes are slightly larger than females. The hyrax gives birth to two to four young after 6 to 7 months gestation period. The young are well developed at birth with fully-opened eyes and a complete pelage. The young can ingest solid food after two weeks and are weaned at ten weeks. They are sexually mature after 16 months, and reach adult size at three years. Their typical lifespan is about ten years. Hyraxes are found in Africa and the Middle East. In Israel they are found mostly on the Hermon and the Carmel, in the Judean desert and the Negev. Hyraxes live in family groups of up to 100 individuals. Hyraxes have poorly developed body temperature regulation and compensate by basking in the sun like reptiles. Hyraxes are sometimes described as being the closest living relative of the elephant. This is because they shared a common ancestor in the distant past when hyraxes were larger and more diverse. However, the details of this relationship remain open to debate.
V o l u m e 63 (4) 2008
website: www.isrvma.org
115