bovine ephemeral fever
- Host Animals
- Hosts/Species Affected
- Systems Affected
- Distribution Table
- List of Symptoms/Signs
- Disease Course
- Impact: Economic
- Zoonoses and Food Safety
- Disease Treatment
- Prevention and Control
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- bovine ephemeral fever
International Common Names
- English: bovine ephemeral fever - exotic; dengue fever of cattle; ephemeral fever; lazy man's disease; stiff sickness; three-day sickness
Local Common Names
- China: dragon boat disease
- India: vil
- Japan: bovine epizootic fever
- South Africa: drei-tag-siekte; stiffsiekte
Pathogen/sTop of page bovine ephemeral fever virus
OverviewTop of page
Bovine ephemeral fever (BEF) is probably an ancient disease of cattle and buffalo in Asia and Africa. The disease becomes more evident and economically important, wherever cattle populations increase or production systems intensify. In Pacific countries, where the introduction of cattle followed European settlement, the disease is more recent. Fat cattle, lactating cows in late pregnancy, bulls and steers in heavy condition suffer more severely than non-lactating thin or young animals. Draught cattle or buffaloes need rest for at least a week after recovery or they may die.
A disease with very similar clinical signs has been reported from Nigeria (Tomori et al., 1974; Fagbami and Ojeh, 1983). The disease is produced by Kotonkan virus, which is also a rhabdovirus. This virus is not well studied but has antigenic relationships with BEF virus.
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Bos indicus (zebu)||Domesticated host||Cattle & Buffaloes: All Stages|
|Bos javanicus||Domesticated host||Cattle & Buffaloes: All Stages|
|Bos taurus (cattle)||Domesticated host||Cattle & Buffaloes: All Stages|
|Bubalus bubalis (Asian water buffalo)||Domesticated host||Cattle & Buffaloes: All Stages|
Hosts/Species AffectedTop of page
Long before the scientific investigation of bovine ephemeral fever (BEF), owners of cattle stated that the fattest animals and the best milkers suffered the worst disease and were most likely to die. Heavy bulls and feedlot cattle in very fat condition suffer the highest mortality. Cows in the eighth or ninth month of pregnancy may abort (Uren et al., 1987). Very hot weather increases mortality, probably due to the effects of dehydration. Many fevered animals will not drink, even if offered water (St-George, 1994). No objective evidence has been produced to show whether any breed is genetically more susceptible than another. In Asia, Africa and the Middle East local cattle and buffalo may suffer less severe disease in comparison with imported European cattle, but the latter are usually much better fed and produce more milk. No clinical disease due to ephemeral fever has been reported in wildlife. However, neutralizing antibodies have been found in other species of African wildlife (Davies et al., 1975).
Vectors and Intermediate Hosts
The vectors of BEF have not been satisfactorily identified over most of its range. Epidemiological and other evidence suggest that mosquitoes are be the most likely vectors but there is a possibility that Culicoides spp may also be involved. BEF virus has been isolated from a pool of uncommon species of culicine mosquitoes (Culex and Aedes species) (St-George et al., 1976). The anopheline mosquito Anopheles bancroftii, from which BEF virus has also been isolated, has a distribution limited to the tropics so is not a major vector in Australia (Standfast et al., 1984). In Australia, experimental studies have indicated that a widely distributed species of mosquito Culex annulirostris is a vector. In experimental studies, BEF virus has been demonstrated to appear in the saliva of Culex annulirostris 6-8 days after infection of the mosquito (Muller and Standfast, 1993).
BEF virus has been isolated from several species of Culicoides (C. brevitarsis, C. imicola and C. coarctatus) but they are unlikely to be effective vectors (Davies & Walker, 1974; Cybinski and Muller, 1990; Blackburn et al., 1985). In New South Wales, Australia, it has been demonstrated that Culicoides brevitarsis, which transmits many other arboviruses infecting cattle, was not present in large areas during an epidemic (Kirkland, 1993). BEF virus is not secreted into the saliva of C. brevitarsis (Muller and Standfast, 1993) but may transmit the virus mechanically if a blood vessel is penetrated on feeding.
Systems AffectedTop of page blood and circulatory system diseases of large ruminants
digestive diseases of large ruminants
mammary gland diseases of large ruminants
nervous system diseases of large ruminants
reproductive diseases of large ruminants
respiratory diseases of large ruminants
skin and ocular diseases of large ruminants
DistributionTop of page
The list and map provides information on the countries from which ephemeral fever has been reported at a particular time. The disease has been reported from most African and Asian countries and has probably occurred in others. Papua New Guinea had a brief incursion in 1956 but the disease died out in the small and discontinuous cattle population (St-George et al., 1977). A country from which ephemeral fever has been reported in a particular year may be free in other years. Australia represents the present eastern boundary of the distribution in Oceania. The vectors of bovine ephemeral fever (BEF) virus in Kenya are highly dependent on temperature and rainfall (Davies et al., 1975, 1990) or river flooding, so that the prevalence varies greatly from sporadic to massive epidemics in different years. It would appear to be similar elsewhere. In general terms, the epidemics move in directions away from the equator and within regions in the direction of prevailing winds (Murray, 1970; Shirakawa et al., 1994). A broad band of countries in Africa, Asia, plus Australia are infected but not all regions within those countries. A map published by Odend’hal (1983) illustrates the band effect of the distribution of ephemeral fever north and south of the equator. North and South America and most of Europe are free of infection or disease.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|China||Present||Present based on regional distribution.|
|-Anhui||Present||Bai et al., 1991; Bai, 1993|
|-Fujian||Present||Bai et al., 1991; Bai, 1993|
|-Gansu||Present||Bai et al., 1991; Bai, 1993|
|-Guangdong||Widespread||Bai et al., 1991; Bai, 1993|
|-Guangxi||Present||Bai et al., 1991; Bai, 1993|
|-Hainan||Present||Bai et al., 1991; Bai, 1993|
|-Hebei||Present||Bai et al., 1991; Bai, 1993|
|-Henan||Present||Bai et al., 1991; Bai, 1993|
|-Hubei||Present||Bai et al., 1991; Bai, 1993|
|-Hunan||Present||Bai et al., 1991; Bai, 1993|
|-Jiangsu||Present||Bai et al., 1991; Bai, 1993|
|-Jiangxi||Present||Li et al., 1985; Bai et al., 1991; Bai, 1993|
|-Jilin||Present||Bai et al., 1991; Bai, 1993|
|-Liaoning||Present||Bai et al., 1991; Bai, 1993|
|-Nei Menggu||Present||Bai et al., 1991; Bai, 1993|
|-Ningxia||Present||Bai et al., 1991; Bai, 1993|
|-Shaanxi||Present||Bai et al., 1991; Bai, 1993|
|India||Present||Sen, 1931; FAO, et al., 1970; Prasad et al., 1997|
|-Gujarat||Present||Patel et al., 1992|
|Indonesia||Present||FAO, et al., 1970; Ronohardjo and Rastiko, 1982|
|-Java||Present||Soleha et al., 1993|
|Iran||Present||FAO, et al., 1970; Hazrati et al., 1975|
|Iraq||Present||FAO, et al., 1970|
|Israel||Present||Yeruham et al., 2010|
|-Honshu||Present||Tanaka and Inaba, 1986|
|-Kyushu||Present||Tanaka and Inaba, 1986|
|-Shikoku||Present||Tanaka and Inaba, 1986|
|Jordan||Present||FAO, et al., 1970|
|Korea, Republic of||Present||Shirakawa et al., 1994|
|Kuwait||Present||FAO, et al., 1970|
|Laos||Present||FAO, et al., 1970|
|Malaysia||Present||Present based on regional distribution.|
|-Peninsular Malaysia||Present||FAO, et al., 1970; OIE, 1981|
|Nepal||Present||FAO, et al., 1970|
|Pakistan||Present||Meadows, 1919; FAO, et al., 1970; Asi et al., 1999|
|Philippines||Present||FAO, et al., 1970; Dumag, 1977|
|Saudi Arabia||Present||Abu-Elzein et al., 1997; Elzein et al., 1999|
|Sri Lanka||Present||Balanchrandan, 1965; FAO, et al., 1970|
|Syria||Present||FAO, et al., 1970; Abu-Elzein et al., 1997|
|Taiwan||Present||Otte, 1968; Chiu and Lu, 1986|
|Thailand||Present||Wongwatcharadumrong et al., 1984|
|Turkey||Present||Tonbak et al., 2013|
|Angola||Present||FAO, et al., 1970|
|Botswana||Present||FAO, et al., 1970|
|Burundi||Present||FAO, et al., 1970|
|Central African Republic||Present||FAO, et al., 1970|
|Chad||Present||FAO, et al., 1970|
|Congo||Present||FAO, et al., 1970|
|Egypt||Present||Davies et al., 1993|
|Ethiopia||Present||FAO, et al., 1970|
|Kenya||Present||FAO, et al., 1970; Davies and Walker, 1974; Davies et al., 1990|
|Lesotho||Present||FAO, et al., 1970|
|Malawi||Present||FAO, et al., 1970|
|Mauritania||Present||FAO, et al., 1970|
|Namibia||Present||Directorate of Veterinary Services Namibia, 1978; St-George, 1994|
|Nigeria||Present||FAO, et al., 1970; Kemp et al., 1973|
|Rwanda||Present||FAO, et al., 1970; St-George, 1994|
|South Africa||Present||FAO, et al., 1970; St-George, 1994|
|Tanzania||Present||FAO, et al., 1970|
|Uganda||Present||FAO, et al., 1970|
|Zambia||Present||FAO, et al., 1970|
|Zimbabwe||Present||FAO, et al., 1970; Odiawo, 1989|
|Russian Federation||Present||Present based on regional distribution.|
|-Western Siberia||Present||Chunikin and Alekseev, 1989|
|Australia||Widespread||Seddon, 1938; Murray, 1970|
|-Australian Northern Territory||Present||Uren et al., 1987|
|-New South Wales||Present||Kirkland, 1982|
|-Queensland||Present||Newton and Wheatley, 1970|
|-South Australia||Present||Kirkland, 1993|
|-Victoria||Present||Morgan and Murray, 1969|
|-Western Australia||Present||Uren et al., 1987|
|Papua New Guinea||Present||St-George et al., 1977|
PathologyTop of page
Most of the material published on the pathology of ephemeral fever is derived from experimental infections (Basson et al., 1970; Theodoridis and Coetzer, 1979; Young, 1979; Young and Chung, 1986). In summary, the pathology is that of a generalised inflammatory disease. There is an increase in permeability of small blood vessels with an escape of neutrophils into the tissues. Muscle necrosis can occur. Joint capsules, pleural, peritoneal cavities and the pericardial sac contain straw coloured fibrinous fluid. There may be lung congestion or pneumonia. In some rare cases with prolonged paralysis, Wallerian degeneration is found high in the spinal cord (Hill and Schultz, 1977; Murphy et al., 1986).
Many other limb lesions may occur. Serofibrinous inflammation of the limb joints, polysinovitis, polyarthritis, polytendinitis, cellulites and focal necrosis of skeletal muscles has been observed. It is also possible to see lesions in the upper cervical region of the spinal cord. Subcutaneous emphysema over the thorax has been frequently observed in cattle following BEF infection in Africa.
DiagnosisTop of page
Diagnosis of ephemeral fever is based upon the clinical observations and the history of the sudden onset of outbreaks in a herd, neighbouring herds or more extensively, where vectors are dispersed by wind (Morgan and Murray, 1969). Usually various stages of the disease are seen at any one time.
There is fever, slight ocular and nasal discharge, loss of appetite, lameness in one or more limbs, with recovery in 1-2 days. Usually seen in animals less than 18 months old.
Fever and severe depression occur, with animals in sternal recumbency, some may rise if stimulated. Serous ocular and nasal discharges are present, which may become cloudy. Salivation and dehydration occur if swallowing reflex is lost. There is rapid respiration in episodes. Other signs are rhâles, tachycardia, swelling of leg joints with lameness or refusal to bear weight, ruminal atony and sometimes bloat, and constipation. Milk secretion falls suddenly and is often (with fever) the first presenting sign of the disease (Theodoridis et al., 1973b; Davis et al., 1984). Recovery occurs abruptly after 2-4 days. Abortion may follow if illness occurs in the eighth or ninth month of pregnancy (St-George et al., 1986).
The signs progress to lateral recumbency, paralysis and progressive loss of reflexes. A high respiration rate and tachycardia become continuous. Swelling with crepitation due to a subcutaneous emphysema may be felt under the skin of the backline after 3-4 days of fever (Theodoridis and Coetzer, 1979). Death may occur or recovery may be rapid or slow. Residual paresis may remain after fever has resolved and the animal is eating and drinking normally. The paresis may resolve in days, weeks or never. Hindquarter weakness may prevent bulls serving cows. Dehydration under range conditions may be important in determining the outcome.
The sudden onset of fever and fall in milk yield in the African range of BEF may be a presenting sign of many tick-borne and other diseases, but BEF is most often confused with Rift Valley fever. This has a sudden acute onset in dairy cattle exactly similar to BEF, with epidemic proportions. Single cases may be difficult to diagnose but usually various stages of disease are present especially completely recovered cases, which aid diagnosis. Blackleg and botulism can cause confusion (St-George, 1994). If a hand is run over the skin, the area affected by blackleg can be found. Paralysis due to botulism does not resolve as it does in most ephemeral fever cases. Differential diagnosis should include parturient hypocalcaemia, babesiosis, anaplasmosis, black-leg, limb damage due to trauma and hoof infections.
The isolation of bovine ephemeral fever (BEF) virus in Aedes albopictus cell cultures from blood taken during fever is the most efficient method available (Uren et al., 1992). Other cell cultures such as BHK 21 C 13 or Vero cells may be used but they are less sensitive and require serial passage. The virus can be identified by immunofluorescent or other immuno-staining techniques or by serum virus-neutralisation. Isolation of the virus is possible in the brains of suckling mice (van der Westhuizen, 1967) but this is only 25% efficient. A rise in titre of neutralizing antibodies between serum taken during fever and one taken 2 weeks later is confirmatory. However, there are no objective standards of antibody rise to confirm diagnosis. This is because of antigenic variability and the effects of cross-reacting rhabdoviruses in nature (Cybinski and Zakrzewski, 1984; St-George et al., 1984; Cybinski, 1987). Antibody can also be measured by a tissue culture neutralization test or a blocking ELISA test using a monoclonal antibody (Zakrzewski et al., 1992). This ELISA test is specific to BEF virus infection. Polymerase chain reaction (PCR) assays have been developed (Stram et al., 2005; Stram et al., 2011; Blasdell et al., 2013; Finlaison et al., 2014) and are used for diagnosis in some countries, such as Australia.
Blood clot contraction is interfered with from the second day of fever in BEF infections for 2-4 days. This can provide a field diagnosis method. A sample of blood is drawn without anticoagulants and is allowed to clot in a glass or plastic vial. This abnormal clot is surrounded by a gel, and differs from blood taken from a normal cow. Several cattle should be bled. If the clots all contract normally, the disease is highly unlikely to be ephemeral fever.
List of Symptoms/SignsTop of page
|Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate||Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox||Diagnosis|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sign|
|Digestive Signs / Decreased amount of stools, absent faeces, constipation||Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox||Diagnosis|
|Digestive Signs / Decreased borborygmi, gut sounds, ileus||Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox||Diagnosis|
|Digestive Signs / Diarrhoea||Sign|
|Digestive Signs / Dysphagia, difficulty swallowing||Sign|
|Digestive Signs / Excessive salivation, frothing at the mouth, ptyalism||Sign|
|Digestive Signs / Rumen hypomotility or atony, decreased rate, motility, strength||Diagnosis|
|General Signs / Abnormal proprioceptive positioning, knuckling||Sign|
|General Signs / Ataxia, incoordination, staggering, falling||Sign|
|General Signs / Back swelling, mass back region||Sign|
|General Signs / Dehydration||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Cattle & Buffaloes:All Stages||Diagnosis|
|General Signs / Forelimb lameness, stiffness, limping fore leg||Diagnosis|
|General Signs / Forelimb swelling, mass in fore leg joint and / or non-joint area||Diagnosis|
|General Signs / Forelimb weakness, paresis, paralysis front leg||Sign|
|General Signs / Generalized lameness or stiffness, limping||Diagnosis|
|General Signs / Generalized weakness, paresis, paralysis||Cattle & Buffaloes:All Stages||Diagnosis|
|General Signs / Hindlimb lameness, stiffness, limping hind leg||Diagnosis|
|General Signs / Hindlimb swelling, mass in hind leg joint and / or non-joint area||Diagnosis|
|General Signs / Inability to stand, downer, prostration||Diagnosis|
|General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes||Sign|
|General Signs / Neck swelling, mass cervical region||Sign|
|General Signs / Overweight, obese, weight gain||Cattle & Buffaloes:All Stages||Sign|
|General Signs / Paraparesis, weakness, paralysis both hind limbs||Diagnosis|
|General Signs / Reluctant to move, refusal to move||Diagnosis|
|General Signs / Trembling, shivering, fasciculations, chilling||Cattle & Buffaloes:All Stages||Diagnosis|
|General Signs / Weakness of one hindlimb, paresis paralysis rear leg||Sign|
|Musculoskeletal Signs / Forelimb spasms, myoclonus||Sign|
|Musculoskeletal Signs / Hindlimb spasms, myoclonus||Sign|
|Nervous Signs / Coma, stupor||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Diagnosis|
|Nervous Signs / Tremor||Sign|
|Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes||Cattle & Buffaloes:All Stages||Diagnosis|
|Ophthalmology Signs / Purulent discharge from eye||Sign|
|Reproductive Signs / Abortion or weak newborns, stillbirth||Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow||Sign|
|Reproductive Signs / Agalactia, decreased, absent milk production||Cattle & Buffaloes:Cow||Diagnosis|
|Reproductive Signs / Female infertility, repeat breeder||Sign|
|Reproductive Signs / Male infertility||Cattle & Buffaloes:Bull||Sign|
|Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs||Diagnosis|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Sign|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Diagnosis|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Diagnosis|
|Respiratory Signs / Purulent nasal discharge||Sign|
|Skin / Integumentary Signs / Skin edema||Sign|
|Skin / Integumentary Signs / Subcutaneous crepitation, skin emphysema||Sign|
Disease CourseTop of page
The infection of a cow begins with the insertion of the proboscis of a mosquito infected with bovine ephemeral fever (BEF) virus into a venule (St-George, 1993; Muller and Standfast, 1993). Under experimental conditions, the disease can only be produced by injecting infective blood directly into a vein (Mackerras et al., 1940). BEF virus is not present in the lymphatic system at least for the first half of clinical disease. This means that a Culicoides bite is ineffective in transferring virus. It also means that vaccines containing live virus and injected subcutaneously or intramuscularly cannot produce an adequate stimulus to the immune system.
The cell type within the circulatory system in which BEF virus multiplies has not been determined. However, virus can be detected by culture of blood in Aedes albopictus tissue cultures 54 h after infection and at least 24 h before fever begins (Uren et al., 1992). It appears to be concentrated in neutrophils (Young and Spradbrow, 1980).
BEF virus does not damage host tissues directly. The host response is to the high level of interferons (interleukins) triggered by the virus (St-George et al., 1986; Uren and Zakrzewski, 1989). The interleukins in turn cause an inflammatory response. The wide range of haematological and biochemical dyscrasias (Uren and Murphy, 1985; Murphy et al., 1986; Hill et al., 1988; Murphy et al., 1989) that occur with the clinical signs are illustrated some of the accompanying figures. There is a hypocalcaemia of varying depth. The rise in blood pH lowers the level of available calcium ions. The calcium deficit is responsible for muscle fasiculation, ruminal stasis and some of the paralysis (St-George et al., 1984). All the clinical signs can be completely prevented by early treatment with anti-inflammatory drugs (St-George et al., 1986; Uren et al., 1989; St-George, 1997). They are also useful for treating established disease (St-George et al., 1984).
The fever is in two or more phases. In the first febrile stage, when interleukins predominate, the clinical signs are milder than in the later phase(s). The febrile stages may be completely distinct with a period of apparent normality for 3 to 26 h or merge into each other. In the later phases clinical signs are severe lasting 2 to 4 days. Recovery follows the disappearance of interferons (interleukins) from the circulation (St-George et al., 1986). In experimental cases, and a proportion of natural cases, neutralising antibodies do not appear for a further 3-5 days. Once they do, immunity is usually life-long with no residual infection. There is no carrier state (St-George, 1993).
The pathogenesis of natural cases of BEF can be complicated by non-protective antigenically related viruses with a similar distribution. These are Kimberley and Adelaide River virus (Cybinski and Zakrzewski, 1983, 1984; Gard et al., 1983, 1984). These viruses appear to be non-pathogenic in themselves. However, they generate heterotypic antibodies to BEF viruses and an anamnestic response during clinical ephemeral fever (St-George et al., 1984; Cybinski, 1987). It is possible that the heterotypic antibody response plus high interferon levels (St-George et al., 1986) contributes to the prolonged paralysis after fever resolves in natural cases, which is rarely seen under experimental conditions (St-George, 1993).
Lactation in dairy cows can decline suddenly or stop completely. Lactation returns slowly during the recovery period but never reached the pre-disease level.
EpidemiologyTop of page
The epidemiology of bovine ephemeral fever (BEF) has been described in relatively few countries: Australia, South Africa, Kenya, China and Japan (Seddon, 1938; Murray, 1970; St-George et al., 1973; Davies et al., 1975 ; St-George et al., 1977; Uren et al., 1987; Tanaka and Inaba, 1986; St-George, 1986; Uren et al., 1983; St-George and Standfast, 1988; Davies et al., 1990; Bai et al., 1991; Bai, 1993; St-George, 1994). BEF virus spreads only after multiplication in mosquito vectors and never by contact, aerosols, urine, faeces, meat, milk or fomites. The incubation period varies between 2-5 days, very occasionally, 7. The viraemia is short, 3 and 5 days in most cases, and natural immunity is normally life-long. There is no carrier state (St-George, 1994).
The disease occurs in the wet season in tropical regions with distinct wet-dry seasons, and in the spring, summer and autumn in subtropical and temperate countries. In endemic areas, cases may occur in focal outbreaks annually or semi-annually. This means that younger animals tend to be infected, which lessens the economic impact, for the clinical effects are less severe in younger, lighter or non-lactating cattle. In other parts of the world, BEF appears as periodic epidemics, with clear inter-epidemic periods of 5-10 years. Epidemic activity appears to be associated with the periodic cycles of prolonged and excessive precipitation, which is greater than the mean expected rainfall. For this reason it often occurs simultaneously with epizootic Rift Valley fever virus activity. Little or no virus activity may be detected in the inter-epidemic periods (Davies et al., 1990), although seroconversions have been found in sentinel animals, at periods when no clinical manifestation of BEF has been observed.
The passage of BEF virus through a herd can be blocked by other arboviruses being transmitted in the same time frame (St-George, 1985). The mechanism is not fully understood, but interferons (interleukins) (St-George et al., 1986), generated by the virus which establishes first, are the likely reason. The immune response occurs at the end of the viraemia (St-George, 1985) so cannot be involved. This means that part of a susceptible age group can miss being infected in a particular outbreak and experience disease in a subsequent epidemic. The blocking effect of other arboviruses decreases with age, as cattle acquire antibodies to other endemic arboviruses.
The main routes of transmission between countries and continents have been studied (Aziz-Boaron et al., 2012). Both winds and animal transport were found to be important factors in transboundary transmission of BEF virus. Most epidemic areas or countries are adjacent to others where ephemeral fever is epidemic. The less frequent the epidemics are, the more severe they tend to be. Since the previous epidemic, the susceptible population will have grown and involve all age groups. The speed and pattern of spread depends heavily on climate and wind directions. In eastern Australia, the same north to south distance of approximately 3000 km took 6 weeks to cover in 1967-68 (Murray, 1970) or 3 years in 1972-1974 (St-George et al., 1977). The most severe epidemic in Asia moved from south to north in China in a single summer (Bai, 1993). This epidemic crossed 150 km of the straits of Pohai to the Lioniang Peninsula. All movement was in the direction of the prevailing winds.
The overwintering mechanism has not been defined. BEF virus does not overwinter in cattle (Knott et al., 1983). BEF virus does not infect sheep, pigs, horses, dogs, cats or marsupials as judged by serology (St-George, 1994). Wild ruminant species in Africa, inhabiting the same ecozones as cattle severely affected with BEF, have not been observed to suffer any clinical disease syndrome. Antibody to BEF has been found in several of these wild ruminant species, notably the buffalo (Syncercus caffer), wildebeest (Connochaetes taurinus), hartebeest (Alcelaphus buselaphus) and waterbuck (Kobus ellipsiprymnus) (Davies et al., 1975).
Experimental studies have not demonstrated transovarial transmission in possible insect vectors, although this must remain a possibility (Muller and Standfast, 1986). The current hypothesis is that infected adult mosquitoes may survive through the short winters of subtropical areas, however this does not explain the long inter-epidemic periods encountered in many countries. Vaccination is considered to affect the severity of epidemics in Japan (Tanaka and Inaba, 1986) but not in South Africa (Erasmus, 1986).
In Africa, BEF occurs across a wide range of ecological zones. It is found in the humid tropical forests, through temperate type highland grasslands, bushed and wooded savannahs both wet and dry, to the dry scrub and thorn bush of the semi desert zones (Davies et al., 1975, 1990).
Impact: EconomicTop of page
The overall mortality is between 1 and 2% (Newton and Wheatley, 1970; St-George, 1986). However, most of this mortality is from the most productive animals. Abortion rate is 5.1% of sick pregnant cattle (St-George et al., 1986; Uren et al., 1987) or 6% (Li et al., 1985). As this occurs just before the lactation period, the whole of the following year’s milk production is lost. Lactation is sharply reduced during fever (Theodoridis et al., 1973). On recovery, production resumes at approximately 15% below the rate before illness (Davis et al., 1984; Tanaka and Inaba, 1986). Gray (1938) commented on the lower price obtained for milk from affected cows. The quality is also affected (Theodoridis et al., 1973). Davis et al. (1984) estimated from daily measurement of milk yield during illness that the total identifiable loss for 15 high-producing Sahiwahl Friesian cattle was US $1440 (1983 value). Malviya and Prasad (1977) estimated losses of milk production in individual dairy cows at between 33% and 84%.
The total direct economic loss in Australia has been estimated as between US $2 million in a year with small focal outbreaks, and US $38 million in a major epidemic (1986 values). The indirect costs caused by disruptions of milk supplies and husbandry procedures cannot be estimated. Also, loss of fertility with abnormal spermatozoa (Parsonson and Snowdon, 1974; Burgess and Chenoweth, 1975) in untreated bulls can persist for 6 months. There are other indirect economic consequences. Movement of live cattle from countries where ephemeral fever is endemic is subject to embargoes, testing requirements or expensive quarantine procedures (Delahunty, 1986).
In Indonesia, the deaths of 264 adult and 65 young cattle between 1978 and 1982 was valued at Rupiahs 186,600,000 (1982 values). The cost of loss of labour of draught animals was Rupiahs 128,400,000. The total loss equated to US $400,000 (Ronohardjo and Rastiko, 1982).
All vaccines are expensive and give short-term protection. Costs vary but range from between US $1 and US $10 per dose, depending on the country.
Zoonoses and Food SafetyTop of page
Ephemeral fever is not a zoonosis (St-George, 1994). There have been no reports of infection of humans in proximity to natural cases during epidemics and none of laboratory infections.
Disease TreatmentTop of page
The basic inflammatory pathology is responsible for the fever and most of the clinical signs. Early treatment with phenylbutazone and through the expected duration of the disease completely blocks these signs (St-George et al., 1986; Uren et al., 1989; St-George, 1997). Later treatment reduces fever and modifies signs (Fenwick and Daniel, 1996). Cheaper anti-inflammatory drugs such as aspirin could be useful. Nothing should be given by mouth unless the swallowing reflex is observed to be working. The secondary effect of inflammation on plasma calcium levels is responsible for ruminal stasis and loss of the swallowing reflex, muscular fasiculation; paresis, tachycardia and rapid respiration in the latter stages of severe infections can be reversed by the injection of calcium borogluconate (St-George et al., 1984). The dose is according to response. The treatment must be supplemented by anti-inflammatory drugs otherwise relapse will occur (St-George et al., 1984). Rest is essential during illness and for at least a week after recovery for draught cattle or buffaloes. Time is necessary for tissue repair whether or not treatment is successful in preventing or relieving clinical signs.
Prevention and ControlTop of page
Several forms of live attenuated, inactivated and recombinant vaccines have been reported but with variable efficacy and durability of protection (Liu and Munir, 2013). None of the bovine ephemeral fever (BEF) vaccines produced so far, confer a life-long immunity and the proportion of cattle protected in the face of an epidemic is unpredictable Vaccines developed include:
- live, killed - Japan (Tanaka and Inaba, 1986)
- live - South Africa (Theodoridis et al., 1973)
- live - Australia (Tzipori and Spradbrow, 1973)
- live - Australia (Vanselow, 1986; Walthall and Vanselow, 1986)
- killed - Australia
- subunit - Australia (Uren et al., 1994)
The live virus vaccines are two-part vaccines and must be kept cool until combined for injection. Two doses are essential with annual boosters with any vaccine (Uren and Zakrzewski, 1989). All are too expensive for use in the developing countries but may be economically justifiable in high input/high output livestock systems.
Ephemeral fever is likely to be transmitted by mosquitoes over most of its range of distribution. Their identity is not certain, so no targeted vector control is possible. The spread of infection is largely downwind from adjacent infected areas. Quarantine within an infected country has no impact upon the local spread of BEF. International regulations on movement of cattle and buffaloes from infected to uninfected countries vary with country and time. As the regulations are not usually based on what is known of the pathogenesis of the disease, no improvement is likely in the short term. In the western hemisphere, ephemeral fever would be handled as an exotic disease. In objective terms, an animal, which has recovered from ephemeral fever, presents no risk 2 weeks after recovery. Meat, semen and embryos are not a risk on first principles for BEF virus must be injected intravenously to transfer disease (St-George, 1994). Intra-cervical transfer of BEF virus has not been successful (Burgess, 1973).
ReferencesTop of page
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