Ephemeral fever is an insect-transmitted, noncontagious, viral disease of cattle and water buffalo that is seen in Africa, the Middle East, Australasia (excluding Papua New Guinea and New Zealand), and Asia south of the former USSR. Inapparent infections can develop in Cape buffalo, hartebeest, waterbuck, wildebeest, deer, and possibly goats. Low levels of antibody have been recorded in several other antelope species and giraffe, but the specificity has not been confirmed.
Etiology and Epidemiology
Ephemeral fever virus is classified as a member of the genus Ephemerovirus in the family Rhabdoviridae (single-stranded, negative sense RNA). The virus is ether-sensitive and readily inactivated at pH levels below 5 and above 10. Although no evidence of immunogenic diversity is reported, antigenic variation has been demonstrated using panels of monoclonal antibodies and by epitope mapping.
The virus can be transmitted from infected to susceptible cattle by IV inoculation; as little as 0.005 mL of blood collected during the febrile stage is infective. Although the virus has been recovered from several Culicoides species and from Anopheline and Culicine mosquito species collected in the field, the identity of the major vectors has not been proved. Transmission by contact or fomites does not occur. The virus does not appear to persist in recovered cattle, which often have a lifelong immunity.
The prevalence, geographic range, and severity of the disease vary from year to year, and epidemics occur periodically. During epidemics, onset is rapid; many animals are affected within days or 2–3 wk. Ephemeral fever is most prevalent in the wet season in the tropics and in summer to early autumn in the subtropics or temperate regions (when conditions favor multiplication of biting insects); it disappears abruptly in winter. Virus spread appears to be limited by latitude rather than topography or availability of susceptible hosts. Morbidity may be as high as 80%; overall mortality is usually 1–2%, although it can be higher in lactating cows, bulls in good condition, and fat steers (10–30%).
Signs, which occur suddenly and vary in severity, can include biphasic to polyphasic fever (40–42°C), shivering, inappetence, lacrimation, serous nasal discharge, drooling, increased heart rate, tachypnea or dyspnea, atony of forestomachs, depression, stiffness and lameness, and a sudden decrease in milk yield. Clinical signs are generally milder in water buffalo. Affected cattle may become recumbent and paralyzed for 8 hr to >1 wk. After recovery, milk production often fails to return to normal levels until the next lactation. Abortion, with total loss of the season's lactation, occurs in ∼5% of cows pregnant for 8–9 mo. The virus does not appear to cross the placenta or affect the fertility of the cow. Bulls, heavy cattle, and high-lactating dairy cows are the most severely affected, but spontaneous recovery usually occurs within a few days. More insidious losses may result from decreased muscle mass and lowered fertility in bulls.
Ephemeral fever is an inflammatory disease. The most common lesions include polyserositis affecting pleural, pericardial, and peritoneal surfaces; serofibrinous polysynovitis, polyarthritis, polytendinitis, and cellulitis; and focal necrosis of skeletal muscles. Generalized edema of lymph nodes and lungs, and atelectasis may also be present.
Diagnosis is based almost entirely on clinical signs in an epidemic. All clinical cases have a neutrophilia with the presence of many immature forms, although this is not pathognomonic. Serofibrinous inflammation in the tendon sheaths, fasciae, and joints, together with pulmonary lesions, may substantiate a presumptive diagnosis.
Laboratory confirmation is by serology, rarely by virus isolation. Whole blood should be collected from sick and apparently healthy cattle in affected herds and must be sufficient to provide 2 air-dried blood smears, 5 mL of whole blood in anticoagulant (not EDTA), and ~10 mL of serum. A differential leukocyte count on blood smears can either support or refute a presumptive field diagnosis.
Virus is best isolated by inoculation of mosquito (Aedes albopictus) cell cultures with defibrinated blood, followed by transfer to baby hamster kidney (BHK-21) or monkey kidney (Vero) cell cultures after 15 days. Suckling mice may also be used for primary isolation by intracerebral inoculation. Isolated viruses are identified by PCR, neutralization tests using specific ephemeral fever virus antisera, and ELISA using specific monoclonal antibodies. The neutralization test and the blocking ELISA are recommended for antibody detection and give similar results. A 4-fold rise in antibody titer between paired sera collected 2–3 wk apart confirms infection.
Treatment and Control
Complete rest is the most effective treatment, and recovering animals should not be stressed or worked because relapse is likely. Anti-inflammatory drugs given early and in repeated doses for 2–3 days are effective. Oral dosing should be avoided unless the swallowing reflex is functional. Signs of hypocalcemia are treated as for milk fever (see Parturient Paresis in Cows). Antibiotic treatment to control secondary infection and rehydration with isotonic fluids may be warranted.
Attenuated virus vaccines appear to be effective but should be used only in endemic areas. Inactivated virus vaccines have not produced longterm protection against experimental challenge with virulent virus and cannot guarantee lasting immunity, but they may boost the immunity produced by live virus vaccine. Although a subunit vaccine that protects against field and laboratory challenge has been described, it is not commercially available. The efficacy of vector control remains uncertain because the insect vectors have not been fully identified. There is no evidence that humans can be infected.
Last full review/revision March 2012 by Christopher Hamblin, CBiol, MSB