East Coast Fever

Also known as

Theileriosis, corridor disease, January disease

Description

This is an acute disease of cattle and domestic buffalo caused by Theileria parva (family Theileridae), a microscopic protozoan parasite that lives within the blood cells of the host’s body and transmitted by a tick vector, Rhipicephalus appendiculatus.

East coast fever is a serious problem in eastern, central and southern Africa. Infected cattle usually develop high fever, swollen lymph nodes, and difficult breathing—coughing frequently. They become listless, lose weight, and generally die. In later stages of the disease some of these animals may have diarrhea and mucous discharges from the eyes and nose. Mortality may exceed 90% in adults but survival rate is higher in calves

T. parva causes a severe illness in some cattle that has been called corridor disease. In other cattle, it produces a much milder illness known as January disease. Scientists at first thought these differences were caused by separate subspecies of this parasite, but recent molecular studies show that the two conditions represent different expressions of the same disease.

This disease was first reported in southern Africa--south of the Zambezi River--in 1902. It became known as East Coast fever since it originated in cattle imported to that area from the East Coast of Africa.

Cattle and buffalo are the usual hosts, with zebu cattle more resistant than British breeds. Native cattle are often resistant to the parasite, but still show some signs of disease. They are often hosts, but do not suffer as severely. There are also significant variations in virulence (ability to infect/damage) between different strains of this parasite.

Many species of Theileria are found in domestic and wild animals in tick-infested areas of Africa, Asia and Europe. The most important species affecting cattle are T. parva and T. annulata, which cause widespread cattle deaths in tropical and subtropical areas. In some endemic areas, local cattle have a degree of resistance. Mortality in these animals is relatively low, but introduced cattle are quite vulnerable to severe infections.

Signs

• Fever
• Depression
• Lack of appetite
• Abnormal appetite
• Lymph node enlargement
• Weakness
• Emaciation
• Discharges from eyes and nose
• Difficult breathing
• Diarrhea (often bloody) in severe cases
• Sometimes nervous signs (convulsions, circling, head-pressing) if the brain is affected

Cause

Both Theileria and Babesia are members of the suborder Piroplasmorina. Although Babesia are primarily parasites of red blood cells, Theileria use white blood cells and later the red blood cells for completion of their life cycle in their host mammals. The infective sporozoite stage of the parasite is transmitted in the saliva of infected ticks as they feed on the animal.

The parasite goes through early developmental stages in the tick, then sporozoites are injected into the host by the tick’s saliva while feeding on blood. In tick-infested regions all animals become infected. Transmission can also occur via reused hypodermic needles, transferring the parasite from the infected animal’s bloodstream to a susceptible animal.

The sporozoites introduced by tick saliva or a contaminated needle invade the white blood cells and then within a few days become schizonts. In the most pathogenic species of Theileria (T. parva and T. annulata), the parasite multiplication occurs predominantly within the host’s white blood cells. The less pathogenic species multiply mainly in the red blood cells.

Development of the schizont stage of the pathogenic Theileria causes the host’s white blood cell to divide, and with each cell division, the parasite also divides. Thus, the parasitized cell population expands and the pathogen becomes disseminated throughout the lymph system.

Later in the course of infection, some of the schizonts undergo merogony (asexual reproduction), releasing merozoites that infect red blood cells and become available to be spread to other animals. Uptake of infected red blood cells by vector ticks feeding on infected animals is the beginning of a complex cycle of development within the tick itself, culminating in transmission of infection by ticks feeding on other host animals in their own next stage of development.

Following ingestion of host blood by larval or nymphal ticks, gamete formation (male and female cells) and fertilization occur in the tick’s midgut, after which the parasites invade the lining of the tick’s midgut and migrate to the salivary glands so transmission to another animal can occur when the tick bites and feeds again. After their molt, the nymphal or adult ticks can also transmit the infection to another host.

The African or cape buffalo (Syncerus caffer) is an important wildlife reservoir of this parasite, but these buffalo do not show any signs of the disease. T. parva transmitted by ticks from either buffalo or other cattle cause severe disease in cattle. T. parva is usually highly pathogenic in cattle, causing high levels of mortality. Cattle that do survive usually have solid immunity afterward but often remain carriers.

The incubation period for this disease is 1 to 3 weeks, depending on the virulence of the strain and amount of infecting dose (how many parasites are injected into the host animal via tick saliva). Fever usually occurs 7 to 10 days after parasites are introduced by the feeding ticks, continues throughout the course of infection, and may be as high as 106°F or more.

Lymph node swelling becomes pronounced and generalized. The animal goes off feed and rapidly loses weight. There may be cloudiness of the cornea and lacrimation (watering eyes), and nasal discharge. In late stages some animals develop diarrhea and anemia.

Terminally, the animal has trouble breathing. Just before death, there is a sharp decrease in body temperature, and lung fluid pours from the nostrils. Death may also occur following blocked capillaries affecting the central nervous system, causing neurological signs.

Mortality rate in calves is 5 to 50% whereas the disease is adult cattle is usually fatal, with 95% mortality rate. Death usually occurs about 18 to 30 days after the initial attachment of infected ticks.

Corridor disease occurs outside the known range of R. appendiculatus but within the geographic range of another competent tick vector, R. zambesiensis. The occurrence of East Coast fever coincides with the distribution of its primary wild reservoir, the cape buffalo.

Movement of cattle has played a major role in periodic outbreaks in cattle during the 20th century. Outbreaks tend to occur when highly susceptible breeds are introduced into areas endemic for this parasite.

Endemic cattle that are treated early in the course of the disease sometimes recover to varying degrees, and may become carriers.

For diagnosis, post mortem findings include damage to the lymph and respiratory systems. The main cause of death is pulmonary edema (excess fluid in the lungs).

Prevention

Incidence of East Coast fever can be reduced by rigid tick control on domestic cattle, but this is not feasible in many areas because of cost and the high frequency of chemical pesticide treatment required. The pesticides for controlling ticks (acaricides) are applied via dipping baths or sprays. In high risk areas, cattle breeds with ability to acquire some immune resistance are used. Cattle that have been exposed and recovered have lifelong immunity unless stressed.

In May 2010, a vaccine to protect cattle against East Coast fever was reportedly approved and registered by the governments of Kenya, Malawi and Tanzania. The vaccine consists of frozen preserved sporozoites from crushed ticks, but is expensive and sometimes can cause disease.

Immunization of cattle against T. parva using an infection-and-treatment procedure is gaining acceptance in some regions. The components for this procedure include a cryopreserved (frozen) sporozoite product that is alive and stable--derived from infected ticks--and a single dose of long-acting oxytetracycline given simultaneously.

Though oxytetracycline has little therapeutic effect when administered after onset of the disease, it inhibits development of the parasite when given at the very beginning of the infection. Cattle should be immunized 3–4 weeks before being moved into infected pastures.

Animals that recover from the actual disease are immune to subsequent challenge with the same strains but may be susceptible to some related strains. Most recovered or immunized animals remain carriers of the infection.

Treatment

Treatment with parvaquone and its derivative buparvaquone is highly effective when administered in the early stages of clinical disease but less effective in the advanced stages--where there is extensive destruction of lymph and blood cell-forming tissues.

Halofuginone lactate has also been shown to have an 80.5% efficacy against Theirelia infections.