Heartwater or Cowdriosis is a disease of cattle, sheep, goats and wild ruminants endemic to Sub-Sahara Africa, Madagascar, and portions of the Caribbean such as Antigua and Guadeloupe. Heartwater is caused by obligate intracellular rickettsial organisms that parasitize macrophages (a type of white blood cell). After initially replicating in macrophages, the organism will move to the vascular endothelium where it undergoes additional replication. The rickettsial organism is now classified as Ehrlichia ruminantium, and was previously known as Cowdria ruminantium.

E. ruminantium is transmitted by Amblyomma ticks with A. variegatum, also known as the tropical bont tick, and A. habraeum, the bont tick, being the top transmitters. These are 3-host ticks that undergo transstadial transmission (any stage of the tick life-cycle from the time of infection forward may transmit the rickettsial organism). In the Caribbean, cattle egrets are suspected to cause the spread of the A. variegatum tick between the various islands. The American mainland is currently not affected by heartwater but it is feared that vectors spreading the rickettsia could still be introduced. Vertical transmission (from cow to calf) through colostrum has also been reported. Researchers in South Africa have recently obtained evidence that the E. ruminantium may be capable of causing infection in dogs and people (zoonotic). It is feared that infected people or dogs may lead to the spread of heartwater to other parts of the globe. The worldwide spread of heartwater would have serious consequences to global cattle production. Heartwater is already regarded as the most important disease of ruminants in southern Africa.

Native breeds of cattle and wildlife such as the N’Dama breed in West Africa are said to be resistant to the clinical effects of heartwater. Animals having recovered from infection are typically immune to reinfection for 6 months to 4 years but may be carriers of the disease for 8 months or longer. Apparently an age-dependent resistance has long been demonstrated, recognizing that young animals have an innate resistance. This resistance has been shown to be due to a low-grade infection of E. ruminantium obtained in colostral cells.

The incubation period is 1-3 weeks after transmission by an infected tick.

Clinical disease is produced by an increase in vascular permeability which leads to a leakage of fluid from blood vessels. This leakage of fluid results in edema formation, especially in the lungs, body cavities, and the brain. In goats, disease is often characterized by renal ischemia (lack of blood to the kidneys) and nephrosis (disease of the kidneys). Irreversible kidney damage may cause death in infected goats.

Clinical disease may be classified as peracute, acute, subacute or mild and inapparent. The clinical syndrome exhibited depends on the susceptibility of the animal infected and the virulence of the rickettsia involved. Peracute disease is characterized by a high fever that quickly leads to prostration (extreme exhaustion) and death within 1-2 days.

These animals may have terminal convulsions shortly before death. The mortality rate may be near 100% with peracute disease. Acute disease is more common and will have a course of approximately 6 days. Initially the animal will appear febrile (feverish) followed by anorexia (inappetance), rapid breathing, lethargy, and a classical nervous syndrome characteristic of heartwater. Cattle become ataxic, have empty chewing movements, twitching of the eyelids, circling, aggression, apparent blindness, convulsions, and animals will often become recumbent shortly before death. A profuse, fetid diarrhea often accompanies the neurologic clinical signs. The mortality rate is 50 to 90% in adult animals whereas calves less than 4 weeks of age only have a 5 to 10% mortality rate. Subacute cases are typically less severe with similar clinical signs of disease. With subacute infection, the course of the disease is longer, up to 2 weeks in length after which the animal will gradually recover or die. The mild form of the disease is only seen in indigenous breeds of cattle or native wildlife that have natural resistance. These animals will appear sub-clinical or exhibit mild clinical signs of infection.

Treatment is typically only successful when begun early, before central nervous system signs develop. Tetracyclines and sulphonamides have both been used.

As of yet there is no widely effective or safe vaccine available against E. ruminantium. Various types of vaccines are currently in the experimental development stage but have yet to be released. Tick control may be useful or controversial. Stringent tick control may result in additional losses in endemic areas by interfering with immunity obtained when native species of ruminants are constantly exposed to lower levels of the rickettsial infection. In endemic areas, animals may be better able to deal with field exposure by constant challenge with low levels of infection.


References:

Ettinger, Stephen and Edward Feldman. Textbook of Veterinary Internal Medicine. 6th Edition. Elsevier 2000. Vol.1. pp. 632-636.

Kahn, Cynthia Editor. The Merck Veterinary Manual. 9th Edition. Merck and Co. 2005.
pp. 604-605.

Radostits, Otto and Clive Gay et al. Veterinary Medicine. 10th Edition. Saunders. 2007. pp. 1462-1464.