Anaplasmosis is a noncontagious, infectious, transmissible hemoparasitic disease of cattle. It is caused by Anaplasma marginale in the United States and A. centrale in parts of Africa. Anaplasma marginale is member of the order Rickettsiales and anaplasmosis is characterized by anemia, fever, and icterus.
The agent is enzootic in both cattle and certain wildlife hosts. The prevalence in cattle varies between region of the U.S.
and within regions depending on topography, wildlife hosts, vectors, and management practices. Likewise, the prevalence in
wildlife species can vary by region. For example, Columbian black-tailed deer populations in California have near 100% carrier
status for A. marginale, while the white-tailed deer of the Midwest and southeastern U.S. have prevalence rates of about 1% or less. Wildlife species
such as antelope, elk, and big horn sheep can also be experimentally infected with A. marginale. While ticks are not normally thought of as reservoir hosts—in the case of anaplasmosis, they can "carry" the agent for long
periods of time. While they are usually classified as vectors, from a functional state I tend to think of them as potential
reservoirs of new infections. The most important mammalian reservoirs in the U.S. are cattle and black-tailed deer; however,
this is not to imply that clinical disease is always limited to areas populated by carrier cattle or black-tailed deer.
Boophilus ticks can transmit both babesiosis and anaplasmosis and are extremely important vectors in the areas of the world where they
exist. The eradication of Boophilus annulatus in the U.S. has eliminated this potential vector in terms of transmission. The importance of maintaining that eradication
control is two-fold because of anaplasmosis and babesiosis. In the western U.S. Dermacentor occidentalis and Dermacentor andersoni are both important in the natural transmission of anaplasmosis. They both will feed on deer species and can pass the anaplasmosis
organism from stage to stage (larvae, nymph, and adult) and possibly can have transovarian transmission of the agent. Thus,
these ticks are potent biological vectors of anaplasmosis.
Mechanical vectors of anaplasmosis include horse flies, stable flies, deer flies, and possibly mosquitoes. The most important
of these are the horse flies (Tabanids) as they tend to be interrupted feeders, have large mouth pieces that can contain a
relatively large amount of blood, and can fly long distances. These vectors can all transmit blood from an infected (carrier)
animal to a susceptible animal under practical conditions. Additionally, mechanical transmission can occur iatrogenically
during common management procedures such as dehorning, castration, bleeding, use of nose tongs, ear tagging, vaccination (hypodermic
needles) and other surgical procedures. The routine use of disinfection and cleaning of instruments between uses will help
eliminate this possible route of transmission.
The age of the animal is an important factor in determining susceptibility to clinical disease. Cattle can become infected
at any age; but the older they are the more likely they are to have clinical signs of anaplasmosis. Cattle up to 6 months
of age can become infected but do not develop detectable clinical signs. Cattle 6-12 months of age rarely develop overt illness,
but their PCV will decrease after they become infected. Cattle 12-18 months have a greater chance of developing clinical illness
(1%-20%) and cattle over 24 months of age can experience 50% mortality or more if not treated after infection. The disease
can be divided into four phases which have clinical significance: incubation (prepatent), developmental, convalescent, and
After infection with A. marginale, the organism begins invasion of the erythron and the length of time of the prepatent period is dose dependent with a typical
range of 3-8 weeks. At the end of the incubation phase the organism can be seen in abut 1% of the red blood cells if a blood
smear is examined. However, clinical signs are not apparent at this time. The developmental phase begins at this time and
the % parasitemia doubles each day for 4-11 days. At the end of this phase the animal has recognized the infection and begins
to destroy the infected RBCs and the clinical signs of fever, anemia, and icterus are apparent. Death losses usually occur
during the late developmental phase or early convalescent phase. Convalescence is marked by increased erythropoietin (reticulocytes,
polychromatophilia, and basophilic stippling) and improving clinical signs. The carrier phase begins with clinical recovery
and the disappearance of detectable parasitemia and usually last the life of the animal. The carrier can thus become a reservoir
for infection of other cattle or a source of anaplasma for vector transmission.