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Preventing bovine anaplasmosis


Anaplasmosis is endemic in many parts of the country, causing significant economic losses to beef and dairy industries.

Anaplasmosis, a rickettsial disease characterized by progressive anemia and caused by Anaplasma marginale, is endemic in many parts of the country, causing significant economic losses to beef and dairy industries.

Practitioners in some areas are reporting that they are diagnosing anaplasmosis more frequently in recent years, possibly a reflection of increased cattle movement due to drought and other natural disasters.

The causative organism also can infect sheep, goats and some wild ruminants. These animals usually have inapparent infections and can become a reservoir for the disease.


A. marginale is transmitted from carrier to susceptible cattle via arthropod vectors or iatrogenically (needles, dehorning and castration equipment, tattoo instruments, etc.).

Ticks serve as biological vectors and are more likely to spread the disease from herd to herd. Horse flies are the other major arthropod vector. They are mechanical vectors, so transmission requires close contact of animals. Therefore, they are important in spreading the disease within a herd. Stable flies can transmit the disease, but probably not as effectively as horse flies. Although it is stated in the literature that mosquitoes are vectors, they probably play little part in spreading this disease unless very severe infestations occur.

Iatrogenic spread within a herd also can occur. According to one report, a needle used on an infected animal leads to a 60-percent chance of the next animal getting infected if the same needle is used.

The incubation period can be from one to eight weeks, depending on the infective dose. In natural infections it is usually three to five weeks. The organism replicates in red blood cells (RBCs), which are then removed from circulation by the reticuloendothelial (RE) system. This causes an extravascular hemolysis and progressive anemia.

Animals that survive the anemia usually become chronic carriers. It is unknown where in the body the infection persists, but blood remains infective, even if infected RBCs cannot be detected on a blood smear. Most carrier animals remain immune to subsequent acute disease.

Transplacental transmission is reported to occur and could play a role in the maintenance of the disease within herds. Calves that are infected in utero rarely show clinical signs but become carriers.

The severity of disease is age- and possibly breed-related. Calves less than 1 year old show only mild signs or remain asymptomatic. Cattle up to 2 years of age have acute but rarely fatal disease. Cattle more than 2 years of age are most likely to have severe, acute and potentially fatal disease.

Bos taurus cattle appear to be more likely to develop severe, acute disease than Bos indicus cattle. The reasons for the age and breed susceptibility differences are not known.

Clinical signs

Peracute, acute, chronic and mild forms of anaplasmosis occur. Acute anaplasmosis is most common and usually occurs in summer and fall during peak vector season. If outbreaks occur at other times, iatrogenic transmission should be suspected.

Fever (in some), anorexia, rapid loss of body condition, severe decrease in milk production, pale and icteric mucous membranes, increased heart and respiratory rates, muscle weakness and depression are common.

Aggression from cerebral anoxia is common, especially in beef cattle. Abortions can occur in females and temporary infertility can occur in males. Since the hemolysis is extravascular, hemoglobinuria does not occur.

With peracute anaplasmosis, death occurs within hours of the onset of clinical signs. This is most common in highly susceptible purebred animals and high-producing dairy cows. Cattle may die before icterus occurs.

Chronic disease occurs in severely affected animals that do not die. It may take weeks to months for animals to recover, during which time production losses can be significant (decreased calf weaning weights, infertility). Cattle that have hematocrit levels less than 11 have a poor prognosis. They might live, but severe hypoxia can damage the heart and other organs, leading to a chronic "poor doer." In mild cases, abortion and decreased milk production can be the only problems, which might go unnoticed.


Diagnosis of acute disease is by finding A. marginale bodies at the periphery of the RBCs. Once the acute stage is advanced, it can be difficult to find the organism. Late clinical disease or the chronic carrier state has to be diagnosed with serologic tests.

In the past, the rapid card agglutination and complement-fixation (CF) tests most commonly were run. A new competitive enzyme-linked immunosorbent assay (cELISA) appears to have better sensitivity. However, the sensitivity of the serologic tests depends on the stage of infection. Early in the incubation phase, these tests might be negative.

On necropsy, tissues are pale, turning icteric in later stages. The blood is thin and watery. Splenomegaly occurs in most cases.


Clinical signs usually don't occur until about 50 percent of the RBCs have been destroyed. However, because many of the remaining cells already are infected and will also be destroyed, the clinical course is difficult to change, even with treatment. Oxytetracycline is effective, but it works best in early or preclinical stages. Many times cattle aren't recognized as infected until they are severely anemic, so treatment might not help. In fact, the stress can kill the animal, especially beef cattle. A blood transfusion might be indicated for some animals.

Treatment of the remainder of the herd with long-acting formulations of oxytetracycline should be considered. In endemic areas, the mortality rate is rarely very high, although subclinical disease (abortions, decreased milk production) might still warrant treatment.

For herds in non-endemic areas that are unlikely to have any immunity, mortality rates can be high. Therefore, once the disease is diagnosed, treatment of the entire exposed group should be considered.

Prevention and control

In non-endemic areas, the goal is to prevent the disease from coming into a herd. Herd additions should be screened with the cELISA or purchased from test-negative herds. Because of the potential for possible false negatives on the cELISA during the incubation phase and the potential for wildlife reservoirs, the disease still can sneak in. Therefore, a new needle should be used for all animals and equipment should be washed/disinfected between animals.

If available, vaccination, especially of the most valuable animals, should also be considered. The only vaccine available is produced by University Products and is offered in 14 states via a U.S. Department of Agriculture experimental approval. However, work is ongoing to allow availability nationwide. Visit www.anaplasmosis.com for more information about the vaccine.

In infected herds in non-endemic areas, or in herds in endemic areas, the goal is to minimize losses. Because of potential in utero infections, vector transmission, wildlife reservoirs and false-negative serologic tests in the incubation phase, once a herd is infected it is difficult to eliminate the disease, even in non-endemic areas.

For infected herds in non-endemic areas, periodic testing with the cELISA to continually remove carrier animals and proper needle and equipment use might help decrease losses. Vaccination or tetracycline in feed or mineral supplements during the vector season can help. Neither will prevent animals from becoming carriers but will decrease chances of abortions, milk-production losses and clinical disease.

Supplements containing tetracycline must be labeled for anaplasmosis prevention to contain high enough levels to be effective.

Due to the continual risk of introduction of anaplasmosis in endemic areas, and because carrier cattle are resistant to the disease, it is not recommended that herds in endemic areas remove carriers. And, because young animals are resistant to disease, control of transmission is concentrated on older, more susceptible animals.

A new needle should be used for each pregnant replacement heifer and any animal 2 years of age and older to prevent spread to animals most likely to abort or have acute infections. Tetracycline in feed or mineral supplements might also help. However, intake of these products is variable from animal to animal and, with the high exposure pressure in endemic areas, some animals might still be vulnerable.

If available, vaccination probably is the most effective means of preventing losses in herds in endemic areas. Vector control and good biosecurity practices are important in decreasing spread of anaplasmosis in all herds.

Introducing cattle from non-endemic areas to endemic areas should be done carefully. If possible, introduce new animals during the non-vector season (if there is one). Vaccination on arrival is indicated. If vaccination is not available, consider treatment of the new animals with long-acting oxytetracycline two weeks after arrival if introduced during the vector season.


Anaplasmosis can be devastating for producers and costs the American cattle industry millions of dollars each year. There is still much that is not understood about the disease, including the importance of wildlife reservoirs. However, with the availability of more modern research techniques, these questions can start to be answered. In the near future we hope to gain a greater understanding of the epidemiology of this disease and have better methods of controlling it.

Dr. Navarre works as an extension veterinarian with Louisiana State University's Department of Veterinary Science.

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