Anaplasmosis, caused primarily by Anaplasma marginale, has been traditionally thought of as a disease of southern cattle, but a recent survey shows that it can be found, at least occasionally, in almost every state in the U.S. Annual economic losses are estimated to be well in excess of $100 million, and it is considered to be the second or third most expensive disease to the U.S. cattle industry. It can cause deaths, lowered productivity, a drop in milk production and reproductive disorders. Preventive and curative costs can also be a significant economic factor. In addition, regulatory restrictions on cattle movement can be a burden to livestock producers.
Interstate movement of animals makes the appearance of anaplasmosis possible nationwide and anaplasmosis is often diagnosed outside of the traditional anaplasmosis endemic areas. Feeder cattle, breeding stock and dairy cows are often transported from endemic to non-endemic areas. Because of the increased risk that widespread interstate movement of animals poses, veterinarians in areas not traditionally associated with anaplasmosis should consider it as a differential diagnosis in animals showing clinical signs of disease. It might also be prudent to consider adding anaplasmosis control to any herd biosecurity measures in place.
Previous eradication efforts in endemic areas have failed. Unfortunately, because anaplasmosis does not enjoy the “glamour” status of diseases having human health implications and is not reportable, reliable detailed information on incidence is not available from USDA’s National Animal Health Monitoring System. This is unfortunate for a disease that has such tremendous real and potential negative impacts for the U.S. cattle industries.
Clinical anaplasmosis is strongly seasonal. Outbreaks are more common in the summer and autumn when there is greater arthropod activity. Winter outbreaks have been reported in states as varied geographically as Oklahoma, Illinois, Idaho and Mississippi.
Anaplasmosis is transmitted by certain tick species, horseflies, stable flies mosquitos and other biting insects. Ticks are the most important biological vector and Anaplasma can survive in certain ticks for long periods of time. Biting insects transmit the disease mechanically by transferring blood from an infected (or carrier) animal to a susceptible one. Horseflies can travel long distances and transmit anaplasmosis from neighboring herds or wildlife, allowing the disease to manifest in herds previously free of the disease.
Mechanical transmission also occurs through needles and instruments used on multiple animals for injections, castration and dehorning. Intrauterine transmission is controversial, but it may lead to fetal death and abortion or the calf becoming a life-long carrier of the disease. Late-term cows that develop clinical signs usually abort. Most outbreaks occur either when carrier animals are introduced into naïve herds or naïve animals are introduced into herds where anaplasmosis is endemic.
Any age, breed or sex of cattle is susceptible, and anaplasmosis can also infect and/or cause clincical disease in a wide range of domestic and wild ruminants. Transmission from wildlife is possible. Whitetail deer are thought to play a minor role, but mule deer in some cattle areas have significant infection rates. Bison, sheep, goats and various other domesticated, wild and zoo ruminants are also susceptible to infection and play roles in the epidemiology of the disease.
Calves born to immune or non-immune dams have innate resistance to severe clinical disease; resistance is greatest at six months of age then declines with age. Calves 6-12 months of age usually show no clinical signs or perhaps a mild form of the disease. It’s uncommon to see clinical signs in cattle 1-2 years of age, but they may develop acute, but rarely fatal, disease symptoms. Mature animals (>2 years) often have severe clinical disease and up to 50 percent of infected adult animals may die. Unless treated appropriately, animals of any age that are infected with anaplasmosis remain carriers of the disease for life, effectively becoming “Typhoid Marys” for anaplasmosis.
How it infects
In a natural infection, Anaplasma multiplies in the blood for three to five weeks after transmission, infecting more and more erythrocytes although the animal continues to appear normal. Once the infection is recognized by the immune system, organisms are removed from circulation by erythrophagocytosis, which results in a rapidly developing anemia as infected blood cells are destroyed. Anemia also results from an autoimmune response due to alterations of erythrocyte membrane by the parasite (even uninfected cells are destroyed). Opsonizing and hemagglutinating antibodies result in both infected and uninfected erythrocytes being removed by phagocytosis.
Anemia due to anaplasmosis increases over four to 15 days, and animals may lose 70 percent or more of their circulating RBC’s. Icterus develops, but not hemoglobinemia and hemoglobinuria (hemoglobinuria develops in leptospirosis). In acute clinical cases, icterus is particularly noticeable on the sclera, udder, mucous membranes of the head and perineal regions, but may be difficult to detect on dark skinned animals.
The outcome in adults is determined by the competence of the reticuloendothelial system, immunologic responsiveness of individual animals and percentage of red blood cells destroyed. As stated earlier, recovered animals become reservoirs for the disease and the source of future outbreaks unless treated.
Convalescence after patent infection is slow and may last several months, resulting in lowered production in surviving animals.
Herds with high infection rates can exist in endemic areas with little or no clinical disease being recognized. In these herds, “premunization” occurs because calves are naturally infected at a young age and become carriers, which protects them from developing clinical disease as adults.
Premunization can evolve on a herd or regional basis into “enzootic stability,” where infection rate (carrier state) is high but clinical disease incidence is low. However, disease will often occur when naïve mature cattle, such as new bulls, are introduced into a “stable” herd or if carrier animals from a “stable” herd are moved into naive herds or areas.
As herds in endemic areas strive to improve genetics and import bulls from non-endemic areas, significant problems have occurred, and there have been losses in purchased bulls that were introduced, then contracted the disease.
Premunization, using the intentional inoculation (“vaccination”) of young animals with “live” anaplasmosis organisms, has also been practiced in some endemic areas to reduce losses. It should be noted that these premunized cattle are carriers of the disease and may transmit it to susceptible animals.
Because of the “enzootic stability” phenomenum resulting from carrier status, outbreaks tend to be more severe and costly in herds or regions “free” of anaplasmosis since all mature animals are susceptible to clinical disease if it is introduced.
Most studies do not show Bos indicus breeds to be more resistant to infection than Bos taurus. However, greater resistance to insects may result in field observations to the contrary. Mature bulls of all breeds appear to be more severely affected and more likely to die if clinical signs develop.
Individual treatment should address the parasite (chemotherapy) and anemia (supportive therapy). Chemotherapy before the development of a high parasitemia is essential for a favorable prognosis, and tetracyclines are the most common drugs used. In the absence of specific treatment, recovery is dependent on rate of erythrocyte destruction and bone marrow response. Supportive care, such as blood transfusions and hematinics, is sometimes utilized, especially in valuable animals, with mixed results because of the autoimmune component of the disease.
To be effective, treatment must be administered before a critical number of red blood cells have been infected and/or destroyed. In severely anemic animals, the stress of handling may precipitate death, and the value of chemotherapy may not justify the risk of handling and stressing the animal to administer the treatment.
Prevention and control
USDA-approved vaccines for anaplasmosis (Anaplaz® and PlazVax®) have been withdrawn from the commercial market. In some states, locally-produced vaccines may be available at the discretion of animal health officials. In general, anaplasmosis vaccines have been plagued with efficacy problems and side-effects such as neonatal isoerythrolysis. Vaccinated animals react positively to some diagnostic tests, complicating interstate shipment, export and eradication efforts. In addition, vaccine-protected animals will still develop carrier status if exposed to the disease.
Attempts to control of anaplasmosis through vector (insect) control alone would be expensive and impractical, although it is an important part of an overall control program. Carrier cattle can be eliminated by testing and/or chemotherapy, but this may not be appopriate in all herds, especially if “enzootic stability” exists and the risk is high for future reinfection from neighboring herds or wildlife. (Once the carrier state is eliminated, cattle again become susceptible to clinical disease.)
Consideration should also be given to the impact of anaplasmosis status on future cattle marketing. Positive cattle may be restricted from interstate/international commerce and probably represent a significant economic liability to those selling replacement breeding animals.
Losses and clinical disease can be prevented by feeding chlortetracycline (CTC/Aureomycin) during periods of potential transmission. CTC is not cleared for use in lactating dairy cows, however. In endemic areas, low levels of CTC can be used to prevent clinical disease while still allowing “enzootic stability” to develop. Similar to vaccines, low levels of CTC prevent clinical signs and losses but still allow the protective carrier state to develop. Higher levels of the tetracyclines (multiple injections or feed additives) can be used to eliminate the carrier animals from a herd. Management is important to insure proper consumption of the feed additives to deliver an appropriate dose level to susceptible animals.
In an outbreak situation, injectable oxytetracyline (5 mg/lb bodyweight) and CTC feed additives can be administered to the entire herd to stop disease progression in animals incubating the disease and prevent further losses from clinical disease.
This information provided by Robin Falkner, DVM, Alpharma, Inc.
Clinical signs and diagnosis
Clinical signs of anaplasmosis include fever, increased heart/respiration rate, muscle weakness, watery thin blood, constipation, nervousness, anemia, inappetance, depression, drop in milk yield, dehydration and reproductive disorders.
PERACUTEINFECTIONS are the most severe form and are frequently fatal. An animal may die before icterus develops (60-80 percent of erythrocytes parasitized).
ACUTEINFECTIONS show the classical signs and animals may die within 24-96 hours. Recovery may be very slow, often taking several months, resulting in “chronic anaplasmosis.”
A tentative diagnosis can be made based on geographic region, history, clinical signs, laboratory examination of blood and post-mortem lesions. Tests for subclinical infections include:
- Direct/indirect fluorescent antibody
- Complement fixation: 90% accurate
- Capillary tube agglutination: 90% accurate
- Rapid card agglutination
- DNA probe
- Subinnoculation of blood into a splenectomized calf
Diagnosis during an acute stage can be based on clinical signs, hematologic changes and microscopic examination of stained blood smears. Animals in the incubation stages of the disease may test negative with serological methods.
Chronic or carrier stage diagnosis is more difficult because infected cattle cannot be clinically differentiated from uninfected cattle, and low parasite numbers may not be detectable microscopically. Serologic methods are necessary to detect latent infections. Animals that have been treated successfully to remove carrier status and animals vaccinated for anaplasmosis may react positively to serological testing for a year or more.
Differential diagnoses include rabies, plant toxicities, lead poisoning, sporadic bovine encephalomyelitis, pesticide poisoning, leptospirosis, chronic copper poisoning, bacillary hemoglobinuria and bacterial meningitis.