Anaplasmosis in cattle (Proceedings)

Definition/Etiology

Infectious, transmissible disease of cattle, sheep and goats.

Caused by the Rickettsial organism, Anaplasma marginale in cattle.

A. ovis in sheep/goats

Epidemiology

Most prevalent of the tick borne diseases of cattle

Has been reported in at least 40 states, and is considered endemic to certain areas of the US

Maintained in a population by the presence of a good vector and subclinical carrier animals.

Clinical Signs

Dependent upon:

Age at time of infection

Breed differences in susceptibility

Virulence of the strain

Young calves (6-9 months)

Asymptomatic to mild

Adult cattle

Severity tends to increase with increasing age

4 stages

1. Incubation – 21-45 days

2. Acute disease – signs appear when approximately 1% of red cells or greater are infected.

3. Convalescent stage – 3-4 weeks

4. Carrier stage – for life?

1. Animals are generally asymptomatic during the incubation phase.

2. Acute disease can be characterized by the following:

Fever – 103-106°F for 24-48 hrs, then drops to normal or below

Anorexia

Acute death

Drop in milk production

Lethargy

Rumen stasis

Dry muzzle

Aggressiveness – hypoxia?

Staggering gait – weakness from anemia/hypoxia

Tachycardia

Pale and/or icteric mucous membranes

Constipation with dark brown, mucus covered feces (sometimes I think it is a bronze tinge)

Dark yellow urine

(NO HEMOGLOBINURIA AS THIS IS AN EXTRAVASCULAR HEMOLYTIC EVENT)

Abortion

3. Convalescent period characterized by weight loss, icterus

4. Asymptomatic

Sheep/Goats

Often asymptomatic, but can be severe enough to cause signs similar to infection with cattle.

Clinical Pathology

PCV/total protein:

Acute phase – PCV falls dramatically within the first 24 to 48 hrs. May be as low as 6-10% upon presentation. Total protein is normal (hemolytic anemia). Organism can by detected in peripheral blood films during this phase (dif-quick stain). After anemia is present for several days, the number of organisms detected decreases and signs of regeneration are predominant (polychromasia, reticulocytosis, anisocytosis, basophilic stippling)

Carrier stage – organism is not reliably detected due to extremely low numbers present.

Serology – not reliable for acute disease, but can detect carriers.

Serum Chemistry:

Hyperbilirubinemia

Urinalysis:

Hyperbilirubinuria

Pathophysiology

Transmission occurs most commonly by Boophilus spp. or Dermacentor ssp. ticks, however, direct transfer can occur by iatrogenic means (using blood contaminated needles among animals for vaccinations, medication administration, or non-disinfected castration tools, dehorners, etc.) or mechanically by blood feeding flies. Organisms invade mature erythrocytes and replicate. Signs appear when greater than 1% of the RBC's are infected and correlate with the percentage of cells infected. The anemia is due to phagocytosis of infected red cells by the splenic and hepatic macrophages. In addition, autoantibodies are produced against the red cell surface which activates acute phase reactants and compliment. Regeneration is usually vigorous. Organisms are not completely cleared from the body due to the build up of antigenic variants. Can become re-infected (no long term immunity provided by infection), or can be diseased from an existing infection due to stress. (ie: carrier cow calves, becomes acutely diseased)

Pathology

Blood may be thin, watery in acute disease.

Pale mucous membranes, subcutaneous tissues and skeletal muscle.

Icterus may be present.

Splenomegaly (anthrax!)

NO HEMOGLOBINURIA

Finding organism in RBC's confirms diagnosis.

Treatment

Tetracycline's are the treatment of choice in acute disease.

1 to 2 treatments of LA 200 (long acting oxytetracycline) at 20 mg/kg 72 hrs apart, or 11 mg/kg once daily for 3-5 days

Blood transfusion?

PCV's of 8 or less – poor prognosis

Clearing the carrier state for exportation?

20 mg/kg q 72 hrs for 4 treatments

Some animals still won't clear it.

Try to get them cleared to become seronegative (confirm with PCR?)

Even though they may become negative on CF test, experts believe they never really "clear" the infection.

Prevention and Control

In endemic areas, it is unlikely that we can prevent re-exposure after carrier animals have been culled or cleared via tetracycline. Also, it is probably only possible to maintain negative herds in regions where infected animals are low in number and where transmission potential via vectors is low as well. There is no currently licensed vaccine available in the United States. Therefore, our best plan of attack is preventing clinical signs and reducing transmission.

Providing access to chlortetracycline containing feed or mineral mixes, or top dressing feed with this antibiotic at low levels throughout the year, or during periods of high vector activity (mid to late summer into fall) is highly effective in preventing clinical anaplasmosis. Many commercial products (Aureomycin crumbles, Anaplaz blocks) are available to provide this access. I told my producers that 1 pound of Aureo 50 (50 grams/pound) could prevent clinical anaplasmosis in 10, 1000 pound cows per day. This comes out to be 1.1 mg/kg/animal/day. This DOES NOT treat anaplasmosis or prevent infection. It is effective in preventing clinical disease. Therefore, you may have an entire herd of carrier animals but no cases of anaplasmosis. This is usually OK for commercial herds and many purebred beef herds. In herds that export or ship animals to other countries, or to states with regulations on the transport of this disease into their state, you should test them for a titer via the complement fixation test. (this test is highly specific, but not very sensitive, but is the approved test available for detecting asymptomatic animals) If they are positive, you can try clearing them with oxytetracycline as previously described. For dairies, the fact that oxytetracycline is approved for use in lactating dairy cows allows one to treat them in the acute stage. An effective vector control program is indicated in any region to control transmission.

Reference

BP Smith, Large animal internal medicine. 2002 pp. 1049-1051