Anaplasmosis is caused by a rickettsia called Anaplasma marginale or A. centrale of which A. marginale is the most virulent.

Distribution + Spread:

This is dependant on the vector carrying the disease ie. ticks Boophilus decoloratus + B. microplus (blue tick species) (see attached distribution map), another couple of tick species, biting flies (esp. in high density populations such as dairies), intra uterine and iatrogenic (eg. use of contaminated needles).


By blood smear.

Incubation period:

3 – 6 wks related to:

  • parasite dose injected during infection
  • route of infection


  1. Peracute: This occurs in highly susceptible adult stock and animals die almost without notice. They show a very high parasitaemia on blood smear.
  2. Acute: This is the most common form:
    • milkdrop
    • 40 – 41 temp.
    • anaemia
    • panting
    • constipation
    • jaundice
    • depression
    • rumen stasis
    • death

    Parasites drop drastically in number on bloodsmear and regeneration of red blood cells is seen.

  3. Chronic: This may develop after the acute form and leads to emaciation.


Once parasites invade the red blood cells anaemia develops rapidly.  Parasites alter the red blood cell making it antigenic to the host leading to auto antibody formation and autoimmune anaemia.  The anaemia also leads to secondary liver damage and thus jaundice.  Recovery takes 1 – 3 months.


The earlier the disease is detected and treated the better the prognosis.  Once severe anaemia and/or jaundice has set in the prognosis is poor.  The severity of anaplasmosis is generally age related:

  • 0 – 1 yrs: usually subclinical disease
  • 1 – 2 yrs: moderate disease
  • > 2 yrs: often severe

Source of infection:

  1. Vectors eg. ticks, flies, contaminated needles.
  2. Diseased animals in close contact with susceptible animals.
  3. Carrier cows that developed their status as calves.
  4. Antelope eg. blesbuck that serve as resevoir hosts.
  5. Introduction of contaminated animals into clean herds.


  • Young animals are naturally resistant.
  • Animals that were diseased and survive develop premunity and are immune for 4 – 5 yrs.
  • Regular exposure can lead to life long immunity.
  • Carrier animals that have been sterilized by treatment remain immune for +/- 3 yrs.
  • Subclinically infected calves can become life-long carriers.
  • Calves infected intra-uterine may either become ill or not and may develop into carriers.


  1. Two to three injections of short acting Tetracycline at 10mg/kg @ 24 hrs.
  2. One injection of longacting Tetracycline 20mg/kg.
  3. One injection of Forray 65 at 3mg/kg.
  4. Supportive treatment:
  5. Support for liver, rumen stimulants, haematinics, blood transfusions, good quality food.


  • Ticks:
    • Calves < 9 months of age should be exposed to enough ticks to infect calves naturally and thus cause premunity (but obviously not too many to cause tick worry).
    • With minimal or zero exposure to ticks at a young age calves remain 100% susceptible and need to be vaccinated.
  • Biting flies:
    These are difficult to control but in feedlots and dairies control should be as good as possible.
  • Vaccination:
    • This is a blood vaccine and contains A.centrale which provides good cross-immunity to A.marginale: 2ml/i.m.
    • The best age to vaccinate is about 6 months of age as minimal reaction occurs.
    • Reactions can be expected from 4-6 wks post vaccination and are treated with tetracyclines or all vaccinated animals can be blocked with tetracyclines 5-6 wks after vaccination.
    • Cows more than 5 months pregnant should not be vaccinated.
    • Older animals often show reactions.

Controlling outbreaks:

  • Isolate sick animals and treat them.
  • Prevent transmission by use of contaminated needles.
  • Prevent transmission by biting flies.
  • Control the vectors.
  • Observe other animals.
  • Introduce a calf vaccination program.


We live in an endemic area for anaplasma which means that there should be a relatively good natural immunity in most animals that are exposed to ticks at an early age. An outbreak can be caused by the following reasons:

  • Some calves are susceptible when introduced into the herd.
  • Low tick loads are maintained which mean certain animals may go for years without any contact to anaplama which maintains their susceptibility.
  • Some adult cows may loose their immunity due to lack of exposure.
  • Some animals may loose their sterile immunity.
  • In dry years i.e. fewer ticks herd immunity drops making the next wet year i.e. more ticks a recipe for disaster.


Animals can originate from:

  • calves that had no tick exposure and are 100% susceptible
  • cows that have not been naturally exposed regularly i.e. kept too tick free and have lost their immunity
  • animals that have been treated, developed sterile immunity and have become susceptible +/- 3 years later
  • new susceptible animals that have been introduced to the herd
  • high stress levels that comprimise immunity
  • (life-long carrier status develops in infected calves < 6m old that never develop disease, making them a permanent source of infection)

In principle a decision needs to be made based on herd immunity:  either there needs to be regular controlled tick exposure to stimulate immunity (practical solution) or ticks need to be destroyed 100% leaving vulnerable susceptible animals (an impracticable and impractical solution in an endemic area).

The solution in our opinion lies in introducing calves into the herd with good immunity (i.e. from vaccination and/or tick exposure) and limited tick control in older animals to re-stimulate immunity regularly.  This is a long-term outlook.

In the short-term the solution must lie in treating diseased animals, controlling spread via biting flies, needles and ticks by isolating diseased animals and good observation in susceptible groups.