Anaplasmosis

Gall sickness

 


Nature of the disease

History
Etiology
Hosts
Transmission
Key signs
Lesions
Diagnosis
Immunity
Treatment
Control
References

 

Nature of the disease

  • Anaplasmosis is an infectious, non-contagious, tick-borne hemoparasitic disease of domesticated and wild ruminants in the tropics and subtropics. Bovine anaplasmosis is caused by Anaplasma marginale and it is characterized by progressive weakness, anemia, emaciation and jaundice.

  • Anaplasma marginale, a member of the order Rickettsiales is an obligate intraerythrocytic parasite that replicates causing erythrocytic damage.

  • Once infected, the cattle tend to be carriers of A. marginale for many years if not life, and these animals can serve as a source of infection for other cattle.

  • Bovine anaplasmosis is of economic significance, the disease constrains efficient production and its costs include loss of production of sick and recovered animals, abortion and deaths in some clinical cases, and tick control costs.

  • OIE classification: list "B."

 

History and Occurrence

  • Arnold Theiler in South Africa first described the disease in 1910.

  • Anaplasmosis has a worldwide distribution particularly in tropical and subtropical regions, it also seen in some temperate areas. The disease is endemic in Africa including Egypt, South and Central America, southern Europe, the Far and Middle East, India, Russia, and Australia

 

Etiology

  • Anaplasma spp. are small, pleomorphic, coccobacillary, obligate-erythrocytic parasites belonging to the order Rickettsiales.

  • Four species are of veterinary importance; A. marginale, A. caudatum, A. centrale (cattle), and A. ovis (goats, sheep, deer). A. marginale is the most pathogenic of the Anaplasma spp. listed.

Hosts

  • Cattle and wild ruminants are the natural hosts for A. marginale. Infections have been reported in camels.

  • Cattle are also infected with A. caudatum, which may result in severe disease, and A. centrale, which generally results in mild disease.

  • Sheep, goats, and deer are the natural hosts for A.ovis that may cause mild to severe disease.

  • All cattle may become infected with A. marginale but the severity of illness increases with age. Young cattle, less than 6 months of age are susceptible but seldom show any signs of disease, they will become immune carriers protected against the anemia and clinical disease. Cattle between 6 months and 3 years of age, which become infected are at increasing risk of becoming ill and cattle infected after 3 years of age will die if not treated.

 

Transmission

  • Anaplasmosis is not contagious. Spread from animal to animal occurs chiefly by insect vectors.

  • Most transmission occurs via tick vectors through intrastadial or trans-stadial and rarely transovarial transmission. Boophilus species is the main vectors in Africa.

  • Anaplasmosis may also transmitted mechanically by bloodsucking flies and transplacental in pregnant cows.

  • Contaminated surgical instruments and hypodermic needles are known mechanical vectors.

Key signs

Bovine anaplasmosis:

  • The form of the disease including its duration and severity of signs depends on the age and the previous exposure to infection. Cattle in endemic areas, when infected they undergo inapparent or low-grade reactions whereas cattle in free areas, react severely.

  • The IP period of A. marginale ranges from 2 - 5 weeks. A low number of erythrocytes are parasitized for 5-10 days patently before the onset of fever and 10-30% and sometimes up to 65% of erythrocytes are infected at peak parasitemia and fever.

  • In most cases, the disease is subacute especially in endemic areas and in young animals in which infected animals show a transient, non-fatal illness with fluctuate fever and petechiation of the mucous membranes in a course ranged from several days to 2 weeks.

  • In acute cases, there is incomplete anorexia, depression, reduced milk yield, respiratory distress, rapid pulse, and loss of coordination are usually evident in the late stages. Petechial hemorrhages occur on mucous membranes that appear pale and icteric later in the course of the disease. Normal discharges and faeces may be bloodstained. The urine may be brown without hemoglobinuria. Pregnant cows may abort. Death can occur within several days but many survive and enter a chronic form. Surviving cattle convalesce over several weeks, during which hematological parameters gradually return to normal.

  • The chronic disease may follow an acute form and may persist for several months and often lose their condition.

  • Recently imported cattle to endemic areas often develop a peracute form in which most infected cattle collapse and die within four days.

Ovine and caprine anaplasmosis:

  • A.ovis is more severe in goats than in sheep. Overt clinical signs and mortality is rare and recovered cases remain persistent carriers.

lesions

  • The carcasses of cattle that die from peracute anaplasmosis are in good condition, whereas carcasses of cattle that die after chronic illness are generally markedly anemic and jaundiced.

  • Blood is thin and watery.

  • ُEdema and lymphoid hyperplasia are often present.

  • Epicardial and pericardial petechiae and ecchymoses are often present.

  • The spleen is characteristically enlarged and soft. The splenic pulp is dark in colour.

  • The liver may be mottled and yellow-orange. The gallbladder is often distended and contains thick brown or green bile.

 

Diagnosis

  • A tentative diagnosis of acute anaplasmosis can be made on the bases of history, clinical, pathological, and epidemiological features.

  • Samples and specimens:

  • Blood in anticoagulant should also be obtained for hematologic testing.

  • Acute and convalescent sera for serological studies.

  • At necropsy, thin blood films of liver, kidney, spleen, lungs, and peripheral blood should be prepared for microscopical examination.

  • Detection of Anaplasma spp. in blood smears stained with Giemsa stain or Differential Quick stain is critical to confirm diagnosis of acute cases. It appears as polymorphic coccobacillary bodies, 0.2-1.0 mm in diameter that stains bluish purple.

  • Chronically infected carriers are difficult to confirm by Giemsa-stained blood films and may be identified by either complement fixation, card agglutination tests, IFA, PCR, dot-ELISA, and DNA-based detection methods can be also used.

  • Hematological changes include significant decreases in erythrocyte count, hematocrit, and hemoglobin concentration.

  • Differential diagnosis: anaplasmosis may be confused with other diseases such as anthrax, haemorrhagic septicaemia, acute trypansomiasis, acute babesiosis, and other conditions that result in anemia and jaundice, such as leptospirosis and theileriosis

  Immunity

  • Resistance to reinfection is attributed to both humoral and cell-mediated immune mechanisms but does not prevent relapses following stress.

 

Treatment

  • The tetracyclines and imidocarb are currently used for treatment. The most effective time to treat is during the IP when tetracyclines prevent disease.

  • Blood transfusion greatly improves the survival rate of more severely affected cattle.

  • Prompt administration of tetracycline, chlortetracycline, or oxytetracycline in the early stages of acute disease usually ensures survival. A commonly used treatment consists of a single IM injection of long-acting oxytetracycline at 20 mg/kg or 6-10 mg/kgm BW dialy for 3 days. The carrier state may be eliminated by administration of a long-acting oxytetracycline preparation (20 mg/kg, IM), at least two injections with a 1-wk interval.

  • Imidocarb is also highly efficacious against A. marginale as a single injection as the dihydrochloride salt at 1.5 mg/kg, SC. Elimination of the carrier state requires the use of higher repeated doses (5 mg/kg, IM or SC, two injections of the dihydrochloride salt 2 wk apart).

  • To stop or prevent an outbreak a temporary protection in the face of an exposure risk can be achieved by a single IM injection of long-acting oxytetracycline at 20 mg/kg. Prolonged protection can be achieved by a single IM injection of long-acting oxytetracycline at 20 mg/kg every 28 days or by chlortetracycline in the feed at 1.1mg/ kgm BW daily for at least 60 days.

 

Prevention and control measure

  • Eradication of anaplasmosis is very difficult because of the diversity of vectors.

  • Control programs in endemic areas are aimed only to limit outbreaks and to restrict the spread of disease. The control program should be based on; the control of tick and other vectors by periodic spraying and dipping, prevention of iatrogenic transmissions, vaccination of susceptible animals prior adding to the herd and limiting the introductions to animals less than two years, and increasing the resistance of the population by immunization.

  • Vaccination: Most control programs in enzootic areas are based on increasing the resistance of the population by immunization. The most effective vaccines are:

  • Live attenuated A. marginale ovine-origin vaccine are available gives good protection.

  • living A. centrale, which causes mild inapparent disease.

  • killed A. marginale vaccine, has lower protectivity and needs two injections at least 4 - 6 weeks apart.

References

  1. Bron, C.G.D.; Hunter, A.G. and Luckins, A.G.(1992): "Diseases caused by Protozoa in:  "Handbook on Animal Diseases in the tropics" (Sewell, M. M. H., and Brocklesby, D. W., eds) 4 th Edit. Bailliere Tindall, London, Philadelphia, Tokyo.

  2. El Sawalhy, A. A. (1999): "Veterinary Infectious Diseases" 2nd Edit. Ahram Distribution Agency, Egypt.

  3. Kuttler, K.L. (1984): "Anaplasma infections in wild and domestic ruminants ". A review J. of wild life diseases, 20:12-20.

  4. Losos, G.J. (1986): "Protozoal diseases in Infectious tropical diseases of demostic animals ". longman Scientific & Technical longman Group UK. limited. 

  5. Munz, E. and Dumbell, K.. (1994): "Anaplasmosis In: Infectious Diseases of Livestock with special reference to Southern Africa. Volume I (Coetzer, J. H. W.; Thomson, G. R. and Tustin, R. C.), Chapter 53 pp. 613-615. CAPE Tow, Oxford, New York, Oxford University Press

  6.  Radostits, O.M.; Gay, C.C.; Blood, D.C. and Hinchcliff, K.W. (2000): "Veterinary Medicine A textbook of the diseases of cattle, sheep, pigs, goats and horses".9th Edit.W. B. Saunders Company Ltd. London, New York, Philadelphia, San Francisco St Louis, Sydney.