Selected content from the Animal Health and Production Compendium (© CAB International 2013). Distributed under license by African Union – Interafrican Bureau for Animal Resources.
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Identity Pathogen/s Overview Distribution Distribution Map for Africa Distribution Table for Africa Hosts/Species Affected Host Animals Systems Affected Epidemiology Impact : Economic Zoonoses and Food Safety Pathology Diagnosis Disease Course Disease Treatment Table Disease Treatment Vaccines Prevention and Control References Links to Websites OIE Reference Experts and Laboratories
Preferred Scientific Name
International Common Names
anaplasma bovis in cattle
Anaplasmosis is a disease of ruminants caused by obligate intraerythrocytic parasites of the order Rickettsiales, family Anaplasmataceae (Ristic and Kreier, 1984). Cattle, sheep, goats, deer, antelope, giraffes and buffalo may be infected. Anaplasma marginale is the causative agent in cattle and wild ruminants and Anaplasma ovis in sheep and goats.
Anaplasma centrale causes mild anaplasmosis in cattle and was originally isolated in Africa, but is now widely used as an immunizing agent for cattle (Theiler, 1912). Appendages associated with the Anaplasma body have been observed in certain isolates (Kreier and Ristic, 1963) and this parasite has been named Anaplasma caudatum, but its status as a valid species is questionable. Anaplasma mesaeterum is closely related to A ovis and may also cause disease in sheep and goats, however it appears to be less pathogenic for goats (Uilenberg et al., 1979; Nakamura et al., 1993).
Despite widespread distribution and severe losses, effective control of anaplasmosis has not been achieved on a sustainable basis in most affected areas.
This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's WAHID database on disease occurrence. Please see the AHPC library for further information on this disease from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.
Anaplasmosis occurs in tropical and subtropical regions worldwide (approximately 40o N to 32o S), including South and Central America, the USA, southern Europe, Africa, Asia and Australia. It is transmitted by a diverse group of biological and mechanical vectors and is endemic in tropical and subtropical areas that support these vectors, with sporadic distribution in temperate climate areas.
For current information on disease incidence, see OIE's WAHID Interface.
Anaplasmosis was reported to AU-IBAR by 14 countries in Africa in 2011 (AU-IBAR, 2011). During 2011, 983 outbreaks were recorded involving 872 deaths. The highest number of outbreaks were reported by Zimbabwe (533), followed by Zambia (100) and Kenya (88). The geographical distribution of the disease shows that it was mainly recorded in the southern parts of the continent.
Countries reporting anaplasmosis to AU-IBAR in 2011:
= Present, no further details = Widespread = Localised
= Confined and subject to quarantine = Occasional or few reports
= Evidence of pathogen = Last reported... = Presence unconfirmed
|The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further information for individual references may be available in the Animal Health and Production Compendium. A table for worldwide distribution can also be found in the Animal Health and Production Compendium.|
|Country||Distribution||Last Reported||Origin||First Reported||Invasive||References||Notes|
|Algeria||No information available||OIE, 2012|
|Angola||Reported present or known to be present||OIE, 2012|
|Benin||OIE, 2012; Pangui & Salifou, 1992|
|Reported present or known to be present||OIE, 2012; Carmichael & Hobday, 1975; Fanikiso & Ndzinge, 1992; OIE Handistatus, 2005|
|Burkina Faso||No information available||Belem et al., 1994; OIE, 2012|
|Burundi||Reported present or known to be present||OIE, 2012|
|Cameroon||No information available||Verhulst et al., 1983; Ndi et al., 1991; Chollet, 1995; OIE, 2012|
|Cape Verde||Disease never reported||OIE, 2012|
|Central African Republic||Reported present or known to be present||OIE, 2012|
|Chad||No information available||OIE, 2012|
|Comoros||Present, no further details||AU-IBAR, 2011|
|Congo Democratic Republic||No information available||Ndahiriwe et al., 1994; OIE, 2012|
|Côte d'Ivoire||Reported present or known to be present||Office International des Epizooties1999; OIE, 2012|
|Djibouti||Disease not reported||OIE, 2012|
|Egypt||Reported present or known to be present||El-Seify & Eissa, 1990; OIE, 2012|
|Equatorial Guinea||No information available||OIE, 2012||Disease suspected|
|Eritrea||Reported present or known to be present||Office International des Epizooties1999; OIE, 2012|
|Ethiopia||Present, no further details||2002||Mekonnen et al., 1992; Yilma et al., 1995; Solomon et al., 1998; OIE, 2012|
|Gambia||Present||Mattioli et al., 1993; Mattioli et al., 1997|
|Ghana||Disease not reported||OIE, 2012|
|Guinea||Reported present or known to be present||OIE, 2012|
|Guinea-Bissau||No information available||Rosa et al., 1998; OIE, 2012|
|Kenya||Reported present or known to be present||Ndarathi et al., 1989; Deem et al., 1993; Latif et al., 1995; Ndung'u et al., 1995; Gitau et al., 1997; OIE, 2012|
|Libya||Last reported||2009||OIE, 2012|
|Madagascar||Reported present or known to be present||Office International des Epizooties1999; OIE, 2012|
|Malawi||Reported present or known to be present||Lawrence et al., 1996; Tjornehoj et al., 1997; OIE, 2012|
|Mali||No information available||OIE, 2012|
|Mauritius||Last reported||2001||Office International des Epizooties1999; OIE, 2012|
|Morocco||No information available||Verhulst et al., 1983; Sahibi et al., 1998; OIE, 2012|
|Mozambique||Reported present or known to be present||Office International des Epizooties1999; OIE, 2012|
|Namibia||Reported present or known to be present||Office International des Epizooties1999; OIE, 2012|
|Niger||No information available||OIE, 2012|
|Nigeria||Reported present or known to be present||Akinboade & Dipeolu, 1984; Ajayi & Dipeolu, 1986; Akinboade et al., 1986; Ilemobade, 1992; Egbe-Nwiyi et al., 1997; OIE, 2012|
|Réunion||Reported present or known to be present||Poulin et al., 1991; Office International des Epizooties1999; OIE, 2012|
|Rwanda||Reported present or known to be present||Kabagambe et al., 1988; OIE, 2012|
|Sao Tome and Principe||Last reported||1991||OIE, 2012|
|Senegal||Reported present or known to be present||OIE, 2012|
|Seychelles||Disease not reported||Office International des Epizooties1999; OIE, 2012|
|Somalia||Present, no further details||Schoepf et al., 1984; OIE, 2012|
|South Africa||Present, no further details||Potgieter, 1979; Barry & Niekerk, 1990; Dreyer et al., 1998; OIE, 2012|
|Sudan||Reported present or known to be present||Osman, 1997; OIE, 2012|
|Swaziland||Reported present or known to be present||Office International des Epizooties1999; OIE, 2012|
|Tanzania||Reported present or known to be present||Office International des Epizooties1999; OIE, 2012|
|- Zanzibar||Present||Woodford et al., 1988|
|Togo||No information available||OIE, 2012|
|Tunisia||CAB Abstracts data mining||Office International des Epizooties1999; OIE, 2012|
|Uganda||Present, no further details||Ssenyonga et al., 1991; Ssenyonga et al., 1992; Office International des Epizooties1999; OIE, 2012|
|Zambia||Reported present or known to be present||Jongejan et al., 1988; Ahmadu et al., 1997; OIE, 2012|
|Zimbabwe||Reported present or known to be present||Norval et al., 1984; Lawrence & Norval, 1987; OIE, 2012|
Use of Bos indicus cattle as a means of controlling cattle ticks and tick borne diseases has been advocated for many years. The evidence on the relative susceptibility of Bos taurus and Bos indicus cattle to infection by A. marginale is complicated by variation in resistance of individuals within breeds of both species (Callow, 1984).
Some studies (Parker et al., 1985; Bock et al., 1997) found Bos indicus cattle to be marginally more resistant to disease than Bos taurus cattle. However others have reported no difference in susceptibility to A. marginale of Bos taurus and Bos indicus crossbred cattle (½ to ¾ Bos indicus) (Otim et al., 1980; Wilson et al., 1980) or Bos indicus and Bos indicus crossbred cattle (Bock et al., 1999). It is apparent that A. marginale can be a significant cause of disease in any breed, but the resistance of Bos indicus cattle to the tick vectors could reduce the rate of transmission in some circumstances.
Calves from immune mothers receive partial protection from the colostral-derived antibody (Corrier and Guzman, 1977). This protection lasts about 3 months and, in most cases, is followed by an age resistance, which lasts until the animals are about 9 to 12 months old (Jones et al., 1968; Paull et al., 1980). Calves exposed to anaplasmosis when the maternal or age resistance is high, rarely show clinical symptoms but develop a solid, long-lasting immunity. It is therefore possible to have both A. marginale and vectors present on a property without animal losses or clinical disease. This situation is known as endemic stability.
If cattle are not exposed to A. marginale as calves, the age resistance gradually wanes and these animals will become increasingly susceptible to the disease. If these susceptible adult cattle are mixed with infected cattle in the presence of a vector, serious losses due to anaplasmosis can occur.
Cattle that recover from anaplasmosis remain persistent carriers of the organism and are usually immune to further disease particularly from homologous challenge. Persistent infections are characterized by sequential rickettsaemic cycles occurring at 6 to 8 week intervals and this is fundamental to continued reinfection of vectors and thus transmission (Palmer et al., 1999).
Unlike the situation in bovine anaplasmosis, there appears to be no marked age susceptibility to A ovis infection in sheep and goats. Both young and adult animals usually develop only a mild form of the disease although various stress factors can exacerbate this in individual cases (Stoltsz, 1994).
Immune-compromized animals whether by splenectomy or treatment with immunosuppressants, such as cyclophosphamide and corticosteroids, have been shown experimentally to be susceptible to heterologous challenge (Kuttler et al., 1984). It has also been suggested that the immunity of cattle could be compromised under conditions of environmental stress or other stressors (Kuttler et al., 1984), however, Wilson (Wilson, 1979) showed that cattle on a good plane of nutrition developed more severe primary Anaplasma reactions than ones on a starvation ration.
Mixing cattle from different regions, migration of wildlife carriers and seasonal increases in vector activity can also facilitate transmission especially in temperate climates.
|Bos indicus (zebu)||Domesticated host|
|Bos taurus (cattle)||Domesticated host|
|Bubalus bubalis (buffalo)||Wild host|
|Capra hircus (goats)||Domesticated host, Wild host|
|Giraffa camelopardalis||Wild host|
|Ovis aries (sheep)||Domesticated host|
Blood and Circulatory System - Large Ruminants
Blood and Circulatory System - Small Ruminants
Digestive - Large Ruminants
Digestive - Small Ruminants
The complete development cycle of A. marginale in the vertebrate host occurs in mature erythrocytes. When infected erythrocytes are disrupted, initial bodies are released to invade other erythrocytes by invagination of their cytoplasmic membranes to form vacuoles containing organisms. The initial bodies then undergoes a series of binary fissions to form structures, known as inclusion bodies, which are made up of between four and eight initial bodies (Ristic, 1981).
Anaplasmosis is not contagious and most transmission occurs via ticks with over 20 species being incriminated worldwide as biological vectors (Kocan, 1995). However experimental demonstration of vector competence does not necessarily imply a role in transmission in the field. Any stage of the tick's life cycle can become infected after feeding on an animal carrying Anaplasma organisms in its blood stream.
After feeding on an infected animal the organism undergoes a complex development cycle in the gut cells of ticks and the final infective stage is present in the salivary glands (Kocan et al., 1992; Kocan et al., 1993). Transmission mainly takes place trans-stadially or intrastadially via interhost transfer of ticks (Potgieter and Stoltsz, 1994). The few reported cases of trans-ovarial transmission by ticks reported in the literature are generally regarded as being exceptional (Potgieter and Stoltsz, 1994). The male tick is more mobile and lives longer than other stages, so it is thought to be the most likely stage to transmit the disease (Stiller and Coan, 1995). Male Dermacentor andersoni can act as effective vectors for at least 120 days (Stiller and Coan, 1995). Because an infected stage of the tick must transfer to a susceptible animal, it is considered necessary to have Anaplasma infected animals in close contact with susceptible animals for transmission to occur.
Transmission by biting dipterans is considered to be important in parts of the USA (Kuttler, 1979), but less important elsewhere (Rogers and Shiels, 1979; Potgieter and Stoltsz, 1994). There appears to be no developmental cycle of Anaplasma spp. in biting dipterans (Roberts and Love, 1977; Foil, 1989). The rickettsia remain viable and infective in arthropods for at least 2 to 3 days after ingestion, but it is believed that successful mechanical transmission can only be achieved where there is minimal time lapse (a few minutes) between consecutive feeds (Potgieter and Stoltsz, 1994).
Trans-placental transmission occurs and is probably underestimated (Zaugg, 1987; Potgieter and Stoltsz, 1994; Barry and Niekerk, 1990). It is usually associated with infection of the dam in the second or third trimester of gestation. Anaplasmosis may also be spread through blood transfer on contaminated needles, dehorning, castration or other surgical instruments (iatrogenic transmission) unless care is taken to clean instruments between use on each animal (Ristic, 1968; Hungerford and Smith, 1997; Abdala et al., 1998).
The impact of anaplasmosis on production is affected by the intensity of the production system. Impact is smaller under low input-low output production methods than under more intensive systems. Estimates of total cost are most useful if the disease is eradicable and for most countries where Anaplasma is endemic this is not feasible. When comparing the costs of using/developing a control technique or strategy to expected benefits a number of factors need considering. These include opportunity costs, feasibility, adoption rate, impacts on wider benefits such as lost potential, acaricide resistance, residues, environmental pollution and market effects (Perry and Randolph, 1999). Such wide reaching economic estimates are not available for anaplasmosis so the cost will usually be underestimated.
Anaplasmosis is often associated with other tick borne diseases so one control technique (e.g. use of acaricides) may prevent several diseases. Also fluctuating vector populations can lead to varying levels of natural immunity so the susceptible population is often difficult to estimate. Therefore any form of control in local resistant livestock is not always cost-effective, whereas intensive and expensive control measures are often required for valuable exotic breeds.
In the USA where bovine anaplasmosis costs are not complicated by other haemoparasites the annual loss of 50,000 to 100,000 head of cattle was estimated in 1986 at US $300 million (Palmer, 1989). More specifically, in 1983 it was estimated that the annual cost of treatment and prevention of bovine anaplasmosis, losses in milk production and deaths or culling were valued at US $0.5 million in the Red River Plains and south-east areas of Louisiana (Morley and Hugh-Jones, 1989).
Using a disease prediction-vaccination model (Ramsay, 1997), annual A. centrale vaccination of Bos indicus and Bos indicus cross Bos taurus weaners in a representative beef herd in north west Queensland, Australia was estimated to yield a benefit to cost ratio over 8 years in the range of four to 22 and seven to 39, respectively (Bock et al., 1999). The range depended on the estimated annual seroprevalence of Anaplasma in yearling cattle in the herd.
Anaplasma spp. poses no known zoonotic or food safety problems.
Animals that die of anaplasmosis are generally emaciated, very anaemic and jaundiced. Blood is thin and watery and the spleen is enlarged with soft pulp. The liver may be mottled and yellow-orange and the gall bladder is often enlarged and contains thick brown or green bile. The kidneys are congested and there may be myocardial haemorrhages. There are serous effusions in body cavities, pulmonary oedema and often evidence of severe gastrointestinal stasis especially of the rumen, omasum and colon. The omasal contents are dry and impacted, and the colon contains hard, dry, often bile stained faecal balls. The urine is yellow to dark brown due to the presence of bilirubin and there is a variable degree of red marrow hyperplasia in the long bones (Potgieter and Stoltsz, 1994).
Histological changes in parenchymal organs characteristic of anaemic and hypoxic states may be seen in various organs. There is centrilobular degeneration and necrosis of varying intensity in the liver, with distension of the liver canaliculi due to bile stasis. Also varying degrees of degeneration, necrosis and pigmentation of the tubule cells of the kidneys. There is evidence of haemosiderosis and erythrophagocytosis by the reticulo endothelial system (especially the spleen) and the red bone marrow is usually hyperplastic, but in chronic cases may show signs of depletion (Potgieter and Stoltsz, 1994; Stoltsz, 1994).
History, clinical signs and post-mortem lesions are often suggestive of anaplasmosis, but microscopical identity of the agent in thin blood films stained with either Giemsa or proprietary stains is required for an accurate diagnosis (Wright and Leatch, 1996). To ensure a diagnosis, scrupulously clean, thin blood films on grease free glass slides should be prepared and stained with a batch of stain that does not precipitate out onto the smear during staining (Callow, 1984). A positive result is usually reported as being significant for bovine anaplasmosis if more than 5% of red blood cells are infected, or where the infection is accompanied by marked anaemic changes of the cells. Badly degenerated babesia or theileria parasites can resemble Anaplasma spp. Organ smears are often unsuitable for diagnosis of Anaplasma spp. because small pieces of tissue debris can look like anaplasms.
Erythrocyte count, packed cell volume and haemoglobin values are all severely depressed. Macrocytic anaemia with circulating reticulocytes may be present late in the disease. There is moderate aniscytosis, slight polychromasia, and an increase in unconjugated bilirubin in the serum.
The clinical signs of anaplasmosis are non-specific and laboratory support is needed to confirm a diagnosis.
Anaplasmosis is commonly confused with babesiosis, as many of the epidemiological features are similar. Haemoglobinuria is a distinguishing feature of babesiosis, but is not always present in the early stages of Babesia bovis infection.
Anaemia and progressive weight loss are also clinical signs associated with Trypanosoma spp. infections. Trypanosomiasis in Africa (nagana), generally occurs within well defined, tsetse-infested areas (Potgieter and Stoltsz, 1994).
Some forms of theileriosis should be differentiated from anaplasmosis, and are usually associated with enlarged lymph nodes and the microscopic presence of schizonts in lymph node biopsy smears (Potgieter and Stoltsz, 1994).
Anaemia and icterus may be encountered in cattle suffering from leptospirosis, post-parturient haemoglobinuria, chronic copper poisoning and intoxications with Brassica and Allium spp. In these conditions haemoglobinaemia and haemoglobinuria are present. Causes of hepatotoxicity, such as Lantana camara and Microcystis aeruginosa poisoning in which icterus is one of the principal signs, should also be considered (Potgieter and Stoltsz, 1994).
Changes in behaviour, such as aggression are occasionally manifested in anaplasmosis and need to be differentiated from diseases like heartwater, cerebral babesiosis and cerebral theileriosis, rabies as well as conditions such as lead poisoning.
Sheep and Goats
Many of the differential diagnoses listed for cattle also need to be considered for sheep and goats.
Ehlichiosis, eperythrozoonosis and verminosis (eg haemonchosis) need also to be considered and may occur concurrently.
Wright and Leatch (1996) give a review of diagnostic techniques available for anaplasmosis. Chronically infected carriers may be detected with a fair degree of accuracy by serological testing, but most tests fail to distinguish between species.
The complement fixation test is currently the standard international test for detection of carrier animals for movement controls, but it lacks sensitivity. In a comparison of the indirect fluorescent antibody test, card agglutination tests and the complement fixation test, Gonzalez et al. (1978) found the sensitivity to be 97%, 84% and 79%, respectively while the specificity was 90%, 98% and 100%, respectively.
A recombinant MSP-5 competitive inhibition A. marginale ELISA (McGuire et al., 1991; Knowles et al., 1996; Torioni de Echaide et al., 1998) was recently compared with the card agglutination test and the sensitivity was 98.0%, and 98.0%, and the specificity 99.5% and 98.6%, respectively (Molloy et al., 1999). This ELISA is therefore a useful alternative to the card agglutination test, but reagents are expensive and it requires much more sophisticated laboratory facilities than the card agglutination test.
The sub-inoculation of blood from suspected carrier animals into naïve splenectomized animals (Wright and Leatch, 1996) is a very sensitive method to detect carriers, but too expensive for routine use. DNA-based detection methods are being developed but at this stage are restricted to research use (Gale et al., 1996; Wu et al., 1997; Torioni de Echaide et al., 1998).
Immunology of disease
The protective immune mechanism for anaplasma is not fully understood nor is the mechanism for establishment of persistent infection in the face of an immune response. Cattle that have recovered from acute infection or been immunized with vaccines are solidly protected against challenge with the homologous A. marginale strain, but protection against acute rickettsaemia after challenge with heterologous strains is variable and partial (Palmer et al., 1999). Although antibody alone is not sufficient for protection it is proposed that it provides specificity for macrophage phagocytosis of infected erythrocytes (Palmer et al., 1999).
The number of infected erythrocytes doubles every 24 to 48 hours and the infection is patent within 2 to 8 weeks after infection (Richey and Palmer, 1990), the time influenced by the initial challenge dose (Gale et al., 1996). Connell (Connell and Hall, 1972; Connell, 1974) showed that the prepatent period averaged 27 and 44 days following intrastadial and transstadial transmission by B. microplus, respectively. When transmission is iatrogenic or by biting insects, the prepatent period would be expected to be long, because of the usually low infective dose (Ristic, 1968). Davis et al. (1970) put 0.25 ml of A. marginale infected blood under the lower lid of both eyes in four calves, each of which developed a patent, A. marginale infection, which peaked in 40, 69, 78 and 144 days.
Generally, 10 to 30% of erythrocytes are infected at peak parasitaemia although it can be as high as 90%. Extensive erythrophagocytosis in the reticular endothelial system, initiated by parasite induced red blood cell damage, leads to anaemia (Potgieter and Stoltsz, 1994). This also leads to the release of acute phase inflammatory reactants and consequent development of fever (Radostits et al., 1999). In addition, antibodies produced against the infected and altered erythrocytes sensitize them, thus aiding their removal by the reticular endothelial system. The discrepancy between the number of infected erythrocytes and losses of up to 70% of circulating erythrocytes can probably be explained by an auto-immune mechanism whereby normal erythrocytes are also removed (Potgieter and Stoltsz, 1994). Maximum anaemia develops 1 to 6 days after peak parasitaemia and convalescence usually lasts 1 to 2 months.
The severity of symptoms is age related, but acutely affected animals will show rapid loss of weight, transient fever (40 to 41oC at peak parasitaemia), weakness and respiratory distress, particularly after exercise. There is also depression, loss of appetite and pale mucous membranes (anaemia) followed by jaundice. The urine is often brown due to bile pigments, but not red as in babesiosis. Pregnant cows may abort.
Losses during an outbreak can be as high as 20 to 50%, although a mortality rate of 5 to 10% in newly infected herds is more common. In persistently infected herds, mortalities of 1 to 2% each year are common if control procedures are not instituted.
The pathogenesis of ovine anaplasmosis is very similar to that of bovine anaplasmosis, but parasitaemias are usually lower, reaching 0.1 to 4% in sheep and 1 to 12% in goats (Stoltsz, 1994).
|Drug||Dosage, administration and withdrawal times||Life stages||Adverse affects||Drug resistance||Type|
|Anaplasma centrale||Prepared from blood of infected splenectomized calves. Chilled or Frozen forms. Administered as a single vaccination.||All Stages||Can cause severe clinical reactions. Risk of contamination with pathogens unless high standards applied.||No||Vaccine|
|doxycycline||10 mg/kg intramuscularly daily for 3-5 days. Seek veterinary advice before using.||All Stages||No||Drug|
|imidocarb diproprionate||3 mg/kg subcutaneously once only. Not registered for use in some countries. Seek veterinary advice before use and always follow maufacturers instructions.||All Stages||No||Drug|
|inactivated Anaplasma marginale vaccine||2 doses 4 weeks apart with annual booster. Withdrawn in 1998.||All Stages||May cause neonatal isoerthrolysis in calves from some vaccinated Dams.||No||Vaccine|
|killed Anaplasma marginale vaccine||2 doses 4 weeks apart with annual booster. Withdrawn in 1998.||All Stages||No||Vaccine|
|Louisiana State University experimental vaccine||2 doses given 4 weeks apart, with yearly booster. Given subcutaneously. Vaccine does not prevent infection but aids in prevention or reduction in the severity.||All Stages||No||Vaccine|
|minocycline||10 mg/kg intramuscularly daily for 3-5 days. Seek veterinary advice before using.||All Stages||No||Drug|
|modified live ovine Anaplasma marginale vaccine||2 ml intramuscularly in a single dose. No longer available outside California, USA.||All Stages||May have severe clinical reactions especially in cattle over 2 years of age. Risk of contamination with pathogens unless high standards applied.||No||Vaccine|
|oxytetracycline||Long acting: 20mg/kg intramuscularly in a single dose. Short acting: 10mg/kg intramuscularly or intravenously daily for 3-5 days. Always seek veterinary advice prior to use.||All Stages/All Stages||Products containing povidone as a carrier can cause anaphylaxis.||No||Drug|
|rolitetracycline||10 mg/kg intramuscularly daily for 3-5 days. Seek veterinary advice before using.||All Stages||No||Drug|
|tetracycline||10mg/kg intramuscularly or intravenously daily for 3-5 days. Registered withdrawal times vary. Seek veterinary advice before use.||All Stages||No||Drug|
Treatment of anaplasmosis can be with oxytetracycline at 6 to 10 mg/kg body weight daily for 3 to 5 days, or a single injection of long-acting oxytetracycline at a dose of 20 mg/kg intramuscularly (Rogers and Shiels, 1979; Stewart et al., 1979). Imidocarb dipropionate as a single injection at 3mg/kg body weight is also highly efficacious for bovine anaplasmosis and does not interfere with acquired immunity (Vos et al., 1987), but is not approved for use in some countries.
Prompt treatment in the early stages (PCV > 15%) of acute disease usually ensures survival, but severely infected animals may die in spite of treatment. Symptomatic treatments such as blood transfusions, administration of haematonics, tonics and fluids as well as appetite stimulants, rumenotonics and mild laxatives may also be beneficial (Stoltsz, 1994).
|Vaccine||Dosage, Administration and Withdrawal Times||Life Stages||Adverse Affects|
|Anaplasma centrale||Prepared from blood of infected splenectomized calves. Chilled or Frozen forms. Administered as a single vaccination.||-Cattle & Buffaloes: All Stages||Can cause severe clinical reactions. Risk of contamination with pathogens unless high standards applied.|
|inactivated Anaplasma marginale vaccine||2 doses 4 weeks apart with annual booster. Withdrawn in 1998.||-Cattle & Buffaloes: All Stages||May cause neonatal isoerthrolysis in calves from some vaccinated Dams.|
|killed Anaplasma marginale vaccine||2 doses 4 weeks apart with annual booster. Withdrawn in 1998.||-Cattle & Buffaloes: All Stages|
|Louisiana State University experimental vaccine||2 doses given 4 weeks apart, with yearly booster. Given subcutaneously. Vaccine does not prevent infection but aids in prevention or reduction in the severity.||-Cattle & Buffaloes: All Stages|
|modified live ovine Anaplasma marginale vaccine||2 ml intramuscularly in a single dose. No longer available outside California, USA.||-Cattle & Buffaloes: All Stages||May have severe clinical reactions especially in cattle over 2 years of age. Risk of contamination with pathogens unless high standards applied.|
Immunization and Vaccines
All current vaccines are derived from blood of infected cattle resulting in a high cost of production and difficulties in standardization. There is no vaccine routinely available for ovine anaplasmosis, but if required artificial infection followed by treatment may be useful.
A. centrale is used in vaccine, prepared from blood of infected splenectomized calves, in Australia (Rogers and Shiels, 1979) South Africa, (Potgieter, 1979) Argentina, (Anziani et al., 1987) Uruguay, (Nari et al., 1979) Israel, (Pipano et al., 1986) and more recently Zimbabwe (Turton et al., 1998) and Malawi (Tjornehoj et al., 1997). The only known vector of A. centrale is the African tick Rhipicephalus simus (Potgieter and van Rensburg, 1987). The protective potential of A. centrale isolates against A. marginale is partial and variable (Kuttler, 1967; Potgieter and van Rensburg, 1983; Anziani et al., 1987; Payne et al., 1990; Brizuela et al., 1998; Turton et al., 1998).
A modified live, A. marginale vaccine of ovine origin (Anavac) is also available, but is currently restricted for use to California only (Ristic et al., 1968; Osorno et al., 1975; Corrier et al., 1980; Vizcaino et al., 1980; Henry et al., 1983).
With these live blood-derived vaccines there is a risk of widespread transmission of unknown or newly emerging pathogens and strict production standards need to be adhered to in order to minimize this (Rogers et al., 1988).
A. centrale vaccine cannot be used in the USA, but non-living vaccines purified from infected bovine erythrocytes have been used (Vizcaino et al., 1980; Kuttler et al., 1984; Figueroa Millan et al., 1999), but were withdrawn from the US market in 1998. These vaccines reduced the severity of the disease but may cause neonatal isoerythrolysis in calves from some vaccinated Dams.
An experimental killed vaccine that does not cause neonatal isoerythrolysis in calves may be available in Louisiana, USA from Louisiana State University but is in its experimental stages (Hart et al., 1987; Luther et al., 1990; Luther et al., 1990).
Elimination of carriers
In non-endemic regions, movement controls, serological detection and culling or treating of carriers as well as vector control can be used to ensure freedom from anaplasmosis. Movement of wildlife can complicate such control programs.
The carrier-state has been eliminated by various regimes (Potgieter and Stoltsz, 1994). The administration of three injections of long acting oxytetracycline (20 mg/kg) at 1 week intervals combined with two injections of imidocarb dipropionate at 3mg/kg at a 2 week interval has proven very reliable for sterilizing carrier cattle in Australia.
Reduction of transmission
In some areas stringent control or elimination of the vectors may be a viable if expensive strategy particularly in Africa were a number of tick-borne diseases can be controlled by this strategy.
Attention should also be given to preventing iatrogenic transmission by disinfecting instruments after use on each animal.
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