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anaplasmosis

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anaplasmosis

Summary

  • Last modified
  • 14 July 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • anaplasmosis
  • Overview
  • Anaplasmosis is a disease of ruminants caused by obligate intraerythrocytic parasites of the order Rickettsiales, family Anaplasmataceae (

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    OX10 8DE
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    compend@cabi.org
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Identity

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Preferred Scientific Name

  • anaplasmosis

International Common Names

  • English: anaplasma bovis in cattle - exotic; anaplasmosis in ruminants; anaplasmosis in ruminants, anaplasma marginale, centrale, ovis; gall sickness; gallsickness

Local Common Names

  • Australia: tick fever
  • Portugal: tristeza

Overview

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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.

Bovine anaplasmosis is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). For information on this disease from OIE, see the website: www.oie.int.

Hosts/Species Affected

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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.

Distribution

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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.

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:

Country

Outbreaks

Cases

Deaths

Slaughtered

Destroyed

Botswana

7

19

61

0

0

Comoros

1

2

0

0

0

Congo DRC

1

12

 NS

 NS

 NS

Egypt

69

291

 NS

NS

NS

Kenya

88

93

1

0

0

Lesotho

19

41

13

0

0

Madagascar

18

102

8

 

5

Mozambique

7

45

6

0

0

Namibia

3

6

6

0

0

Somalia

57

592

30

1

4

Swaziland

42

57

30

3

0

Tanzania

38

18,264

42

 NS

 NS

Zambia

100

1713

387

 NS

 NS

Zimbabwe

533

1086

288

 NS

 NS

Total (14)

983

22,323

872

4

9

NS=Not specified

Distribution Table

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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 details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

ArmeniaDisease not reportedMarutyan and Zaratsyan, 1986
AzerbaijanNo information availableMovsum-zade and Agaev, 1976; OIE Handistatus, 2005
BahrainDisease never reportedOIE, 2012
BhutanReported present or known to be presentOIE Handistatus, 2005
Brunei DarussalamCAB Abstracts data mining, 1999; OIE Handistatus, 2005
ChinaPresentLu et al., 1995; Lu et al., 1997; Shen YinSheng, 1998
-GansuPresentLu et al., 1995; Lu et al., 1997
-GuizhouPresentLu et al., 1995
-Hong KongNo information availableOIE Handistatus, 2005
-HubeiPresentLu et al., 1995
-HunanPresentLu et al., 1995
-Nei MengguPresentLu et al., 1997
-NingxiaPresentLu et al., 1995; Lu et al., 1997
-QinghaiPresentLu et al., 1995; Lu et al., 1997
-ShaanxiPresentLu et al., 1995; Lu et al., 1997; Shen YinSheng, 1998
-YunnanPresentLu et al., 1995
Georgia (Republic of)Last reported1997OIE Handistatus, 2005
IndiaMohan and Pathak, 1967; Miranpuri, 1988; Chitravel et al., 1998; OIE Handistatus, 2005
-Andhra PradeshPresentSurendran and Bhaskara, 1989
-Himachal PradeshPresentJithendran, 1997
-Madhya PradeshWidespreadMisraulia et al., 1988
-Tamil NaduPresentRao et al., 1991; Srinivasan et al., 1995; Ramprabhu et al., 1999
-West BengalPresentRay, 1992
IndonesiaReported present or known to be presentTravassos Santos Dias JA, 1988; Siswansyah, 1990; Payne et al., 1991; OIE Handistatus, 2005
-JavaPresentPayne et al., 1991
-KalimantanPresentSiswansyah, 1990; Tarmudji, et al., 1990
-Nusa TenggaraPresentTravassos Santos Dias JA, 1988
-SumatraPresentPayne et al., 1988
IranReported present or known to be presentHashemi-Fesharki, 1997; OIE Handistatus, 2005
IraqReported present or known to be presentOIE Handistatus, 2005
IsraelReported present or known to be presentShkap et al., 1990; Pipano, 1991; Shkap et al., 1991; OIE Handistatus, 2005
JapanLast reported1991OIE Handistatus, 2005
JordanLast reported1991Sherkov et al., 1977; Majaj-Büscher, 1992; OIE Handistatus, 2005
KazakhstanDisease not reportedOIE Handistatus, 2005
Korea, DPRDisease not reportedOIE Handistatus, 2005
Korea, Republic ofSerological evidence and/or isolation of the agentBaek et al., 1989; Baek et al., 1989; Baek et al., 1994; Baek and Son, 1995; Lee et al., 1997; OIE Handistatus, 2005
KuwaitDisease not reportedOIE Handistatus, 2005
LebanonDisease not reportedOIE Handistatus, 2005
MalaysiaPresentPresent based on regional distribution.
-Peninsular MalaysiaDisease not reportedOIE Handistatus, 2005
-SabahReported present or known to be presentOIE Handistatus, 2005
-SarawakNo information availableOIE Handistatus, 2005
MongoliaNo information availableOIE Handistatus, 2005
MyanmarDisease not reportedOIE Handistatus, 2005
NepalNo information availableMiranpuri, 1988; OIE Handistatus, 2005
OmanReported present or known to be presentOIE Handistatus, 2005
PakistanReported present or known to be presentBuriro et al., 1994
PhilippinesDisease not reportedMolina and Montenegro, 1997; OIE Handistatus, 2005
QatarReported present or known to be present, 1999; OIE Handistatus, 2005
Saudi ArabiaDisease not reportedEl-Metenawy, 2000; OIE Handistatus, 2005
SingaporeDisease never reportedOIE Handistatus, 2005
Sri LankaReported present or known to be presentJorgensen et al., 1988; Jorgensen et al., 1992; OIE Handistatus, 2005
SyriaDisease not reportedOIE Handistatus, 2005
TaiwanLast reported2002Otte and Kiltz, 1969; Su and Hsu, 1993; OIE Handistatus, 2005
TajikistanNo information availableBadalov, 1989; OIE Handistatus, 2005
ThailandReported present or known to be presentDissamarn et al., 1968; Chansiri, 1997; OIE Handistatus, 2005
TurkeyNo information availableHoffmann et al., 1971; cetindag, 1996; Sayin et al., 1997; OIE Handistatus, 2005
TurkmenistanNo information availableOIE Handistatus, 2005
United Arab EmiratesReported present or known to be present, 1999; OIE Handistatus, 2005
UzbekistanDisease not reportedOIE Handistatus, 2005
VietnamReported present or known to be presentHa^dot and Nguyên, 1996; Ha et al., 1997; Nguyen et al., 1999; Pham et al., 1999; OIE Handistatus, 2005
YemenNo information availableOIE Handistatus, 2005

Africa

AlgeriaNo information availableOIE, 2012
AngolaReported present or known to be presentOIE, 2012
BeninPangui and Salifou, 1992; OIE, 2012
BotswanaReported present or known to be presentCarmichael and Hobday, 1975; Fanikiso and Ndzinge, 1992; OIE Handistatus, 2005; OIE, 2012
Burkina FasoNo information availableBelem et al., 1994; OIE, 2012
BurundiReported present or known to be presentOIE, 2012
CameroonNo information availableVerhulst et al., 1983; Ndi et al., 1991; Chollet, 1995; OIE, 2012
Cape VerdeDisease never reportedOIE, 2012
Central African RepublicReported present or known to be presentOIE, 2012
ChadNo information availableOIE, 2012
ComorosPresentAU-IBAR, 2011
Congo Democratic RepublicNo information availableNdahiriwe et al., 1994; OIE, 2012
Côte d'IvoireReported present or known to be present, 1999; OIE, 2012
DjiboutiDisease not reportedOIE, 2012
EgyptReported present or known to be presentEl-Seify and Eissa, 1990; OIE, 2012
Equatorial GuineaNo information availableOIE, 2012Disease suspected
EritreaReported present or known to be present, 1999; OIE, 2012
EthiopiaPresent2002Mekonnen et al., 1992; Yilma et al., 1995; Solomon et al., 1998; OIE, 2012
GambiaPresentMattioli et al., 1993; Mattioli et al., 1997
GhanaDisease not reportedOIE, 2012
GuineaReported present or known to be presentOIE, 2012
Guinea-BissauNo information availableRosa et al., 1998; OIE, 2012
KenyaReported present or known to be presentNdarathi et al., 1989; Deem et al., 1993; Latif et al., 1995; Ndung'u et al., 1995; Gitau et al., 1997; OIE, 2012
LibyaLast reported2009OIE, 2012
MadagascarReported present or known to be present, 1999; OIE, 2012
MalawiReported present or known to be presentLawrence et al., 1996; Tjornehoj et al., 1997; OIE, 2012
MaliNo information availableOIE, 2012
MauritiusLast reported2001, 1999; OIE, 2012
MoroccoNo information availableVerhulst et al., 1983; Sahibi et al., 1998; OIE, 2012
MozambiqueReported present or known to be present, 1999; OIE, 2012
NamibiaReported present or known to be present, 1999; OIE, 2012
NigerNo information availableOIE, 2012
NigeriaReported present or known to be presentAkinboade and Dipeolu, 1984; Ajayi and Dipeolu, 1986; Akinboade et al., 1986; Ilemobade, 1992; Egbe-Nwiyi et al., 1997; OIE, 2012
RéunionReported present or known to be present, 1999; Poulin et al., 1991; OIE, 2012
RwandaReported present or known to be presentKabagambe et al., 1988; OIE, 2012
Sao Tome and PrincipeLast reported1991OIE, 2012
SenegalReported present or known to be presentOIE, 2012
SeychellesDisease not reported, 1999; OIE, 2012
SomaliaPresentSchoepf et al., 1984; OIE, 2012
South AfricaPresentPotgieter, 1979; Barry and Niekerk, 1990; Dreyer et al., 1998; OIE, 2012
SudanReported present or known to be presentOsman, 1997; OIE, 2012
SwazilandReported present or known to be present, 1999; OIE, 2012
TanzaniaReported present or known to be present, 1999; OIE, 2012
-ZanzibarPresentWoodford et al., 1988
TogoNo information availableOIE, 2012
TunisiaCAB Abstracts data mining, 1999; OIE, 2012
UgandaPresent, 1999; Ssenyonga et al., 1991; Ssenyonga et al., 1992; OIE, 2012
ZambiaReported present or known to be presentJongejan et al., 1988; Ahmadu et al., 1997; OIE, 2012
ZimbabweReported present or known to be presentNorval et al., 1984; Lawrence and Norval, 1987; OIE, 2012

North America

BermudaDisease not reportedOIE Handistatus, 2005
CanadaLast reported2000Schofield and Saunders, 1987; Stiller and Coan, 1995; OIE Handistatus, 2005
MexicoTeclaw et al., 1985; Cavazzani, 1989; Fragoso Sánchez, 1991; Pena and Spross, 1991; Azuara et al., 1993; Tapia et al., 1996; Cossío-Bayúgar et al., 1997; OIE Handistatus, 2005
USAReported present or known to be presentPalmer, 1989; Stiller and Coan, 1995; Keirans et al., 1996; OIE Handistatus, 2005
-CaliforniaWidespreadBehymer et al., 1991; Clark et al., 1993; Jessup et al., 1993; Chomel et al., 1994; Elliott et al., 1994
-ColoradoPresentAguirre et al., 1992
-FloridaWidespreadPalmer et al., 1986
-IdahoPresentRenshaw and Vaughn, 1977; Stauber et al., 1980; Magonigle et al., 1981; Maas et al., 1986; Zaugg, 1990
-IllinoisWidespreadSmith et al., 1982; Hungerford and Smith, 1996; Hungerford and Smith, 1997
-LouisianaPresentHugh-Jones and Hubbert, 1988; Morley and Hugh-Jones, 1989; Morley and Hugh-Jones, 1989
-MississippiPresentHidalgo et al., 1989
-MissouriPresentMaas et al., 1981
-MontanaPresentZaugg and Kuttler, 1985
-OklahomaPresentKocan, 1994; Rodgers et al., 1994; Ewing et al., 1997; Ge et al., 1997
-OregonPresentPeterson et al., 1977; Zaugg, 1990; Torioni de Echaide et al., 1998
-TexasWidespreadWaldrup et al., 1989
-UtahPresentRenshaw and Vaughn, 1977; Zaugg, 1990
-VirginiaPresentZaugg, 1985
-WashingtonPresentSweet and Stauber, 1978; Goff and Winward, 1985
-WyomingPresentTaylor et al., 1997

Central America and Caribbean

Antigua and BarbudaDisease not reportedCamus and Montenegro-James, 1994; Camus and Barré, 1995
BarbadosReported present or known to be presentCamus and Montenegro-James, 1994; Camus and Barré, 1995; OIE Handistatus, 2005
BelizeLast reported2003OIE Handistatus, 2005
British Virgin IslandsDisease not reportedOIE Handistatus, 2005
Cayman IslandsReported present or known to be presentOIE Handistatus, 2005
Costa RicaNo information availableMcCauley and Pérez, 1980; Hermans et al., 1994; Perez et al., 1994; Perez et al., 1994; Alvarez and Herrero, 1996; Herrero et al., 1998; OIE Handistatus, 2005
CubaReported present or known to be presentDelgado et al., 1976; Roman Suárez HdlN, 1984; Cordoves et al., 1989; Rodriguez et al., 1989; Rodriguez et al., 1989; Cordovés et al., 1991; Fadraga et al., 1991; Camus and Barré, 1995; OIE Handistatus, 2005
CuraçaoDisease not reportedOIE Handistatus, 2005
DominicaReported present or known to be presentCamus and Montenegro-James, 1994; Camus and Barré, 1995; OIE Handistatus, 2005
Dominican RepublicOIE Handistatus, 2005
El SalvadorReported present or known to be presentMirón, 1978; Payne and Scott, 1982; OIE Handistatus, 2005
GrenadaReported present or known to be presentCamus and Montenegro-James, 1994; Camus and Barré, 1995
GuadeloupeReported present or known to be presentMorel, 1967; Camus and Montenegro-James, 1994; Camus and Barré, 1995; Barré, 1997; OIE Handistatus, 2005
GuatemalaReported present or known to be presentGuglielmone, 1995; Andel et al., 1997; OIE Handistatus, 2005
HaitiReported present or known to be presentOIE Handistatus, 2005
HondurasReported present or known to be presentOIE Handistatus, 2005
JamaicaLast reported2003Bundy et al., 1983; McGinnis et al., 1988; Camus and Barré, 1995; OIE Handistatus, 2005
MartiniqueReported present or known to be presentMorel, 1967; Alonso et al., 1992; Camus and Montenegro-James, 1994; Camus and Barré, 1995; Barré, 1997; OIE Handistatus, 2005
MontserratWidespreadCamus and Montenegro-James, 1994; Camus and Barré, 1995
NicaraguaReported present or known to be presentOIE Handistatus, 2005
PanamaNo information availableObaldía, 1992; OIE Handistatus, 2005
Puerto RicoReported present or known to be presentCamus and Barré, 1995; Barré, 1997
Saint Kitts and NevisReported present or known to be presentCamus and Montenegro-James, 1994; Camus and Barré, 1995; OIE Handistatus, 2005
Saint LuciaWidespreadKnowles and Montrose, 1982; Hugh-Jones and Hubbert, 1988; Camus and Montenegro-James, 1994; Camus and Barré, 1995
Saint Vincent and the GrenadinesReported present or known to be presentCamus and Montenegro-James, 1994; Camus and Barré, 1995; OIE Handistatus, 2005
Trinidad and TobagoReported present or known to be presentCamus and Barré, 1995; OIE Handistatus, 2005

South America

ArgentinaSpäth, 1987; Rios et al., 1990; Späth et al., 1990; Guglielmone, 1994; Guglielmone et al., 1997; OIE Handistatus, 2005
BoliviaNicholls et al., 1980; Behymer et al., 1991; Cuéllar and Carrique, 1998; Carrique and Widdowson, 2000; OIE Handistatus, 2005
BrazilReported present or known to be presentHorn, 1983; OIE Handistatus, 2005
-BahiaWidespreadAraújo et al., 1998
-GoiasWidespreadSantos et al., 1998
-Mato Grosso do SulWidespreadMadruga et al., 1983; Madruga et al., 1984; Madruga et al., 1985; Kessler et al., 1987; Madruga et al., 1987; Kessler et al., 1991
-Minas GeraisWidespreadRibeiro and Reis, 1981; Ribeiro et al., 1984; Kano and Vidotto, 1999; Melo et al., 1999; Goncalves, 2000
-ParaibaWidespreadAthayde et al., 1994; Dantas and Nascimento, 1999
-ParanaWidespreadVidotto and Yamamura, 1995; Vidotto et al., 1997; Vidotto et al., 1998; Kano and Vidotto, 1999
-PernambucoWidespreadMelo et al., 1993; Oliveira et al., 1999
-Rio de JaneiroWidespreadTokarnia and Döbereiner, 1962; Massard, 1986; Nogueira et al., 1991; Souza et al., 2000
-Rio Grande do SulWidespreadGloss, 1964; Braccini et al., 1992; Artiles and Alves-Branco, 1995; Lagaggio and Correa, 1997
-Santa CatarinaWidespreadDalagnol et al., 1995; Serra-Freire and Nuernberg, 1995
-Sao PauloWidespreadAmaral and Valente, 1971; Franzolin et al., 1989; Guido et al., 1994; Benesi and Howard, 1999
-SergipeWidespreadOliveira et al., 1992
ChileDisease never reportedOIE Handistatus, 2005
ColombiaReported present or known to be presentKuttler et al., 1970; Corrier and Guzman, 1977; Zararaz and Parra, 1977; Patarroyo et al., 1978; Corrier et al., 1983; OIE Handistatus, 2005
EcuadorNo information availableOIE Handistatus, 2005
Falkland IslandsDisease never reportedOIE Handistatus, 2005
French GuianaReported present or known to be presentOIE Handistatus, 2005
GuyanaReported present or known to be presentOIE Handistatus, 2005
ParaguayReported present or known to be presentPayne and Osorio, 1990; OIE Handistatus, 2005
PeruLora and Koechlin, 1969; OIE Handistatus, 2005
UruguayBerdie et al., 1979; Cardozo et al., 1981; Quintana et al., 1992; Solari, 1994; Guglielmone, 1995; OIE Handistatus, 2005
VenezuelaReported present or known to be presentSchroeder et al., 1970; James et al., 1985; Meléndez and Forlano, 1997; Alfaro et al., 1998; OIE Handistatus, 2005

Europe

AndorraDisease never reportedOIE Handistatus, 2005
AustriaNo information availableFumicz, 1991; Bäumgartner et al., 1992; OIE Handistatus, 2005
BelarusNo information available, 1999; OIE Handistatus, 2005
BelgiumLast reported1996OIE Handistatus, 2005
Bosnia-HercegovinaDisease not reportedOIE Handistatus, 2005
BulgariaLast reported1996OIE Handistatus, 2005
CroatiaNo information available, 1999; OIE Handistatus, 2005
CyprusDisease never reportedOIE Handistatus, 2005
Czech RepublicDisease not reportedOIE Handistatus, 2005
DenmarkDisease never reportedOIE Handistatus, 2005
EstoniaDisease not reportedOIE Handistatus, 2005
FinlandDisease never reportedOIE Handistatus, 2005
FranceDisease never reportedPoncet, 1990; Levasseur, 1991; OIE Handistatus, 2005
GermanyDisease never reportedOIE Handistatus, 2005
GreeceLast reported2001Papadopoulos et al., 1996; OIE Handistatus, 2005
HungaryNo information availableOIE Handistatus, 2005
IcelandDisease never reportedOIE Handistatus, 2005
IrelandDisease never reportedOIE Handistatus, 2005
Isle of Man (UK)Disease never reportedOIE Handistatus, 2005
ItalyNo information availableCeci et al., 1997; Ceci et al., 1997; Ceci and Carelli, 1999; OIE Handistatus, 2005
JerseyDisease never reportedOIE Handistatus, 2005
LatviaDisease never reportedOIE Handistatus, 2005
LiechtensteinDisease not reportedOIE Handistatus, 2005
LithuaniaDisease never reportedOIE Handistatus, 2005
LuxembourgDisease never reportedOIE Handistatus, 2005
MacedoniaOIE Handistatus, 2005
MaltaDisease not reportedOIE Handistatus, 2005
MoldovaDisease not reportedOIE Handistatus, 2005
NetherlandsDisease never reportedUilenberg et al., 1980; OIE Handistatus, 2005
NorwayDisease never reportedOIE Handistatus, 2005
PolandDisease not reportedOIE Handistatus, 2005
PortugalReported present or known to be present, 1999; OIE Handistatus, 2005
RomaniaSerological evidence and/or isolation of the agentOIE Handistatus, 2005
Russian FederationReported present or known to be presentOIE Handistatus, 2005
-Russia (Europe)Present, 1999
SlovakiaDisease not reportedOIE Handistatus, 2005
SloveniaLast reported1990Borko, 1997; OIE Handistatus, 2005
Spain, 1999; OIE Handistatus, 2005
SwedenDisease never reportedOIE Handistatus, 2005
SwitzerlandLast reported2002OIE Handistatus, 2005
UKDisease never reportedOIE Handistatus, 2005
-Northern IrelandDisease never reportedOIE Handistatus, 2005
Ukraine, 1999; Artemenko, 1973; Artemenko, 1977; OIE Handistatus, 2005
Yugoslavia (former)No information availableOIE Handistatus, 2005
Yugoslavia (Serbia and Montenegro)Disease never reportedOIE Handistatus, 2005

Oceania

AustraliaOIE Handistatus, 2005
-Australian Northern TerritoryLocalisedCallow, 1984
-QueenslandLocalisedRogers et al., 1978; Callow, 1984
-Western AustraliaLocalisedCallow, 1984
French PolynesiaDisease not reportedOIE Handistatus, 2005
New CaledoniaDisease never reportedOIE Handistatus, 2005
New ZealandDisease never reportedOIE Handistatus, 2005
Papua New GuineaPresentOwen, 1990
SamoaDisease never reportedOIE Handistatus, 2005
VanuatuDisease never reportedOIE Handistatus, 2005
Wallis and Futuna IslandsNo information availableOIE Handistatus, 2005

Pathology

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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).

Diagnosis

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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.


Differential diagnosis


The clinical signs of anaplasmosis are non-specific and laboratory support is needed to confirm a diagnosis.


Cattle


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.


Laboratory Diagnosis


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).

List of Symptoms/Signs

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SignLife StagesType
Acoustic Signs / Purulent, mucoid discharge, excess wax, foul odour, ears Sign
Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Diagnosis
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Sign
Digestive Signs / Congestion oral mucous membranes, erythema, redness oral mucosa Sign
Digestive Signs / Decreased amount of stools, absent faeces, constipation Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Sign
Digestive Signs / Diarrhoea Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Sign
Digestive Signs / Excessive salivation, frothing at the mouth, ptyalism Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Sign
Digestive Signs / Mucous, mucoid stools, faeces Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Sign
Digestive Signs / Rumen hypomotility or atony, decreased rate, motility, strength Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Sign
General Signs / Ataxia, incoordination, staggering, falling Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Sign
General Signs / Dehydration Sign
General Signs / Empty abdomen on internal palpation Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Sign
General Signs / Exercise intolerance, tires easily Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Diagnosis
General Signs / Fever, pyrexia, hyperthermia Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Diagnosis
General Signs / Generalized weakness, paresis, paralysis Sign
General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass Sign
General Signs / Icterus, jaundice Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Diagnosis
General Signs / Lack of growth or weight gain, retarded, stunted growth Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Sign
General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes Sign
General Signs / Pale mucous membranes or skin, anemia Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Diagnosis
General Signs / Sudden death, found dead Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Diagnosis
General Signs / Trembling, shivering, fasciculations, chilling Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Sign
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Diagnosis
General Signs / Weight loss Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Sign
Nervous Signs / Abnormal behavior, aggression, changing habits Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Sign
Nervous Signs / Seizures or syncope, convulsions, fits, collapse Sign
Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes Sign
Reproductive Signs / Abortion or weak newborns, stillbirth Cattle & Buffaloes:Cow,Sheep & Goats:Mature female Sign
Reproductive Signs / Agalactia, decreased, absent milk production Sign
Reproductive Signs / Anestrus, absence of reproductive cycle, no visible estrus Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Sheep & Goats:Gimmer,Sheep & Goats:Mature female Sign
Reproductive Signs / Female infertility, repeat breeder Sign
Reproductive Signs / Male infertility Cattle & Buffaloes:Bull,Sheep & Goats:Breeding male Sign
Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs Sign
Respiratory Signs / Coughing, coughs Sign
Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping Sign
Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Diagnosis
Respiratory Signs / Mucoid nasal discharge, serous, watery Sign
Respiratory Signs / Purulent nasal discharge Sign
Skin / Integumentary Signs / Rough hair coat, dull, standing on end Sign
Urinary Signs / Red or brown urine, pink Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Cattle & Buffaloes:Bull,Cattle & Buffaloes:Ox,Sheep & Goats:All Stages Diagnosis

Disease Course

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Bovine anaplasmosis


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.


Ovine anaplasmosis


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).

Epidemiology

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Vertebrate host


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).


Transmission


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).

Impact: Economic

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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.

Zoonoses and Food Safety

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Anaplasma spp. poses no known zoonotic or food safety problems.

Disease Treatment

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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).

Prevention and Control

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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.


Live vaccines

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).


Killed vaccines

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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Links to Websites

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WebsiteURLComment
Anaplasmosis – Dept Agriculture Australiahttp://www.daff.qld.gov.au/4790_5839.htm
Anaplasmosis – OIE Codehttp://www.oie.int/index.php?id=169&L=0&htmfile=chapitre_1.11.1.htm
Anaplasmosis – OIE Manualhttp://www.oie.int/fileadmin/Home/eng/Health_standards/tahm/2.04.01_BOVINE_ANAPLASMOSIS.pdf
Anaplasmosis case report – Purdue USAhttps://www.addl.purdue.edu/newsletters/2005/Summer/finaldx.htm
Anaplasmosis in Beef Cattle – Texas A&Mhttp://icwdm.org/PDF's/anaplasmosisTXA&M.pdf
OIE Manual of Diagnostic Tests and Vaccines for Terrestrial Animalshttp://www.oie.int/en/international-standard-setting/terrestrial-manual/access-online/The Manual of Diagnostic Tests and Vaccines for Terrestrial Animals (Terrestrial Manual) aims to facilitate international trade in animals and animal products and to contribute to the improvement of animal health services world-wide. The principal target readership is laboratories carrying out veterinary diagnostic tests and surveillance, plus vaccine manufacturers and regulatory authorities in Member Countries. The objective is to provide internationally agreed diagnostic laboratory methods and requirements for the production and control of vaccines and other biological products.

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