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Anaplasmosis in Bison


Murray Woodbury DVM, MSc.

Specialized Livestock Health and Production
Department of Large Animal Clinical Sciences
Western College of Veterinary Medicine,
University of Saskatchewn
Saskatoon,Saskatchewan    S7N 5B4

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Contents

Introduction
Cause
Species at risk
Transmission
Clinical signs
Diagnosis
Treatment and prevention
Significance
References


Introduction

Anaplasmosis is an infectious, transmissible disease of many domestic and wild ruminant species including North American bison. It is mainly a disease of cattle, manifesting itself as a progressive anemia associated with red blood cell destruction resulting from infection by an organism called Anaplasma marginale, or in sheep, Anaplasma ovis. Anaplasmosis is infrequently found in Canada making it a “Reportable disease” under Canada’s Health of Animals Act and Regulations (http://laws.justice.gc.ca./en/H-3.3/fulltoc.html). Reportable diseases are those of significant importance to human or animal health or to the Canadian economy. Animal owners, veterinarians, and laboratories are required to immediately report to a CFIA veterinarian the presence of an animal that is contaminated or suspected of being contaminated with one of these diseases so that control or eradication measures can be applied immediately (http://www.inspection.gc.ca). In June 2000 several bison from a herd in central Saskatchewan were destroyed to prevent the spread to herd mates or to local cattle. Since under most circumstances bison are not severely affected by anaplasmosis, the issue is not whether bison themselves become infected and sick from anaplasmosis but whether they can act as a reservoir of infective organisms which can be transmitted to cattle.


Cause

In North America anaplasmosis in cattle and bison is caused by a bacterial (Rickettsia) organism named Anaplasma marginale. A similar organism, Anaplasma ovis, affects domestic and wild sheep, most notably the Bighorn sheep of North America. Anaplasma caudatum and A. centrale may also infect cattle and wildlife elsewhere in the world. Anaplasma organisms infect red blood cells, leading to varying degrees of anemia depending on the age, immune status, and species of the host animal. Young animals and animals from populations not previously exposed to organisms are most severely affected. Animals in herds residing in anaplasmosis endemic areas of North America are thought to carry some immunity to infection or at least to clinical disease.


Species at risk

In addition to domestic cattle and sheep, various wild species such as deer (white-tailed, mule and black-tailed), and elk become infected but do not usually exhibit disease (Kuttler 1984). These species, as well as pronghorn antelope and Bighorn sheep have been experimentally infected (Davidson and Goff 2001) as have bison (Zaugg 1985, 1986). Bison are also know to carry natural infections but with minimal signs of disease (de la Fuente 2003). Humans are not at risk from anaplasmosis and further, it appears that only ruminants can become infected (Summers and Gonzales 1965, Zaugg and Newman 1985).

Transmission

Anaplasmosis is not contagious. It is transmitted biologically between animals by ticks and mechanically by insect vectors and blood contaminated instruments such as those used in dehorning, castration, ear tagging, drug implantation, and blood sampling or drug injection. Several species of ticks, including some that are found in Canada, carry anaplasma organisms in their tissues and infect cattle or bison through feeding activity at different stages of their life cycle. There is evidence that Anaplasma spp. are transmitted from one generation of tick to the next through infection of their eggs. Biting insects such as horseflies, stable flies, and mosquitoes can mechanically transmit organisms in blood on their mouthparts but transfer must occur within minutes after first biting an infected animal.

Animals infected with A marginale without becoming sick and survivors of clinical anaplasmosis can carry the organism in their system, serving as a reservoir. Cattle can remain carriers for years and are major sources of infection for other animals. Mule deer and white-tailed deer remain infected for weeks to months and although in the eastern United States white-tailed deer are not considered a significant reservoir, mule deer and black-tailed deer in Idaho and California respectively are thought to be sources of infection for domestic cattle (Keel 1995, Maas et al 1986, Kuttler, 1984).

Elk are susceptible to experimental infection with A. marginale and A. ovis without showing visible signs of disease and apparently develop chronic infections lasting 5 months or more (Harland et al 1979, Zaugg et al 1996). Possibly because of poor diagnostic test performance, establishing the prevalence of anaplasma infection or the recovery of Anaplasma organisms from wild elk populations has been problematic and there are very few published reports of success in this regard. Nonetheless, Davidson and Goff (2001) suggest that antibody to Anaplasma spp. can be found in over 50% of elk in some populations and due to persistent infections there is potential at some locations for elk to be important reservoirs of anaplasmosis.

Similarly, bison are known to be susceptible to experimental infection and to remain carriers for as long as 496 days (Zaugg and Kuttler 1985, Zaugg 1986). Natural infection has been documented both through evidence of antibody and isolation of the organism (Taylor et al 1997, Davidson and Goff 2001, de la Fuente et al 2003). Isolates from the 2000 discovery of anaplasmosis in farmed bison in Saskatchewan were shown to be similar to those found in domestic cattle (de la Fuente et al 2003). The Saskatchewan animals were killed due to the potential for spread to other susceptible animals but it may be that the risk of successful transmission in such northern latitudes is less than in other, more temperate areas of North America. In fact, the principle factor preventing natural infection among Canadian wildlife may be that the major route of transmission is probably through biting flies rather than by ticks. Mechanical transfer of infective organisms on the mouthparts of biting insects is much less effective than though tick transfer. However, both vectors of disease communication are no doubt limited and made less efficient by the low temperatures experienced in Canadian winter, spring, and fall. Although never established, the original source of the outbreak is thought to be herd additions imported from an endemic area of the United States.

Clinical signs

 
Clinical signs result from the infection and subsequent removal of red blood cells from circulation, resulting in anemia and eventually jaundice (Lincoln 1996). Hemoglobinuria (brown urine) is not a feature since there is no intravascular hemolysis (rupture of red cells in blood vessels). Rather, infected cells are removed from circulation by the spleen and liver. There is fever, loss of appetite, and depression. Constipation is a feature, with dark mucous covered feces when bowel movements do occur. The anemia causes weakness, respiratory distress, debility, and sometimes death. Reproductive losses resulting from abortion and poor conception occur in endemic areas. In cattle the severity of signs varies with age and previous exposure. Younger cattle less than 1 year of age are not badly affected but can become carriers of the disease. Animals over 2 years of age with no previous exposure to anaplasma are usually severely ill and mortality rates can reach 50% percent. Experimentally infected bison have been shown to suffer anemia but in general, they are only unapparent carriers with few outward signs of disease (Zaugg 1985).


Diagnosis

Anaplasmosis can be diagnosed by the detection of the organism in red blood cells in stained blood smears from affected animals, and confirmed by injection of suspect blood into susceptible cattle. More commonly, serologic tests are performed on samples from suspect animals looking for antibody evidence of present or past infections. However these tests have been developed to detect anaplasmosis in cattle and have not been validated in other species such as bison. The Rapid Card Test (RCT), compliment fixation test (CF), indirect immunofluorescence test (IIF) and ELISA, have been used to test for evidence of Anaplasma spp infections. There are mixed opinions about the cross reactivity and possible insensitivity of these tests when used to detect anaplasmosis in species other than domestic cattle (Davidson 2001). Recently protein sequencing techniques have been used to confirm and characterize Anaplasma spp infections in bison (de la Fuente 2003). Davidson and Goff (2001) made reference to a competitive inhibition ELISA test (Torioni de Echaide et al 1998) used to establish an 11% prevalence rate on previously CF tested and presumed negative sera from a survey of Yellowstone Park bison.

Treatment and prevention


Anaplasma organisms are relatively sensitive to antibiotic therapy and the use of tetracycline group antibiotics often relieves clinical signs within a few days. Severely affected animals may need blood transfusion and/or fluid therapy. Successfully treated and recovered animals as well as untreated survivors can become chronic asymptomatic carriers of disease if relatively high-dose antibiotic therapy is not provided for an extended period. (Magonigle and Newby 1982, Zaugg and Lincoln 1987). Affected bison are slaughtered because there are no antibiotics licensed in Canada for use in bison and treatment of infected animals is not part of the CFIA’s control strategy for this disease (http://www.inspection.gc.ca).

In countries where anaplasmosis is found and especially endemic areas vector control, sanitary measures and vaccination are used to decrease the incidence of disease. Sanitary measures are directed at surgical or management implements such as syringes and needles to prevent the transfer of blood and infective organisms between animals. Vector control measures include animal and environmental anti-parasitic treatments and in Canada these are assisted by the annual appearance of winter, during which vector activity generally ceases.

Since anaplasmosis is not currently found in Canada, prevention strategies involve preventing infected animals from entering the country. Animal importation requirements include serological testing for anaplasmosis prior to shipment and in the case of bison, retesting after arrival. Should anaplasmosis be diagnosed in Canadian bison, Canada’s current foreign animal disease strategy calls for its eradication through testing of infected and exposed herds and the removal (slaughter) of test positive animals (http://www.inspection.gc.ca).

 
Significance

Anaplasmosis is an economically important disease in subtropical and temperate United States where it is endemic. This disease causes cattle losses through decreased productivity as well as mortality. It is not often found in Canadian cattle, and when it occurs it is from animals imported from endemic areas of the US. It is doubtful whether anaplasmosis could actually become established in most of Canada because cold Canadian winters decrease vector populations, and Canadian populations of potential reservoirs such as mule deer, black-tailed deer, and bison are anaplasmosis free. Import testing of bison remains an important means of keeping anaplasmosis out of the Canadian cattle herd.

Following a CFIA economic analysis of the introduction and establishment of anaplasmosis in Canada (http://www.inspection.gc.ca/english/anima/heasan/import/anaplasmose.shtml) and the subsequent publication of a discussion paper on the import policies for importation of “feeder cattle” from the US (http://www.inspection.gc.ca/english/anima/heasan/import/bovine.shtml) the rules for importing cattle and bison destined for slaughter in Canada have changed. In the past it was only possible to import animals destined for slaughter without prior testing for anaplasmosis during the colder months from October until the end of March. Under new regulations effective April 1, 2004 it will be possible to import feeder animals year round, provided they originate from a “low risk” or non endemic area of the US. These changes do not include animals used for breeding and other permanent additions to the Canadian cattle and bison herd.

Only time will tell if this is a wise change to import regulations. The shared losses associated with Anaplasma marginale becoming established in Canada are estimated between $12 and $36 million. On the other hand, the estimated cost to the CFIA for eradication of an anaplasmosis outbreak is only $3 million (http://www.inspection.gc.ca/english/anima/heasan/import/anaplasmose.shtml).


References

Davidson WR, Goff WL. 2001. Anaplasmosis. Chapter 27- Order Rickettsiales. In: Infectious Diseases of Wild Mammals. Williams ES, Barker IK eds. Iowa State Press, Ames. pp 455-466.

de la Fuente J, Golsteyn Thomas EJ, van den Bussche RA, Hamilton RG, Tanaka EE, Druhan SE, Kocan KM. 2003. Characterization of Anaplasma marginale isolated from North American bison. Applied and Environmental Microbiology 69(8):5001-5005.


Keel MK, Goff WL, Davidson WR. 1995. An assessment of the role of white-tailed deer in the epizootiology of anaplasmosis in the southeastern United States. Journal of Wildlife Diseases 31:378-385.

Kuttler KL. 1984. Anaplasma infections in wild and domestic ruminants: A review. Journal of Wildlife Diseases 20:12-20.


Lincoln SD. 1996. Anaplasmosis Ch 35. Diseases of the Hemopoetic and Hemolymphatic System. In: Large Animal Internal Medicine: Diseases of Horses Cattle Sheep and Goats (2nd edition). Smith B (ed). Mosby-Year Book , St Louis. Pp. 1214-1217.

Magonigle RA, Newby MS. 1982. Elimination of naturally acquired chronic Anaplasma marginale infections with a long-acting oxytetracycline injectable. American Journal of Veterinary Research 43:2170-2172


Mass J, Lincoln SD, Coan ME, Kuttle KL. 1986. Epidemiologic aspects of bovine anaplasmosis in semi-arid range conditions of south central Idaho. American Journal of Veterinary Research 47:528-533.

Summers WA, Gonzales LL. 1965. Attempts to transmit bovine anaplasmosis to small laboratory animals. Experimental Parasitology 16:57-63.


Taylor Sk, Lane VM, Hunter DL, Eyre KG, Frye S, Johnson MR. 1997. Serologic Survey for infectious pathogens in free-ranging American bison. Journal of Wildlife Diseases 33:308-311.

Torioni de Eschaide S, Knowles DP, McGuire TC, Palmer GH, Suarez CE, McElwain TF. 1998. Detection of cattle naturally infected with Anaplasma marginale in a region of endemicity by nested PCR and competitive enzyme-linked immunosorbent assay using recombinant major surface protein 5. Journal of Clinical Microbiology 36:777-782.


Zaugg JL. 1986. Experimental anaplasmosis in American bison: Persistence of infections of Anaplasma marginale and non-susceptibility to A. ovis. Journal of Wildlife Diseases 22:169-172.

Zaugg JL, Kuttler KL. 1985. Anaplasma marginale infections in American bison: Experimental infection and serologic study. American Journal of Veterinary Research 46:699-670.


Zaugg JL, Lincoln SD. 1987. How susceptible are anaplasmosis cleared cattle to reinfection? Veterinary Medicine 82(2);184-190.

Zaugg JL, Newman BA. 1985. Evaluation of jackrabbits as non-ruminant hosts for Anaplasma marginale. American Journal of Veterinary Research. 46:669-670.