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Anaplasma phagocytophilum

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Synonym(s): Ehrlichia equi, Equine granulocytic anaplasmosis


Introduction

Classification

Taxonomy

  • Phylum: Proteobacteria.
  • Order: Rickettsiales. 
  • Family: Anaplasmataceae. 
  • Genus:Anaplasma.
  • Species:phagocytophilum.
  • Several host adapted variants exist.
  • Distinct host species correlate withAnaplasma phagocytophilumankA gene clusters.
  • Variants may behave differently from one another in their interaction/pathogenicity within the host.
  • For example, in ruminants different variants may exist within the same herd and even simultaneously in the same animal; while different horse variants exist it is yet unknown whether they can occur simultaneously in the same animal.

Etymology

  • Formerly known asEhrlichia equiandEhrlichia phagocytophila  Anaplasmataceae  .
  • Gk. an-, without; plasma-, anything formed or molded; phagein-, to eat up, devour; phylum-, friend, loving. Literally: A thing (a bacterium) without form, attractive to phagocytes.
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Clinical Effects

Epidemiology

Habitat

  • Reservoir hosts are mammalian cells.
  • Wildlife such as rodents, and other small mammals act as the reservoir hosts, with transmission to domestic animals and man as a result of tick bites.
  • Wild ruminants such as deer may also act as reservoirs for selected strains.

Lifecycle

  • Alternate infection of two distinct hosts, ticks and mammals. 
  • In ticks the bacteria resides in the salivary glands using upregulation selected tick salivary protein (SALP 16) to establish themselves. The bacteria persists through the nymphal molts but is not passed on transovarially. 

Transmission

  • Transmitted by bites from Ixodes spp tick vectors, especially:
    • Ixodes pacificuson the Pacific coast of USA (same spp that transmit Lymes disease   Borreliosis  in North America).
    • Ixodes scapularisin the eastern and mid-western United States (same spp that transmit Lymes disease   Borreliosis   in North America).
    • Ixodes ricinusin Europe (same spp that transmits Lymes disease   Borreliosis  , and the flavivirus that causes tick borne encephalitis (TBE) in Europe).
  • It has been suggested that the infection can be introduced into disease-free areas by migrating birds; thrushes in particular.
  • Additionally, the presence of swallows at a stable is a risk factor for infections in horses.
  • Time of tick bite transmission; some suggestions are that ticks need at least 24 h feeding to transmit, but in the field situation ticks may be able to transmit in <24 h.

Pathological effects

  • The seroprevalence of anaplasmosis is related to organism prevalence in the tick populations, animal density, and the variety ofA. phagocytophiliumfound within the geographic area.
  • Infects granulocytes    →   initiation of  a cascade of pro-inflammatory events, and cytokine/chemokine (IL-1beta, TNF-alpha, and IL-8 upregulation)   →    vasculitis    →    thrombocytopenia    →    interstitial inflammation, edema and petechial hemorrhages    →    ataxia.
  • The cytopenic effects are likely a combination of shortened half-life, sequestration and consumption of blood elements. As well, despite normal diffuse hypercellularity of the bone marrow, it appears that infection can, via myelosuppresive chemokines, induce a transient failure of hemopoietic colony formation affecting all lineages of hematopoiesis.
  • Vasculitis appears to be due to inflammatory endothelial barrier dysfunction; pathologically most obvious on skeletal extremities, thus reflected in limb edema.
  • Most severe in older horses, especially >4 years.
  • Heaviest burden of infection is in the spleen, liver and lungs.
  • Bacterial surface proteins are expected to have a critical role in the bacteriums pathogenicity. They undergo antigenic variation within the hosts tissues, reducing the effectiveness of the hosts immune response; they can also inhibit neutrophil killing by subverting O2 dependent killing, and as well delay apoptosis and manipulate the chemokine expression by granulocytes to help disseminate the infection.
  • Antibodies are produced during infection, and recovered horses are immune for at least one year.
  • Clinical signs:
    • Pyrexia.
    • Anorexia.
    • Mild anemia.
    • Icterus.
    • Lower limb edema.
    • Locomotor problems: ataxia.
    • Moderate to marked thrombocytopenia, mild short-term lymphopenia/neutropenia.
  • Seldom fatal unless complicated self-trauma (fractures) during ataxia of acute illness, or by other infections. Other uncommon signs, recumbency, rhabdomyolysis.
  • Sudden death can occur in acute disease due to DIC-like reaction (as in mortality in people).

Other Host Effects

  • Infection may be very mild and go unrecognized, especially infection in foals.
  • Complications:
    • As for all febrile diseases, impaired spermatogenesis for several months.
    • In ruminants a predisposing factor for other infections, however the evidence for this existing in equine infection is weak.

Control

Control via animal

  • Minimise exposure to tick bites by use of topical tick repellents.
  • Carefully examine for and remove ticks on return from infected areas.
  • Regular tick removal may be effective to minimize infection by other tick-borne organisms (such asBorreliaspp) but is probably not sufficient to avoid infection byA. phagocytophilumas field work suggests transmission can occur within the first 24 h.

Control via chemotherapies

  • Tetracycline   Therapeutics: tetracyclines  is very effective at treating the infection: signs of acute infection (fever) should abate within 12-24 h.
  • Importantly, if fever does not abate with treatment one should reconsider the diagnosis.

Control via environment

  • Widespread elimination of ticks by use of acaricides is impractical in endemic areas.
  • Locally, vegetation where ticks can breed can be removed from grazing areas.

Vaccination

  • No vaccine is currently available againstA. phagocytophilium.

Diagnosis

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Granquist E G et al (2010) A morphological and molecular study of Anaplasma phagocytophilum transmission events at the time of Ixodes ricinus tick bite. Acta Vet Scand 52, 43 PubMed.
  • Franzén P, Aspan A, Egenvall A, Gunnarsson A, Karlstam E & Pringle J (2009) Molecular evidence for persistence of Anaplasmaphagocytophilum in the absence of clinical abnormalities in horses after recovery from acute experimental infection. J Vet Intern Med  23 (3), 636-642 PubMed.
  • Franzén P, Aspan A, Egenvall A, Gunnarsson A, Aberg L & Pringle J (2005) Acute clinical, hematologic, serologic, and polymerase chain reaction findings in horses experimentally infected with a European strain of Anaplasma phagocytophilumJ Vet Intern Med  19 (2), 232-239 PubMed.
  • Lepidi H, Bunnell J E, Martin M E, Madigan J E, Stuen S & Dumler J S (2000) Comparative pathology, and immunohistology associated with clinical illness after Ehrlichiaphagocytophila-group infections. Am J Trop Med Hyg  62 (1), 29-37 PubMed.
  • Pusterla N et al (1998) Experimental infection of four horses with Ehrlichia phagocytophilaVet Rec 143 (11), 303-305 PubMed
  • Reubel G H, Kimsey R B, Barlough J E & Madigan J E (1998) Experimental transmission of Ehrlichia equi to horses through naturally infected ticks (Ixodes pacificus) from Northern California. J Clin Microbiol  36 (7), 2131-2134 PubMed.
  • Korbutiak E & Schneiders D (1994) Equine granulocytic ehrlichiosis in the UK. Vet Rec 135 (16), 387-388 PubMed

Other sources of information

  • Franzén P (2008) On Anaplasma phagocytophilum in Horses. In: Doctoral Diss, Dept of Clinical Sciences, SLU. Acta Universitatis Agriculturae Sueciae 81.

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