Tick-Borne Fever

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Also Known As: Pasture FeverTickborne FeverRuminant AnaplasmosisTBF

Caused By: Anaplasma phagocytophilum, previously known as Ehrlichia phagocytophila

Contents

Introduction

Rickettsia spp. inside tick haemolymph cells. Sourced from Wikimedia Commons
Ixodes tick. Sourced from Wikimedia commons

Tick Borne Fever is a rickettsial disease affecting the white blood cells of sheep and cattle, causing anaemia and seasonal “pasture fever”.

Seasonal pasture fever occurs in cattle that are returned to tick infected pasture in the Spring.

Human granulocytic ehrlichiosis, the zoonotic form of TBF is a potentially fatal disease reported in the UK, Europe and USA.

Signalment

TBF naturally affects primarily sheep and cattle, and less commonly, deer, horses and dogs.

Distribution

TBF has worldwide distribution including the UK. It is transmitted by Ixodes ticks. Both adults and nymphs can transmit the disease. Transmission is trans-stadial.

Clinical Signs

TBF causes multisystemic disease, causing cardiovascular, gastrointestinal, respiratory, reproductive and neurological signs, and also lymphadenopathy and wasting disease.

Severe haematological changes including profound anaemia and leucopaenia cause significant clinical signs.

Initial lymphocytopaenia and prolonged neutropaenia are also features of TBF.

A profound eosinophilia will occur for 17-20 days post-infection. [1]

Low serum Alkaline Phosphatase (ALP) and decreased zinc, iron and albumin are also common biochemical findings, along with high urea, creatinine and bilirubin.

Recovered animals develop immunity but it is unknown how long this is effective for.

Diagnosis

Haematological and Biochemical changes as listed above along with marked pyrexia are highly suggestive, especially if historical findings are conducive.

Demonstration of the organism in the leucocytes in peripheral blood is confirmative.

On post-mortem examination, the spleen is enlarged and mild liver damage is common. Lesions within the lung are present and contain mononuclear infiltrate on histopathology. Thickening, ulceration and haemorrhage of the gastrointestinal tract become worse distally.

The parasites may be visible within the neutrophils in sections of liver and lung.

Antibodies can be detected using Indirect Immunofluorescence (IFAT), Complement Fixation and Immunoelectrophoresis (CIEP).

Treatment

A. phagocytophilum is susceptible to oxytetracycline, sulphamethazine, sulphadimidine, doxycycline and trimethoprim-sulphonamides.

Control

Control of the tick vector is expensive but effective. Use of ectoparasiticides and tick resistant breeds is also valuable.

Human Granulocytic Ehrlichiosis

Causes fever, malaise, headaches, sweats, nausea, confusion, anorexia, vomiting, weakness, diarrhoea, pneumonia, vertigo, seizures, GI bleeding and a skin rash.[2]



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References

  1. Miert, A. S. J. P. A. Mvan., Duin, C. T. Mvan., Schotman, A. J. H., Franssen, F. F. (1984) Clinical, haematological and blood biochemical changes in goats after experimental infection with tick-borne fever. Vet Parasitology, 16(3/4):225-233; 29
  2. Bakken, J. S., Krueth, J., Tilden, R. L., Dumler, J. S., Kristiansen, B. E. (1996). Serological evidence of human granulocytic ehrlichiosis in Norway. Eur J Clin Microbiol Inf Dis, 15(10):829-832; 12


CABIlogo

This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project.

Datasheet(s) used: tick-borne fever accessed on 6 June 2011










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