Difference between revisions of "Tick-Borne Fever"
| Line 1: | Line 1: | ||
| − | Also Known As – Pasture Fever – Tickborne Fever – Ruminant Anaplasmosis – TBF | + | Also Known As – '''''Pasture Fever''''' – '''''Tickborne Fever''''' – '''''Ruminant Anaplasmosis''''' – '''''TBF''''' |
| − | Caused By – | + | Caused By – ''[[Anaplasma phagocytophila]]'', previously known as ''Ehrlichia phagocytophila'' |
==Introduction== | ==Introduction== | ||
| − | Tick Borne Fever is a [[Rickettsiales | rickettsial]] disease | + | Tick Borne Fever is a '''[[Rickettsiales | rickettsial]]'' disease affecting the '''[[Leucocytes | 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. | 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. | + | Human granulocytic ehrlichiosis, the '''zoonotic''' form of TBF is a potentially '''fatal''' disease reported in the UK, Europe and USA. |
==Signalment== | ==Signalment== | ||
TBF naturally affects primarily sheep and cattle, and less commonly, deer, horses and dogs. | TBF naturally affects primarily sheep and cattle, and less commonly, deer, horses and dogs. | ||
| Line 14: | Line 14: | ||
TBF has worldwide distribution including the UK. | TBF has worldwide distribution including the UK. | ||
| − | TBF is transmitted by [[Ixodes spp]] ticks. Both adults and nymphs can transmit disease. | + | TBF is transmitted by '''[[Ixodes spp. | ixodes]]''' ticks. Both adults and nymphs can transmit disease. |
| − | Transmission is [[Tick Disease Transmission | trans-stadial]]. | + | Transmission is '''[[Tick Disease Transmission | trans-stadial]].''' |
==Clinical Signs== | ==Clinical Signs== | ||
| − | TBF causes multisystemic disease, causing cardiovascular, gastrointestinal, respiratory, reproductive and neurological signs, and also lymphadenopathy and wasting disease. | + | 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. | + | '''Severe haematological changes''' including profound '''anaemia''' and '''leucopaenia''' cause significant clinical signs. |
| − | Initial lymphocytopaenia and prolonged neutropaenia are also features of TBF. | + | Initial lymphocytopaenia and '''prolonged neutropaenia''' are also features of TBF. |
| − | A profound eosinophilia will occur for 17-20 days post-infection. <ref>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 </ref> | + | A profound '''eosinophilia''' will occur for 17-20 days post-infection. <ref>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 </ref> |
Low serum Alkaline Phosphatase (ALP) and decreased zinc, iron and albumin are also common biochemical findings, along with high urea, creatinine and bilirubin. | Low serum Alkaline Phosphatase (ALP) and decreased zinc, iron and albumin are also common biochemical findings, along with high urea, creatinine and bilirubin. | ||
| Line 29: | Line 29: | ||
Recovered animals develop immunity but it is unknown how long this is effective for. | Recovered animals develop immunity but it is unknown how long this is effective for. | ||
==Diagnosis== | ==Diagnosis== | ||
| − | Haematological and Biochemical changes as listed above along with marked pyrexia are highly suggestive, especially if historical findings are conducive. | + | 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 | leucocytes]] in peripheral blood is confirmative. | + | Demonstration of the '''organism''' in the '''[[Leucocytes | leucocytes]]''' in peripheral blood is confirmative. |
| − | On post-mortem examination, the [[Spleen | spleen]] is | + | On '''post-mortem''' examination, the '''[[Spleen | spleen]]''' is enlarged and mild liver damage is common. |
| − | Lesions within the lung are present and contain mononuclear infiltrate on histopathology. | + | Lesions within the '''lung''' are present and contain mononuclear infiltrate on histopathology. |
Thickening, ulceration and haemorrhage of the gastrointestinal tract become worse distally. | 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. | 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). | + | Antibodies can be detected using '''Indirect Immunofluorescence''' (IFAT), '''Complement Fixation''' and Immunoelectrophoresis (CIEP). |
==Treatment== | ==Treatment== | ||
| − | E. phagocytophila is susceptible to oxytetracycline, sulphamethazine, sulphadimidine, doxycycline and trimethoprim-sulphonamides. | + | ''E. phagocytophila'' is susceptible to '''oxytetracycline, sulphamethazine, sulphadimidine, doxycycline''' and '''trimethoprim-sulphonamides'''. |
==Control== | ==Control== | ||
Control of the [[Ticks | tick]] vector is expensive but effective. | Control of the [[Ticks | tick]] vector is expensive but effective. | ||
| Line 49: | Line 49: | ||
==References== | ==References== | ||
<references/> | <references/> | ||
| − | Animal Health & ProductIon Compendium, Tick Borne Fever datasheet, accessed 06/06/2011 @ http://www.cabi.org/ahpc/ | + | Animal Health & ProductIon Compendium, '''Tick Borne Fever datasheet''', accessed 06/06/2011 @ http://www.cabi.org/ahpc/ |
Revision as of 12:41, 6 June 2011
Also Known As – Pasture Fever – Tickborne Fever – Ruminant Anaplasmosis – TBF
Caused By – Anaplasma phagocytophila, previously known as Ehrlichia phagocytophila
Introduction
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.
TBF is transmitted by ixodes ticks. Both adults and nymphs can transmit 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
E. phagocytophila 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]
References
- ↑ 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
- ↑ 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
Animal Health & ProductIon Compendium, Tick Borne Fever datasheet, accessed 06/06/2011 @ http://www.cabi.org/ahpc/
Literature Search
Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation except for full text articles).
Tick-borne disease testing: canine erhlichiosis and anaplasmosis. Alleman, R.; The North American Veterinary Conference, Gainesville, USA, Small animal and exotics. Proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 17-21 January, 2009, 2009, pp 629-631 - Full Text Article