Tick-borne fever and pasteurellosis in sheep

Gilmour, J. L.; Brodie, TA; Holmes, P.H.

doi:10.1136/vr.111.22.512-b

Cited by 22 publications

(4 citation statements)

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“…However, this appeared to have stressed the goats enough to induce sufficient immunosuppression to allow the development of the experimentally induced pneumonic pasteurellosis. Similar observations have been made with viral infections in the respiratory tract or infection by Ehrlichia phagocytophilia (Davies et al, 1982;Gilmour et al, 1982;Buddle et al, 1990) but not previously with a gastrointestinal helminth infection.…”

Section: Discussionsupporting

confidence: 72%

The role of concurrent haemonchosis in the development of pneumonic pasteurellosis in goats

et al. 1994

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Section: Discussionsupporting

confidence: 72%

The role of concurrent haemonchosis in the development of pneumonic pasteurellosis in goats

et al. 1994

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“…These have been best documented in sheep and cattle with tick‐borne fever in Europe. A. phagocytophilum may predispose lambs to tick pyemia, which is characterized by lameness and paralysis caused by Staphylococcus aureus , 110 Pasteurella spp., 111,112 and Listeria monocytogenes 113 . Opportunistic infections also have been documented and suggested as a potential cause of mortality in humans and dogs with granulocytic anaplasmosis, 49,94,114 but are less well described than those in ruminants.…”

Section: Pathogenesismentioning

confidence: 99%

Canine Granulocytic Anaplasmosis: A Review

Carrade

Foley

Borjesson

et al. 2009

Veterinary Internal Medicne

175

183

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Anaplasma phagocytophilum is an emerging pathogen of humans, horses, and dogs worldwide that is transmitted by Ixodid ticks and maintained in a variety of small wild mammal species. Recent studies suggest that multiple strains of A. phagocytophilum may be circulating in wild and domestic animal populations, and these strains may have differential host tropisms and pathogenicity. The organism infects and survives within neutrophils by disabling key neutrophil functions, including neutrophil motility, phagocytosis, the oxidative burst mechanism, and neutrophil‐endothelial cell interactions, as well as interfering with neutrophil apoptosis. Coinfections with other tick‐borne pathogens may occur, especially Borrelia burgdorferi. A. phagocytophilum causes an acute febrile illness in dogs with lethargy and inappetence. Less frequent signs include lameness, coughing, polydipsia, intermittent vomiting, and hemorrhages. Diagnosis is based on finding morulae within granulocytes in the peripheral blood, the combination of acute and convalescent serology using immunofluorescent antibody techniques, and detection of the DNA of A. phagocytophilum using specific polymerase chain reaction assays. Whether persistent infection or reinfection with A. phagocytophilum occurs after natural infection requires additional study, with most reports suggesting that anaplasmosis is a self‐limiting disease in dogs that responds well to a 2‐week course of doxycycline therapy.

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“…Other workers have observed similar clinical signs in cattle 8,73 . Further studies in the UK and Scandinavia have clearly established that TBF variants of A. phagocytophilum are immunosuppressive, resulting in several disease syndromes including tick pyemia, 72,74 abortions, 74–79 pasteurellosis, 80–81 and septicemic listeriosis 82–83…”

Section: Immunosuppressionmentioning

confidence: 99%

“…Other workers have observed similar clinical signs in cattle. 8,73 Further studies in the UK and Scandinavia have clearly established that TBF variants of A. phagocytophilum are immunosuppressive, resulting in several disease syndromes including tick pyemia, 72,74 abortions, [74][75][76][77][78][79] pasteurellosis, [80][81] and septicemic listeriosis. [82][83] Neutrophils form the first line of defence against invading bacteria and fungi and possess a powerful array of cytotoxic enzymes, reactive oxidants, and associated processes, but neutrophils have high rates of spontaneous apoptosis and a very short half-life in the circulation of only 6-12 h. [84][85] In view of this high cytotoxic potential and short half-life, the neutrophil would seem to be an unlikely and unsuitable target for intracellular pathogens such as A. phagocytophilum.…”

Section: Immunosuppressionmentioning

confidence: 99%

Anaplasma phagocytophilum in Ruminants in Europe

Woldehiwet

2006

Annals of the New York Academy of Sciences

116

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The agent that causes tick-borne fever (TBF) in sheep was first described in 1940, 8 years after the disease was first recognized in Scotland. The same agent was soon shown to cause TBF in sheep and pasture fever in cattle in other parts of the UK, Scandinavia, and other parts of Europe. After the initial use of the name Rickettsia phagocytophila, the organism was given the name Cytoecetes phagocytophila to reflect its association with granulocytes and its morphological similarity with Cytoecetes microti. This name continued to be used by workers in the UK until the recent reclassification of the granulocytic ehrlichiae affecting ruminants, horses, and humans as variants of the same species, Anaplasma phagocytophilum. TBF and pasture fever are characterized by high fever, recurrent bacteremia, neutropenia, lymphocytopenia, thrombocytopenia, and general immunosuppression, resulting in more severe secondary infections such as tick pyemia, pneumonic pasteurellosis, listeriosis, and enterotoxemia. During the peak period of bacteremia as many as 90% of granulocytes may be infected. The agent is transmitted transtadially by the hard tick Ixodes ricinus, and possibly other ticks. After patent bacteremia, sheep, goats, and cattle become persistently infected "carriers," perhaps playing an important role in the maintenance of infection, in the flock/herd. Little is known about how efficiently ticks acquire and maintain infection in ruminant populations or whether "carrier" domestic ruminants play an important role as reservoirs of infection, but deer, other free-living ruminants, and wild rodents are also potential sources of infection. During the late 1990s serological evidence of infection of humans was demonstrated in several European countries, creating a renewed interest and increased awareness of the zoonotic potential of TBF variants. More recently, a few cases of human granulocytic anaplasmosis (HGA) have been reported in some European countries, but it remains to be established whether the variants causing HGA in Europe are genetically and biologically different from those causing TBF in ruminants. TBF is readily diagnosed by demonstrating intracytoplasmic inclusions in peripheral blood granulocytes or monocytes of febrile animals or by detecting specific DNA by polymerase chain reaction (PCR), and TBF variants of A. phagocytophilum can be cultivated in tick cell lines, but the differentiation of TBF variants from HGA variants awaits further investigations.

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Tick-borne fever and pasteurellosis in sheep

Cited by 22 publications

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The role of concurrent haemonchosis in the development of pneumonic pasteurellosis in goats

The role of concurrent haemonchosis in the development of pneumonic pasteurellosis in goats

Canine Granulocytic Anaplasmosis: A Review

Anaplasma phagocytophilum in Ruminants in Europe

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