6 research outputs found

    A review on the eco-epidemiology and clinical management of human granulocytic anaplasmosis and its agent in Europe

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    Anaplasma phagocytophilum is the agent of tick-borne fever, equine, canine and human granulocytic anaplasmosis. The common route of A. phagocytophilum transmission is through a tick bite, the main vector in Europe being Ixodes ricinus. Despite the apparently ubiquitous presence of the pathogen A. phagocytophilum in ticks and various wild and domestic animals from Europe, up to date published clinical cases of human granulocytic anaplasmosis (HGA) remain rare compared to the worldwide status. It is unclear if this reflects the epidemiological dynamics of the human infection in Europe or if the disease is underdiagnosed or underreported. Epidemiologic studies in Europe have suggested an increased occupational risk of infection for forestry workers, hunters, veterinarians, and farmers with a tick-bite history and living in endemic areas. Although the overall genetic diversity of A. phagocytophilum in Europe is higher than in the USA, the strains responsible for the human infections are related on both continents. However, the study of the genetic variability and assessment of the difference of pathogenicity and infectivity between strains to various hosts has been insufficiently explored to date. Most of the European HGA cases presented as a mild infection, common clinical signs being pyrexia, headache, myalgia and arthralgia. The diagnosis of HGA in the USA was recommended to be based on clinical signs and the patient’s history and later confirmed using specialized laboratory tests. However, in Europe since the majority of cases are presenting as mild infection, laboratory tests may be performed before the treatment in order to avoid antibiotic overuse. The drug of choice for HGA is doxycycline and because of potential for serious complication the treatment should be instituted on clinical suspicion alone

    Genetic variability of Anaplasma phagocytophilum and its implication in the ecology of anaplasmosis in Central Europe

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    Anaplasma phagocytophilum is the causative agent of granulocytic anaplasmosis of both medical and veterinary importance. In Europe, A. phagocytophilum is transmitted by the Ixodid ticks, mostly Ixodes ricinus. It is mantained in nature by specific assciation to the several vertebrate hosts. In order to understand the ecology of this pathogen in Central Europe we have analyzed and compared the genetic variability of different A. phagocytophilum strains from questing and feeding ticks collected from vegetation and different vertebrate hosts (roe deers, rodents, birds, sheeps, dogs), as well as blood and biological samples of some vertebrate hosts (rodents and birds), from several sites in two regions of Central Europe (Slovakia and Northern Italy). A. phagocytophilum was detected in questing and host feeding I. ricinus ticks from all studied sites, as well as from feeding I. trianguliceps on rodents and rodents’ ear and spleen biopsies. Prevalence of A. phagocytophilum in areas with rodents was much lower (1.1%, 0.6%) than in areas without rodents (6%). In areas where I. trianguliceps ticks were absent we did not detect A. phagocytophilum in rodents. Phylogenetic analyses of A. phagocytophilum positive samples have shown that A. phagocytophilum genotypes in questing I. ricinus and feeding I. ricinus from ungulates, birds and dogs were distinct from genotypes found in rodents and feeding I. trianguliceps. our study from Central Europe confirms that A. phagocytophilum strains have specific associations with two vectors and different reservoir hosts. unlike in the uSA, A. phagocytophilum genotypes that are associated with rodents are probably transmitted solely by I. trianguliceps ticks, therefore these strains may be not of risk for human

    Ecology of Anaplasmosis in Central Europe

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    Anaplasma phagocytophilum is the causative agent of granulocytic anaplasmosis of both medical and veterinary importance. In Europe, it is transmitted by the Ixodid ticks, mostly Ixodes ricinus, however other tick species such as Ixodes trianguliceps probably contribute to the enzootic cycle of this bacterium. According to some studies, the intraspecific variability of A. phagocytophilum plays an important role in the ecology of this pathogen. In order to understand the ecology of this pathogen in Central Europe we have analyzed and compared the genetic variability of different A. phagocytophilum strains from questing and feeding ticks collected from vegetation and different vertebrate hosts (roe deers, rodents, birds, sheeps, dogs) as well as blood and biological samples of some vertberate hosts (rodents and birds) from two regions of Central Europe (Slovakia and Northern Italy). A. phagocytophilum was detected in questing and host feeding I. ricinus ticks from all studied sites, rodent feeding I. trianguliceps, ear and spleen biopsies of rodents. Prevalence of A. phagocytophilum in areas with rodents was much lower (1.1%, 0.6%) than in areas without rodents (6%). In areas where I. trianguliceps were absent we did not detect A. phagocytophilum in rodents. Phylogenetic analysis of four genetic loci in positive samples have shown that genotypes in questing I. ricinus and feeding I. ricinus from ungulates, birds and dogs were distinct from genotypes found in rodents and feeding I. trianguliceps. Msp4, DOV and GroESL sequences of A. phagocytophilum genotypes showed considerable heterogeneity but none of the positive questing I. ricinus tick was infected with the rodent genotype that was identical to the genotype found in I. trianguliceps. GroESL sequences from rodents were closely related to the sequences found in questing I. persulcatus. Our study from Central Europe confirms the previous findings from UK that A. phagocytophilum strains have specific associations with two vectors and different reservoir hosts. Unlike in the US, A. phagocytophilum ecotypes that are associated with rodents are probably transmitted solely by I.trianguliceps ticks, therefore these strains are not of risk for human
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