scholarly journals Seasonal Prevalence of Lyme Disease Spirochetes in a Heterothermic Mammal, the Edible Dormouse (Glis glis)

2014 ◽  
Vol 80 (12) ◽  
pp. 3615-3621 ◽  
Author(s):  
Joanna Fietz ◽  
Jürgen Tomiuk ◽  
Franz-Rainer Matuschka ◽  
Dania Richter

ABSTRACTIn Europe, dormice serve as competent reservoir hosts for particular genospecies of the tick-borne agent of Lyme disease (LD) and seem to support them more efficiently than do mice or voles. The longevity of edible dormice (Glis glis) and their attractiveness for ticks may result in a predominance of LD spirochetes in ticks questing in dormouse habitats. To investigate the role of edible dormice in the transmission cycle of LD spirochetes, we sampled skin tissue from the ear pinnae of dormice inhabiting five different study sites in south western Germany. Of 501 edible dormice, 12.6% harbored DNA of LD spirochetes. Edible dormice were infected most frequently with the pathogenic LD spirocheteBorrelia afzelii. The DNA ofB. gariniiandB. bavariensiswas detected in ca. 0.5% of the examined individuals. No spirochetal DNA was detectable in the skin of edible dormice until July, 6 weeks after they generally start to emerge from their obligate hibernation. Thereafter, the prevalence of spirochetal DNA in edible dormice increased during the remaining period of their 4 to 5 months of activity, reaching nearly 40% in September. Males were more than four times more likely to harbor LD spirochetes than females, and yearlings were almost twice more likely to be infected than adults. The seasonality of the prevalence of LD spirochetes in edible dormice was pronounced and may affect their role as a reservoir host in respect to other hosts.

2004 ◽  
Vol 72 (4) ◽  
pp. 2442-2444 ◽  
Author(s):  
Dania Richter ◽  
Birte Klug ◽  
Andrew Spielman ◽  
Franz-Rainer Matuschka

ABSTRACT We compared the relative reservoir competence of European wood mice for two genospecies of Lyme disease spirochetes by analyzing susceptibility, intrinsic incubation period, and degree and duration of infectivity. Borrelia afzelii, specializing in particular reservoir hosts, is better adapted to those hosts than is the more generalist genospecies B. burgdorferi sensu stricto.


1994 ◽  
Vol 170 (1) ◽  
pp. 122-127 ◽  
Author(s):  
F.-R. Matuschka ◽  
H. Eiffert ◽  
A. Ohlenbusch ◽  
A. Spielman

2011 ◽  
Vol 77 (16) ◽  
pp. 5716-5721 ◽  
Author(s):  
M. Marsot ◽  
M. Sigaud ◽  
J. L. Chapuis ◽  
E. Ferquel ◽  
M. Cornet ◽  
...  

ABSTRACTLittle attention has been given in scientific literature to how introduced species may act as a new host for native infectious agents and modify the epidemiology of a disease. In this study, we investigated whether an introduced species, the Siberian chipmunk (Tamias sibiricus barberi), was a potentially new reservoir host forBorrelia burgdorferisensu lato, the causative agent of Lyme disease. First, we ascertained whether chipmunks were infected by all of theB. burgdorferisensu lato genospecies associated with rodents and available in their source of infection, questing nymphs. Second, we determined whether the prevalence and diversity ofB. burgdorferisensu lato in chipmunks were similar to those of a native reservoir rodent, the bank vole (Myodes glareolus). Our research took place between 2006 and 2008 in a suburban French forest, where we trapped 335 chipmunks and 671 voles and collected 743 nymphs of ticks that were questing for hosts by dragging on the vegetation. We assayed forB. burgdorferisensu lato with ear biopsy specimens taken from the rodents and in nymphs using PCR and restriction fragment length polymorphism (RFLP). Chipmunks were infected by the threeBorreliagenospecies that were present in questing nymphs and that infect rodents (B. burgdorferisensu stricto,B. afzelii, andB. garinii). In contrast, voles hosted onlyB. afzelii. Furthermore, chipmunks were more infected (35%) than voles (16%). These results may be explained by the higher exposure of chipmunks, because they harbor more ticks, or by their higher tolerance of otherB. burgdorferisensu lato genospecies than ofB. afzelii. If chipmunks are competent reservoir hosts forB. burgdorferisensu lato, they may spill backB. burgdorferisensu lato to native communities and eventually may increase the risk of Lyme disease transmission to humans.


2005 ◽  
Vol 71 (3) ◽  
pp. 1336-1345 ◽  
Author(s):  
Horacio Gil ◽  
Marta Barral ◽  
Raquel Escudero ◽  
Ana L. García-Pérez ◽  
Pedro Anda

ABSTRACT The role of small mammals as reservoir hosts for Borrelia burgdorferi was investigated in several areas where Lyme disease is endemic in northern Spain. A low rate of infestation by Ixodes ricinus nymphs was found in the small mammal populations studied that correlated with the near-absence of B. burgdorferi sensu lato in 184 animals tested and with the lack of transmission of B. burgdorferi sensu lato to I. ricinus larvae that fed on them. In contrast, questing ticks collected at the same time and in the same areas were found to carry a highly variable B. burgdorferi sensu lato repertoire (B. burgdorferi sensu stricto, Borrelia garinii, Borrelia valaisiana, and Borrelia afzelii). Interestingly, the only isolate obtained from small mammals (R57, isolated from a bank vole) grouped by phylogenetic analyses with other Borrelia species but in a separate clade from the Lyme disease and relapsing fever organisms, suggesting that it is a new species. This new agent was widely distributed among small mammals, with infection rates of 8.5 to 12% by PCR. Moreover, a high seroprevalence to B. burgdorferi sensu lato was found in the animal sera, suggesting cross-reactivity between B. burgdorferi sensu lato and R57. Although small mammals do not seem to play an important role as reservoirs for B. burgdorferi sensu lato in the study area, they seem to be implicated in the maintenance of spirochetes similar to R57.


2018 ◽  
Vol 200 (13) ◽  
Author(s):  
Melissa L. Anacker ◽  
Dan Drecktrah ◽  
Richard D. LeCoultre ◽  
Meghan Lybecker ◽  
D. Scott Samuels

ABSTRACTThe rRNA genes ofBorrelia(Borreliella)burgdorferiare unusually organized; the spirochete has a single 16S rRNA gene that is more than 3 kb from a tandem pair of 23S-5S rRNA operons. We generated anrncnull mutant inB. burgdorferithat exhibits a pleiotropic phenotype, including decreased growth rate and increased cell length. Here, we demonstrate that endoribonuclease III (RNase III) is, as expected, involved in processing the 23S rRNA inB. burgdorferi. The 5′ and 3′ ends of the three rRNAs were determined in the wild type andrncBbmutants; the results suggest that RNase III inB. burgdorferiis required for the full maturation of the 23S rRNA but not for the 5S rRNA nor, curiously, for the 16S rRNA.IMPORTANCELyme disease, the most common tick-borne zoonosis in the Northern Hemisphere, is caused by the bacteriumBorrelia(Borreliella)burgdorferi, a member of the deeply branching spirochete phylum.B. burgdorfericarries a limited suite of ribonucleases, enzymes that cleave RNA during processing and degradation. Several ribonucleases, including RNase III, are involved in the production of ribosomes, which catalyze translation and are a major target of antibiotics. This is the first study to dissect the role of an RNase in any spirochete. We demonstrate that an RNase III mutant is viable but has altered processing of rRNA.


2014 ◽  
Vol 89 (2) ◽  
pp. 1119-1128 ◽  
Author(s):  
Jussi Hepojoki ◽  
Anja Kipar ◽  
Yegor Korzyukov ◽  
Lesley Bell-Sakyi ◽  
Olli Vapalahti ◽  
...  

ABSTRACTBoid inclusion body disease (BIDB) is a fatal disease of boid snakes, the etiology of which has only recently been revealed following the identification of several novel arenaviruses in diseased snakes. BIBD-associated arenaviruses (BIBDAV) are genetically divergent from the classical Old and New World arenaviruses and also differ substantially from each other. Even though there is convincing evidence that BIBDAV are indeed the etiological agent of BIBD, the BIBDAV reservoir hosts—if any exist besides boid snakes themselves—are not yet known. In this report, we use University of Helsinki virus (UHV; a virus that we isolated from aBoa constrictorwith BIBD) to show that BIBDAV can also replicate effectively in mammalian cells, including human cells, provided they are cultured at 30°C. The infection induces the formation of cytoplasmic inclusion bodies (IB), comprised mainly of viral nucleoprotein (NP), similar to those observed in BIBD and in boid cell cultures. Transferring infected cells from 30°C to 37°C ambient temperature resulted in progressive declines in IB formation and in the amounts of viral NP and RNA, suggesting that BIBDAV growth is limited at 37°C. These observations indirectly indicate that IB formation is linked to viral replication. In addition to mammalian and reptilian cells, UHV infected arthropod (tick) cells when grown at 30°C. Even though our findings suggest that BIBDAV have a high potential to cross the species barrier, their inefficient growth at mammalian body temperatures indicates that the reservoir hosts of BIBDAV are likely species with a lower body temperature, such as snakes.IMPORTANCEThe newly discovered boid inclusion body disease-associated arenaviruses (BIBDAV) of reptiles have drastically altered the phylogeny of the familyArenavirus. Prior to their discovery, known arenaviruses were considered mainly rodent-borne viruses, with each arenavirus species having its own reservoir host. BIBDAV have so far been demonstrated in captive boid snakes, but their possible reservoir host(s) have not yet been identified. Here we show, using University of Helsinki virus as a model, that these viruses are able to infect mammalian (including human) and arthropod cells. Our results providein vitroproof of the considerable ability of arenaviruses to cross species barriers. However, our data indicate that BIBDAV growth occurs at 30°C but is inhibited at 37°C, implying that crossing of the species barrier would be hindered by the body temperature of mammalian species.


2016 ◽  
Vol 84 (5) ◽  
pp. 1274-1286 ◽  
Author(s):  
Denny Maaz ◽  
Sebastian Rausch ◽  
Dania Richter ◽  
Jürgen Krücken ◽  
Anja A. Kühl ◽  
...  

Small rodents serve as reservoir hosts for tick-borne pathogens, such as the spirochetes causing Lyme disease. Whether natural coinfections with other macroparasites alter the success of tick feeding, antitick immunity, and the host's reservoir competence for tick-borne pathogens remains to be determined. In a parasitological survey of wild mice in Berlin, Germany, approximately 40% ofIxodes ricinus-infested animals simultaneously harbored a nematode of the genusHeligmosomoides. We therefore aimed to analyze the immunological impact of the nematode/tick coinfection as well as its effect on the tick-borne pathogenBorrelia afzelii. Hosts experimentally coinfected withHeligmosomoides polygyrusand larval/nymphalI. ricinusticks developed substantially stronger systemic type 2 T helper cell (Th2) responses, on the basis of the levels of GATA-3 and interleukin-13 expression, than mice infected with a single pathogen. During repeated larval infestations, however, anti-tick Th2 reactivity and an observed partial immunity to tick feeding were unaffected by concurrent nematode infections. Importantly, the strong systemic Th2 immune response in coinfected mice did not affect susceptibility to tick-borneB. afzelii. An observed trend for decreased local and systemic Th1 reactivity againstB. afzeliiin coinfected mice did not result in a higher spirochete burden, nor did it facilitate bacterial dissemination or induce signs of immunopathology. Hence, this study indicates that strong systemic Th2 responses in nematode/tick-coinfected house mice do not affect the success of tick feeding and the control of the causative agent of Lyme disease.


2011 ◽  
Vol 79 (11) ◽  
pp. 4681-4687 ◽  
Author(s):  
Marije Oosting ◽  
Hadewych ter Hofstede ◽  
Frank L. van de Veerdonk ◽  
Patrick Sturm ◽  
Bart-Jan Kullberg ◽  
...  

ABSTRACTInterleukin-23 (IL-23) is known to play a crucial role in the development and maintenance of T helper 17 cells. It has been previously demonstrated that IL-17 is involved in experimental Lyme arthritis, caused byBorrelia burgdorferibacteria. However, the precise role of the IL-23 receptor (IL-23R) for theB. burgdorferi-induced IL-17 responses or human Lyme disease has not yet been elucidated. IL-23R single nucleotide polymorphism (SNP) rs11209026 was genotyped using the TaqMan assay. Functional studies were performed using peripheral blood mononuclear cells, and cytokines were measured using enzyme-linked immunosorbent assay (ELISA). Dose-dependent production of IL-23 and IL-17 byB. burgdorfericould be observed. Interestingly, when IL-23 bioactivity was inhibited by a specific antibody against IL-23p19, IL-17 production was significantly downregulated. In contrast, production of gamma interferon (IFN-γ) was not affected after the blockade of IL-23 activity. Moreover, individuals bearing a single nucleotide polymorphism in the IL-23R gene (Arg381Gln) produced significantly less IL-17 afterB. burgdorferistimulation compared with that of the individuals bearing the wild type. Despite lower IL-17 production, the IL-23R gene polymorphism did not influence the development of chronic Lyme disease in a cohort of patients with Lyme disease. This study demonstrates that IL-23R signaling is needed forB. burgdorferi-induced IL-17 productionin vitroand that an IL-23R gene SNP leads to impaired IL-17 production. However, the IL-23R gene polymorphism is not crucial for the pathogenesis of chronic Lyme.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Heidi K. Goethert ◽  
Thomas N. Mather ◽  
Richard W. Johnson ◽  
Sam R. Telford

AbstractPowassan virus lineage 2 (deer tick virus) is an emergent threat to American public health, causing severe neurologic disease. Its life cycle in nature remains poorly understood. We use a host-specific retrotransposon-targeted real time PCR assay to test the hypothesis that white-footed mice, considered the main eastern U.S. reservoir of the coinfecting agent of Lyme disease, is the reservoir for deer tick virus. Of 20 virus-infected host-seeking nymphal black-legged ticks 65% fed on shrews and none on mice. The proportion of ticks feeding on shrews at a site is positively associated with prevalence of viral infection, but not the Lyme disease agent. Viral RNA is detected in the brain of one shrew. We conclude that shrews are a likely reservoir host for deer tick virus and that host bloodmeal analysis can provide direct evidence to incriminate reservoir hosts, thereby promoting our understanding of the ecology of tick-borne infections.


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