Duration of tick attachment and Borrelia burgdorferi transmission

Piesman, Joseph; Mather, Thomas N.; Sinsky, Richard J.; Spielman, Andrew

doi:10.1128/jcm.25.3.557-558.1987

Cited by 454 publications

(152 citation statements)

References 16 publications

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“…We determined the extent of genetic heterogeneity within 1t burgdorferi that had been cultured from ticks that had fed on the control mice by means of ILFLP analysis (15) (Table 3). 21 United States tick isolates were tested; all were/g burgdorferi sensu stricto (RFLP group 1) type organisms. The sole exceptions were one California isolate and the JD-1 strain (21) which were considered to be/t burgdorferi sensu stricto variants because of the presence of additional faint bands on Southern blot.…”

Section: Resultsmentioning

confidence: 99%

Vaccination against Lyme disease caused by diverse Borrelia burgdorferi.

Fikrig

Telford

Wallich

et al. 1995

The Journal of Experimental Medicine

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SummaryDiversity and mutations in the genes for outer surface proteins (Osps) A and B ofBorrelia burgdorferi sensu lato (13, burgdorferi), the spirochetal agent of Lyme disease, suggests that a monovalent OspA or OspB vaccine may not provide protection against antigenically variable naturally occurring B, burgdorferi. We now show that OspA or OspB immunizations protect mice from tick-borne infection with heterogeneous/g burgdorferi from different geographic regions. This result is in distinct contrast to in vitro killing analyses and in vivo protection studies using syringe injections of/g burgdorferi as the challenge inoculum. Evaluations of vaccine efficacy against Lyme disease and other vector-borne infections should use the natural mode of transmission and not be predicated on classification systems or assays that do not rely upon the vector to transmit infection.V accination with outer surface proteins (Osps)lA or B from a Borrelia burgdorferi sensu law (13, burgdorferi) isolate (designated N40) protected C3H/HeJ mice from infection when challenged with the same strain (1, 2). Humoral immunity was sufficient for protection as the passive transfer of OspA or OspB antibodies protected C.B.-17 scid or C3H mice from/3; burgdorferi infection (1-4). OspA and OspB variability, including amino acid differences or truncations of the COOH terminus of the Osps, however, allowed/~ burgdorferi to survive in the presence of protective antibody in vitro and in vivo, predicting a lack of vaccine efficacy (2, 5-11). In addition, spirochetes have been identified that lack the 49-kb plasmid encoding ospA and ospB or have chimeric Osps due to homologous recombination between ospA and ospB, suggesting that OspA or OspB mediated immunity would not be protective in the event of infection by these mutants (7,12). The infectivity of these mutant spirochetes in selected hosts has not yet been delineated. RFLP, multilocus enzyme electrophoresis, or nucleic acid hybridization studies distinguished as many as four groups of/t burgdorferi, with the 1 Abbreviation used in this paper: Osp, outer surface protein. 215description of three new proposed species-/g burgdorferi sensu stricto, Borrelia afzelii, and Borrelia garinii (13)(14)(15)(16)(17). Similarly, reactivity with OspA mAbs divided/g burgdorferi into seven serogroups which upon detailed analysis (several of the serotypes were variants of the three species that arose from osp recombination) corresponded to the three new species (13). lg burgdo~feri sensu stricto is prevalent in North America whereasEuropean sites may contain all three species. In vivo passive immunization studies demonstrated that antiserum against spirochetes from individual groups protected scid mice or hamsters against challenge with homologous, but not heterologous/~ burgdorferi (8,18).The in vivo protection studies used single isolates of/~ burgdorferi, and syringe inoculations as the method of spirochete challenge, and therefore do not mimic natural transmission of the agent. Accordingly, we have shown that v...

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Section: Resultsmentioning

confidence: 99%

Vaccination against Lyme disease caused by diverse Borrelia burgdorferi.

Fikrig

Telford

Wallich

et al. 1995

The Journal of Experimental Medicine

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“…In the first experiment, Piesman et al (1987) applied three nymphal ticks with Borrelia infection rates b 907 to each of 18 Golden Syrian female hamsters and 24 white-footed mice. Animal hosts were randomly divided into three groups of 6 hamsters and 8 mice.…”

Section: Datamentioning

confidence: 99%

“…Once an attached tick is found, it can be tested for the presence of Borrelia spirochetes, the causative agent of Lyme disease. However, even if the tick tests positive, the risk of Lyme disease may still be low, as the probability of contracting Lyme disease appears to depend on the duration of tick attachment (Piesman et al, 1987;Piesman et al, 1991;Matuschka and Spielman, 1993;Piesman, 1993). In this paper, we use previously published animal data (Piesman et al, 1987;Piesman et al, 1991;Piesman, 1993) to estimate the probability of contracting Lyme disease from a tick that has been attached for a given duration of time.…”

Section: Introductionmentioning

confidence: 99%

“…The relationship between the duration of tick attachment and the rate of spirochetal transmission was examined in three studies (Piesman et al, 1987(Piesman et al, , 1991Piesman, 1993) by attaching ticks to healthy animal hosts, removing the ticks at specified time intervals and then determining whether the hosts had become infected. These studies report that the probability (pt) of an animal host contracting Lyme disease is low for an attachment time t of 24 hours (p24 0X07) and increases thereafter (p42 0X25, p48 0X52, and p72 0X93).…”

Section: Introductionmentioning

confidence: 99%

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Estimation of the Transmission Probability of Lyme Borreliosis

1999

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Whether physicians should prophylactically treat tick bites in areas endemic for Lyme disease has been debated. The high rates of tick infection (10–50%) found in Lyme disease‐endemic areas suggest that tick bites should be treated; conversely, the low rates of Lyme disease (1–4%) found in recent clinical trials of untreated tick‐bite victims suggest caution in treatment. Medical advice given from Lyme‐disease World Wide Web sites is equally contradictory, ranging from suggesting that all tick bites should be treated to suggesting that no tick bites be treated. To clarify this issue, we estimate the transmission probability of the causative agent of Lyme disease, Borrelia burgdorferi, for different durations of tick attachment. The data used to estimate this transmission probability is obtained from previously published animal studies. The accuracy of these estimates is assessed by comparing model predictions of the number of Lyme disease cases to that actually observed in clinical studies of Lyme disease. Our results suggest that tick bites should be treated only when it is known that the duration of tick attachment is longer than 48 hours.

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“…The risk of spirochete transmission increases with the duration of tick attachment after a bite. 8 After transmission and an incubation period of 3-32 days, the spirochete may move outward from the skin and disseminate in lymph and blood, resulting in eventual spread to other organs. The spirochete has been isolated from samples of ECM lesions, cerebrospinal fluid (CSF), and blood, and was histologically isolated in synovium and myocardium from infected patient~.~-ll The dissemination results in multisystem manifestations as well as characteristic immune abnormalities.…”

Section: Pathophysiologymentioning

confidence: 99%

Clinical Features and Treatment of Lyme Disease

Tortorice

Heim‐Duthoy

1989

Pharmacotherapy

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Lyme disease is caused by the spirochete Borrelia burgdorferi, which is carried by infected ticks. This disorder has a variable clinical course with multisystem manifestations, including dermatologic, neurologic, cardiac, and rheumatologic abnormalities. Although Lyme disease has been commonly associated with stages, the utility of staging may be limited due to the inconsistency of clinical manifestations among patients. Furthermore, stages may overlap as a result of the acute and chronic phases of the disease. The laboratory characteristics of Lyme disease are highly variable. The use of microbiologic cultures in establishing the diagnosis requires several weeks and has a low yield of positivity. Serologic assays using indirect immunofluorescence and enzyme-linked immunosorbence are preferred. Because of the highly variable features of Lyme disease, clinical and laboratory features must be correlated and interpreted in the context of the disease. Treatment should be initiated as early as possible after the onset of illness. Prompt therapeutic intervention may result in early resolution of the dermatologic hallmark, erythema chronicum migrans, as well as prevention and attenuation of subsequent complications.

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Duration of tick attachment and Borrelia burgdorferi transmission

Cited by 454 publications

References 16 publications

Vaccination against Lyme disease caused by diverse Borrelia burgdorferi.

Vaccination against Lyme disease caused by diverse Borrelia burgdorferi.

Estimation of the Transmission Probability of Lyme Borreliosis

Clinical Features and Treatment of Lyme Disease

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