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Future Studies on Lyme Disease

Competent reservoirs for Borrelia burgdorferi are those with a high “realized reservoir competence” (Brunner et al. 2008). This competence is a function of the probability that (1) the host is infected (infection prevalence) and that (2) the infected host will transmit the infection to the vector (infectivity). The white-footed mouse (Peromyscus leucopus) is a competent reservoir for B. burgdorferi in North America as the majority of its population is infected and they are highly infective to feeding ticks (Mather et al. 1989). Larger mammals are generally less competent reservoirs (Tilly et al. 2008). Brunner et al (2008) found that infection prevalence is low in white-tailed deer (Odocoileus virginianus), a large mammal commonly parasitized by infected adult ticks (Magnarelli et al. 2004). In fact, Ullman et al (2003) concluded that sera taken from mule deer (Odocoileus hemionus) was completely borreliacidal for both B. burgdorferi and B. bissettii due to their immune system’s complement pathway. Their infectivity is also significantly lower than that of the white-footed mouse (Brunner et al. 2008).


But what about humans? Nymphs will feed on humans. Can humans infected with B. burgdorferi (or some other Borrelia strain) infect nymphs? And, if so, can these nymphs then infect another host with their next blood-meal? We know there is a decent infection prevalence of B. burgdorferi in humans (Gaito et al. 2014), but can we pass on this infection to other vectors/hosts? I was unable to find an existing study that explored these questions for humans.

In order to address these questions, I would calculate infection prevalence (π) and infectivity (φ) in people according to calculations developed by Brunner et al (2008). This will require blood samples from a number people (as many as possible), preferably from several locations that have different Borrelia species/strains. These blood samples can then be fed into artificial feeders using a silicone membrane proposed by Andrade et al (2014). [Another option is to use humanized mouse models, which will require us to first develop one specifically designed for B. burgdorferi (Vaughan et al. 2012).] Once non-infected nymphs feed on these blood samples, we will let them molt before screening them for B. burgdorferi using a direct immunofluorescent assay (LoGiudice et al. 2003). Results from these tests will be used in the before-mentioned calculations.


This information may be able to tell us whether or not people, who travel more than ordinary animals, are partly responsible for the recent spread in Lyme disease. Many people are unaware that they have Lyme disease, which isn’t helped by the high incidence of false negatives in serological tests (Schutzer et al. 1990). This allows for the infection to persist in many people unknowingly, increasing the infection prevalence within the human population. Additionally, if we can get several Borrelia species/strains involved in the study, we could see whether our competency as hosts differs among Borrelia species/strains.


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References

Andrade, J.J., Xu, G., Rich, S.M. 2014. A silicone membrane for in vitro feeding of Ixodes scapularis (Ixodida: Ixodidae). Journal of Medical Entomology 51: 878-879.

Brunner, J.L., LoGiudice, K., Ostfeld, R.S. 2008. Estimating reservoir competence of Borrelia burgdorferi hosts: prevalence and infectivity, sensitivity, and specificity. Journal of Medical Entomology 45: 139-147.

Gaito, A., Gjivoje, V., Lutz, S., Baxter, B. 2014. Comparative analysis of the infectivity rate of both Borrelia burgdorferi and Anaplasma phagocytophilum in humans and dogs in a New Jersey community. Infection and Drug Resistance 7: 199-201.

LoGiudice, K., Ostfeld, R.S., Schmidt, K.A., Keesing, F. 2003. The ecology of infectious disease: effects of host diversity and community composition on Lyme disease risk. Proceedings of the National Academy of Science USA 100: 567-571.

Magnarelli, L.A., Ijdo, J.W., Ramakrishnan, U., Henderson, D.W., Stafford, K.C., Fikrig, E. 2004. Use of recombinant antigens of Borrelia burgdorferi and Anaplasma phagocytophilum in enzyme-linked immunosorbent assays to detect antibodies in white-tailed deer. Journal of Wildlife Diseases 40: 249-258.

Mather, T.N., Wilson, M.L., Moore, S.I., Ribeiro, J.M.C., Spielman, A. 1989. Comparing the relative potential of rodents as reservoirs of the Lyme disease spirochete (Borrelia burgdorferi). American Journal of Epidemiology 130: 143-150.

Schutzer, S.E., Coyle, P.K., Belman, A.L., Golightly, M.G., Drulle, J. 1990. Sequestration of antibody to Borrelia burgdorferi in immune complexes in seronegative Lyme disease. The Lancet 335: 312-315.

Tilly, K., Rosa, P.A., Stewart, P.E. 2008. Biology of infection with Borrelia burgdorferi. Infectious Diseases Clinics of North America 22: 217-234.

Ullmann, A.J., Lane, R.S., Kurtenbach, K., Miller, M., Schriefer, M.E., Zeidner, N., Piesman, J. 2003. Bacteriolytic activity of selected vertebrate sera for Borrelia burgdorferi sensu stricto and Borrelia bissettii. The Journal of Parasitology 89: 1256-1257.

Vaughan, A.M., Kappe, S.H., Ploss, A., Mikolajczak, S.A. 2012. Development of humanized mouse models to study human malaria parasite infection. Future Microbiology 7: 657-665.

Waladde, S.M., Young, A.S., Morzaria, S.P. 1996. Artificial feeding of Ixodid ticks. Parasitology Today 12: 272-278.