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Population-wide Impacts of Lyme Disease

As mentioned in a previous blog entry, Reservoir host of Lyme Disease, the white-footed mouse (Peromyscus leucopus) is the most competent reservoir for Borrelia burgdorferi (Levine et al. 1985; Ostfeld et al. 1996; CFSPH 2011). The mice do not exhibit any signs when infected, but several researchers found that their bodies do develop a serological response to the bacterium’s proteins (Tilly et al. 2008). The majority of white-footed mice become persistently infected (Magnarelli et al. 1988; Schwan et al. 1988). This blog will discuss how B. burgdorferi impacts the white-footed mouse population. We will also examine how another disease commonly associated with white-footed mice can affect the transmission of Lyme disease.


The incidence of a disease in a population is important when assessing population-wide impacts of a pathogen. Incidence can be defined as the number of new instances of illness, or persons becoming ill, during a given period in a specified population (Porta et al. 2014). In other words, incidence is a measure of the number of new cases of a particular disease in a population. It is basically a measure of how quickly a disease spreads. Bunikis et al (2004) found that the incidence of B. burgdorferi in a natural population of white-footed mice in Connecticut was 0.2 cases/mouse/week. A study in Maryland found an incidence rate of 6-11.5 cases/1,000 mouse-days, pointing out that rates were 10 times greater during periods of high exposure to nymphal Ixodes scapularis ticks (nymph season) (Hofmeister et al. 1999). Interestingly, the incidence rate reported by Hofmeister et al (1999) was 3 times lower than the rate found by Bunikis et al (2004). This may be because Maryland has a lower endemicity of B. burgdorferi than Connecticut (CDC 1997). The high incidence rate of infection with B. burgdorferi in the Connecticut study is unusual for human zoonotic diseases with enzootic transmission cycles. The fact that nearly all mice became infected during their study suggests that it is more typical of an epizootic outbreak. In that way, the spread of Lyme disease among white-footed mice is similar to that of plague (Kartman and Hudson, 1971).


The prevalence is the proportion of cases in the population at a given time and indicates how widespread a disease is (Porta et al. 2014). Anderson et al (1987) found that the prevalence of B. burgdorferi in white-footed mice was about 75% in mice collected between June and August, while it was about 33% during December-March months. This is probably tightly linked with nymph season, which occurs in late spring/early summer. Mather et al (1989) found that the prevalence of infection in white-footed mouse in Massachusetts was 90%, which was a lot higher than the prevalence in chipmunks (Tamia striatus; 75%) and meadow voles (Microtus pennsylvanicus; 5.5%). Another study done in Wisconsin found that the prevalence of B. burgdorferi in white-footed mice was 88% (Anderson et al. 1987). Overall, prevalence of B. burgdorferi is relatively high in white-footed mice, especially during peak nymph season.

Another important thing to consider in white-footed mice is their persistent infection with B. burgdorferi. There is some debate whether or not white-footed mice really do mount an antibody response during infection (Schwan et al. 1989; Barbour et al. 2008). A potential lack of antibodies may allow for the spirochete to stay longer in the mouse host. Another possible reason for the infection’s persistence is that mice experience constant feeding by deer ticks, especially larvae and nymphs, due to their similar wooded habitat requirement. If their bodies were to be able to rid themselves of B. burgdorferi, the high incidence rate would ensure most would be re-infected again. Overall, most white-footed mice have persistent B. burgdorferi infection (Magnarelli et al. 1988). An important side-effect of this high persistence is the resultantly high infectivity. For example, Donahue et al (1987) found that white-footed mice can remain infective for at least 200 days after a single infective tick bite. White-footed mice can infect as many nymphal ticks as 12 chipmunks or 221 voles (Mather et al. 1989), demonstrating how infectious they really are. This is why most B. burgdorferi infections in Ixodes scapularis results from a blood meal from white-footed mice (Ostfeld et al. 1995).


Borrelia burgdorferi is not the only pathogen to use white-footed mice as its host. Another important disease in white-footed mice is Babesiosis, whose etiologic agent is Babesia microti. Anderson et al (1986) found that this protozoan parasite was present in 57% of the white-footed mice sampled. A study done on Nantucket Island found that 31 of the 39 captured white-footed mice were positive for B. microti, giving a prevalence of 80% (Healy et al. 1976). So how do B. microti infections affect B. burgdorferi? It seems that they have no problem co-existing in the same host as several studies found both pathogens present in white-footed mice (Anderson et al. 1986, 1991; Magnarelli et al. 2013). Coleman et al (2005) found that both infections proceed independently of one another suggesting there is no synergism between them. This would mean that a co-infection is not more pathogenic than a single infection. Similar results were found by Wang et al (2000), who reported that coinfections did not worsen the long term outcome with regard to constitutional, musculoskeletal, and neurological symptoms. Other researchers, however, found that babesial infections can enhance Lyme disease myocarditis and that B. microti may impair host defense mechanisms that further supports B. burgdorferi infections in the host (Purvis 1977; De Vos et al. 1987; Kimsey et al. 1990). Coinfections may therefore lead to a longer duration of illness and exacerbated symptoms (in people) including myalgia, fatigue, sweats, anorexia, erythema migrans, and conjunctivitis (Krause et al. 1996; Dos Santos and Kain, 1999). More studies are therefore needed to fully understand how coinfections between these two pathogens differ from regular single infections.


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References

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