Co-Infection
The Problem
Co-infection could represent a major potential problem, mainly because the Ixodes ticks that transmit B. burgdorferi often carry—and simultaneously transmit—other emerging pathogens such as Anaplasma (Ehrlichia) species, the causative agent of human anaplasmosis and Babesia microti, which causes babesiosis. In Europe and Asia, Ixodes ticks also are known to transmit tick-borne encephalitis viruses. Fortunately, this tickborne viral infection has not yet been reported in the United States, although co-infections with Powasan virus and deer tick virus have been reported.
Co-infection by some or all of these other infectious agents may interfere with the clinical diagnosis of Lyme borreliosis and/or adversely influence host defense mechanisms, thereby altering landmark characteristics of the disease and the severity of infection (J. Infect. Dis. 186: 428, 2002; J Infect Dis 186, 428, 2002). Studies conducted by NIAID grantees indicate that co-infection with HGE increases the severity of Lyme borreliosis (Infect Immun 69, 3359, 2001). By contrast, when mice were co-infected with B. microti and B. burgdorferi, neither agent influenced the course of infection induced by the other as evidenced by the percentage of parasitemia, spleen weights, and hematologic and clinical chemistry parameters (J. Infect. Dis. 192, 1634, 2005).
Clinical Studies
In NIAID-supported clinical studies on chronic Lyme disease, patients with persisting symptoms were examined to determine if they might have been co-infected with other tickborne infectious diseases at the time of their acute episode of Lyme disease. Among the tickborne infectious diseases considered were babesioisis (Babesia microti), granulocytic ehrlichiosis (Anaplasma phagocytophilia), and tickborne encephalitis virus infection. The seroprevalence rates for B. microti and A. phagocytophilia were found to be 2.5 percent and 8.6 percent, respectively and no patient examined was found to be positive for tickborne encephalitis viruses (Vector Borne Zoonotic Dis 2: 255, 2002). Thus, the persistence of symptoms in patients with "post-Lyme syndrome" could not be attributed to co-infection with one of these pathogens.
An examination of pathogen distributions in the tissues of mice infected with both B. burgdorferi and A. phagocytophilium, the bacterium that cause anaplasmosis in humans, showed an increase in the numbers of B. burgdorferi in the ears, heart base, and skin of co-infected mice; however, the numbers of A. phagocytophilium remained relatively constant. The serum antibody response to A. phagocytophilium – but not to B. burgdorferi – decreased as a result of co-infection. These findings suggest that co-infection can influence not only pathogen burden but also host antibody responses (Infect Immun 73: 3440, 2005).
NIAID intramural and extramural research programs have initiated clinical studies on chronic Lyme disease. The intramural research program is conducting a comprehensive clinical, microbiological, and immunological assessment of patients with Lyme disease. This involves multiple lines of investigation with emphasis on:
- Defining various biological markers of infection
- Assessing clinical course and outcomes of patients with Lyme borreliosis
- Characterizing the immune response generated in response to B. burgdorferi
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