• Gary P Wormser, Aakanksha Prasad, Ellen Neuhaus, Samit Joshi, John Nowakowski, John Nelson, Abraham Mittleman, Maria Aguero-Rosenfeld, Jeffrey Topal, and Peter J Krause.
• Divisions of 1Infectious Diseases, Departments of Medicine and 3Pathology, New York Medical College, Valhalla, NY 10595, USA. gary_wormser@nymc.edu
• Clin. Infect. Dis. 2010 Feb 1;50(3):381-6.

BackgroundBabesiosis is an emerging tickborne malaria-like infection principally caused by Babesia microti. This infection typically resolves either spontaneously or after administration of a 7-10-day course of azithromycin plus atovaquone or clindamycin plus quinine. Although certain highly immunocompromised patients may respond suboptimally to these drug regimens, unlike the situation with malaria there has been no reported evidence that the cause of treatment failure is infection with drug-resistant strains of B. microti.MethodsEmergence of drug resistance in B. microti was defined as the development of a microbiologic relapse (recurrent parasitemia or a marked increase in parasitemia) in association with both clinical and laboratory abnormalities indicative of active babesiosis in a patient after 28 days of uninterrupted antibabesia drug therapy and while still receiving treatment.ResultsThe clinical case histories of 3 highly immunocompromised patients who received a subcurative course of azithromycin-atovaquone associated with the eventual development of resistance to this drug regimen are described. One of the 3 patients died of complications related to babesiosis.ConclusionsB. microti may become resistant to azithromycin-atovaquone during the treatment of babesiosis with this combined drug regimen in highly immunocompromised patients. Although research is needed to determine the optimal therapy for highly immunocompromised patients with babesiosis, reducing the level of immunosuppression when possible would appear to be a desirable strategy.

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