Case Presentation: A healthy, pleasant 25 years old male, dog-owner, with Down syndrome presented with generalized malaise, intermittent fevers, chills, sweating, abdominal pain, intermittent neck pain that progressively worsened over a week. His fever was ranging from 101-105 Fahrenheit and spiked nocturnally. He had raked the yard 2 weeks ago and his parents were concerned about a tick bite, however no tick or rash was ever found. Physical exam was remarkable for hepatosplenomegaly.Upon admission he was found to be in septic shock; he was fluid resuscitated with 4.5L saline, however his systolic blood pressure remained in his 90’s and hence he was started on pressor support. Lab work revealed severe pancytopenia and mildly elevated transaminases. CT scan of abdomen and pelvis showed mild hepatosplenomegaly and fatty liver. Given the severity of presentation he was started empirically on broad spectrum coverage including vancomycin, piperacillin/tazobactam, doxycycline, atovaquone, azithromycin, clindamycin and quinine to cover tick-borne disease. Positive buffy coat and intra-erythrocytic inclusions suggesting co-infection of babesia and anaplasmosis were found. Babesia microti DNA was positive and Anaplasma phagocytophilum DNA was negative in serum. Lyme disease titer was negative, but could be falsely during first 1-2 of infection. Septic shock with severe anemia resolved after 3 days. He received intermittent blood transfusions, and he was continued on doxycycline for anaplasma and suspected Lyme disease and on azithromycin, atovaquone and clindamycin for severe babesia infection. Quinine was discontinued give possible quinine ototoxicity. He had daily peripheral smears for babesia to assess for level of parasitemia – on admission it was at 1%, and then peaked to 2% and after adding clindamycin it decreased to less than 1% at the time of discharge. He became clinically more stable and discharged on on azithromycin, atovaquone, and doxycycline. Repeat serological testing for Lyme disease was not performed as an outpatient.

Discussion: Since the late 1980s, Babesia spread from the New England coast to the mainland and other continents. The etiological agents responsible for Lyme disease (Borrelia burgorferi), human granulocytic anaplasmosis (Anaplasma phagocytophilum), and babesiosis (Babesia microti) are primarily transmitted by the backlegged tick, Ixodes scapularis. Babesiosis is a malaria-like protozoan infection of erythrocytes that is transmitted by Ixodes.
Babesia microti is the commonest piroplasm infecting humans.
Symptoms of babesiosis are similar to those of Lyme disease, but babesiosis often starts with high fever and chills. As the infection progresses, patients may develop fatigue, headache, drenching sweats, muscle aches, chest pain, hip pain and shortness of breath. Babesiosis is often so mild it is not noticed but can be life-threatening to people with no spleen, the elderly, and people with weak immune systems.
Level of babesia parasitemia was low in our patient however co-infection with anaplasmosis likely contributed to development of sepsis.

Conclusions: Ticks can carry multiple infective agents including Lyme, babesia, and anaplasma, placing patients at risk for a more severe presentation and complications, which include hypotension, severe hemolytic anemia and kidney failure. Clinicians should be aware of a possibility of co-infection with different tick-borne pathogens especially if a patient presented with septic shock who has slow response to initial therapy.