Case Presentation: A 54-year-old male with no past medical history presented with chief complaint of generalized weakness, fatigue, headache, loss of appetite and intermittent fever and chills for 5 days. On arrival to the ED, his vitals were notable for temperature was 102.3F.. Labs notable for a hemoglobin 12.5 g/dL, platelets 55×109/L, sodium 128 mmol/L, AST 56 units/L, total bilirubin 2.2 mg/dL. Chest x-ray did not show acute findings. EKG showed normal sinus rhythm. Peripheral blood smear showed red blood cell (RBC) inclusions. Infectious disease was consulted and he was started on atovaquone, azithromycin and doxycycline for presumed babesiosis and possible Lyme. Initial parasitemia level on blood smear was 5.2% with RBC inclusions. On hospital day 3, he suffered a syncopal event due to orthostatic hypotension, with a drop in his hemoglobin to 6.5 mg/dL. He received 4 units of packed RBCs over the next 2 days. Labs notable for low haptoglobin at 12 mg/dL, elevated reticulocytes at 4.80%, elevated ESR at 125 mm/hr and decreased parasitemia to 0.08%. Symptoms were accompanied by new-onset abdominal distension and pain with deep inspiration prompting a CT abdomen which demonstrated an enlarged spleen and perisplenic hematoma. Due to concern for splenic rupture, he underwent celiac and splenic artery angiography with embolization of the proximal splenic artery. His course was further complicated by persistent fevers ranging from 99.6 to 102.0 F due to a suspected intra-abdominal infection. He underwent a diagnostic laparotomy with extensive washout and subsequent JP drain placement. He was discharged with outpatient follow-up.
Discussion: Babesia microti is the predominant protozoan responsible for babesiosis and is transmitted by the Ixodes scapularis tick – most commonly seen in the Northeast and upper Midwest between May and September. [1] Clinical manifestations can include fever, chills, myalgias, headache, nausea and vomiting to severe anemia due to hemolysis, acute respiratory distress syndrome, disseminated intravascular coagulation, splenic rupture and shock. Severe symptoms are associated with high levels of parasitemia, elevated lactate dehydrogenase, low haptoglobin, reticulocytosis and thrombocytopenia. [2,3] Definitive diagnosis is via thin blood smear on Giemsa or Wright stains, by visualization of the intraerythrocytic trophozoites or merozoites with typical RBC inclusions – Maltese cross tetrad (figure 1). [2] PCR is another diagnostic tool with 100% sensitivity to the Babesia 180 rRNA gene. [3] Splenic infarct or rupture is a rare complication and occurs more frequently in younger, healthier individuals. The presumed mechanism is thought to be secondary to excessive erythrophagocytosis in the red pulp of the spleen. [5] Most common presentation is severe abdominal pain which may be diffuse or in the left upper quadrant. Splenic artery embolization and splenectomy is the mainstay of treatment. Classic antibiotic therapy includes oral atovaquone and azithromycin for 7 to 10 days. In cases of an allergy to azithromycin or atovaquone, an alternative regimen includes intravenous clindamycin and oral quinine. Symptom improvement is typically seen within the 24-48 hours of initiation of therapy. [2]
Conclusions: Babesiosis is a common tickborne infection that can be treated with antibiotics but can progress rapidly to serious illness including hemolysis, DIC and splenic rupture. We hope to educate physicians about identifying life-threatening complications of babesiosis.
