Babesia microti Infection Presenting as Acute Splenic Laceration

Case Report

A 48-year-old male presented one week after being struck in the left upper quadrant of the abdomen with a wooden board. He complained of general malaise, weakness, and headache as well as left upper quadrant abdominal pain. Admission vital signs were temperature 37.1°C, pulse 79 beats/min, blood pressure 116/51 mm Hg, ventilatory rate 17 breaths/min, and oxygen saturation 98% on room air. There was no abdominal distention or external sign of injury. The left upper quadrant was full and tender. The remainder of the physical examination was unremarkable.

Abnormal laboratory values included a hemoglobin concentration of 10.5 g/dL and a platelet count of 137,000 mcL. A focused assessment by sonography for trauma (FAST) was positive for pelvic fluid, and a computed tomographic (CT) scan identified a 14.6 cm×9.5-cm spleen (normal up to 11×7 cm) with wedge-shaped defects consistent with a Grade III splenic laceration, accompanied by pelvic hemoperitoneum (Fig. 1). The enlarged spleen prompted a peripheral smear that identified intra-erythrocytic parasites. A detailed travel history revealed a camping trip one month earlier to a heavily tick-infested area, suggesting the diagnosis of babesiosis; no tick bites could be recalled. The diagnosis of babesiosis was supported by the finding of 10% parasitemia on a peripheral blood smear (Fig. 2) and validated by polymerase chain reaction (PCR) testing. Tests for immunoglobulin (Ig) M and Ig G antibodies for the other likely infecting tick-borne organism, Borrelia burgdorferi, were negative.

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FIG. 1.

Axial computed tomography scan demonstrating wedge-shaped splenic opacities.

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FIG. 2.

Peripheral blood smear with intra-erythrocyte Babesia microti.

Treatment with azithromycin and atovaquone (antiparasitic) was initiated. Within 96 h, the parasitic load had decreased to 1%, along with a general improvement in the patient's constitutional symptoms and abdominal pain.

Discussion

There are seven reports of spontaneous splenic rupture secondary to babesiosis [2–7]; four cases were managed non-operatively [3,5,6]. One report describes the diagnosis of babesiosis after splenectomy for trauma [8]. Our patient appears to be the initial report of blunt injury-associated splenic laceration managed non-operatively and leading to the diagnosis of established babesiosis. Babesia are malaria-like parasites that reproduce within exclusively mammalian erythrocytes and were first identified by Victor Babes in 1888. It is likely that B. microti-induced hypersplenism increased this patient's risk of splenic laceration by increasing parenchymal mass and capsular tension.

Splenic injury presents most commonly after blunt-force abdominal kinetic energy transfer, with myriad clinical presentations ranging from non-specific abdominal pain to catastrophic hemorrhage [9,10]. Prompt identification and triage of those with splenic injury is essential in preventing morbidity and death. Current management embraces non-operative techniques spanning observation and bedrest to angioembolization, as these techniques are highly successful, reduce morbidity compared with operation, and preserve splenic immune function, including the crucial ability to opsonize encapsulated organisms [11,12].

Failure of non-operative management occurs in approximately 10% of adults and leads most commonly to splenectomy when associated with hemodynamic instability. Hypersplenism is a risk factor for failure of non-operative management and may impede attempts at splenic salvage. Accordingly, prompt diagnosis and therapy of conditions that either induce or promote hypersplenism should be corrected as part of a non-operative approach to splenic injury. Infectious causes such as babesiosis are encountered uncommonly in surgical practice; hematologic malignant tumors, splenic vein thrombosis, and portal hypertension are encountered more commonly. The surgeon's index of suspicion for infectious causes should be heightened by constitutional symptoms and a suggestive travel history and time interval. Therefore, the surgeon should be aware of endemic infecting organisms within the typical referral region.

Babesiosis is spread by parasites carried by the tick Ixodes scapularis; the most common parasite is B. microti in North America; that organism is endemic to New England and the upper Midwest. This patient was camping in New England in the month prior to presentation. Transfusion-associated babesiosis also has been reported, including in a patient receiving a transfusion after splenectomy [7,13]. Patients with babesiosis generally present with acute but non-specific symptoms that may be confused with viral infection; the mean time from inoculation to symptoms is 1–4 wks [14]. More severe but less common manifestations are hemolytic anemia, jaundice, and acute respiratory dysfunction associated with severe anemia and congestive heart failure. Most Babesia infections are not fatal, although greater virulence is noted in the immunoincompetent and in those infected with B. divergens.

Microscopic examination rarely identifies intra-erythrocytic parasites in merozoite tetrads that create the pathognomonic “Maltese cross” configuration. More commonly, single trophozoites that appear circular, oval, or teardrop-shaped are noted, as is anemia. Definitive diagnosis relies on PCR for Babesia DNA or 18S rRNA. The differential diagnosis of parasitemia and hypersplenism includes ehrlichiosis and anaplasmosis, and less commonly rickettsial and Lyme disease, and may be assessed by IgG and IgM assay. Immunofluorescence for babesia IgM or IgG antibodies can persist for months after parasite eradication and is less useful in diagnosing active babesial infection.

Babesia microti therapy is a dual-pronged anti-infective approach, most commonly with atovaquone plus azithromycin for mild-to-moderate disease or quinine (oral) plus clindamycin (IV) for severe disease [15]. Therapy for 7–10 days is appropriate in uncomplicated disease. Follow-up to confirm parasite eradication is essential because of persistent parasitemia in those treated inadequately, with potential recrudescence years after the index infection [16]. For complicated disease, treatment continues for two weeks after peripheral blood smears document resolution of parasitemia.

Conclusion

Babesiosis is an uncommon surgeon-managed parasitic infection that can increase the risk of splenic injury by inducing hypersplenism. Rapid diagnosis is aided by obtaining a history of travel to an endemic area, noting splenic enlargement, and confirming parasitemia microscopically; the final diagnosis relies on confirmation. PCR by dual-agent therapy should be instituted to aid in non-operative management of those with splenic injury, and follow-up is essential to ensure eradication.