Dr. James Schaller, MD
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Babesiosis and Lyme Disease Diagnosed in Ontario

Introduction

Human babesiosis (caused by Babesia microti) and Lyme disease (caused by Borrelia burgdorferi) are among the most common tick-transmitted zoonoses. Recent evidence indicates that both diseases are emerging in the northeastern and Great Lakes regions of the United States as the deer tick (Ixodes scapularis), which transmits both infections, increases in geographic distribution(1,2). Because B. microti and B. burgdorferi reside in the same rodent reservoir (Peromyscus leucopus) and are transmitted by the same tick vector, human co-infection may be relatively common in endemic areas. In support of this contention, up to two-thirds of Long Island residents with Lyme disease have antibodies to Babesia species (3). However, until recently, only three episodes of co-infection had been described and, in each case, a particularly severe illness was experienced and one individual died (4-6). A recent report from New England found that the severity of symptoms and duration of illness in patients with concurrent babesiosis and Lyme disease was greater than for either infection alone (7).

Ixodes scapularis ticks have been found in a number of provinces in Canada and 205 cases of Lyme disease were reported to public-health officials from 1984-1994 (105 locally acquired) (8). However, there have been no previous reports of co-infections in Canada and, to our knowledge, no case of babesiosis has ever been reported in Canada. This report describes a co-infection of babesiosis and Lyme disease acquired by a Canadian traveler.

Case Report

A 59-year-old male from Toronto presented to The Toronto Hospital on 27 July 1997 because of persistent fever and night sweats. The patient had recently returned from a 6-week trip to Nantucket, where he had vacationed in a summer home. There was no history of rural travel nor hiking or walking in the woods. Additional travel history included a trip to Hong Kong, Indonesia, and Singapore 7 months ealier.

The patient was well until 21 June 1997 when he noticed a small black "pinhead" lesion on his left biceps, which he removed. He subsequently developed a spreading erythema surrounding this lesion that spontaneously resolved after 2 to 3 days. On 26 June, he experienced a 2-day episode of fever, sweats, chills, myalgia, and fatigue, which was treated symptomatically with acetaminophen. He was then well until 21 July 1997 when the fever and chills returned. In addition, he developed rigors, extreme fatigue, headache, myalgia, nausea, vomiting, and drenching night sweats. On 22 July, he saw his family physician who diagnosed a "viral infection". On presentation to The Toronto Hospital 5 days later, he was febrile (38.8o C), pale, and appeared ill. He had a tachycardia of 130 beats/minute, mild splenomegaly, and occasional petechia on his extremities. The remainder of his examination was unremarkable.

Initial laboratory investigations revealed a normochromic, normocytic anemia of 106 g/L, leukopenia of 4.2 billion/L (normal 4.5 to 11.0), thrombocytopenia of 14 billion/L (normal 150 to 400), elevated lactate dehydrogenase at 799 U/L (normal 45 to 90), bilirubin 26 µmol/L (normal 2 to 17), aspartate aminotransferase 151 U/L (normal < 35), fibrinogen 4.22 g/L (normal 1.5 to 3.5), fibrin degradable products > 10 µg/mL (normal < 2.5), international normalized ratio 4.89 (normal 1.00), decreased haptoglobin < 0.12 g/L (normal 0.6 to 2.9), and D-dimers < 250 ng/mL (normal 500 to 1,000). Urinalysis was positive for blood and hemoglobin.

His past medical history was significant for nephritis of unknown etiology at the age of 3 years, atrial fibrillation diagnosed in 1995, and a myocardial infarction in 1996 complicated by congestive heart failure. He had not previously undergone splenectomy nor had he ever received a blood transfusion. The patient's medications included coumadin 7.5 mg po od, cozaar 50 mg po od, lanoxin 0.125 mg po od, and acetylsalicylic acid 325 mg po od. He had no known allergies.

His travel history to southeast Asia, fever, and hemolytic picture suggested malaria; thick and thin films were ordered. Thick and thin films revealed many tiny ring forms, initially interpreted as Plasmodium falciparum malaria at 4% parasitemia. However, an astute senior technologist noted morphologic differences from P. falciparum malaria and correctly identified the protozoan organisms on the smears as trophozoites of B. microti. [Babesia microti]

Source: C dos Santos, MD, K Kain, MD, Tropical Disease Unit, The Toronto Hospital and University of Toronto, Toronto, ON.

[We have found many patients in Canada have Babesia, and not merely this species. It is a shame that some physicians in the United States treating Canadians have seen more Babesia than the entire collection of provinces].

TRANSFUSION-TRANSMITTED BABESIOSIS IN ONTARIO: FIRST REPORTED CASE IN CANADA

Introduction

Human babesiosis is a tick-borne zoonosis caused by protozoa of the genus Babesia. While the genus comprises over one hundred species, most cases of human babesiosis in North America are caused by Babesia microti (1-4). The great majority of these cases are transmitted by the bite of the deer or blacklegged tick, Ixodes scapularis (2-4). The clinical manifestations of babesiosis range from asymptomatic to severe and occasionally fatal disease characterized by fever, intravascular hemolysis, hemoglobinuria, and renal failure. Severe disease is more common in asplenic individuals, elderly patients, and those with underlying immunodeficiency states including the acquired immunodeficiency syndrome(5,6).

Babesia parasites invade and survive within erythrocytes. They remain viable under blood bank conditions and there have been several well documented cases of babesiosis acquired from blood transfusion in the United States(7-11). We report the first transfusion-transmitted case of babesiosis in Canada.

Case report of the blood recipient

The recipient was a 53-year-old... She initially presented on 23 October 1998 with... a hemoglobin was 69 g/L and on 6 November 1998 she was transfused with three units of packed red blood cells (PRBCs). Her post-transfusion hemoglobin was 106 g/L...Her colonoscopy was normal but a small bowel follow-through examination revealed an annular tumor of her small intestine. On 9 March 1999 she underwent laproscopic resection of the tumor without complication. However, she was readmitted on 11 April 1999 following a 7-day history of high fever, chills, diaphoresis, nausea, and weakness.

Her physical examination on admission was unremarkable with the exception of a temperature of 40° C... Her lactate dehydrogenase level was elevated at 161 U/L (normal 45 U/L to 90 U/L) and her aspartate aminotransferase level was elevated at 63 U/L (normal < 35 U/L). Examination of peripheral blood smears revealed intraerythrocytic ring forms initially attributed to Plasmodium falciparum infection at a parasitemia of 2.5%. However, smears were reviewed at the Tropical Disease Unit of the Toronto Hospital; a diagnosis of babesiosis was confirmed by the presence of typical intraerythrocytic forms of babesiosis and by PCR results which were positive for B. microti DNA...

Investigation of blood donors

The recipient received a total of five units of PRBCs from five donors during hospitalizations in November 1998 and February 1999.

[Her] last donor was a 40-year-old male who had donated blood twice previously. He gave a history of camping in rural and forested areas in Cape Cod in August 1998. He did not remember receiving any tick bites and he denied any febrile illnesses during or after his return from Cape Cod. He donated a unit of blood on 6 February 1999 which was transfused into the recipient on 25 February 1999. He also gave a travel history of visiting the United States (Arizona, St. Louis, New York City, and Michigan) in the previous year. He provided a follow-up blood sample. His blood sample was positive for B. microti by blood smear and by PCR. His Babesia serology was also positive at a titer of 1:1024 by IFA...

Discussion

This is the first report of transfusion-transmitted babesiosis in Canada and only the third and fourth cases of B. microti infection recognized in this country.

[It is amazing that states bordering Canada have large numbers of Babesia. Perhaps they respect the Canadian border?]

As was the case for the donor in this report, individuals infected with babesiosis may remain asymptomatic but parasitemic for months to years following tick-transmitted disease(13). Since the parasite remains infective under blood-banking conditions, transfusion associated babesiosis is a risk of transfusion with blood components including platelet concentrates, PRBCs, and frozen, thawed, and deglycerolized erythrocytes(7-11). The risk of acquiring babesiosis from a blood transfusion in Canada is unknown but would be expected to be very low. A study of transfusion recipients in Connecticut, an area endemic for babesiosis, reported a risk of 0.17% per unit of transfused PRBCs(11).

In Canada, blood banks do not routinely inquire of donors about travel to Babesia-endemic areas (e.g. Cape Cod, Martha's Vineyard, Connecticut), tick bites, or a past history of babesiosis. However, since most immunocompetent individuals who acquire babesiosis do not remember a tick bite and since most will have either minimal or no symptoms, this deferral practice would be unlikely to identify most Babesia-infected donors... infected individuals may remain parasitemic for up to years and since PRBCs are stored for up to 42 days, even seasonal deferral of potential high-risk donors would not be expected to prevent transfusion-associated babesiosis.

Similar to previously reported cases of transfusion-associated babesiosis in the United States, the recipient of Babesia-infected blood products in this case developed moderate to severe manifestations of infection(7)?. Both the donor and recipient in this series were treated with a combination of quinine and clindamycin, and both had a satisfactory clinical and or parasitologic response. However, there have been a number of recent reports including a case of imported babesiosis in our own experience that have not responded optimally to this traditional therapy...

Given the millions of Canadians who visit Babesia-endemic regions of the United States each year, we must anticipate an increase in the number of cases of imported babesiosis and the potential for transfusion-transmitted disease in this country. Our own anecdotal experience with five documented cases of babesiosis in Toronto residents within the last 2 years supports this contention. Canadian physicians must consider babesiosis in the differential diagnosis of a patient who developing fever or a hemolytic reaction after a recent blood transfusion. Prompt recognition and an accurate diagnosis are important since Babesia infections respond to therapy and may be severe or fatal in certain risk groups. Improved strategies to prevent transfusion-associated babesiosis are required.


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