Although many people who are infected with Babesia do not have symptoms, for those who do effective treatment is available. Babesiosis is preventable, if simple steps are taken to reduce exposure to ticks.
Babesia microti is transmitted by the bite of infected Ixodes scapularis ticks typically, by the nymph stage of the tick, which is about the size of a poppy seed. AnIxodes scapularis nymph is shown on the face of a penny
To the Editor: Human babesiosis, caused by Babesia microti, was ini- tially described in the eastern United States in 1970 in a woman vacation- ing on Nantucket Island, Massachusetts (1). With few excep- tions, almost all subsequent cases were recorded from islands in the northeastern United States and Cape Cod, Massachusetts (2), until this ill- ness was diagnosed in 13 patients liv- ing in New London County in south- eastern Connecticut (3,4). B. microti was isolated from white-footed mice, Peromyscus leucopus, captured from 1988 to 1990 in the yards of patients. Babesiosis also was diagnosed in per- sons living in Wisconsin (5) and in New Jersey (6) who acquired the organism locally. The number of
cases of babesiosis reported by health departments on their Web sites and by personal communication in Massa- chusetts, Rhode Island, and New York State, was 330 from 1988 to 2002, 121 from 1994 to 2002, and 542 from 1986 to 2001, respectively. The num- ber of cases reported by the New York City Health Department from 1991 to 2000 was 75.
From 1991 to 2000, babesiosis was diagnosed in 230 persons residing in New London County and adjacent Middlesex County, Connecticut (7). Fifty-three additional cases were reported in five other counties in Connecticut, but epidemiologic data did not indicate that these infections likely were acquired within Connecticut. We now note a new and distinct geographic focus by reporting the isolation of B. microti from rodents captured in the yards of two patients in whom babesiosis was diag- nosed at Greenwich Hospital in 2002. These patients lived in Greenwich, Connecticut, which is located in Fairfield County in the extreme south- western part of the state. Neither patient had traveled outside of the immediate area of Greenwich, Connecticut, before onset of illness. We also trapped rodents in the yards of two additional patients in whom babesiosis was diagnosed. These two patients had traveled to Rhode Island shortly before becoming ill. Patients became ill from June 23 to July 7, 2002, and none reported a tick bite.
Attempts to trap small mammals on the properties of the four patients were made on July 22, 23, and 29, 2002. Rodents were captured in Sherman box traps baited with peanut butter and apple. Approximately 0.3 mL of blood was drawn from the heart of each animal into a syringe coated with heparin or uncoated. Blood was kept on ice in the field and then returned to the laboratory. A 3- to 5- week-old male Syrian hamster was injected intraperitoneally with 0.1 mL of each blood sample.
Blood smears were obtained from a drop of blood taken from the tail of each hamster on weeks 3 to 6 after injection. Blood cells were stained with Giemsa and examined for B. microti at a magnification of 1,008x. Hamsters were considered uninfected when no parasites were found in 75 fields of stained erythrocytes.
B. microti was isolated from rodents captured at the residences of two of the patients who did not travel outside of the Greenwich area 6 weeks before onset of illness. Blood from two of three white-footed mice and from the two eastern chipmunks, Tamias striatus, captured in the yards of the patients, produced infections in injected hamsters. Infections did not develop in hamsters injected with blood from 10 white-footed mice cap- tured at the residences of two patients who visited Wakefield and Charles- town, Rhode Island, shortly before becoming ill.
B. microti is prevalent in rodent populations in Greenwich, Connec- ticut, and causes human disease. Establishing evidence of B. microti in rodents and documenting this proto- zoan parasite as the cause of human disease in Greenwich are important. Relatively high populations of the vector tick, Ixodes scapularis, are present in Greenwich and nearby towns. In 2002, the health depart- ments of Greenwich, Stamford, New Canaan, and Darien submitted 1,671 I. scapularis ticks removed from per- sons to the Connecticut Agricultural Experiment Station for identification and testing for Borrelia burgdorferi. Two hundred and thirty cases of Lyme disease were reported from these four towns in 2002 (Connecticut Department of Public Health, unpub. data). With such extensive human exposure to ticks and a relatively large number of Lyme disease cases in these four towns and elsewhere in Fairfield County, the number of cases of babesiosis is likely to increase appreciably in the future.
Emerging Infectious Diseases www.cdc.gov/eid Vol. 10, No. 3, March 2004 545
LETTERS
B. microti has been transmitted through blood transfusion in Connec- ticut (8). Blood collection agencies in southwestern Connecticut and adja- cent Westchester County, New York, should be aware of the possibility that blood donors could be infected with this pathogen. Physicians should also be alert to the possibility that patients could be coinfected with the etiologic agents of Lyme disease or human granulocytic ehrlichiosis. Some patients in whom Lyme disease was diagnosed have been simultaneously infected with B. microti (9,10).
Acknowledgments
We thank Michael Vasil and Bonnie Hamid for their technical assistance; the staff of Greenwich Hospital for assistance; Caroline Baisley and Doug Serafin for helping coordinate the trapping of rodents in Greenwich; and Michael Gosciminski, Palma Caron, and Dennis White for pro- viding documentation of several cases of babesiosis from the states of Rhode Island, Massachusetts, and New York, respectively.
This study was supported in part by Hatch funds administered by the U.S. Department of Agriculture.
John F. Anderson* and Louis A.
Magnarelli*
*Connecticut Agricultural Experiment Station, New Haven, Connecticut, USA
References
- Western KA, Benson GD, Gleason NN, Healy GR, Schultz MG. Babesiosis in a Massachusetts resident. N Engl J Med 1970;283:8546.
- Healy G, Ristic M. Human babesiosis. In: Babesiosis of domestic animals and man. Boca Raton (FL): CRC Press, Inc; 1988. p. 20925.
5. Herwaldt BL, Springs FE, Roberts PP, Eberhard ML, Case K, Persing DH, et al. Babesiosis in Wisconsin: a potentially fatal disease. Am J Trop Med Hyg 1995; 14651.
6. Herwaldt BL, McGovern PC, Gerwel MP, Easton RM, MacGregor RR. Endemic babesiosis in another eastern state: New Jersey. Emerg Infect Dis 2003;9:184
7. Cartter ML, Ertel SH. Lyme disease Connecticut, 2000, and babesiosis Connecticut, 19912000. Connecticut Epidemiologist Newsletter [serial online] 2001;21:912. Available from: http://www.dph.state.ct.us/Publications/BC H/Infectious%20Diseases/ce72001.pdf
8. Mintz ED, Anderson JF, Cable RG, Hadler JL. Transfusion-transmitted babesiosis: a case report from a new endemic area. Transfusion 1991;31:3658.
9. Krause PJ. Babesiosis. In: The medical clinics of North America: tick-borne dis- eases. Philadelphia: W. B. Saunders Co.; 2002. p. 36173.
10. Grunwaldt E, Barbour AG, Benach JL. Simultaneous occurrence of babesiosis and Lyme disease. N Engl J Med 1983;308:1166.
Address for correspondence: John F. Anderson, Connecticut Agricultural Experiment Station, PO Box 1106, New Haven, CT 06504, USA; fax: 203-974-8502; email: John.F.Anderson@ po.state.ct.us
Migratory Thrombophlebitis and Acute Q Fever
To the Editor: Q fever is a world- wide zoonosis particularly common in some cattle- raising countries such as Great Britain, France, Spain, Australia, and Canada (1). Wide- spread use of diagnostic serologic tests has led to increasing recognition of the disease in many other parts of the world. For example, Q fever has been recently described in Southeast Asia (2).
Acute Q fever usually manifests as a febrile syndrome with hepatic abnormalities or pneumonia; chronic
Q fever is commonly associated with endocarditis (3,4). When the disease manifests with an atypical clinical picture, diagnosis becomes difficult.
We describe a patient in whom Trousseau’s syndrome developed as the sole manifestation of acute Q fever. To the best of our knowledge, this complication has not been found previously in patients with Q fever.
A 39-year-old, previously healthy man was admitted to the hospital because of fever and subcutaneous painful induration in the legs and arms. Ten days previously, he had fever, generalized aches, and malaise. Forty-eight hours after the onset of these symptoms, he noticed a painful induration and redness along the right calf that spontaneously subsided in a few days. He remained febrile, and additional swollen, painful indurated lesions appeared on his thighs and arms. Pleuritic chest pain developed, and he was taken to the emergency room.
On admission, he was febrile (38.7C). A tender, indurated cord, 10 cm long, was felt on the greater saphenous vein of the right thigh. The cephalic vein of the left arm and the basilic vein of the right arm were also tender and indurated.
The leukocyte count was 9,800/mm3; hemoglobin 14.5 g/dL, and platelets 441,000/mm3. The fib- rinogen levels (385 mg/dL) and pro- thrombin time (12 s, control 1014 s) were normal. The partial thrombo- plastin time (40 s, control 2636 s) was mildly prolonged. Serum aspar- tate aminotransferase was 75 U/L, serum alanine aminotransferase was 110 UL, and I?-glutamyltranspeptidase was 230 U/L. Antibodies to phospho- lipids (aPL) measured by enzyme- linked immunosorbent assay were positive (titer of 95 for antibodies of class IgG/titer of 19 for antibodies of class IgM. Results of testing for tumor-associated antigens, such as carcinoembryonic antigen, carcinoma antigen 19-9, prostatic specific anti-