Correspondence

Can Ticks Be Vectors for Hepatitis C Virus?

N Engl J Med 2002; 347:1724-1725November 21, 2002

Article

To the Editor:

We describe a case of acute Babesia microti infection temporally associated with hepatitis C virus (HCV) seroconversion in a blood donor in Connecticut. Blood donated on July 9, 1999, tested negative for all markers of infectious diseases for which donated blood is routinely screened. However, as part of a study, this donation and a follow-up specimen from August 6, 1999, tested positive for antibodies against B. microti, and the follow-up specimens subsequently tested positive for B. microti by nested polymerase chain reaction (PCR).

The donor, a resident of southeastern Connecticut, worked as a medical technologist. In September 1999 she noted having fatigue, appetite loss, abdominal cramps, and dark urine. She reported that she had not engaged in activities associated with a high risk of blood-borne infections and that she had not had occupational exposure to blood. A specimen obtained on September 20, 1999, by her employer was reported to be negative for hepatitis B surface antigen, antibodies to the core antigen of hepatitis B virus, and antibodies against both hepatitis A virus and HCV. The serum alanine aminotransferase concentration was 850 U per liter, and it normalized several weeks later. Her symptoms resolved over the course of the next several weeks. The donor had an intact spleen.

Routine testing of a subsequent blood donation in December 1999 revealed infection with HCV as shown by positive test results for anti-HCV antibodies and HCV RNA. The donated blood unit was destroyed, and further donation was deferred. A serum specimen from August 1999 that had been obtained for the B. microti study was positive for HCV RNA as well as positive for B. microti on PCR. In February 2000 the donor's blood tested negative for HCV RNA but remained positive for anti-HCV antibodies. Additional serologic tests for B. microti performed by an outside laboratory (Imugen, Norwood, Mass.) on the samples from July and August 1999 confirmed IgG reactivity on immunofluorescence assay and revealed both IgG and IgM reactivity on Western blotting in both samples. IgG reactivity was stronger in the August sample than in the July sample, but IgM reactivity was stronger in the July sample than in the August sample. Laboratory results are summarized in Table 1Table 1Laboratory Results..

The B. microti serologic pattern observed in the donor is most consistent with acquisition of infection in early June, a month before the donation in July. The time window from the acquisition of HCV infection to the detection of HCV viremia on nucleic acid amplification testing has not been precisely determined (Dodd RY: personal communication). However, the appearance of HCV viremia between the July 9 and August 6 samples is compatible with the acquisition of HCV infection in early June as well.

Several scenarios could account for this temporal association. Most directly, exposure to B. microti through a tick bite could have coincided with a parenteral or sexual exposure to HCV. Although the prevalence of B. microti infection detectable by PCR among Connecticut blood donors is approximately 1 in 1800,1 the rate of seroconversion for HCV antibody among repeated blood donors in the United States is only 1.889 new infections per 100,000 person-years.2 Thus, simultaneous discovery of these two independent infective events in an established blood donor would be highly unusual.

There are two other possibilities: coincidental acquisition of B. microti and HCV from occupational exposure (although occupational acquisition of B. microti has not been reported) or acquisition of both B. microti and HCV from a dually infected tick. Ingestion of host blood by ticks permits efficient transmission of pathogens to the host. The competence of Ixodes scapularis as a vector for HCV has not been established clinically or experimentally. However, several reports demonstrate transmission of other flaviviridae by ticks.3,4

This case suggests the possibility of HCV transmission by a tick vector. Additional epidemiologic investigation of the I. scapularis tick for the presence of the HCV virus is warranted.

Lois Gitlin Wurzel, M.D.
Ritchard G. Cable, M.D.
American Red Cross Blood Services, Farmington, CT 06032
wurzell@usa.redcross.org

David A. Leiby, Ph.D.
American Red Cross, Rockville, MD 20855

4 References

1. 1

   Cable RG, Badon S, Trouern-Trend J, et al. Evidence for transmission of Babesia microti from Connecticut blood donors to recipients. Transfusion 2001;41:Suppl:12S-12S abstract.
   CrossRef | Web of Science

2. 2

   Dodd RY, Notari EP IV, Stramer SL. Current prevalence and incidence of infectious disease markers and estimated window-period risk in the American Red Cross blood donor population. Transfusion 2002;42:975-979
   CrossRef | Web of Science | Medline

3. 3

   Wahlberg P, Saikku P, Brummer-Korvenkontio M. Tick-borne viral encephalitis in Finland: the clinical features of Kumlinge disease during 1959-1987. J Intern Med 1989;225:173-177
   CrossRef | Web of Science | Medline

4. 4

   Costero A, Grayson MA. Experimental transmission of Powassan virus (Flaviviridae) by Ixodes scapularis ticks (Acari:Ixodidae). Am J Trop Med Hyg 1996;55:536-546
   Web of Science | Medline

Citing Articles (1)

Citing Articles

1. 1

   S. Cook, E. C. Holmes. (2006) A multigene analysis of the phylogenetic relationships among the flaviviruses (Family: Flaviviridae) and the evolution of vector transmission. Archives of Virology 151:2, 309-325
   CrossRef