Final Diagnosis -- Babesiosis


FINAL DIAGNOSIS:   BABESIA INFECTION

DISCUSSION:

Babesiosis is an emerging infection caused by protozoal parasites and transmitted by the black-legged tick, the same tick that transmits Lyme disease (Figure 5*). Babesia and its close relatives are members of a group of organisms called piroplasms, a name which comes from their pear-shaped outlines. The babesia organism was named after Viktor Babs, who first recognized it in blood cells of cattle in the late 19th century. Babesiosis, as the disease is known, is found in a wide variety of mammals, but is perhaps most prevalent in rodents, carnivores, and cattle. In excess of 100 species of Babesia have been described from mammals. Babesiosis is found throughout the world, but most cases have been described from the northeastern and northern midwestern United States. Four Babesia species cause disease in human beings, B. microti, WA1, and MO1 in North America, and Babesia divergens in Europe [1-5]. Like the malaria agent, the parasite attacks and damages host erythrocytes. Babesiosis is found throughout the world, but most cases have been described from the northeastern and northern midwestern United States.

The clinical manifestations of babesiosis range from subclinical illness to a fatal fulminating disease [1]. Babesial infections are often not apparent [2]. In most clinically apparent cases, overt signs and symptoms generally commence after an incubation period of 1 6 weeks, measured from the beginning of tick feeding. Although patients may present with a mild flulike illness, the presentation generally is more severe and begins with malaise, anorexia, and fatigue that is followed by intermittent fever with a temperature as high as 40C and 1 of the following symptoms: headache, chills, sweats, myalgia, arthralgia, nausea, and vomiting [6]. Less commonly noted are emotional lability and depression, hyperesthesia, sore throat, abdominal pain, conjunctival infection, photophobia, weight loss, and nonproductive cough [6]. Physical examination findings often consist solely of fever [6]. Splenomegaly, hepatomegaly, or both are noted occasionally. Abnormal laboratory findings reflect lysis of erythrocytes by the parasite; they include mild to moderately severe hemolytic anemia and an elevated reticulocyte count. Findings of liver function tests are elevated for about one-half of patients. Thrombocytopenia is common. The leukocyte count is either normal or slightly low. Complications of babesial infection are limited. The illness usually lasts for a few weeks to as long as several months; recovery sometimes requires as long as 18 months [6]. Patients may remain parasitemic after all symptoms have resolved. As noted with malaria, parasitemia and relapse of illness can occur up to 27 months after the initial episode. Those at greatest risk of fatal disease include individuals older than age 50 years; asplenic individuals; and immunocompromised individuals as a result of immunosuppressive drugs, malignancy, or HIV infection. These patients may have serious illness, characterized by high fever and severe hemolytic anemia, that results in death or a prolonged convalescence. The case fatality rate for human babesiosis approaches 5% [1]. Approximately 20% of the cases of babesiosis have clinical and serologic evidence of concurrent Lyme disease.

A variety of factors are taken into account in diagnosing babesiosis, most importantly patient history and examination of blood smears. Standard diagnostic techniques for human infection, such as examination of Giemsa-stained thin blood smears and serology, have been complemented with molecular techniques, such as PCR. There are, however, drawbacks in reliance upon blood smears alone. Identification of the parasites in thin blood films requires a reasonable level of parasitemia, otherwise the parasites might be missed. Some Babesia, because of their small size, might not be seen in thick blood smears. Polymerase chain reaction detection of B. microti is a more sensitive method and can be used for confirmation if immunofluorescent assay titers are nondiagnostic [7].

Current treatment for babesiosis is focused on a regimen of clindamycin and quinine, although new drugs have shown promise. The combination of clindamycin (20 mg/kg/day, 600 mg every 6 h) for 7 10 days and quinine (25 mg/kg/day, 650 mg every 6 8 h) for 7 10 days was first used for treating babesiosis in 1982 and has subsequently become the treatment of choice [8, 9]. This combination frequently produces untoward reactions, however, such as tinnitus, vertigo, and gastrointestinal upset. Treatment failures have been reported with clindamycin and quinine in patients who are asplenic, infected by HIV, or receiving concurrent corticosteroid therapy. In severe cases, exchange transfusion was used.

The parasite represents a threat to the safety of the blood supply in that blood from asymptomatic humans can transmit Babesia to blood recipients. Such transmissions have occurred.

Prevention of infection relies on self-monitoring for the presence of ticks and, in some locations, targeted application of pesticides to decrease tick abundance. Identification of human infection with Babesia spp. will probably increase as physicians and the public become more aware of the disease, as people live and recreate in rural tick-infested areas, and as the numbers of immunocompromised individuals increase.

REFERENCES:

  1. Meldrum, SC, Birkhead GS, White DJ, et al. Human babesiosis in New York state: an epidemiologic description of 136 cases. Clin Infect Dis 1992; 15:1019 23.
  2. Krause PJ, Telford SR, Pollack RJ, et al. Babesiosis: an underdiagnosed disease of children. Pediatrics 1992; 89:1045 8.
  3. Persing D, Herwaldt BL, Glaser C, et al. Infection with a Babesia-like organism in the western United States. N Engl J Med 1995; 332:298 303.
  4. Herwaldt BL, Persing DH, Precigout EA, et al. A fatal case of babesiosis in Missouri: identification of another piroplasm that infects humans. Ann Intern Med 1996; 124:643 50.
  5. Gorenflot A, Moubri K, Precigout E, Carcy B, Schetters TP. Human babesiosis. Ann Trop Med Parasitol 1998; 92:489 501.
  6. Ruebush TK, Cassaday PB, Marsh HJ, et al. Human babesiosis on Nantucket Island. Ann Intern Med 1977; 86:6 9.
  7. D.H. Persing, D. Mathiesen, W.F. Marshall et al., Detection of Babesia microti by polymerase chain reaction. J Clin Microbiol 96 (1992), pp. 601604.
  8. Wittner M, Rowin KS, Tanowitz HB, et al. Successful chemotherapy of transfusion babesiosis. Ann Intern Med 1982; 96:601 4.
  9. Krause PJ, Lepore T, Sikand VJ, et al. Atovaquone and azithromycin for the treatment of human babesiosis. N Engl J Med 2000; 343:1454 8.
* Figure 5: courtesy of http://www.dpd.cdc.gov/dpdx/HTML/Babesiosis.htm

Contributed by Sarah Navina, MD, Ming Yin, MD, PhD, and A. William Pasculle. ScD




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