Congenital transmission of visceral leishmaniasis (kala azar) from an asymptomatic mother to her child

In this article, we report the case of a 16-month-old German boy who was ad mitted to the Children's Hospital of Stuttgart with a 4-week history of int ermittent fever, decreased appetite, weakness, fatigue, and difficulty slee ping. He was healthy at birth and remained so for the first 15 months of hi s life. On admission, physical examination showed enlarged cervical, axilla ry, and inguinal lymph nodes, as well as hepatosplenomegaly. Laboratory dat a revealed pancytopenia, elevated liver function tests, and hypergammaglobu linemia. Blood, stool, and urine culture results were negative. Viral infec tions and rheumatologic and autoimmune disorders were ruled out, but a posi tive titer for Leishmania antibodies was noted. In a liver and bone marrow biopsy, the amastigote form of the parasite could not be seen in cells. The promastigote form of Leishmania was found and the diagnosis of visceral le ishmaniasis was made by combining the cultures of both the liver and the bo ne marrow biopsy material in 5 mL 0.9% saline on brain heart infusion agar, supplemented with defibrinated rabbit blood and incubated at 25 to 26 degr ees C for 5 days. The parasite was identified by Southern blot analysis as Leishmania infantum. Specific therapy with the antimonial compound sodium stibogluconate with a dose of 20 mg/kg body weight was begun immediately. Within 4 days, the pati ent became afebrile. The side effects of treatment, including erosive gastr itis, cholelithiasis, worsening hepatosplenomegaly, elevation of liver enzy mes, pancreatitis, and electrocardiogram abnormalities, necessitated the di scontinuation of treatment after 17 days. On discharge 4 weeks later, the p atient was stabilized and afebrile with a normal spleen, normal complete bl ood count, normal gammaglobulins, and decreasing antibody titers to Leishma nia. During the next 24 months, the patient experienced intermittent episod es of abdominal pain, decreased appetite, recurrent arthralgia, and myalgia . But at his last examination in January 1998, he was well; all symptoms me ntioned above had disappeared. Because the child had never left Germany, nonvector transmission was suspec ted and household contacts were examined. His mother was the only one who h ad a positive antibody titer against Leishmania donovani complex. She had t raveled several times to endemic Mediterranean areas (Portugal, Malta, and Corse) before giving birth to the boy. But she had never been symptomatic f or visceral leishmaniasis. Her bone marrow, spleen, and liver biopsy result s were within normal limits. Culture results and polymerase chain reaction of this material were negative. A Montenegro skin test result was positive, indicating a previous infection with Leishmania. Western blot analysis sho wed specific recognition by maternal antibodies of antigens of Leishmania c ultured from the boy's tissue. Visceral leishmaniasis is endemic to several tropical and subtropical count ries, but also to the Mediterranean region. It is transmitted by the sand f ly (Phlebotomus, Lutzomyia). Occasional nonvector transmissions also have b een reported through blood transfusions, sexual intercourse, organ transpla nts, excrements of dogs, and sporadically outside endemic areas. Only 8 cas es of congenital acquired disease have been described before 1995, when our case occurred. In our patient, additional evaluation showed that the asymptomatic mother m ust have had a subclinical infection with Leishmania that was reactivated b y pregnancy, and then congenitally transmitted to the child. Visceral leish maniasis has to be considered in children with fever, pancytopenia, and spl enomegaly, even if the child has not been to an endemic area and even if th ere is no evidence of the disease in his environment, because leishmaniasis can be transmitted congenitally from an asymptomatic mother to her child.