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Fatal congenital human leptospirosis
Zbl. Bake Hyg. A 257, 548 (1984)
Fatal Congenital Human Leptospirosis S. FAINE I , B. ADLER 1, W. CHRISTOPHER I, and R. VALENTINE 2 1
2
Microbiology, Monash University, Clayton, Australia, 3168 Pathology, Queen Victoria Medical Centre, Melbourne, Australia, 3000
A 33 year old farmer 's wife, 26 weeks pregnant, developed sudden fever, vomiting and abdominal pain. She was milking cows following her husb and 's febrile incapacitating illness, subsequently diagnosed as leptospirosis. She recovered from her illness after 3 days of symptomatic treatment and hydration. The fetal heart was normal. Blood taken 10 days after onset of symptoms had a serum agglutination titre of 512 to 1. interrogans serovar hardio, a locally prevalent cause of leptospirosis in cattle and people. There had recently been an outbreak of an illness amongst cows on the patient's farm , diagnosed retrospectively as leptospirosis hardjo. She was readmitted to hospital 3 weeks later, now 29 weeks pregnant following a period of vomiting, fever, headache and myalgia. She was afebrile on admi ssion, but the fetal heart was not heard follow ing a few days of reduced fetal movements. Fetal death was diagnosed and labor induced. A dead fetus was delivered. At autopsy a 30 week normally developed partly autol yzed fetus was estimated to have been dead for 3-4 days. All tissues were partially aut olyzed, with a few hemorrhages, congested meninges and a small retroplacental hematoma. Histologically there was clear placental villitis, but other tissues were too autolyzed to show histological detail. Special investigations included attempts to culture lepto spires from blood and tissues, special sta ining and serology. Leptospire s, cultured from the placenta, were identified as 1. interrogans serovar hardjo. Cultures of other tissues were negative or contaminated. Leptospires were visualized in the placenta by silver staining and by specific immunofluorescence with ssus-hardjo (but not anti-pomona) anti sera, and also in adrenals, kidney and intestine by anti-hardio specific immunofluorescence. The cord blood had an agglutination titre of 128 to bardjo but no other serovars, and reacted strongly positive when tested for specific IgM against hardio antigen in the enzymelinked immunosorbent assay. The diagnosis was pro ved by cultivation of the organism, specific cord blood IgM antibodies and specific immunofluorescence of the leptospires in the placenta and fetal tissues. This is the first report of fatal intrauterine human infection by serovar bardio. Dr. S. Paine, Dept. of Microbiology, Monash University, Clayton, Victoria 3168, Australia
Fatal Congenital Human Leptospirosis S. FAINE I , B. ADLER 1, W. CHRISTOPHER I, and R. VALENTINE 2 1
2
Microbiology, Monash University, Clayton, Australia, 3168 Pathology, Queen Victoria Medical Centre, Melbourne, Australia, 3000
A 33 year old farmer 's wife, 26 weeks pregnant, developed sudden fever, vomiting and abdominal pain. She was milking cows following her husb and 's febrile incapacitating illness, subsequently diagnosed as leptospirosis. She recovered from her illness after 3 days of symptomatic treatment and hydration. The fetal heart was normal. Blood taken 10 days after onset of symptoms had a serum agglutination titre of 512 to 1. interrogans serovar hardio, a locally prevalent cause of leptospirosis in cattle and people. There had recently been an outbreak of an illness amongst cows on the patient's farm , diagnosed retrospectively as leptospirosis hardjo. She was readmitted to hospital 3 weeks later, now 29 weeks pregnant following a period of vomiting, fever, headache and myalgia. She was afebrile on admi ssion, but the fetal heart was not heard follow ing a few days of reduced fetal movements. Fetal death was diagnosed and labor induced. A dead fetus was delivered. At autopsy a 30 week normally developed partly autol yzed fetus was estimated to have been dead for 3-4 days. All tissues were partially aut olyzed, with a few hemorrhages, congested meninges and a small retroplacental hematoma. Histologically there was clear placental villitis, but other tissues were too autolyzed to show histological detail. Special investigations included attempts to culture lepto spires from blood and tissues, special sta ining and serology. Leptospire s, cultured from the placenta, were identified as 1. interrogans serovar hardjo. Cultures of other tissues were negative or contaminated. Leptospires were visualized in the placenta by silver staining and by specific immunofluorescence with ssus-hardjo (but not anti-pomona) anti sera, and also in adrenals, kidney and intestine by anti-hardio specific immunofluorescence. The cord blood had an agglutination titre of 128 to bardjo but no other serovars, and reacted strongly positive when tested for specific IgM against hardio antigen in the enzymelinked immunosorbent assay. The diagnosis was pro ved by cultivation of the organism, specific cord blood IgM antibodies and specific immunofluorescence of the leptospires in the placenta and fetal tissues. This is the first report of fatal intrauterine human infection by serovar bardio. Dr. S. Paine, Dept. of Microbiology, Monash University, Clayton, Victoria 3168, Australia