374
FATE AFTER 120 DAYS OF RATS TREATED WITH FK 506 FROM DAYS 30 TO 120
Amaurosis
fugax and antiphospholipid antibodies
SiR,—Dr Booy (June 23, p 1538) describes a case of amaurosis fugax in a young woman and discusses whether a carotid angiogram should be done. The far less invasive procedure of phospholipid (aPL) antibody detection may be appropriate. The antiphospholipid antibody syndrome (APS), whose clinical features include thrombosis, thrombocytopenia, and recurrent miscarriages,’ affects mainly young women. The solid phase cardiolipin antibody test and the lupus anticoagulant test are regarded as useful diagnostic toolsAlthough a close pathogenetic link between autoantibodies and neurological diseases is still
*Other 2 animals became diabetic. at 132 and 147 days tOther 3 animals used for breedmg and became diabetic while pregnant at 170,175, and 180 days
During the 90-day treatment period, diabetes developed in 15,3, and none of the tap water, low-dose FK 506, and high-dose FK 506 groups, respectively (figure). Rats with diabetes died within a few days but there was no mortality or inhibition of weight gain among the non-diabetic rats. In these protected animals, blood glucose levels, measured every 2 weeks, and hepatic and renal function tests were always normal. 9 FK 506-treated rats (3 from group 2, 6 from group 3) had intraperitoneal glucose tolerance tests (2 g/kg) on the last day of treatment, and pancreas insulin content was measured by radioimmunoassay in 11of the group 2 and 3 non-diabetic animals which were killed. The results were normal, and not different from those in 6 untreated Wistar-Furth (non-BB) rats. On histopathological examination, the pancreases of the non-diabetic FK 506-treated rats had little or no evidence of the insulitis and periductular mononuclear inflammation which was characteristic of the non-treated diabetic animals. As with cyclosporin3 the protective effect of FK 506 often outlasted the time of active treatment (table). Glucose intolerance, which has been described in BB rats under cyclosporin treatment,9 was not observed with the doses of FK 506 used in this study. These findings support the possibility of clinical trials of immune intervention for recent onset diabetes. Supported by research grants from the Veterans Administration, project grant DK 29961 from the National Institutes of Health, and the Renziehausen grant of the Children’s Hospital of Pittsburgh.
Departments of Surgery, Pathology, Medicine, Neurobiology, and Pediatrics,
University Health Center of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA 1.
N. MURASE I. LIEBERMAN M. NALESNIK D. MINTZ S. TODO A. L. DRASH T. E. STARZL
Stiller CR, Gardell C, et al. Cyclosporin prevents diabetes in BB Wistar Lancet 1983; i: 10-12 Like AA, Dirodi V, Thomas S, Guberski DL, Rossini AA Prevention of diabetes mellitus in the BB W rat cyclosporin-A. Am J Pathol 1984, 117: 92-97. Brayman KL, Armstrong BA, Shaw LM, et al. Prevention of diabetes in BB rats by intermittent administration of cyclosporine. Surgery 1987, 102: 235-41. Stiller CR, Dupre J, Gent M, et al Effects of cyclosporine immunosuppression in insulin-dependent diabetes mellitus of recent onset Science 1984, 223: 1362-67 Assan R, Feutren G, Debray-Sachs M, et al. Metabolic and immunological effects of cyclosporin in recently diagnosed type I diabetes mellitus Lancet 1985; i. 67-71. Stiller CR, Dupre J. Immune interventional studies in type I diabetes: summary of the London (Canada) and Canadian-European experience In. Eisenbarth GS, ed Immunotherapy of diabetes and selected autoimmune diseases. Boca Raton, Florida: CRC Press, 1989: 73-84 Starzl TE, Todo S, Fung J, Demetris AJ, Venkataramanan R, Jam A FK 506 for human liver, kidney and pancreas transplantation Lancet 1989; ii 1000-04. Kino T, Hatanaka H, Miyata S, et al FK 506, a novel immunosuppressant isolated from a streptomyces II immunosuppressive effect of FK 506 in vitro J Antibiotics
Laupacis A, rats.
2.
3. 4. 5.
6.
7.
8
1987; 40: 1256-65 9. Yale JF, Grose M, Seemayer TA, Marliss EB Immunological and metabolic concomitants of cyclosporin prevention of diabetes in BB rats. Diabetes 1987; 36: 749-57.
speculative, the clinical association of phospholipid antibodies and neurological disorders is no longer in dispute. Primary APS (without signs of definite connective-tissue disease) has been reported in association with focal cerebral ischaemia, migraine, transient global amnesia, chorea, myelopathy, and ocular ischaemia.3,4 These antibodies have been described in systemic lupus erythematosus (SLE) in children, the highest levels occurring during neurological events,’ and in children without any underlying pathological condition (primary APS).6 During the past two years we have studied fifteen female patients with primary APS. Amaurosis fugax is the only symptom in one patient; another patient presents with amaurosis fugax during recurrent episodes of migraine; a third has a central retinal artery thrombosis with permanent visual impairment. Asherson et af pointed out that cardiolipin antibodies represent a risk factor for occlusive ocular vascular disease in SLE. Several of our SLE patients with cardiolipin antibodies have migraine with or without visual disturbances. We agree with Booy that carotid angiography is not indicated in young patients with amaurosis fugax, but we suggest that phospholipid antibodies be looked for.
Medical Clinic 1, Università di Roma "La 00161 Rome, Italy
Sapienza",
GUIDO VALESINI ROBERTA PRIORI FU LUNG LUAN MIRELLA FALCO FRANCESCO BALSANO
1 Hughes GRV Thrombosis, abortion, cerebral disease and the lupus anticoagulant Br Med J 1983; 287: 1088-89. 2. Mackworth-Young CG. Antiphospholipid antibodies: more than just a disease marker? Immunol Today 1990, 11: 60-65. 3. Levine S, Welch KMA. The spectrum of neurologic disease associated with antiphospholipid antibodies Arch Neurol 1987, 44: 876-83. 4. Mackworth-Young CG, Loizou S, Walport MJ. Primary antiphospholipid syndrome: features of patients with raised anticardiolipin antibodies and no other disorder. Ann Rheum Dis 1989; 48: 362-67 5.
Shergy W, Kredich D, Pisetsky DS. The relationship of aCL antibodies to disease manifestations in pediatric systemic lupus erythematosus J Rheumatol 1988, 15:
1389-94 6 Ravelli A, Caporali R, Bianchi E, et al. Anticardiolipin syndrome in childhood: report of two cases Clin Exp Rheumatol 1990, 8: 95-98. 7 Asherson RA, Merry P, Acheson JF, Harris EN, Hughes GRV Antiphospholipid antibodies a risk factor for occlusive ocular vascular disease in systemic lupus erythematosus and the primary antiphospholipid antibodies syndrome Ann Rheum Dis 1989; 48: 358-61.
Acute viral
hepatitis B in children: lack of chronicity
SIR,-Chronic hepatitis B virus infection had been shown to evolve acute viral hepatitis B (AVHB) in 5-10% of cases.’ However, recent studies in adults have shown that chronic infection develops after AVHB in only 1-3% of patients.2v To evaluate the rate of progression to chronic infection after AVHB in children of less than 15 years old we followed prospectively 154 patients classified as having AVHB on hospital admission. All the children were positive for hepatitis B surface antigen (HBsAg) and/or IgM anti-HBs on admission, and were followed for between 3 and 24 months after admission. Diagnosis of acute viral hepatitis was made from clinical, biochemical, and serological features. Enzyme immunoassay (EIA) was used to detect HBsAg (Abbott) and anti-HBV antibodies (Institute of Organic Synthesis, Riga, USSR; Behring), antihepatitis A virus (HAV) antibody (Abbott), and anti-hepatitis D from
375
virus
(HDV) antibodies (Institute of Virology, Moscow, USSR; Abbott). With the above methods, 129 children were diagnosed as having AVHB, and 25 as having chronic HBV infection. All children exhibited symptomatic viral hepatitis. 115 of the AVHB children had a self-limiting disease and recovered during follow-up. Of these, 104 were initially HBsAg-positive but cleared HBsAg;
A 23-year-old primigravida was admitted to our hospital during week 20 of gestation. She had uterine contractions and a 1-week history of febrile influenza-like syndrome. Her pregnancy had previously been uneventful and she had not received any antibiotics. The patient’s temperature was 38’6°C, the leucocyte count was 25 500/1; there was no vaginal bleeding, but the cervix was dilated to 2 cm and spontaneous rupture of the membranes occurred. Blood
anti-HBs developed in 86. 11 were HBsAg-negative but IgM anti-HBc positive, and anti-HBs developed in all. 20 of the AVHB
cultures
children had fulminant hepatitis B and 14 died, all at less than 6 months of age. 25 children were classified as having chronic HBV infection because they remained HBsAg positive during follow-up. 10 children from this group (age range 5-12 years) had serum IgM anti-HAV on admission, but not anti-HDV (total and IgM). In 5 of these 10 children IgM anti-HBc was not detected, and in the other 5 it was found at a titre of not more than 10 000. These children were regarded as previously unrecognised HBsAg-carriers with superimposed acute viral hepatitis A. 14 of the chronic HBV infection children (age range 6 months to 6 years) had been admitted to hospital after casual testing. All had hepatomegaly and/or raised serum alanine aminotransferase with normal bilirubin. In 9 patients IgM anti-HBc was not found and in 5 it was detected at a titre of not more than 1000. These 14 patients were thought to be previously unrecognised HBsAg carriers. The remaining child in the chronic HBV infection group (a 12-year-old boy) presented with a clinical picture of acute moderate viral hepatitis. He was positive for HBsAg, hepatitis B early antigen (HBeAg), and IgM anti-HBc at a titre of 100, and negative for IgM anti-HAV and anti-HDV (IgM and total). After 1 month his symptoms had improved, but he remained HBsAg-positive and HBeAg-positive. After 1 year he was still HBsAg-positive but had become anti-HBe-positive. A liver biopsy taken at this time revealed chronic persistent hepatitis. This patient was diagnosed as having spontaneous reactivation of previously unrecognised chronic HBV infection. The exacerbation of chronic hepatitis B might be associated with seroconversion of HBeAg to anti-HBe.4 In this study none of 129 children with AVHB progressed to chronic viral hepatitis. We suspect that acute clinical HBV infection rarely if ever leads to the development of chronic liver disease. Chronic HBV infection in children seems to be a latent disease with an asymptomatic course and is not associated with clinical AVHB.
Department of Children’s
Infectious Diseases,
2nd Medical Institute, Moscow 117869, USSR
B. S. KAGANOV N. I. NISEVICH V. F. UCHAIKIN V. A. KONEV E. I. LEVINA N. N. SIZICH G. V. CHAPLIGINA
and prognostic aspects of hepatitis A, B and 17 (suppl): 1-44. Tassopoulos NC, Papaevangelou GJ, Sjogren MH, et al. Natural history of acute hepatitis B surface antigen-positive hepatitis in Greek adults. Gastroenterology
1 Norkrans J Clinical,
epidemiological
therapy with cephalothin (3 g few hours, the patient had a spontaneous incomplete abortion, delivering a non-macerated 470 g male fetus. A shredded foul-smelling placenta was removed. The patient’s temperature had fallen to 37 2°C by the next day, and cephalothin was replaced by oral cefadroxil. 5 days after admission, she was discharged afebrile and well. At necropsy the fetus showed no gross abnormalities but an early autolysis. Histological examination revealed placentitis, and multiple microabscesses in the lungs suggestive of listeriosis. Blood and placental tissue cultures yielded gram-positive bacilli, which were identified as L monocytogenes type 4b. Minimum inhibitory concentrations of 39 antibiotics against this strain and thirty other clinical isolates of L monocytogenes were determined by dilution in Mueller-Hinton agar supplemented with 5% horse blood, and found to be similar except for chloramphenicol (64 and 4-8 mg/1, respectively), tetracycline (64 and 1 mg/1), minocycline (8 and 01-02 mg/1), erythromycin (>512 and 0-1mg/1), spiramycin (> 512 and 4 mg/1), and clindamycin (512 and 2 mg/1). were
taken and intravenous
in 24 h) started. Within
a
Resistance to chloramphenicol, tetracycline, and erythromycin was eliminated in 44 to 100% of cells by all curing agents tested (acridine orange, ethidium bromide, pefloxacin, novobiocin, rifampicin and sodium dodecylsulphate). All three resistance markers were lost simultaneously, which suggests that they were encoded by the same
plasmid. shows that antibiotic-resistant L monocytogenes may be encountered, even in an untreated patient. Resistance transfer may also occur in the human bowel and vagina/cervix. The assumption that all L monocytogenes are antibiotic sensitive needs modification, and monitoring for the emergence of resistant strains is required. This
case
Departments of Bacteriology, and Obstetrics and Gynaecology, Hôpital Pellegrin, 33076 Bordeaux, France
CLAUDINE QUENTIN MARIE CLAUDE THIBAUT JACQUES HOROVITZ CHRISTIANE BEBEAR
Espoaze EP, Reynaud AE. Antibiotic susceptibilities of Listeria. m vitro studies. Infection 1988; 16 (suppl 2): 160-64. 2. Larsson S, Walder MH, Cronberg SN, Forsgren AB, Moestrup T. Antimicrobial susceptibilities of Listeria monocytogenes strains isolated from 1958 to 1982 in Sweden Antimicrob Agents Chemother 1985; 28: 12-14 3 Flamm RK, Hinrichs DJ, Thomashow MF Introduction of pAM&bgr;1 into Listeria monocytogenes by conjugation and homology between native L monocytogenes plasmids. Infect Immun 1984, 44: 157-61. 5. Vicente MF, Baquero F, Perez-Diaz JC Conjugative acquisition and expression of antibiotic resistance determinants in Listeria spp. J Antimicrob Chemother 1988; 21: 1
309-18
non-A, non-B Scand J Infect Dis 1978;
2
1987, 92: 1844-50 3 Bortolotti F, Bertaggia A, Crivellaro C, et al. Chronic evolution of acute hepatitis type B prevalence and predictive markers Infection 1986, 14: 64-67. 4 Tong MJ, Sampliner RE, Govindarajan S, et al Spontaneous reactivation of hepatitis B in Chinese patients with HBsAg-positive chronic active hepatitis Hepatology 1987; 7: 713-18
Multiresistant strain of Listeria monocytogenes in septic abortion SIR, Listerra monocytogenes was thought to be susceptible to all antibiotics active against gram-positive bacteria, except for the newer cephalosporins and fosfomycin. The antibiotic susceptibility of this organism had not varied,12 and no resistant clinical strain had been reported until Dr Poyart-Salmeron and colleagues did so (June 16, p 1422), although resistance determinants are easily transferred in vitro from streptococci..3,1 We report the isolation of a multiresistant strain of L morwcytogenes responsible for septic abortion.
Experience with toxin bead ELISA in cholera outbreak SIR,-An outbreak of acute secretory diarrhoea occurred among passengers in two families aboard the MV Harshavardhan while sailing from Calcutta to Port Blair, in the Andaman Islands, from July 5 to 8, 1990. Two passengers died and were buried at sea. The ship was advised not to berth at Port Blair but to await clearance by the port health officer and health staff. On July 8, doctors and health inspectors boarded the vessel. Stool samples from the affected passengers were sent to the National Institute of Cholera and Enteric Diseases (NICED), where they arrived on July 10. The samples were immediately plated on selective media for isolation of Vibrio cholerae, diarrhoeogenic Escherichia coli, Campylobacter, Salmonella and Shigella spp, and Clostridium difficile. Samples were also inoculated into alkaline peptone water and a double enrichment protocol was followed to isolate cholera vibrios. Microscopy did not yield any clue as to the causative agent seven
FATE AFTER 120 DAYS OF RATS TREATED WITH FK 506 FROM DAYS 30 TO 120
Amaurosis
fugax and antiphospholipid antibodies
SiR,—Dr Booy (June 23, p 1538) describes a case of amaurosis fugax in a young woman and discusses whether a carotid angiogram should be done. The far less invasive procedure of phospholipid (aPL) antibody detection may be appropriate. The antiphospholipid antibody syndrome (APS), whose clinical features include thrombosis, thrombocytopenia, and recurrent miscarriages,’ affects mainly young women. The solid phase cardiolipin antibody test and the lupus anticoagulant test are regarded as useful diagnostic toolsAlthough a close pathogenetic link between autoantibodies and neurological diseases is still
*Other 2 animals became diabetic. at 132 and 147 days tOther 3 animals used for breedmg and became diabetic while pregnant at 170,175, and 180 days
During the 90-day treatment period, diabetes developed in 15,3, and none of the tap water, low-dose FK 506, and high-dose FK 506 groups, respectively (figure). Rats with diabetes died within a few days but there was no mortality or inhibition of weight gain among the non-diabetic rats. In these protected animals, blood glucose levels, measured every 2 weeks, and hepatic and renal function tests were always normal. 9 FK 506-treated rats (3 from group 2, 6 from group 3) had intraperitoneal glucose tolerance tests (2 g/kg) on the last day of treatment, and pancreas insulin content was measured by radioimmunoassay in 11of the group 2 and 3 non-diabetic animals which were killed. The results were normal, and not different from those in 6 untreated Wistar-Furth (non-BB) rats. On histopathological examination, the pancreases of the non-diabetic FK 506-treated rats had little or no evidence of the insulitis and periductular mononuclear inflammation which was characteristic of the non-treated diabetic animals. As with cyclosporin3 the protective effect of FK 506 often outlasted the time of active treatment (table). Glucose intolerance, which has been described in BB rats under cyclosporin treatment,9 was not observed with the doses of FK 506 used in this study. These findings support the possibility of clinical trials of immune intervention for recent onset diabetes. Supported by research grants from the Veterans Administration, project grant DK 29961 from the National Institutes of Health, and the Renziehausen grant of the Children’s Hospital of Pittsburgh.
Departments of Surgery, Pathology, Medicine, Neurobiology, and Pediatrics,
University Health Center of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA 1.
N. MURASE I. LIEBERMAN M. NALESNIK D. MINTZ S. TODO A. L. DRASH T. E. STARZL
Stiller CR, Gardell C, et al. Cyclosporin prevents diabetes in BB Wistar Lancet 1983; i: 10-12 Like AA, Dirodi V, Thomas S, Guberski DL, Rossini AA Prevention of diabetes mellitus in the BB W rat cyclosporin-A. Am J Pathol 1984, 117: 92-97. Brayman KL, Armstrong BA, Shaw LM, et al. Prevention of diabetes in BB rats by intermittent administration of cyclosporine. Surgery 1987, 102: 235-41. Stiller CR, Dupre J, Gent M, et al Effects of cyclosporine immunosuppression in insulin-dependent diabetes mellitus of recent onset Science 1984, 223: 1362-67 Assan R, Feutren G, Debray-Sachs M, et al. Metabolic and immunological effects of cyclosporin in recently diagnosed type I diabetes mellitus Lancet 1985; i. 67-71. Stiller CR, Dupre J. Immune interventional studies in type I diabetes: summary of the London (Canada) and Canadian-European experience In. Eisenbarth GS, ed Immunotherapy of diabetes and selected autoimmune diseases. Boca Raton, Florida: CRC Press, 1989: 73-84 Starzl TE, Todo S, Fung J, Demetris AJ, Venkataramanan R, Jam A FK 506 for human liver, kidney and pancreas transplantation Lancet 1989; ii 1000-04. Kino T, Hatanaka H, Miyata S, et al FK 506, a novel immunosuppressant isolated from a streptomyces II immunosuppressive effect of FK 506 in vitro J Antibiotics
Laupacis A, rats.
2.
3. 4. 5.
6.
7.
8
1987; 40: 1256-65 9. Yale JF, Grose M, Seemayer TA, Marliss EB Immunological and metabolic concomitants of cyclosporin prevention of diabetes in BB rats. Diabetes 1987; 36: 749-57.
speculative, the clinical association of phospholipid antibodies and neurological disorders is no longer in dispute. Primary APS (without signs of definite connective-tissue disease) has been reported in association with focal cerebral ischaemia, migraine, transient global amnesia, chorea, myelopathy, and ocular ischaemia.3,4 These antibodies have been described in systemic lupus erythematosus (SLE) in children, the highest levels occurring during neurological events,’ and in children without any underlying pathological condition (primary APS).6 During the past two years we have studied fifteen female patients with primary APS. Amaurosis fugax is the only symptom in one patient; another patient presents with amaurosis fugax during recurrent episodes of migraine; a third has a central retinal artery thrombosis with permanent visual impairment. Asherson et af pointed out that cardiolipin antibodies represent a risk factor for occlusive ocular vascular disease in SLE. Several of our SLE patients with cardiolipin antibodies have migraine with or without visual disturbances. We agree with Booy that carotid angiography is not indicated in young patients with amaurosis fugax, but we suggest that phospholipid antibodies be looked for.
Medical Clinic 1, Università di Roma "La 00161 Rome, Italy
Sapienza",
GUIDO VALESINI ROBERTA PRIORI FU LUNG LUAN MIRELLA FALCO FRANCESCO BALSANO
1 Hughes GRV Thrombosis, abortion, cerebral disease and the lupus anticoagulant Br Med J 1983; 287: 1088-89. 2. Mackworth-Young CG. Antiphospholipid antibodies: more than just a disease marker? Immunol Today 1990, 11: 60-65. 3. Levine S, Welch KMA. The spectrum of neurologic disease associated with antiphospholipid antibodies Arch Neurol 1987, 44: 876-83. 4. Mackworth-Young CG, Loizou S, Walport MJ. Primary antiphospholipid syndrome: features of patients with raised anticardiolipin antibodies and no other disorder. Ann Rheum Dis 1989; 48: 362-67 5.
Shergy W, Kredich D, Pisetsky DS. The relationship of aCL antibodies to disease manifestations in pediatric systemic lupus erythematosus J Rheumatol 1988, 15:
1389-94 6 Ravelli A, Caporali R, Bianchi E, et al. Anticardiolipin syndrome in childhood: report of two cases Clin Exp Rheumatol 1990, 8: 95-98. 7 Asherson RA, Merry P, Acheson JF, Harris EN, Hughes GRV Antiphospholipid antibodies a risk factor for occlusive ocular vascular disease in systemic lupus erythematosus and the primary antiphospholipid antibodies syndrome Ann Rheum Dis 1989; 48: 358-61.
Acute viral
hepatitis B in children: lack of chronicity
SIR,-Chronic hepatitis B virus infection had been shown to evolve acute viral hepatitis B (AVHB) in 5-10% of cases.’ However, recent studies in adults have shown that chronic infection develops after AVHB in only 1-3% of patients.2v To evaluate the rate of progression to chronic infection after AVHB in children of less than 15 years old we followed prospectively 154 patients classified as having AVHB on hospital admission. All the children were positive for hepatitis B surface antigen (HBsAg) and/or IgM anti-HBs on admission, and were followed for between 3 and 24 months after admission. Diagnosis of acute viral hepatitis was made from clinical, biochemical, and serological features. Enzyme immunoassay (EIA) was used to detect HBsAg (Abbott) and anti-HBV antibodies (Institute of Organic Synthesis, Riga, USSR; Behring), antihepatitis A virus (HAV) antibody (Abbott), and anti-hepatitis D from
375
virus
(HDV) antibodies (Institute of Virology, Moscow, USSR; Abbott). With the above methods, 129 children were diagnosed as having AVHB, and 25 as having chronic HBV infection. All children exhibited symptomatic viral hepatitis. 115 of the AVHB children had a self-limiting disease and recovered during follow-up. Of these, 104 were initially HBsAg-positive but cleared HBsAg;
A 23-year-old primigravida was admitted to our hospital during week 20 of gestation. She had uterine contractions and a 1-week history of febrile influenza-like syndrome. Her pregnancy had previously been uneventful and she had not received any antibiotics. The patient’s temperature was 38’6°C, the leucocyte count was 25 500/1; there was no vaginal bleeding, but the cervix was dilated to 2 cm and spontaneous rupture of the membranes occurred. Blood
anti-HBs developed in 86. 11 were HBsAg-negative but IgM anti-HBc positive, and anti-HBs developed in all. 20 of the AVHB
cultures
children had fulminant hepatitis B and 14 died, all at less than 6 months of age. 25 children were classified as having chronic HBV infection because they remained HBsAg positive during follow-up. 10 children from this group (age range 5-12 years) had serum IgM anti-HAV on admission, but not anti-HDV (total and IgM). In 5 of these 10 children IgM anti-HBc was not detected, and in the other 5 it was found at a titre of not more than 10 000. These children were regarded as previously unrecognised HBsAg-carriers with superimposed acute viral hepatitis A. 14 of the chronic HBV infection children (age range 6 months to 6 years) had been admitted to hospital after casual testing. All had hepatomegaly and/or raised serum alanine aminotransferase with normal bilirubin. In 9 patients IgM anti-HBc was not found and in 5 it was detected at a titre of not more than 1000. These 14 patients were thought to be previously unrecognised HBsAg carriers. The remaining child in the chronic HBV infection group (a 12-year-old boy) presented with a clinical picture of acute moderate viral hepatitis. He was positive for HBsAg, hepatitis B early antigen (HBeAg), and IgM anti-HBc at a titre of 100, and negative for IgM anti-HAV and anti-HDV (IgM and total). After 1 month his symptoms had improved, but he remained HBsAg-positive and HBeAg-positive. After 1 year he was still HBsAg-positive but had become anti-HBe-positive. A liver biopsy taken at this time revealed chronic persistent hepatitis. This patient was diagnosed as having spontaneous reactivation of previously unrecognised chronic HBV infection. The exacerbation of chronic hepatitis B might be associated with seroconversion of HBeAg to anti-HBe.4 In this study none of 129 children with AVHB progressed to chronic viral hepatitis. We suspect that acute clinical HBV infection rarely if ever leads to the development of chronic liver disease. Chronic HBV infection in children seems to be a latent disease with an asymptomatic course and is not associated with clinical AVHB.
Department of Children’s
Infectious Diseases,
2nd Medical Institute, Moscow 117869, USSR
B. S. KAGANOV N. I. NISEVICH V. F. UCHAIKIN V. A. KONEV E. I. LEVINA N. N. SIZICH G. V. CHAPLIGINA
and prognostic aspects of hepatitis A, B and 17 (suppl): 1-44. Tassopoulos NC, Papaevangelou GJ, Sjogren MH, et al. Natural history of acute hepatitis B surface antigen-positive hepatitis in Greek adults. Gastroenterology
1 Norkrans J Clinical,
epidemiological
therapy with cephalothin (3 g few hours, the patient had a spontaneous incomplete abortion, delivering a non-macerated 470 g male fetus. A shredded foul-smelling placenta was removed. The patient’s temperature had fallen to 37 2°C by the next day, and cephalothin was replaced by oral cefadroxil. 5 days after admission, she was discharged afebrile and well. At necropsy the fetus showed no gross abnormalities but an early autolysis. Histological examination revealed placentitis, and multiple microabscesses in the lungs suggestive of listeriosis. Blood and placental tissue cultures yielded gram-positive bacilli, which were identified as L monocytogenes type 4b. Minimum inhibitory concentrations of 39 antibiotics against this strain and thirty other clinical isolates of L monocytogenes were determined by dilution in Mueller-Hinton agar supplemented with 5% horse blood, and found to be similar except for chloramphenicol (64 and 4-8 mg/1, respectively), tetracycline (64 and 1 mg/1), minocycline (8 and 01-02 mg/1), erythromycin (>512 and 0-1mg/1), spiramycin (> 512 and 4 mg/1), and clindamycin (512 and 2 mg/1). were
taken and intravenous
in 24 h) started. Within
a
Resistance to chloramphenicol, tetracycline, and erythromycin was eliminated in 44 to 100% of cells by all curing agents tested (acridine orange, ethidium bromide, pefloxacin, novobiocin, rifampicin and sodium dodecylsulphate). All three resistance markers were lost simultaneously, which suggests that they were encoded by the same
plasmid. shows that antibiotic-resistant L monocytogenes may be encountered, even in an untreated patient. Resistance transfer may also occur in the human bowel and vagina/cervix. The assumption that all L monocytogenes are antibiotic sensitive needs modification, and monitoring for the emergence of resistant strains is required. This
case
Departments of Bacteriology, and Obstetrics and Gynaecology, Hôpital Pellegrin, 33076 Bordeaux, France
CLAUDINE QUENTIN MARIE CLAUDE THIBAUT JACQUES HOROVITZ CHRISTIANE BEBEAR
Espoaze EP, Reynaud AE. Antibiotic susceptibilities of Listeria. m vitro studies. Infection 1988; 16 (suppl 2): 160-64. 2. Larsson S, Walder MH, Cronberg SN, Forsgren AB, Moestrup T. Antimicrobial susceptibilities of Listeria monocytogenes strains isolated from 1958 to 1982 in Sweden Antimicrob Agents Chemother 1985; 28: 12-14 3 Flamm RK, Hinrichs DJ, Thomashow MF Introduction of pAM&bgr;1 into Listeria monocytogenes by conjugation and homology between native L monocytogenes plasmids. Infect Immun 1984, 44: 157-61. 5. Vicente MF, Baquero F, Perez-Diaz JC Conjugative acquisition and expression of antibiotic resistance determinants in Listeria spp. J Antimicrob Chemother 1988; 21: 1
309-18
non-A, non-B Scand J Infect Dis 1978;
2
1987, 92: 1844-50 3 Bortolotti F, Bertaggia A, Crivellaro C, et al. Chronic evolution of acute hepatitis type B prevalence and predictive markers Infection 1986, 14: 64-67. 4 Tong MJ, Sampliner RE, Govindarajan S, et al Spontaneous reactivation of hepatitis B in Chinese patients with HBsAg-positive chronic active hepatitis Hepatology 1987; 7: 713-18
Multiresistant strain of Listeria monocytogenes in septic abortion SIR, Listerra monocytogenes was thought to be susceptible to all antibiotics active against gram-positive bacteria, except for the newer cephalosporins and fosfomycin. The antibiotic susceptibility of this organism had not varied,12 and no resistant clinical strain had been reported until Dr Poyart-Salmeron and colleagues did so (June 16, p 1422), although resistance determinants are easily transferred in vitro from streptococci..3,1 We report the isolation of a multiresistant strain of L morwcytogenes responsible for septic abortion.
Experience with toxin bead ELISA in cholera outbreak SIR,-An outbreak of acute secretory diarrhoea occurred among passengers in two families aboard the MV Harshavardhan while sailing from Calcutta to Port Blair, in the Andaman Islands, from July 5 to 8, 1990. Two passengers died and were buried at sea. The ship was advised not to berth at Port Blair but to await clearance by the port health officer and health staff. On July 8, doctors and health inspectors boarded the vessel. Stool samples from the affected passengers were sent to the National Institute of Cholera and Enteric Diseases (NICED), where they arrived on July 10. The samples were immediately plated on selective media for isolation of Vibrio cholerae, diarrhoeogenic Escherichia coli, Campylobacter, Salmonella and Shigella spp, and Clostridium difficile. Samples were also inoculated into alkaline peptone water and a double enrichment protocol was followed to isolate cholera vibrios. Microscopy did not yield any clue as to the causative agent seven
