- Email: [email protected]
PROPHYLACTIC ANTIBIOTICS IN ERYSIPELAS
1401
erythema migrans in the right loin 10 weeks earlier but did not recall having been bitten by a tick. 4 weeks after this episode he had had joint pains in his neck and shoulders and dysaesthesias in the chest and back with mild fever (38°C) and asthenia. He had been treated by spiramycin 6 million IU for 8 days and had recovered completely a few days. Besides the Bell’s palsy, a diminution of the tendon reflexes of the lower limbs was noted. Leg joints were painful but not swollen. CSF contained 100 cells/1 (100% lymphocytes), protein 1 - 6 g/l, glucose 3 - 6 mmol/1. Electrophoresis of CSF showed an increase of IgG (0 - 23g/1) with an IgG/albumin ratio of-31. There was a striking neutrophilia (12 500 white cells1, 63% neutrophils). The ESR was 15 mm/h. Other blood tests were normal. The patient, being allergic to penicillin, was treated with doxycycline 200 mg daily for 3 weeks and recovered rapidly. 4 weeks later his reflexes were normal and the pains had disappeared. A mild right facial palsy remained. Serial sera were tested for specific IgG and IgM antibody to B burgdorferi by indirect immunofluorescence by Dr Bettina Wilske (Max van Pettenkofer Institute, Munich). The first patient had significant IgG and IgM antibody whereas the second patient had high IgG titres without IgM (figure). In the first patient IgM titres decreased rapidly after the onset of the facial paralysis. An IgM response may have been missed in patient 2, who was seen later in the course of the disease and had been treated by antibiotics. Typical erythema chronicum migrans has long been recognised in France. However, only recently has it been possible to confirm its association with an infection by the Lyme-disease spirochaete. The broad clinical spectrum of the disease makes it an unobvious diagnosis when neurological involvements are the prime symptoms. These two French cases of lymphocytic meningoradiculitis provide argument for including a search for antibody to B burgdorferi in the laboratory work-up of patients presenting with meningoradiculitis whether or not they report a history of tick-bite. Early serological diagnosis permits high-dose penicillin, therapy that significantly shortens neurological disorders in Lyme disease.6
EFFECT OF ANTIBIOTIC PROPHYLAXIS
in
We thank Prof Friedrich Deinhart who put disease research group at his institute. Internal Medicine Service B, and Virology Laboratory,
CHRU Bretonneau, 370444 Tours, France
us
in touch with the
Lyme
O. WEILL
J. P. AVIGNON A. GOUDEAU
1. Garin
C, Bujadoux. Paralysie par lestiques. J Med Lyon 1922; 3: 765-67. AC, Malawista SE, Hardin JA, Ruddy S, Askenase PW, Andiman WA. Erythema chronicum migrans and Lyme arthritis: the enlarging clinical spectrum. Ann Intern Med 1977; 86: 685-98. Barbour AG, Burgdorfer W, Hayes SF, Peter O, Aeschlimann A. Isolation of a cultivable spirochete from Ixodes ricinus ticks of Switzerland. Curr Microbiol 1983;
2. Steere
3.
8: 123-26. 4.
Ryberg B, Nilsson B, Burgdorfer W, Barbour AG Antibodies to Lyme-disease spirochaete in European lymphocytic meningoradiculitis (Bannwarth’s syndrome). Lancet
1983; ii: 519. F, Lecomte F, Humbert G, Dournon E. La maladie de Lyme un cas autochtone confirmé sérologiquement Méd Mal Inf 1985; 15: 44-45 Steere AC, Pachner AR, Malawista SE Neurologic abnormalities of Lyme disease: successful treatment with high-dose intravenous penicillin. Ann Intern Med 1983,
5. Borsa-Lebas 6.
99: 767-72.
PROPHYLACTIC ANTIBIOTICS IN ERYSIPELAS
SIR,-Dr Bitnun (Feb 9, p 345) and Dr Thind (April 27, p 986) suggest that prolonged antibiotic prophylaxis reduces the number of attacks in recurrent erysipelas. However, their conclusions were based on only two cases and one case, respectively, and there was a mild relapse during prophylaxis in Bitnun’s second case. We have observations on seventeen patients. Since 1982 our policy has been to institute long-term antibiotic prophylaxis after a first attack of erysipelas. We administer benzathine penicillin G 2-44 megaunits intramuscularly every 3 weeks. Data on these seventeen patients (ten females, seven males; mean age 59 years) seen in our clinic between 1982 and 1984 for a first attack of erysipelas are shown in the table. Because of a history of allergy to penicillin five patients were not treated. Prophylaxis with intramuscular benzathine penicillin prevented relapses but when prophylaxis stopped the risk of recurrence
returned. We are tempted to conclude that prevention of recurrent necessitates treatment for very long periods. Questions about the cost-benefit ratio of long-term prophylactic regimens now need to be addressed.
erysipelas
Dermatology Clinic, Hôpital Cantonal Universitaire, 1211 Geneva
4, Switzerland
T. DUVANEL Y. MÉROT M. HARMS J.-H. SAURAT
EPIDEMIC OF APLASTIC CRISIS IN PATIENTS WITH HEREDITARY SPHEROCYTOSIS IN JAPAN
SiR,-Dr Shiraishi and his colleagues (April 27, p 982) describe a large outbreak of erythema infectiosum (fifth disease) in Japan. We report here an epidemic of aplastic crisis in patients with hereditary spherocytosis in Japan. Hereditary spherocytosis is the most frequent of the congenital chronic haemolytic anaemias in this country. However, aplastic crises in hereditary spherocytosis used to be very rare and up to 1980 few reports had been published in Japan. However, nine such reports appeared between August, 1980, and 1982. There have been none since 1983. This pattern suggests that the aplastic crises in 1980-82 were due to a single transmissible agent. In Niigata we saw four patients with hereditary spherocytosis in aplastic crisis between June, 1981, and March, 1982. The aplastic crises of both chronic haemolytic anaemia and erythema infectiosum are caused principally by human parvovirus (HPV).2-4 Cryopreserved serum from one of our patients in the acute phase was available and was found to contain both HPV antigens (countercurrent immunoelectrophoresis) and HPV-like virus particles (electron microscopy). Moreover, the serum inhibited colony formation by both late erythroid progenitors (CFU-E) and more primitive erythroid progenitors (BFU-E). There was also a large outbreak of erythema infectiosum between 1981 and 1982 in Niigata.’ Epidemic aplastic crisis in congenital chronic haemolytic anaemia has been reported in Britain,3Jamaica,and the United States,5 and the causative agent has been identified as HPV. We suggest that the epidemic of aplastic crises in patients with hereditary spherocytosis in Japan was also due to HPV.
Division of Haematology, Niigata Shimin Hospital, Niigata, Japan
TSUNEYASU TSUKADA TADASHI KOIKE* RYOKO KOIKE MASAYOSHI SANADA
First Department of Internal Medicine, Niigata University School of Medicine
MASUHIRO TAKAHASHI AKIRA SHIBATA
School of Health Sciences, Kyushu University, Fukuoka
TADASU NUNOUE
*Present address: First
Department of Internal Medicine, Niigata University, Asahi machi
don, Niigata, Japan. T, Koike T, Sanada M. Epidemic outbreak of aplastic crises in the patients hereditary spherocytosis in Japan. Igaku no ayumi 1985, 133: 123-25 (in Japanese). Pattison JR, Jones SE, Hodgson J, et al. Parvovirus infection and hypoplastic crisis in
1. Tsukada
with
2.
sickle-cell anaemia. Lancet 1981; ii: 664-65. MJ, Davis LR, Hodgson J, et al. Occurrence of infection with parvovirus-like agent in children with sickle cell anaemia during a two-year period. J Clin Pathol 1982; 35: 744-49. 4. Serjeant GR, Topley JM, Mason K, et al. Outbreak of aplastic crises in sickle cell anaemia associated with parvovirus-like agent Lancet 1981; ii: 595-97. 5. Rao KRP, Patel AR, Anderson MJ, et al. Infection with parvovirus-like agent and aplastic crisis in adults with chronic hemolytic anemia. Ann Intern Med 1983; 98: 930-32. 3. Anderson
erythema migrans in the right loin 10 weeks earlier but did not recall having been bitten by a tick. 4 weeks after this episode he had had joint pains in his neck and shoulders and dysaesthesias in the chest and back with mild fever (38°C) and asthenia. He had been treated by spiramycin 6 million IU for 8 days and had recovered completely a few days. Besides the Bell’s palsy, a diminution of the tendon reflexes of the lower limbs was noted. Leg joints were painful but not swollen. CSF contained 100 cells/1 (100% lymphocytes), protein 1 - 6 g/l, glucose 3 - 6 mmol/1. Electrophoresis of CSF showed an increase of IgG (0 - 23g/1) with an IgG/albumin ratio of-31. There was a striking neutrophilia (12 500 white cells1, 63% neutrophils). The ESR was 15 mm/h. Other blood tests were normal. The patient, being allergic to penicillin, was treated with doxycycline 200 mg daily for 3 weeks and recovered rapidly. 4 weeks later his reflexes were normal and the pains had disappeared. A mild right facial palsy remained. Serial sera were tested for specific IgG and IgM antibody to B burgdorferi by indirect immunofluorescence by Dr Bettina Wilske (Max van Pettenkofer Institute, Munich). The first patient had significant IgG and IgM antibody whereas the second patient had high IgG titres without IgM (figure). In the first patient IgM titres decreased rapidly after the onset of the facial paralysis. An IgM response may have been missed in patient 2, who was seen later in the course of the disease and had been treated by antibiotics. Typical erythema chronicum migrans has long been recognised in France. However, only recently has it been possible to confirm its association with an infection by the Lyme-disease spirochaete. The broad clinical spectrum of the disease makes it an unobvious diagnosis when neurological involvements are the prime symptoms. These two French cases of lymphocytic meningoradiculitis provide argument for including a search for antibody to B burgdorferi in the laboratory work-up of patients presenting with meningoradiculitis whether or not they report a history of tick-bite. Early serological diagnosis permits high-dose penicillin, therapy that significantly shortens neurological disorders in Lyme disease.6
EFFECT OF ANTIBIOTIC PROPHYLAXIS
in
We thank Prof Friedrich Deinhart who put disease research group at his institute. Internal Medicine Service B, and Virology Laboratory,
CHRU Bretonneau, 370444 Tours, France
us
in touch with the
Lyme
O. WEILL
J. P. AVIGNON A. GOUDEAU
1. Garin
C, Bujadoux. Paralysie par lestiques. J Med Lyon 1922; 3: 765-67. AC, Malawista SE, Hardin JA, Ruddy S, Askenase PW, Andiman WA. Erythema chronicum migrans and Lyme arthritis: the enlarging clinical spectrum. Ann Intern Med 1977; 86: 685-98. Barbour AG, Burgdorfer W, Hayes SF, Peter O, Aeschlimann A. Isolation of a cultivable spirochete from Ixodes ricinus ticks of Switzerland. Curr Microbiol 1983;
2. Steere
3.
8: 123-26. 4.
Ryberg B, Nilsson B, Burgdorfer W, Barbour AG Antibodies to Lyme-disease spirochaete in European lymphocytic meningoradiculitis (Bannwarth’s syndrome). Lancet
1983; ii: 519. F, Lecomte F, Humbert G, Dournon E. La maladie de Lyme un cas autochtone confirmé sérologiquement Méd Mal Inf 1985; 15: 44-45 Steere AC, Pachner AR, Malawista SE Neurologic abnormalities of Lyme disease: successful treatment with high-dose intravenous penicillin. Ann Intern Med 1983,
5. Borsa-Lebas 6.
99: 767-72.
PROPHYLACTIC ANTIBIOTICS IN ERYSIPELAS
SIR,-Dr Bitnun (Feb 9, p 345) and Dr Thind (April 27, p 986) suggest that prolonged antibiotic prophylaxis reduces the number of attacks in recurrent erysipelas. However, their conclusions were based on only two cases and one case, respectively, and there was a mild relapse during prophylaxis in Bitnun’s second case. We have observations on seventeen patients. Since 1982 our policy has been to institute long-term antibiotic prophylaxis after a first attack of erysipelas. We administer benzathine penicillin G 2-44 megaunits intramuscularly every 3 weeks. Data on these seventeen patients (ten females, seven males; mean age 59 years) seen in our clinic between 1982 and 1984 for a first attack of erysipelas are shown in the table. Because of a history of allergy to penicillin five patients were not treated. Prophylaxis with intramuscular benzathine penicillin prevented relapses but when prophylaxis stopped the risk of recurrence
returned. We are tempted to conclude that prevention of recurrent necessitates treatment for very long periods. Questions about the cost-benefit ratio of long-term prophylactic regimens now need to be addressed.
erysipelas
Dermatology Clinic, Hôpital Cantonal Universitaire, 1211 Geneva
4, Switzerland
T. DUVANEL Y. MÉROT M. HARMS J.-H. SAURAT
EPIDEMIC OF APLASTIC CRISIS IN PATIENTS WITH HEREDITARY SPHEROCYTOSIS IN JAPAN
SiR,-Dr Shiraishi and his colleagues (April 27, p 982) describe a large outbreak of erythema infectiosum (fifth disease) in Japan. We report here an epidemic of aplastic crisis in patients with hereditary spherocytosis in Japan. Hereditary spherocytosis is the most frequent of the congenital chronic haemolytic anaemias in this country. However, aplastic crises in hereditary spherocytosis used to be very rare and up to 1980 few reports had been published in Japan. However, nine such reports appeared between August, 1980, and 1982. There have been none since 1983. This pattern suggests that the aplastic crises in 1980-82 were due to a single transmissible agent. In Niigata we saw four patients with hereditary spherocytosis in aplastic crisis between June, 1981, and March, 1982. The aplastic crises of both chronic haemolytic anaemia and erythema infectiosum are caused principally by human parvovirus (HPV).2-4 Cryopreserved serum from one of our patients in the acute phase was available and was found to contain both HPV antigens (countercurrent immunoelectrophoresis) and HPV-like virus particles (electron microscopy). Moreover, the serum inhibited colony formation by both late erythroid progenitors (CFU-E) and more primitive erythroid progenitors (BFU-E). There was also a large outbreak of erythema infectiosum between 1981 and 1982 in Niigata.’ Epidemic aplastic crisis in congenital chronic haemolytic anaemia has been reported in Britain,3Jamaica,and the United States,5 and the causative agent has been identified as HPV. We suggest that the epidemic of aplastic crises in patients with hereditary spherocytosis in Japan was also due to HPV.
Division of Haematology, Niigata Shimin Hospital, Niigata, Japan
TSUNEYASU TSUKADA TADASHI KOIKE* RYOKO KOIKE MASAYOSHI SANADA
First Department of Internal Medicine, Niigata University School of Medicine
MASUHIRO TAKAHASHI AKIRA SHIBATA
School of Health Sciences, Kyushu University, Fukuoka
TADASU NUNOUE
*Present address: First
Department of Internal Medicine, Niigata University, Asahi machi
don, Niigata, Japan. T, Koike T, Sanada M. Epidemic outbreak of aplastic crises in the patients hereditary spherocytosis in Japan. Igaku no ayumi 1985, 133: 123-25 (in Japanese). Pattison JR, Jones SE, Hodgson J, et al. Parvovirus infection and hypoplastic crisis in
1. Tsukada
with
2.
sickle-cell anaemia. Lancet 1981; ii: 664-65. MJ, Davis LR, Hodgson J, et al. Occurrence of infection with parvovirus-like agent in children with sickle cell anaemia during a two-year period. J Clin Pathol 1982; 35: 744-49. 4. Serjeant GR, Topley JM, Mason K, et al. Outbreak of aplastic crises in sickle cell anaemia associated with parvovirus-like agent Lancet 1981; ii: 595-97. 5. Rao KRP, Patel AR, Anderson MJ, et al. Infection with parvovirus-like agent and aplastic crisis in adults with chronic hemolytic anemia. Ann Intern Med 1983; 98: 930-32. 3. Anderson