943
will remain essentially unchanged. Bleeding is and the cycle length is unchanged. The most induced usually obvious effect is on the development of the endometrium. Six days after the LH surge (ie, 84 h after mifepristone intake) all endometrial specimens are highly asynchronous with the time of the cycle.2 At the same time, the uterine contractility pattern is also substantially changed and corresponds to that usually seen late in the luteal phase.3After in-vitro fertilisation a successful implantation will take place only between days 17 and 19 of a 28-day cycle.4 Thus changes in endometrial development and in uterine contractility might be sufficient to prevent implantation.
hormone
(FSH)
not
In
a
continuing study
18 fertile,
sexually active
women were
treated with a single dose of 200 mg mifepristone 2 days after the LH surge, on a monthly basis. All women had had at least one delivery and one termination of pregnancy. The occurrence of urinary LH surge and day of treatment was monitored by the women with an LH colour test. Recording of sexual activity revealed that intercourse was not avoided at the time of ovulation. The overall number of months of treatment is at present 80 and the duration of treatment in individuals is between 2 and 12 months. 5 women had slight bleeding or spotting on the second or third day after mifepristone. Length of menstrual cycle was not different from pretreatment cycles, and no other changes in cycle were noted. So far, there has been only one pregnancy, indicating that a single dose of mifepristone could be sufficient to prevent implantation. Glasier et als reported that mifepristone given within 72 h of unprotected intercourse was highly effective in preventing pregnancy, which supports the hypothesis that the effect of mifepristone on the endometrium is sufficient to do this. Postcoital treatment with this drug, although very valuable in an emergency, cannot be used repeatedly since the menstrual cycle will be upset in different ways, depending on the time of treatment. Postovulatory treatment on day LH + 2 can be repeated monthly and be used as the only contraceptive method. The most important advantage of the method is the lack of effect on plasma oestrogen and progesterone concentrations. The need for the woman to monitor her cycle is a slight disadvantage. Department of Obstetric and Gynaecology, Karolinska Hospital, S-10401 Stockholm, Sweden
M. L. SWAHN K. GEMZELL M. BYGDEMAN
1. Silvestre L, Dubois C, Renault M, Rezvani Y, Baulieu EE, Ulmann A. Voluntary interruption of pregnancy with mifepristone (RU 486) and a prostaglandin 1990; 322: 145-48. J analogue. N Engl Med 2. Swahn ML, Bygdeman M, Cekan S, Xing S, Masironi B, Johannisson E. The effect of RU 486 administered during the early luteal phase on bleeding pattern, hormonal parameters and endometrium. Hum Reprod 1990; 5: 402-08 3. Gemzell K, Swahn ML, Bygdeman M. Regulation of non-pregnant human uterine contractility: effects of antihormones. Contraception 1990; 42: 323-35. 4. Navot D, Scott RT, Droesch K, Veeck LL, Liw H-C, Rosenwaks Z. The window of embryo transfer and the efficiency of human contraception in vitro. Fertil Steril
1991; 55: 114-18. 5. Glasier A, Thong KJ, Dewar M, Mackie M, Baird DT. Postcoital contraception with mifepristone. Lancet 1991; 337: 1444.
Characteristics of successive
epidemics of respiratory syncytial virus infection
SIR,-We would like to report our experience of infections caused by respiratory syncytial virus (RSV) in paediatric inpatients over the past two winters. We examined, by direct immunofluorescence, 461 and 429 specimens (more than 95 % were nasopharyngeal aspirates) between November and April in 1989/90 and in 1990/91; 39% and 34% of these, respectively, were positive for RSV. We observed a shift in the peak incidence of RSV infections (figure) from December in 1989/90 to March in 1990/91. Although national data concur with a December peak, the incidence of RSV infection in Sheffield in the last winter was greatest almost 3 months after the peak reported by the Communicable Disease Surveillance Centre, which was the first week in January.1 Belshe et al2 in the United States noted that RSV epidemics tend to alternate between early and late winter months in successive years. This pattern has not been reflected in the figures for England and Wales, where the peak has shifted 2 weeks or so later in the past three winters. Clearly, data presented in a national format may hide
Comparison of numbers of RSV-positive paediatric inpatients during the winters 1989/90 and 1990/91. wide geographical variations such as those seen in Sheffield. However, several other groups have failed to observe the pattern described by Belshe et al,2 and in general it appears that different RSV subgroups can predominate in both diverse geographical
locations and within individual communities.3,4 For these reasons caution should be exercised when extrapolating nationally compiled data to the local situation. Unfortunately, our method of RSV detection precludes any information on subgroups. Subgroup A RSV has previously been shown to be more virulent than subgroup B.5 At the height of the epidemic in Sheffield in 1989/90 we had 30 RSV-positive inpatients in one week (the hospital has 150 beds), constituting a major potential source of cross-infection. Guidelines advise that RSV-positive patients be isolated-or cohort nursed by staff without other patient contact. We frequently find that neither of these options is practicable, and as a compromise we attempt to ensure that RSV-positive patients are nursed separately from high-risk individuals, such as those with chronic respiratory disease or who are immunocompromised. Management during the epidemic of 1989/90 was compounded by an increase in December to three times winter baseline levels in the number of new cases of respiratory tract illness in nurses (absentees per week 20 [SE 5] vs 6 [1]). Whether this increase in staff illness was due at least in part to RSV infection acquired in the hospital remains unknown. An epidemic of influenza A in 1989/90 may have been a confounding factor. However, transmission of RSV from patients to hospital staff with resulting symptomatic respiratory disease has been described? We examined the details of children with RSV infection who were admitted to intensive care (table). 12 cases were managed on the unit in both winter epidemics, with similar numbers of males (13) and females (11). A preponderance of severe RSV infection in males has been noted elsewhere.8 The average length of stay was similar, although more ventilatory support was given in 1989/90, perhaps because in 1990/91 nasal continuous positive airway pressure was introduced earlier, following our experince of the RSV-POSITIVE PATIENTS MANAGED IN INTENSIVE CARE
CPAP continuous
positive airway pressure
944
previous year. Ribivirin was not used. For 82% and 67% of the days in between the first admission and the last discharge, there was at least 1 patient (maximum 4) being managed on intensive care in 1989/90 and 1990/91. This consitutes a major drain on specialist support services. Planning for RSV epidemics is not made any easier by the great variability in timing of outbreaks. Paediatric units should be aware of the local epidemiology of RSV infection and not be misled by figures that sum up the situation over large areas, ’1l IC
T T
"TT_-
M. H. WILCOX Departments of Bacteriology and Anaesthetics, Royal Hallamshire Hospital,
Sheffield S10 2JF, UK, and Sheffield Children’s Hospital
----
O. WILLIAMS S. J. CAMP R. C. SPENCER I. BARKER
1 Public Health Laboratory Service. Commun Dis Rep 1991, 1: 66-69. 2. Belshe RB, Bernstein JM, Dansby KN. Respiratory syncytial virus. In: Belshe RB, ed.
Textbook of human virology. Chicago: PSG/Biomedical, 1984: 361-84. 3. Hendry RM, Pierik LT, McIntosh K. Prevalence of respiratory syncytial virus subgroups over six consecutive outbreaks: 1981-1987. J Infect Dis 1989; 160: 185-90 4. Hendry RM, Talis AL, Godfrey E, Anderson LJ, Femie BF, McIntosh K. Concurrent circulation of antigenically distinct strains of respiratory syncytial virus during community outbreaks. J Infect Dis 1986, 153: 291-97 5. Taylor CE, Morrow S, Scott M, Young B, Toms GL. Comparative virulence of respiratory syncytial virus subgroups A and B. Lancet 1989, i: 777-78. 6. Breuer J, Jeffries DJ. Control of viral infections in hospitals. J Hosp Infect 1990; 16: 191-221. 7. Hall WJ, Hall CB, Speers DM. Respiratory syncytial virus infections in adults: clinical virologic and serial pulmonary function studies. Ann Intern Med 1978; 88: 203-05. 8. Parrott RH, Kim HW, Arrobis JO, et al Epidemiology of respiratory syncytial virus infection in Washington DC II: infections and disease with respect to age, immunologic status, race and sex. Am J Epidemiol 1973; 98: 289-700.
Progressive flaccid myelopathy associated with HTLV-I SIR,-Human T-lymphotropic virus type I (HTLV-I) is to have a key role in the pathogenesis of chronic tropical spastic myelopathy.1 The diagnosis requires the presence of spastic paraparesis or paraplegia with no evidence of spinal cord compression, multiple sclerosis, or hereditofamilial degeneration.2 We describe a patient with a progressive flaccid paraparesis believed
associated with HTLV-1 infection in whom spasticity or flexor spasms has not developed in 13 years’ follow-up. A 67-year-old Jamaican-born woman presented to the orthopaedic clinic in 1978 with right-sided sciatic pain and backache. Neurological findings at that time were unremarkable. However, she became progressively weak over the following 10 years such that she could only shuffle about at home on her bottom. In 1988, she was referred to the diabetic clinic with thirst, glycosuria, and a random blood glucose of 22-4 mmolll. She then needed a wheelchair. Examination of the cranial nerves and arms was normal. She had a flaccid paraparesis with symmetrically wasted legs. There was bilateral grade 3 weakness of ankle plantar flexion and grade 0-2 weakness of the other leg muscle groups. Tendon reflexes were present at the knees and absent at the ankles. The right plantar response was equivocal and the left was extensor. Patchy stocking sensory loss to pin prick and light touch was noted. Investigations, including tests for syphilis, serum vitamin B12 and folate, myelography, computed tomographic 5 mm cuts through the foramen magnum, and magnetic resonance imaging of the whole spine were normal. Electromyography showed evidence of a mild peripheral neuropathy, compatible with diabetic neuropathy. Cerebrospinal fluid (CSF) contained 6 white blood cells/1, less than 1 red blood cells1, protein 0-29 gll, IgG 216 mgll (normal < 40 mg/1), and oligoclonal IgG bands (absent in serum). Antibodies to HTLV-I were present in serum and CSF by ELISA and confirmed by western blot. HTLV-I DNA sequences were identified in mononuclear cells from blood and CSF by polymerase chain reaction analysis. Southern blot analysis of genomic DNA extracted from CSF T cells cultured in vitro confirmed the presence of several HTLV-1 proviruses in these cells (figure). She remains wheelchair bound and has lately needed urinary catheterisation. Her diabetes is controlled by diet. The signs in her legs remain
unchanged.
Southern blot analysis of CSF T cells. 5 I1g of DNA from CSF clone Ph1 was digested with EcoR1 (E) or Sac1 (S) and hybridised with a full-length HTLV-I probe EcoR1 cuts outside the provirus and Sac1 cuts within the long terminal repeat.
In the only previous report of which we are aware, of non-spastic paraparesis associated with HTLV-1the clinical onset was acute and febrile, occurring before the age of 5 years in most instances. Since HTLV-I antibodies could not be demonstrated in the CSF, Kazadi et aP postulated that non-spastic paraparesis represents a non-active manifestation of HTLV-1 infection acquired in childhood. We do not think that this can be the case in our patient, in whom intrathecal synthesis of IgG antibody to HTLV-1 was seen. Furthermore, proviral DNA was identified in CSF lymphocytes. Although the pathogenesis of HTLV-1 associated myelopathy is not known, we presume that the flaccidity and wasting of the legs in our patient resulted from damage to anterior horn cells or their efferents. The presentation with sciatic pain, suggesting a radiculopathy, has been noted previously at the onset of tropical spastic paraparesis.’’ This patient further extends the spectrum of clinical features of HTLV-1 infection. Clinicians seeing patients with paraparesis and epidemiologists studying the prevalence of this virus should consider HTLV-1 infection
even
in the absence of
spasticity. Departments of Biochemical Medicine, Neurology, and Communicable Diseases, St George’s Hospital Medical School, London SW17 0RE, UK
S. HYER J. H. RICHARDSON M. BROWN A. M. L. LEVER S. S. NUSSEY
Tropical neuromyelopathies and retroviruses: a review. Rev Infect Dis 1990; 12: 890-99. 2. Vemant JC, Gessain A, Gout O, et al. Endemic tropical spastic paraparesis associated with human T-lymphotropic virus type I: a clinical and seroepidemiological study of 25 cases. Ann Neurol 1987; 21: 123-30. 3. Kazadi K, Garin B, Goussard B, Salaun JJ, De-The G. Non-spastic paraparesis associated with HTLV-I. Lancet 1990; 336: 260. 4. Cruickshank JK, Rudge P, Dalgleish AG, et al. Tropical spastic paraparesis and human T cell lymphotropic virus type I in the United Kingdom. Brain 1989; 112: 1057-90 1 Bucher B, Poupard JA, Vernant JC, DeFreitas EC.
HTLV-II and HTLV-I associated
myelopathy
SiR,—Dr Kira and colleagues (July 6, p 64) used polymerase chain amplification (PCR) to demonstrate a surprisingly high rate of co-infection with HTLV-II (12/18, 67%) in patients with HTLV-1 associated myelopathy or tropical spastic paraparesis (HAM/TSP). They also found a significantly lower rate of co-infection (1/18) in healthy HTLV-1-positive persons. Kira et al suggest that co-infection with HTLV-11 may be important for the development of HAM/TSP among HTLV-1 infected persons and indicate that this is the "first clear report" of an association of HTLV-IIwith a neurological disease. Because of the important implications of these conclusions, which stand alone amidst a large amount of evidence implicating HTLV-I exclusively in the pathogenesis of HAM/TSP/.2we believe that the HTLV-II PCR positivity should be verified by ruling out the contamination problems that are so inherently
will remain essentially unchanged. Bleeding is and the cycle length is unchanged. The most induced usually obvious effect is on the development of the endometrium. Six days after the LH surge (ie, 84 h after mifepristone intake) all endometrial specimens are highly asynchronous with the time of the cycle.2 At the same time, the uterine contractility pattern is also substantially changed and corresponds to that usually seen late in the luteal phase.3After in-vitro fertilisation a successful implantation will take place only between days 17 and 19 of a 28-day cycle.4 Thus changes in endometrial development and in uterine contractility might be sufficient to prevent implantation.
hormone
(FSH)
not
In
a
continuing study
18 fertile,
sexually active
women were
treated with a single dose of 200 mg mifepristone 2 days after the LH surge, on a monthly basis. All women had had at least one delivery and one termination of pregnancy. The occurrence of urinary LH surge and day of treatment was monitored by the women with an LH colour test. Recording of sexual activity revealed that intercourse was not avoided at the time of ovulation. The overall number of months of treatment is at present 80 and the duration of treatment in individuals is between 2 and 12 months. 5 women had slight bleeding or spotting on the second or third day after mifepristone. Length of menstrual cycle was not different from pretreatment cycles, and no other changes in cycle were noted. So far, there has been only one pregnancy, indicating that a single dose of mifepristone could be sufficient to prevent implantation. Glasier et als reported that mifepristone given within 72 h of unprotected intercourse was highly effective in preventing pregnancy, which supports the hypothesis that the effect of mifepristone on the endometrium is sufficient to do this. Postcoital treatment with this drug, although very valuable in an emergency, cannot be used repeatedly since the menstrual cycle will be upset in different ways, depending on the time of treatment. Postovulatory treatment on day LH + 2 can be repeated monthly and be used as the only contraceptive method. The most important advantage of the method is the lack of effect on plasma oestrogen and progesterone concentrations. The need for the woman to monitor her cycle is a slight disadvantage. Department of Obstetric and Gynaecology, Karolinska Hospital, S-10401 Stockholm, Sweden
M. L. SWAHN K. GEMZELL M. BYGDEMAN
1. Silvestre L, Dubois C, Renault M, Rezvani Y, Baulieu EE, Ulmann A. Voluntary interruption of pregnancy with mifepristone (RU 486) and a prostaglandin 1990; 322: 145-48. J analogue. N Engl Med 2. Swahn ML, Bygdeman M, Cekan S, Xing S, Masironi B, Johannisson E. The effect of RU 486 administered during the early luteal phase on bleeding pattern, hormonal parameters and endometrium. Hum Reprod 1990; 5: 402-08 3. Gemzell K, Swahn ML, Bygdeman M. Regulation of non-pregnant human uterine contractility: effects of antihormones. Contraception 1990; 42: 323-35. 4. Navot D, Scott RT, Droesch K, Veeck LL, Liw H-C, Rosenwaks Z. The window of embryo transfer and the efficiency of human contraception in vitro. Fertil Steril
1991; 55: 114-18. 5. Glasier A, Thong KJ, Dewar M, Mackie M, Baird DT. Postcoital contraception with mifepristone. Lancet 1991; 337: 1444.
Characteristics of successive
epidemics of respiratory syncytial virus infection
SIR,-We would like to report our experience of infections caused by respiratory syncytial virus (RSV) in paediatric inpatients over the past two winters. We examined, by direct immunofluorescence, 461 and 429 specimens (more than 95 % were nasopharyngeal aspirates) between November and April in 1989/90 and in 1990/91; 39% and 34% of these, respectively, were positive for RSV. We observed a shift in the peak incidence of RSV infections (figure) from December in 1989/90 to March in 1990/91. Although national data concur with a December peak, the incidence of RSV infection in Sheffield in the last winter was greatest almost 3 months after the peak reported by the Communicable Disease Surveillance Centre, which was the first week in January.1 Belshe et al2 in the United States noted that RSV epidemics tend to alternate between early and late winter months in successive years. This pattern has not been reflected in the figures for England and Wales, where the peak has shifted 2 weeks or so later in the past three winters. Clearly, data presented in a national format may hide
Comparison of numbers of RSV-positive paediatric inpatients during the winters 1989/90 and 1990/91. wide geographical variations such as those seen in Sheffield. However, several other groups have failed to observe the pattern described by Belshe et al,2 and in general it appears that different RSV subgroups can predominate in both diverse geographical
locations and within individual communities.3,4 For these reasons caution should be exercised when extrapolating nationally compiled data to the local situation. Unfortunately, our method of RSV detection precludes any information on subgroups. Subgroup A RSV has previously been shown to be more virulent than subgroup B.5 At the height of the epidemic in Sheffield in 1989/90 we had 30 RSV-positive inpatients in one week (the hospital has 150 beds), constituting a major potential source of cross-infection. Guidelines advise that RSV-positive patients be isolated-or cohort nursed by staff without other patient contact. We frequently find that neither of these options is practicable, and as a compromise we attempt to ensure that RSV-positive patients are nursed separately from high-risk individuals, such as those with chronic respiratory disease or who are immunocompromised. Management during the epidemic of 1989/90 was compounded by an increase in December to three times winter baseline levels in the number of new cases of respiratory tract illness in nurses (absentees per week 20 [SE 5] vs 6 [1]). Whether this increase in staff illness was due at least in part to RSV infection acquired in the hospital remains unknown. An epidemic of influenza A in 1989/90 may have been a confounding factor. However, transmission of RSV from patients to hospital staff with resulting symptomatic respiratory disease has been described? We examined the details of children with RSV infection who were admitted to intensive care (table). 12 cases were managed on the unit in both winter epidemics, with similar numbers of males (13) and females (11). A preponderance of severe RSV infection in males has been noted elsewhere.8 The average length of stay was similar, although more ventilatory support was given in 1989/90, perhaps because in 1990/91 nasal continuous positive airway pressure was introduced earlier, following our experince of the RSV-POSITIVE PATIENTS MANAGED IN INTENSIVE CARE
CPAP continuous
positive airway pressure
944
previous year. Ribivirin was not used. For 82% and 67% of the days in between the first admission and the last discharge, there was at least 1 patient (maximum 4) being managed on intensive care in 1989/90 and 1990/91. This consitutes a major drain on specialist support services. Planning for RSV epidemics is not made any easier by the great variability in timing of outbreaks. Paediatric units should be aware of the local epidemiology of RSV infection and not be misled by figures that sum up the situation over large areas, ’1l IC
T T
"TT_-
M. H. WILCOX Departments of Bacteriology and Anaesthetics, Royal Hallamshire Hospital,
Sheffield S10 2JF, UK, and Sheffield Children’s Hospital
----
O. WILLIAMS S. J. CAMP R. C. SPENCER I. BARKER
1 Public Health Laboratory Service. Commun Dis Rep 1991, 1: 66-69. 2. Belshe RB, Bernstein JM, Dansby KN. Respiratory syncytial virus. In: Belshe RB, ed.
Textbook of human virology. Chicago: PSG/Biomedical, 1984: 361-84. 3. Hendry RM, Pierik LT, McIntosh K. Prevalence of respiratory syncytial virus subgroups over six consecutive outbreaks: 1981-1987. J Infect Dis 1989; 160: 185-90 4. Hendry RM, Talis AL, Godfrey E, Anderson LJ, Femie BF, McIntosh K. Concurrent circulation of antigenically distinct strains of respiratory syncytial virus during community outbreaks. J Infect Dis 1986, 153: 291-97 5. Taylor CE, Morrow S, Scott M, Young B, Toms GL. Comparative virulence of respiratory syncytial virus subgroups A and B. Lancet 1989, i: 777-78. 6. Breuer J, Jeffries DJ. Control of viral infections in hospitals. J Hosp Infect 1990; 16: 191-221. 7. Hall WJ, Hall CB, Speers DM. Respiratory syncytial virus infections in adults: clinical virologic and serial pulmonary function studies. Ann Intern Med 1978; 88: 203-05. 8. Parrott RH, Kim HW, Arrobis JO, et al Epidemiology of respiratory syncytial virus infection in Washington DC II: infections and disease with respect to age, immunologic status, race and sex. Am J Epidemiol 1973; 98: 289-700.
Progressive flaccid myelopathy associated with HTLV-I SIR,-Human T-lymphotropic virus type I (HTLV-I) is to have a key role in the pathogenesis of chronic tropical spastic myelopathy.1 The diagnosis requires the presence of spastic paraparesis or paraplegia with no evidence of spinal cord compression, multiple sclerosis, or hereditofamilial degeneration.2 We describe a patient with a progressive flaccid paraparesis believed
associated with HTLV-1 infection in whom spasticity or flexor spasms has not developed in 13 years’ follow-up. A 67-year-old Jamaican-born woman presented to the orthopaedic clinic in 1978 with right-sided sciatic pain and backache. Neurological findings at that time were unremarkable. However, she became progressively weak over the following 10 years such that she could only shuffle about at home on her bottom. In 1988, she was referred to the diabetic clinic with thirst, glycosuria, and a random blood glucose of 22-4 mmolll. She then needed a wheelchair. Examination of the cranial nerves and arms was normal. She had a flaccid paraparesis with symmetrically wasted legs. There was bilateral grade 3 weakness of ankle plantar flexion and grade 0-2 weakness of the other leg muscle groups. Tendon reflexes were present at the knees and absent at the ankles. The right plantar response was equivocal and the left was extensor. Patchy stocking sensory loss to pin prick and light touch was noted. Investigations, including tests for syphilis, serum vitamin B12 and folate, myelography, computed tomographic 5 mm cuts through the foramen magnum, and magnetic resonance imaging of the whole spine were normal. Electromyography showed evidence of a mild peripheral neuropathy, compatible with diabetic neuropathy. Cerebrospinal fluid (CSF) contained 6 white blood cells/1, less than 1 red blood cells1, protein 0-29 gll, IgG 216 mgll (normal < 40 mg/1), and oligoclonal IgG bands (absent in serum). Antibodies to HTLV-I were present in serum and CSF by ELISA and confirmed by western blot. HTLV-I DNA sequences were identified in mononuclear cells from blood and CSF by polymerase chain reaction analysis. Southern blot analysis of genomic DNA extracted from CSF T cells cultured in vitro confirmed the presence of several HTLV-1 proviruses in these cells (figure). She remains wheelchair bound and has lately needed urinary catheterisation. Her diabetes is controlled by diet. The signs in her legs remain
unchanged.
Southern blot analysis of CSF T cells. 5 I1g of DNA from CSF clone Ph1 was digested with EcoR1 (E) or Sac1 (S) and hybridised with a full-length HTLV-I probe EcoR1 cuts outside the provirus and Sac1 cuts within the long terminal repeat.
In the only previous report of which we are aware, of non-spastic paraparesis associated with HTLV-1the clinical onset was acute and febrile, occurring before the age of 5 years in most instances. Since HTLV-I antibodies could not be demonstrated in the CSF, Kazadi et aP postulated that non-spastic paraparesis represents a non-active manifestation of HTLV-1 infection acquired in childhood. We do not think that this can be the case in our patient, in whom intrathecal synthesis of IgG antibody to HTLV-1 was seen. Furthermore, proviral DNA was identified in CSF lymphocytes. Although the pathogenesis of HTLV-1 associated myelopathy is not known, we presume that the flaccidity and wasting of the legs in our patient resulted from damage to anterior horn cells or their efferents. The presentation with sciatic pain, suggesting a radiculopathy, has been noted previously at the onset of tropical spastic paraparesis.’’ This patient further extends the spectrum of clinical features of HTLV-1 infection. Clinicians seeing patients with paraparesis and epidemiologists studying the prevalence of this virus should consider HTLV-1 infection
even
in the absence of
spasticity. Departments of Biochemical Medicine, Neurology, and Communicable Diseases, St George’s Hospital Medical School, London SW17 0RE, UK
S. HYER J. H. RICHARDSON M. BROWN A. M. L. LEVER S. S. NUSSEY
Tropical neuromyelopathies and retroviruses: a review. Rev Infect Dis 1990; 12: 890-99. 2. Vemant JC, Gessain A, Gout O, et al. Endemic tropical spastic paraparesis associated with human T-lymphotropic virus type I: a clinical and seroepidemiological study of 25 cases. Ann Neurol 1987; 21: 123-30. 3. Kazadi K, Garin B, Goussard B, Salaun JJ, De-The G. Non-spastic paraparesis associated with HTLV-I. Lancet 1990; 336: 260. 4. Cruickshank JK, Rudge P, Dalgleish AG, et al. Tropical spastic paraparesis and human T cell lymphotropic virus type I in the United Kingdom. Brain 1989; 112: 1057-90 1 Bucher B, Poupard JA, Vernant JC, DeFreitas EC.
HTLV-II and HTLV-I associated
myelopathy
SiR,—Dr Kira and colleagues (July 6, p 64) used polymerase chain amplification (PCR) to demonstrate a surprisingly high rate of co-infection with HTLV-II (12/18, 67%) in patients with HTLV-1 associated myelopathy or tropical spastic paraparesis (HAM/TSP). They also found a significantly lower rate of co-infection (1/18) in healthy HTLV-1-positive persons. Kira et al suggest that co-infection with HTLV-11 may be important for the development of HAM/TSP among HTLV-1 infected persons and indicate that this is the "first clear report" of an association of HTLV-IIwith a neurological disease. Because of the important implications of these conclusions, which stand alone amidst a large amount of evidence implicating HTLV-I exclusively in the pathogenesis of HAM/TSP/.2we believe that the HTLV-II PCR positivity should be verified by ruling out the contamination problems that are so inherently
