80
3. Hirschel
B, Chang HR, Mach N,
et
al. Fatal infection with
a
novel
mycobacterium in a man with the acquired immunodeficiency syndrome. N Engl J Med 1990; 323: 109-13. 4. Woese CR. Bacterial evolution. Microbiol Rev 1987; 51: 221-71. 5. Edwards U, Rogall T, Blocker H, Emde M, Böttger EC. Isolation and direct complete nucleotide determination of entire genes. Characterization of a gene coding for 16S ribosomal RNA. Nucleic unidentified
Acids Res 1989; 17: 7843-53.
Relman DA, Loutit JS, Schmit TM, Falkow S, Tompkins LS. The agent of bacillary angiomatosis. N Engl J Med 1990; 323: 1573-80. 7. Rogall T, Wolters J, Flohr T, Böttger EC. Towards a phylogeny and definition of species at the molecular level within the genus Mycobacterium. Int J Syst Bacteriol 1990; 40: 323-30. 8. Maniatis T, Fritsch EF, Sambrook J. Molecular cloning. A laboratory manual. Cold Spring Harbor, N.Y.: Cold Spring Harbor Laboratory, 6.
1982. 9.
Böddinghaus B, Rogall T, Flohr T. Detection and identification of mycobacteria by amplification of rRNA. J Clin Microbiol 1990; 28:
1751-59. 10. Stahl DA, Urbance
JW. The division between fast- and slow-growing species corresponds to natural relationships among the mycobacteria. J Bacteriol 1990; 172: 116-24. 11. Rogall T, Flohr T, Böttger EC. Differentiation of Mycobacterium
species by direct sequencing of amplified DNA. J Gen Microbiol 1990; 136: 1915-20. 12. Teske A, Wolters J,
Böttger EC. The 16S RNA nucleotide sequence of Mycobacterium leprae: phylogenetic position and development of DNA probes. FEMS Microbiol Lett 1991; 64: 231-37. 13. Jacobson MA. Mycobacterial diseases. In: Sande MA, Volberding PA, eds. The medical management of AIDS, 3rd ed. Philadelphia: Saunders, 1990: 291-303. 14. Brenner DJ. Impact of modern taxonomy of clinical microbiology. ASM News 1983; 49: 58-63. 15. Brenner DJ. Taxonomy, classification, and nomenclature of bacteria. In: Lennette EH, Balows A, Hausler WJ, Truant JP, eds. Manual of clinical microbiology, 3rd ed. Washington: American Society for Microbiology, 1980: 1-6. 16. Böttger EC. Frequent contamination of Taq polymerase with DNA. Clin Chem 1990; 36: 1258. 17. Rand KH, Houck H. Taq polymerase contains bacterial DNA of unknown origin. Mol Cell Probes 1990; 4: 445-50. 18. Fischl MA, Richman DD, Causey DM, et al. Prolonged zidovudine therapy in patients with AIDS and advanced AIDS-related complex. JAMA 1989; 262: 2405-10. 19. Graham NM, Zeger SL, Park LP, et al. Effect of zidovudine and Pneumocystis carinii pneumonia prophylaxis on progression of HIV-1 infection to AIDS. Lancet 1991; 338: 265-69.
SHORT REPORTS Low cerebrospinal fluid concentration of free gammaaminobutyric acid in startle disease
The
pathophysiology of startle disease (hyperekplexia) is unknown. Hyperactivity of the brainstem reticular formation has been suggested as a cause. We report a newborn infant with classic features of startle disease in whom cerebrospinal fluid (CSF) concentrations of gamma-aminobutyric acid (GABA) were substantially lower than normal during the first weeks of life. She improved greatly on clonazepam treatment. We suggest that the signs of
this disorder may be due to a genetic defect or to delayed maturation resulting in low CSF GABA.
Startle disease (hyperekplexia), first described in a family who sustained violent falls precipitated by fright, stress, or surprise,1 is inherited as an autosomal dominant trait with incomplete penetrance.2.3 Most patients present in the neonatal period, either with "stiff baby syndrome", or with a seizure disorder4,5 characterised by myoclonic jerks, increased muscle tone, and severe apnoea but without concomitant discharges on electroencephalography (EEG). This disorder is easily mistaken for neonatal convulsion,4 since the EEG changes due to ocular movement or other muscle artifact are frequent,6 so its true incidence is probably underestimated. The pathophysiology is unknown. The startle response is thought to be mediated through the brainstem. Hyperactivity of the brainstem reticular formation, due either to intrinsic hyperexcitability or to insufficient cortical
inhibition could lead to startle disease. Delayed maturation of these systems has also been suggested since the signs abate with age.2 No biochemical abnormality has been found. We report an infant with classic features of startle disease who had an abnormality of cerebrospinal fluid (CSF) gamma-aminobutyric acid (GABA). The baby girl, born at 38 weeks’ gestation, was the first child of non-consanguinous parents. The mother was a 24-year-old Asian primigravida. Pregnancy and labour were uneventful. Birthweight was 2560 g (10th centile), length 48 cm (50th centile), and head circumference 36 cm (97th centile). Apgar scores at 1 and 5 min were 6 and 9, respectively, and cord-blood pH was 7-4. 1 h after birth the infant had generalised jerks which were diagnosed as convulsions. She was given 20 mg/kg phenobarbitone before transfer to the neonatal unit. 8 h later she was very hypotonic. On day 3 she still had pronounced truncal hypotonia but the tone in the limbs was abnormally hgh. She had exaggerated tendon reflexes and became jittery when touched. The limb hypertonia diminished during sleep, but increased when she was touched. She had poor visual fixation and pursuit but responded to auditory stimuli without startle. Physical examination was otherwise normal. On day 5 there were seizure-like episodes, consisting of myoclonic movement of the limbs, rigidity of the trunk and limbs, flexion of the upper limbs, fisting of the hands, and extension of the lower extremities. Some episodes were accompanied by apnoea and upward deviation of the eyes. The heart rate initially increased, but arterial oxygen saturation (SaOz) fell to 60%, so episodes were followed by brief bradycardia, which was corrected by administration of oxygen. The jerks and stiffening could be inhibited by holding the infant tightly or by bending her forward, but were precipitated by handling, tapping, and especially by turning her into the prone position. No seizure discharges could be recorded on standard EEG or on four-channel continuous monitoring. No abnormalities in organicacid or aminoacid measurements and no infections were found. Cranial ultrasound showed a small intraventricular haemorrhage on day 2 but magnetic resonance imaging at 1 week and 3 months was normal, as were proton spectroscopy, auditory brainstem responses, and visual evoked responses. Latency of the somatosensory responses was normal, but the amplitude was larger than expected for age. Empirical treatment with pyridoxine during an attack produced a doubtful response and 10 mg/kg intravenous phenobarbitone did
81
stop an episode. We therefore continued pyridoxine and began maintenance treatment with phenobarbitone, which reduced the frequency and severity of the attacks but did not relieve the touch-induced myoclonus. All episodes could be stopped by forcibly flexing the infant. These findings led to a diagnosis of startle disease. Although no defmite family history could be obtained because the father and his family do not live in the UK, two first cousins (paternal) had had neonatal convulsions but are now healthy
REFERENCES 1. Kirstein L, Silfverskiold B. A family with emotionally precipitated drop seizures. Acta Psychiatr Scand 1958; 33: 471-76. 2. Suhren O, Bruyn GW, Tuynman JA. Hyperekplexia: a hereditary startle syndrome. J Neurol Sci 1966; 3: 577-605. 3. Andermann F, Andermann E. Startle disorders of man: hyperekplexia,
jumping and startle epilepsy. Brain Dev 1988; 10: 213-22. C, Roze JC, David A, Veccierini MF, Renaud P, Mouzard A. Hyperekplexia or stiff baby syndrome. Arch Dis Child 1991; 66:
4. Tohier
on no treatment.
We speculated that the abnormalities might be due to low GABA concentrations. A CSF sample was taken on day 14. Free GABA, measured by ion-exchange chromatography with fluorescence detection, was abnormally low (11nmol/1 compared with normal range for newborn infants of 20-100 mnolfl).8 Clonazepam was introduced on day 28 and phenobarbitone was gradually withdrawn. The infant showed great improvement; a normal tone pattern developed and she now has only a few nocturnal myoclonic episodes, though nose tappingb can still elicit a startle response. At 9 weeks, the CSF free GABA concentration was 35 nmol/1, in the low normal range for this age. The infant is now 3 months old and is at home with an apnoea alarm in use. She has mild general hypotonia with greater tone in the upper limbs, but no fisting.
Hyperactivity of the brainstem centres, especially of the rhomboencephalic reticular formation, has been suggested as the cause of startle disease.2,3,7 Several nuclei in the medullary and pontine reticular formation are primary sources of serotoninergic innervation in the brain; thus it is possible that serotoninergic hyperexcitability is a primary cause of the disorder, especially since it has been successfully treated with the serotonin antagonist clonazepam.2 Some of the symptoms of startle disease are similar to those of opioid-induced hypertonicity, so it could be a defect of the endogenous opiate pathway.9 A genetic defect resulting in low brain and CSF GABA is another possibility. GABA is an important inhibitory neurotransmitter, and low concentrations could produce hyperexcitability in the nervous system. A low threshold to epileptic stimulil3 and high amplitude of somatosensory responses5 have also been described in this disorder. The improvement with clonazepam could be explained by potentiation of GABA transmission, brought about by increasing the sensitivity of the GABA receptor, which in turn could lead to an increase in free CSF GABA. If startle disease is primarily due to low GABA concentrations, the best treatment should be vigabatrin. However, this drug can produce microvacuolation in myelinated tracts in animals, so it could interfere with myelination in very immature infants. The mechanism by which acute flexion of the trunk10 abolishes the signs of this disorder remains a mystery. Our case also illustrates the difficulties of clinical diagnosis of startle disease. Although the infant had all the classic signs, we were initially cautious. The myoclonic movements produced a lot of artifacts on the EEG so it was difficult to rule out electrical seizures. The apnoea and abnormal eye movements also hinted at an epileptiform basis. However, the production of myoclonic jerks in response to touch and their inhibition by swaddling and flexing, together with the persistent startle response to nose tapping,6 helped to clinch the diagnosis. We suggest that measurement of CSF GABA concentration is helpful in the diagnosis of this disorder and that the GABA neurotransmitter system is implicated in its pathogenesis. L. M. S. D. is supported by the Medical Research Council. We thank Dr D. Wertheim and Miss M. Hayden for electrophysiological investigation, the Magnetic Resonance Imaging Unit for MRI and MRS studies, and our colleagues for helpful discussions.
460-61. 5. Markand ON,
Garg BP, Weaver (hyperekplexia): electrophysiological
DD. Familial startle disease studies. Arch Neurol 1984; 41:
71-74. 6. Shahar E, Brand
N, Uziel Y, Barak Y. Nose tapping test inducing a generalized flexor spasm: a hallmark of hyperekplexia. Acta Paediatr Scand 1991; 80: 1073-77.
7.
Morley DJ, Weaver DD, Garg BP, Markand O. Hyperekplexia:
an
inherited disorder of the startle response. Clin Genet 1982; 21: 388-96. 8. Carchon HA, Jaeken J, Jansen E, Eggermont E. Reference values for free gamma-aminobutyric acid determined by ion-exchange chromatography and fluorescence detection in the cerebrospinal fluid of children. Clin Chim Acta 1991; 201: 83-88. 9. Weinger MB. "Stiff baby" syndrome: an expression of the same neural circuitry responsible for opiate-induced muscle rigidity? Anesthesiology
1987; 66: 580-81. 10.
Dalla Bernardina B. Startle disease: avoidable cause of sudden infant death. Lancet 1989; i: 216.
Vigevano F, Di Capua M,
an
ADDRESSES: Department of Paediatrics and Neonatal Medicine, Hammersmith Hospital, Du Cane Road, London W12 0HS, UK (L. M. S. Dubowitz, MD, H. Bouza, MD, M. F. Hird, MRCP), and Department of Paediatrics, Universitair Ziekenhuis Gasthuisberg, Leuven, Belgium (J. Jaeken, PhD). Correspondence to Dr L. M. S. Dubowitz.
Detection of Chlamydia trachomatis DNA in joints of reactive arthritis patients by polymerase chain reaction
In 1986, Chlamydia trachomatis elementary bodies were found by direct immunofluorescence (DIF) in synovial-fluid cell deposits and synovialmembrane biopsy samples from five of eight patients with sexually acquired reactive arthritis (SARA) but in none of eight controls with other types of arthritis. Cells from the original slides (stored at 4°C) have now been examined by a polymerase chain reaction (PCR) that amplifies DNA for the major outer membrane protein of C trachomatis. Chlamydial DNA was found in samples from four DIF-positive patients, one DIF-negative patient, and one DIFnegative control. Overall, there was 80% concordance for DIF and PCR results. This study supports our previous finding of chlamydiae in joints in reactive arthritis.
in about 1 % of men with and disease definitely associated non-gonococcal urethritis, with sexually transmitted infection has been called sexually acquired reactive arthritis (SARA).1 Serovars of Chlamydia trachomatis account for up to 50% of cases of nongonococcal urethritis and for other genital-tract diseases
Reactive arthritis
develops
3. Hirschel
B, Chang HR, Mach N,
et
al. Fatal infection with
a
novel
mycobacterium in a man with the acquired immunodeficiency syndrome. N Engl J Med 1990; 323: 109-13. 4. Woese CR. Bacterial evolution. Microbiol Rev 1987; 51: 221-71. 5. Edwards U, Rogall T, Blocker H, Emde M, Böttger EC. Isolation and direct complete nucleotide determination of entire genes. Characterization of a gene coding for 16S ribosomal RNA. Nucleic unidentified
Acids Res 1989; 17: 7843-53.
Relman DA, Loutit JS, Schmit TM, Falkow S, Tompkins LS. The agent of bacillary angiomatosis. N Engl J Med 1990; 323: 1573-80. 7. Rogall T, Wolters J, Flohr T, Böttger EC. Towards a phylogeny and definition of species at the molecular level within the genus Mycobacterium. Int J Syst Bacteriol 1990; 40: 323-30. 8. Maniatis T, Fritsch EF, Sambrook J. Molecular cloning. A laboratory manual. Cold Spring Harbor, N.Y.: Cold Spring Harbor Laboratory, 6.
1982. 9.
Böddinghaus B, Rogall T, Flohr T. Detection and identification of mycobacteria by amplification of rRNA. J Clin Microbiol 1990; 28:
1751-59. 10. Stahl DA, Urbance
JW. The division between fast- and slow-growing species corresponds to natural relationships among the mycobacteria. J Bacteriol 1990; 172: 116-24. 11. Rogall T, Flohr T, Böttger EC. Differentiation of Mycobacterium
species by direct sequencing of amplified DNA. J Gen Microbiol 1990; 136: 1915-20. 12. Teske A, Wolters J,
Böttger EC. The 16S RNA nucleotide sequence of Mycobacterium leprae: phylogenetic position and development of DNA probes. FEMS Microbiol Lett 1991; 64: 231-37. 13. Jacobson MA. Mycobacterial diseases. In: Sande MA, Volberding PA, eds. The medical management of AIDS, 3rd ed. Philadelphia: Saunders, 1990: 291-303. 14. Brenner DJ. Impact of modern taxonomy of clinical microbiology. ASM News 1983; 49: 58-63. 15. Brenner DJ. Taxonomy, classification, and nomenclature of bacteria. In: Lennette EH, Balows A, Hausler WJ, Truant JP, eds. Manual of clinical microbiology, 3rd ed. Washington: American Society for Microbiology, 1980: 1-6. 16. Böttger EC. Frequent contamination of Taq polymerase with DNA. Clin Chem 1990; 36: 1258. 17. Rand KH, Houck H. Taq polymerase contains bacterial DNA of unknown origin. Mol Cell Probes 1990; 4: 445-50. 18. Fischl MA, Richman DD, Causey DM, et al. Prolonged zidovudine therapy in patients with AIDS and advanced AIDS-related complex. JAMA 1989; 262: 2405-10. 19. Graham NM, Zeger SL, Park LP, et al. Effect of zidovudine and Pneumocystis carinii pneumonia prophylaxis on progression of HIV-1 infection to AIDS. Lancet 1991; 338: 265-69.
SHORT REPORTS Low cerebrospinal fluid concentration of free gammaaminobutyric acid in startle disease
The
pathophysiology of startle disease (hyperekplexia) is unknown. Hyperactivity of the brainstem reticular formation has been suggested as a cause. We report a newborn infant with classic features of startle disease in whom cerebrospinal fluid (CSF) concentrations of gamma-aminobutyric acid (GABA) were substantially lower than normal during the first weeks of life. She improved greatly on clonazepam treatment. We suggest that the signs of
this disorder may be due to a genetic defect or to delayed maturation resulting in low CSF GABA.
Startle disease (hyperekplexia), first described in a family who sustained violent falls precipitated by fright, stress, or surprise,1 is inherited as an autosomal dominant trait with incomplete penetrance.2.3 Most patients present in the neonatal period, either with "stiff baby syndrome", or with a seizure disorder4,5 characterised by myoclonic jerks, increased muscle tone, and severe apnoea but without concomitant discharges on electroencephalography (EEG). This disorder is easily mistaken for neonatal convulsion,4 since the EEG changes due to ocular movement or other muscle artifact are frequent,6 so its true incidence is probably underestimated. The pathophysiology is unknown. The startle response is thought to be mediated through the brainstem. Hyperactivity of the brainstem reticular formation, due either to intrinsic hyperexcitability or to insufficient cortical
inhibition could lead to startle disease. Delayed maturation of these systems has also been suggested since the signs abate with age.2 No biochemical abnormality has been found. We report an infant with classic features of startle disease who had an abnormality of cerebrospinal fluid (CSF) gamma-aminobutyric acid (GABA). The baby girl, born at 38 weeks’ gestation, was the first child of non-consanguinous parents. The mother was a 24-year-old Asian primigravida. Pregnancy and labour were uneventful. Birthweight was 2560 g (10th centile), length 48 cm (50th centile), and head circumference 36 cm (97th centile). Apgar scores at 1 and 5 min were 6 and 9, respectively, and cord-blood pH was 7-4. 1 h after birth the infant had generalised jerks which were diagnosed as convulsions. She was given 20 mg/kg phenobarbitone before transfer to the neonatal unit. 8 h later she was very hypotonic. On day 3 she still had pronounced truncal hypotonia but the tone in the limbs was abnormally hgh. She had exaggerated tendon reflexes and became jittery when touched. The limb hypertonia diminished during sleep, but increased when she was touched. She had poor visual fixation and pursuit but responded to auditory stimuli without startle. Physical examination was otherwise normal. On day 5 there were seizure-like episodes, consisting of myoclonic movement of the limbs, rigidity of the trunk and limbs, flexion of the upper limbs, fisting of the hands, and extension of the lower extremities. Some episodes were accompanied by apnoea and upward deviation of the eyes. The heart rate initially increased, but arterial oxygen saturation (SaOz) fell to 60%, so episodes were followed by brief bradycardia, which was corrected by administration of oxygen. The jerks and stiffening could be inhibited by holding the infant tightly or by bending her forward, but were precipitated by handling, tapping, and especially by turning her into the prone position. No seizure discharges could be recorded on standard EEG or on four-channel continuous monitoring. No abnormalities in organicacid or aminoacid measurements and no infections were found. Cranial ultrasound showed a small intraventricular haemorrhage on day 2 but magnetic resonance imaging at 1 week and 3 months was normal, as were proton spectroscopy, auditory brainstem responses, and visual evoked responses. Latency of the somatosensory responses was normal, but the amplitude was larger than expected for age. Empirical treatment with pyridoxine during an attack produced a doubtful response and 10 mg/kg intravenous phenobarbitone did
81
stop an episode. We therefore continued pyridoxine and began maintenance treatment with phenobarbitone, which reduced the frequency and severity of the attacks but did not relieve the touch-induced myoclonus. All episodes could be stopped by forcibly flexing the infant. These findings led to a diagnosis of startle disease. Although no defmite family history could be obtained because the father and his family do not live in the UK, two first cousins (paternal) had had neonatal convulsions but are now healthy
REFERENCES 1. Kirstein L, Silfverskiold B. A family with emotionally precipitated drop seizures. Acta Psychiatr Scand 1958; 33: 471-76. 2. Suhren O, Bruyn GW, Tuynman JA. Hyperekplexia: a hereditary startle syndrome. J Neurol Sci 1966; 3: 577-605. 3. Andermann F, Andermann E. Startle disorders of man: hyperekplexia,
jumping and startle epilepsy. Brain Dev 1988; 10: 213-22. C, Roze JC, David A, Veccierini MF, Renaud P, Mouzard A. Hyperekplexia or stiff baby syndrome. Arch Dis Child 1991; 66:
4. Tohier
on no treatment.
We speculated that the abnormalities might be due to low GABA concentrations. A CSF sample was taken on day 14. Free GABA, measured by ion-exchange chromatography with fluorescence detection, was abnormally low (11nmol/1 compared with normal range for newborn infants of 20-100 mnolfl).8 Clonazepam was introduced on day 28 and phenobarbitone was gradually withdrawn. The infant showed great improvement; a normal tone pattern developed and she now has only a few nocturnal myoclonic episodes, though nose tappingb can still elicit a startle response. At 9 weeks, the CSF free GABA concentration was 35 nmol/1, in the low normal range for this age. The infant is now 3 months old and is at home with an apnoea alarm in use. She has mild general hypotonia with greater tone in the upper limbs, but no fisting.
Hyperactivity of the brainstem centres, especially of the rhomboencephalic reticular formation, has been suggested as the cause of startle disease.2,3,7 Several nuclei in the medullary and pontine reticular formation are primary sources of serotoninergic innervation in the brain; thus it is possible that serotoninergic hyperexcitability is a primary cause of the disorder, especially since it has been successfully treated with the serotonin antagonist clonazepam.2 Some of the symptoms of startle disease are similar to those of opioid-induced hypertonicity, so it could be a defect of the endogenous opiate pathway.9 A genetic defect resulting in low brain and CSF GABA is another possibility. GABA is an important inhibitory neurotransmitter, and low concentrations could produce hyperexcitability in the nervous system. A low threshold to epileptic stimulil3 and high amplitude of somatosensory responses5 have also been described in this disorder. The improvement with clonazepam could be explained by potentiation of GABA transmission, brought about by increasing the sensitivity of the GABA receptor, which in turn could lead to an increase in free CSF GABA. If startle disease is primarily due to low GABA concentrations, the best treatment should be vigabatrin. However, this drug can produce microvacuolation in myelinated tracts in animals, so it could interfere with myelination in very immature infants. The mechanism by which acute flexion of the trunk10 abolishes the signs of this disorder remains a mystery. Our case also illustrates the difficulties of clinical diagnosis of startle disease. Although the infant had all the classic signs, we were initially cautious. The myoclonic movements produced a lot of artifacts on the EEG so it was difficult to rule out electrical seizures. The apnoea and abnormal eye movements also hinted at an epileptiform basis. However, the production of myoclonic jerks in response to touch and their inhibition by swaddling and flexing, together with the persistent startle response to nose tapping,6 helped to clinch the diagnosis. We suggest that measurement of CSF GABA concentration is helpful in the diagnosis of this disorder and that the GABA neurotransmitter system is implicated in its pathogenesis. L. M. S. D. is supported by the Medical Research Council. We thank Dr D. Wertheim and Miss M. Hayden for electrophysiological investigation, the Magnetic Resonance Imaging Unit for MRI and MRS studies, and our colleagues for helpful discussions.
460-61. 5. Markand ON,
Garg BP, Weaver (hyperekplexia): electrophysiological
DD. Familial startle disease studies. Arch Neurol 1984; 41:
71-74. 6. Shahar E, Brand
N, Uziel Y, Barak Y. Nose tapping test inducing a generalized flexor spasm: a hallmark of hyperekplexia. Acta Paediatr Scand 1991; 80: 1073-77.
7.
Morley DJ, Weaver DD, Garg BP, Markand O. Hyperekplexia:
an
inherited disorder of the startle response. Clin Genet 1982; 21: 388-96. 8. Carchon HA, Jaeken J, Jansen E, Eggermont E. Reference values for free gamma-aminobutyric acid determined by ion-exchange chromatography and fluorescence detection in the cerebrospinal fluid of children. Clin Chim Acta 1991; 201: 83-88. 9. Weinger MB. "Stiff baby" syndrome: an expression of the same neural circuitry responsible for opiate-induced muscle rigidity? Anesthesiology
1987; 66: 580-81. 10.
Dalla Bernardina B. Startle disease: avoidable cause of sudden infant death. Lancet 1989; i: 216.
Vigevano F, Di Capua M,
an
ADDRESSES: Department of Paediatrics and Neonatal Medicine, Hammersmith Hospital, Du Cane Road, London W12 0HS, UK (L. M. S. Dubowitz, MD, H. Bouza, MD, M. F. Hird, MRCP), and Department of Paediatrics, Universitair Ziekenhuis Gasthuisberg, Leuven, Belgium (J. Jaeken, PhD). Correspondence to Dr L. M. S. Dubowitz.
Detection of Chlamydia trachomatis DNA in joints of reactive arthritis patients by polymerase chain reaction
In 1986, Chlamydia trachomatis elementary bodies were found by direct immunofluorescence (DIF) in synovial-fluid cell deposits and synovialmembrane biopsy samples from five of eight patients with sexually acquired reactive arthritis (SARA) but in none of eight controls with other types of arthritis. Cells from the original slides (stored at 4°C) have now been examined by a polymerase chain reaction (PCR) that amplifies DNA for the major outer membrane protein of C trachomatis. Chlamydial DNA was found in samples from four DIF-positive patients, one DIF-negative patient, and one DIFnegative control. Overall, there was 80% concordance for DIF and PCR results. This study supports our previous finding of chlamydiae in joints in reactive arthritis.
in about 1 % of men with and disease definitely associated non-gonococcal urethritis, with sexually transmitted infection has been called sexually acquired reactive arthritis (SARA).1 Serovars of Chlamydia trachomatis account for up to 50% of cases of nongonococcal urethritis and for other genital-tract diseases
Reactive arthritis
develops
