- Email: [email protected]
Mycoplasma pneumoniae–Associated Transverse Myelitis and Rhabdomyolysis
Mycoplasma pneumoniae– Associated Transverse Myelitis and Rhabdomyolysis Wen-Chin Weng, MD*, Steven Shinn-Forng Peng, MD†, Shi-Bing Wang, MD*, Yen-Ting Chou, MD‡, and Wang-Tso Lee, MD, PhD* Mycoplasma pneumoniae is a common cause of respiratory tract infection. Extrapulmonary manifestations of M. pneumoniae infection are also common. The present case is that of a previously healthy 4-year-old boy who displayed a novel simultaneous onset of both acute rhabdomyolysis and transverse myelitis associated with an infection of M. pneumoniae. He had no preceding symptoms or signs of respiratory tract infection. Intravenous immunoglobulin (1 g/kg per day) for 2 days was prescribed initially for the deterioration of neurologic condition. His rhabdomyolysis resolved without complication, but neurologic sequelae remained during 2 years of follow-up. Evaluation for M. pneumoniae infection is recommended in patients with idiopathic rhabdomyolysis and transverse myelitis, even if in the absence of antecedent respiratory symptoms. Ó 2009 by Elsevier Inc. All rights reserved. Weng WC, Peng SS, Wang SB, Chou YT, Lee WT. Mycoplasma pneumoniae–associated transverse myelitis and rhabdomyolysis. Pediatr Neurol 2009;40:128-130.
From the Departments of *Pediatrics and †Medical Imaging, National Taiwan University Hospital, Taipei, Taiwan, and the ‡Department of Pediatrics, Cardinal Tien Hospital Yung Ho Branch, Taipei, Taiwan.
128 PEDIATRIC NEUROLOGY Vol. 40 No. 2
Introduction Mycoplasma pneumoniae is one of the leading causes of respiratory tract infection of varying severity [1]. Extrapulmonary manifestations of M. pneumoniae infection are also common, and involvement of every organ system has been described [1,2]. Central nervous system involvements are the most frequent complications associated with M. pneumoniae infection [1-3]. With respect to musculoskeletal involvement, polyarthralgia and mild myalgia are common, but rhabdomyolysis is very rare, and only six previous cases, including both adults and children, have been reported [4-8]. The combination of M. pneumoniae-related rhabdomyolysis and transverse myelitis documented with neuroimaging is a novel finding. Described here is the case of a 4-year-old boy presenting with acute rhabdomyolysis in association with M. pneumoniae infection. He also developed symptoms and signs of spinal cord lesions, and neuroimaging documented the existence of transverse myelitis. Based on clinical and laboratory results, Immune-mediated pathophysiology was postulated. Case Report A boy aged 4 years and 10 months was quite healthy until 3 days before his admission, when he developed itching sensation over both legs. On the day of admission, he developed abdominal pain and myalgia over both legs, followed by muscle weakness over both legs and also acute urinary retention. The medical and family histories were unremarkable, except for 1 day of fever occurring 7 days before admission. The patient had no prior episodes similar to this one, and he did not take any medication before admission. There was no history of upper respiratory tract infection, fever, recent travel, recent trauma, pet exposure, or violent exercise. On the first day of admission, the physical examination revealed a supple neck, no skin rash, no hepatosplenomegaly, and no erythema or induration of his joints. He was conscious and well oriented. He was afebrile, with a respiratory rate of 24 breaths per minute, heart rate of 112 beats per minute, and blood pressure of 106/59 mm Hg. Neurologic examination revealed increased deep tendon reflex, over both knees, and ankle jerks. The initial laboratory studies revealed white blood cell count of 10,260/ mL, hemoglobin at 12.8 g/dL, platelet count of 366,000/mL, and C-reactive protein at 2.27 mg/dL (normal value, <0.8 mg/dL). Creatine kinase was elevated, at 15,855 U/L; uric acid was elevated, at 10.4 mg/dL; and lactate dehydrogenase was elevated, at 1233 IU/L. A slight decrease of serum calcium (1.93 mmol/L; normal 2.02-2.60 mmol/L), increases of serum aspartate aminotransferase (113 U/L) and alanine aminotransferase (52 U/L)
Communications should be addressed to: Dr. Lee; Department of Pediatrics; National Taiwan University Hospital; No. 7 Chung-Shan South Road; Taipei, Taiwan. E-mail: [email protected] Received July 30, 2008; accepted October 13, 2008.
Ó 2009 by Elsevier Inc. All rights reserved. doi:10.1016/j.pediatrneurol.2008.10.009 0887-8994/09/$—see front matter
were also found. The serum level of other electrolytes, albumin, bilirubin, amylase, lipase, blood urea nitrogen, and creatinine were normal. Immunological findings for antinuclear antibody, complement 3, and complement 4 were all within normal limit. Under the impression of rhabdomyolysis, intravenous hydration, alkalization, and mannitol were prescribed. On the day of admission, the patient had developed progressive weakness of the upper extremities, and neurologic examination revealed absence of the abdominal reflex and the cremasteric reflex. Magnetic resonance imaging of the spinal cord was performed. The T2-weighted images demonstrated abnormal high signal intensities at the level from cervical to lumbar cord, with mild swelling (Fig 1), which was compatible with the diagnosis of transverse myelitis. Lumbar puncture was performed and cerebrospinal fluid evaluation showed a white blood cell count of 40 leukocytes/mm3 (32 lymphocytes and 8 neutrophils), protein 44.4 mg/ dL, and glucose 50 mg/dL. Results were negative from the rapid tests in cerebrospinal fluid for Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae, Streptococcus group B, and Escherichia coli. Cranial magnetic resonance imaging revealed no abnormal signal, and the visual evoked potentials from both eyes were within normal limits, which excluded the possibility of Devic disease (i.e., neuromyelitis optica) or a first episode of multiple sclerosis. Peripheral nerve conduction velocity testing yielded normal results. For progressive symptoms and signs of spinal cord inflammation, intravenous immunoglobulin (1 g/kg per day) was then administered for 2 days, starting on the 2nd day of admission. Subsequent investigation by polymerase chain reaction and serology for viral infection, including herpes simplex virus, human herpes virus-6 and -7, and enteroviruses, all yielded negative results. Neither virus nor bacteria were isolated from cerebrospinal fluid, throat swab, or rectal swab. At admission, the M. pneumoniae antibody titers determined by enzyme-linked immunosorbent assay using a commercial kit were positive for both immunoglobulin M (>20 Bethesda units [BU]/mL) and for immunoglobulin G (38.32 BU/mL; positive, >20 BU/mL). Four weeks later, the antibody titers for immunoglobulin G remained elevated (53 BU/mL), but M. pneumoniae was not detected in
cerebrospinal fluid and throat swab by cultures or polymerase chain reaction. The chest radiography did not reveal increased infiltration. During the next 2 weeks, the patient’s weakness improved gradually, and the urinary retention also resolved in the following course. The serum creatine kinase level decreased gradually after intravenous immunoglobulin treatment. The patient received rehabilitation at outpatient clinics and his neurological condition improved gradually. Neurological sequelae (weakness over the left upper limb and right lower limb) remained at follow-up at outpatient clinics 2 years later.
Discussion Rhabdomyolysis is characterized by an elevated level of serum creatine kinase, and the level of elevation is dependent on the extent of muscle injury [9]. In the present case, the diagnosis of rhabdomyolysis was based on the elevated serum levels of creatine kinase and a low calcium concentration. The hyperuricemia probably resulted from the breakdown of purine released from destroyed muscle cells. Rhabdomyolysis can be chronic, acute, or recurrent, and the causes vary. For a single episode of acute rhabdomyolysis, it can be induced by multiple factors, including skeletal muscle overuse, heat, crush injury, alcoholism, status epilepticus, drugs, toxins, or metabolic abnormalities (such as hypokalemia, hyponatremia, or hypernatremia) [9]. None of these were applicable in the present case. Various viral and bacterial infections can also be responsible for rhabdomyolysis [9]. In most patients with viral-related rhabdomyolysis, the cause is influenza virus [10], followed by human
Figure 1. Magnetic resonance imaging of the spine shows abnormal high signal intensity on T2-weighted image from the cervical level to the lumbar cord. Mild cord swelling was also noted. (TR/TE = 3500/104 ms; slice thickness = 3 mm; turbo spin echo, turbo factor = 150.).
Weng et al: Transverse Myelitis and Rhabdomyolysis 129
immunodeficiency virus, enterovirus, Epstein-Barr virus, varicella zoster virus, and cytomegalovirus [5,7]. The present patient had no symptoms or signs of bacterial infection, and laboratory findings also excluded the possibility of viral or bacterial infections, until the diagnosis of M. pneumoniae infection was based on serological assays. Rhabdomyolysis as a complication of M. pneumoniae infection is very rare, and only six previous cases, including both adults and children, have been reported [4-8]. The present patient had no impaired renal function and did not require dialysis, probably because of early recognition and early treatment with aggressive hydration, alkalization, and mannitol. Approximately 1-10% of patients hospitalized because of serologically confirmed M. pneumoniae infection have associated neurologic manifestations [3]. Encephalitis is the most frequent manifestation, but cases of myelitis, polyradiculitis, and Guillain-Barre´ syndrome as well as other symptoms, such as stroke or psychosis have also been reported [2,11]. Myelitis is a severe and rare neurological complication associated with M. pneumoniae infection. Various mechanisms explaining neuromuscular and neurologic disease after M. pneumoniae infection have been postulated, including direct invasion by the organism, cytokine storm, immune-mediated complex formation or autoantibodies, toxin effects, vascular injury, and hypercoagulable state [1,10,12,13]. The failure to isolate M. pneumoniae from cerebrospinal fluid by culture and polymerase chain reaction suggested an immune-mediated process as the underlying mechanism. Treatment of mycoplasma infection–related neurologic and neuromuscular complications has been varied [13]. Antimicrobial treatment is questionable, because of low penetration via the blood–brain barrier, and potential immunologic pathophysiology [11]. The use of corticosteroids has been suggested, after the confirmation of M. pneumoniae infection, although the efficacy remains controversial [13]. The present patient received intravenous immunoglobulin treatment because of rapid deterioration of his myelitis. The long-term outcome was reported to be favorable [11]. In the present case, the patient’s rhabdomyolysis resolved without any long-term complication, but he had neurologic deficit secondary to transverse myelitis. An unfavorable prognosis is thought to be associated with rapid onset of neurological symptoms, loss of tendon reflex, and impairment of posterior column functions [11,14]. It remains unclear to what extent the treatment for mycoplasma infection actually influenced the spontaneous course. A unique feature in the present case is the simultaneous onset of both rhabdomyolysis and transverse myelitis in a single patient subsequent to M. pneumoniae infection. Respiratory infection did not precede his rhabdomyolysis and extensive myelitis. Rothstein and Kenny [15] described a similar case, an adult patient with cranial neuropathy, myeloradiculopathy, and myositis as the complications of M. pneumoniae infection. In their report, the diagnosis of neurological disturbance was based on the clinical presentation, without confirmation from neuroimaging. The maximal
130 PEDIATRIC NEUROLOGY Vol. 40 No. 2
creatine kinase in their patient was >40,000 units, and the muscle biopsy disclosed lymphocytic infiltration and neurogenic atrophy. No other serum electrolyte derangement was mentioned, however, so the diagnosis was of acute myositis rather than rhabdomyolysis. The present patient had significant signal abnormalities and spinal cord swelling in spinal MRI, compatible with the diagnosis of transverse myelitis. Furthermore, the laboratory data, including evidence of hyperuricemia and hypocalcemia, implied the destruction of muscle cells and supported the diagnosis of rhabdomyolysis. In the present case, with the unique finding in this young child of concomitant rhabdomyolysis and transverse myelitis in association with M. pneumoniae infection, the failure to yield M. pneumoniae from cerebrospinal fluid via cultures and polymerase chain reaction supported the evidence of direct toxic or immune-mediated mechanism. Experience with this patient suggests that, in cases of concurrent acute transverse myelitis and rhabdomyolysis, an association with M. pneumoniae should be considered even without antecedent respiratory infection. References [1] Cassell GH, Cole BC. Mycoplasmas as agents of human disease. N Engl J Med 1981;304:80-9. [2] Koskiniemi M. CNS manifestations associated with Mycoplasma pneumoniae infections: summary of cases at the University of Helsinki and review. Clin Infect Dis 1993;17(Suppl. 1):S52-7. [3] Ponka A. Central nervous system manifestations associated with serologically verified Mycoplasma pneumoniae infection. Scand J Infect Dis 1980;12:175-84. [4] Decaux G, Szyper M, Ectors M, Cornil A, Franken L. Central nervous system complications of Mycoplasma pneumoniae. J Neurol Neurosurg Psychiatry 1980;43:883-7. [5] Berger RP, Wadowsky RM. Rhabdomyolysis associated with infection by Mycoplasma pneumoniae: a case report. Pediatrics 2000;105:433-6. [6] Daxbo¨ck F, Brunner G, Popper H, et al. A case of lung transplantation following Mycoplasma pneumoniae infection. Eur J Clin Microbiol Infect Dis 2002;21:318-22. [7] Minami K, Maeda H, Yanagawa T, Suzuki H, Izumi G, Yoshikawa N. Rhabdomyolysis associated with Mycoplasma pneumoniae infection. Pediatr Infect Dis J 2003;22:291-3. [8] Gupta R, Gupta A, Goyal V, Guleria R, Kumar A. Mycoplasma pneumonia associated with rhabdomyolysis and the Guillain-Barre syndrome. Indian J Chest Dis Allied Sci 2005;47:305-8. [9] Poels PJP, Gabree¨ls FJM. Rhabdomyolysis: a review of the literature. Clin Neurol Neurosurg 1993;95:175-92. [10] Singh U, Scheld WM. Infectious etiologies of rhabdomyolysis: three case reports and review. Clin Infect Dis 1996;22:642-9. [11] Goebels N, Helmchen C, Abele-Horn M, Gasser T, Pfister HW. Extensive myelitis associated with Mycoplasma pneumoniae infection: magnetic resonance imaging and clinical long-term follow-up. J Neurol 2001;248:204-8. [12] Fernald GW. Immunologic mechanisms suggested in the association of M. pneumoniae infection and extrapulmonary disease: a review. Yale J Biol Med 1983;56:475-9. [13] Abele-Horn M, Franck W, Busch U, Nitschko H, Roos R, Heesemann J. Transverse myelitis associated with Mycoplasma pneumoniae infection. Clin Infect Dis 1998;26:909-12. [14] Ropper AH, Poskanzer DC. The prognosis of acute and subacute transverse myelopathy based on early signs and symptoms. Ann Neurol 1978;4:51-9. [15] Rothstein TL, Kenny GE. Cranial neuropathy, myeloradiculopathy, and myositis: complications of Mycoplasma pneumoniae infection. Arch Neurol 1979;36:476-7.
From the Departments of *Pediatrics and †Medical Imaging, National Taiwan University Hospital, Taipei, Taiwan, and the ‡Department of Pediatrics, Cardinal Tien Hospital Yung Ho Branch, Taipei, Taiwan.
128 PEDIATRIC NEUROLOGY Vol. 40 No. 2
Introduction Mycoplasma pneumoniae is one of the leading causes of respiratory tract infection of varying severity [1]. Extrapulmonary manifestations of M. pneumoniae infection are also common, and involvement of every organ system has been described [1,2]. Central nervous system involvements are the most frequent complications associated with M. pneumoniae infection [1-3]. With respect to musculoskeletal involvement, polyarthralgia and mild myalgia are common, but rhabdomyolysis is very rare, and only six previous cases, including both adults and children, have been reported [4-8]. The combination of M. pneumoniae-related rhabdomyolysis and transverse myelitis documented with neuroimaging is a novel finding. Described here is the case of a 4-year-old boy presenting with acute rhabdomyolysis in association with M. pneumoniae infection. He also developed symptoms and signs of spinal cord lesions, and neuroimaging documented the existence of transverse myelitis. Based on clinical and laboratory results, Immune-mediated pathophysiology was postulated. Case Report A boy aged 4 years and 10 months was quite healthy until 3 days before his admission, when he developed itching sensation over both legs. On the day of admission, he developed abdominal pain and myalgia over both legs, followed by muscle weakness over both legs and also acute urinary retention. The medical and family histories were unremarkable, except for 1 day of fever occurring 7 days before admission. The patient had no prior episodes similar to this one, and he did not take any medication before admission. There was no history of upper respiratory tract infection, fever, recent travel, recent trauma, pet exposure, or violent exercise. On the first day of admission, the physical examination revealed a supple neck, no skin rash, no hepatosplenomegaly, and no erythema or induration of his joints. He was conscious and well oriented. He was afebrile, with a respiratory rate of 24 breaths per minute, heart rate of 112 beats per minute, and blood pressure of 106/59 mm Hg. Neurologic examination revealed increased deep tendon reflex, over both knees, and ankle jerks. The initial laboratory studies revealed white blood cell count of 10,260/ mL, hemoglobin at 12.8 g/dL, platelet count of 366,000/mL, and C-reactive protein at 2.27 mg/dL (normal value, <0.8 mg/dL). Creatine kinase was elevated, at 15,855 U/L; uric acid was elevated, at 10.4 mg/dL; and lactate dehydrogenase was elevated, at 1233 IU/L. A slight decrease of serum calcium (1.93 mmol/L; normal 2.02-2.60 mmol/L), increases of serum aspartate aminotransferase (113 U/L) and alanine aminotransferase (52 U/L)
Communications should be addressed to: Dr. Lee; Department of Pediatrics; National Taiwan University Hospital; No. 7 Chung-Shan South Road; Taipei, Taiwan. E-mail: [email protected] Received July 30, 2008; accepted October 13, 2008.
Ó 2009 by Elsevier Inc. All rights reserved. doi:10.1016/j.pediatrneurol.2008.10.009 0887-8994/09/$—see front matter
were also found. The serum level of other electrolytes, albumin, bilirubin, amylase, lipase, blood urea nitrogen, and creatinine were normal. Immunological findings for antinuclear antibody, complement 3, and complement 4 were all within normal limit. Under the impression of rhabdomyolysis, intravenous hydration, alkalization, and mannitol were prescribed. On the day of admission, the patient had developed progressive weakness of the upper extremities, and neurologic examination revealed absence of the abdominal reflex and the cremasteric reflex. Magnetic resonance imaging of the spinal cord was performed. The T2-weighted images demonstrated abnormal high signal intensities at the level from cervical to lumbar cord, with mild swelling (Fig 1), which was compatible with the diagnosis of transverse myelitis. Lumbar puncture was performed and cerebrospinal fluid evaluation showed a white blood cell count of 40 leukocytes/mm3 (32 lymphocytes and 8 neutrophils), protein 44.4 mg/ dL, and glucose 50 mg/dL. Results were negative from the rapid tests in cerebrospinal fluid for Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae, Streptococcus group B, and Escherichia coli. Cranial magnetic resonance imaging revealed no abnormal signal, and the visual evoked potentials from both eyes were within normal limits, which excluded the possibility of Devic disease (i.e., neuromyelitis optica) or a first episode of multiple sclerosis. Peripheral nerve conduction velocity testing yielded normal results. For progressive symptoms and signs of spinal cord inflammation, intravenous immunoglobulin (1 g/kg per day) was then administered for 2 days, starting on the 2nd day of admission. Subsequent investigation by polymerase chain reaction and serology for viral infection, including herpes simplex virus, human herpes virus-6 and -7, and enteroviruses, all yielded negative results. Neither virus nor bacteria were isolated from cerebrospinal fluid, throat swab, or rectal swab. At admission, the M. pneumoniae antibody titers determined by enzyme-linked immunosorbent assay using a commercial kit were positive for both immunoglobulin M (>20 Bethesda units [BU]/mL) and for immunoglobulin G (38.32 BU/mL; positive, >20 BU/mL). Four weeks later, the antibody titers for immunoglobulin G remained elevated (53 BU/mL), but M. pneumoniae was not detected in
cerebrospinal fluid and throat swab by cultures or polymerase chain reaction. The chest radiography did not reveal increased infiltration. During the next 2 weeks, the patient’s weakness improved gradually, and the urinary retention also resolved in the following course. The serum creatine kinase level decreased gradually after intravenous immunoglobulin treatment. The patient received rehabilitation at outpatient clinics and his neurological condition improved gradually. Neurological sequelae (weakness over the left upper limb and right lower limb) remained at follow-up at outpatient clinics 2 years later.
Discussion Rhabdomyolysis is characterized by an elevated level of serum creatine kinase, and the level of elevation is dependent on the extent of muscle injury [9]. In the present case, the diagnosis of rhabdomyolysis was based on the elevated serum levels of creatine kinase and a low calcium concentration. The hyperuricemia probably resulted from the breakdown of purine released from destroyed muscle cells. Rhabdomyolysis can be chronic, acute, or recurrent, and the causes vary. For a single episode of acute rhabdomyolysis, it can be induced by multiple factors, including skeletal muscle overuse, heat, crush injury, alcoholism, status epilepticus, drugs, toxins, or metabolic abnormalities (such as hypokalemia, hyponatremia, or hypernatremia) [9]. None of these were applicable in the present case. Various viral and bacterial infections can also be responsible for rhabdomyolysis [9]. In most patients with viral-related rhabdomyolysis, the cause is influenza virus [10], followed by human
Figure 1. Magnetic resonance imaging of the spine shows abnormal high signal intensity on T2-weighted image from the cervical level to the lumbar cord. Mild cord swelling was also noted. (TR/TE = 3500/104 ms; slice thickness = 3 mm; turbo spin echo, turbo factor = 150.).
Weng et al: Transverse Myelitis and Rhabdomyolysis 129
immunodeficiency virus, enterovirus, Epstein-Barr virus, varicella zoster virus, and cytomegalovirus [5,7]. The present patient had no symptoms or signs of bacterial infection, and laboratory findings also excluded the possibility of viral or bacterial infections, until the diagnosis of M. pneumoniae infection was based on serological assays. Rhabdomyolysis as a complication of M. pneumoniae infection is very rare, and only six previous cases, including both adults and children, have been reported [4-8]. The present patient had no impaired renal function and did not require dialysis, probably because of early recognition and early treatment with aggressive hydration, alkalization, and mannitol. Approximately 1-10% of patients hospitalized because of serologically confirmed M. pneumoniae infection have associated neurologic manifestations [3]. Encephalitis is the most frequent manifestation, but cases of myelitis, polyradiculitis, and Guillain-Barre´ syndrome as well as other symptoms, such as stroke or psychosis have also been reported [2,11]. Myelitis is a severe and rare neurological complication associated with M. pneumoniae infection. Various mechanisms explaining neuromuscular and neurologic disease after M. pneumoniae infection have been postulated, including direct invasion by the organism, cytokine storm, immune-mediated complex formation or autoantibodies, toxin effects, vascular injury, and hypercoagulable state [1,10,12,13]. The failure to isolate M. pneumoniae from cerebrospinal fluid by culture and polymerase chain reaction suggested an immune-mediated process as the underlying mechanism. Treatment of mycoplasma infection–related neurologic and neuromuscular complications has been varied [13]. Antimicrobial treatment is questionable, because of low penetration via the blood–brain barrier, and potential immunologic pathophysiology [11]. The use of corticosteroids has been suggested, after the confirmation of M. pneumoniae infection, although the efficacy remains controversial [13]. The present patient received intravenous immunoglobulin treatment because of rapid deterioration of his myelitis. The long-term outcome was reported to be favorable [11]. In the present case, the patient’s rhabdomyolysis resolved without any long-term complication, but he had neurologic deficit secondary to transverse myelitis. An unfavorable prognosis is thought to be associated with rapid onset of neurological symptoms, loss of tendon reflex, and impairment of posterior column functions [11,14]. It remains unclear to what extent the treatment for mycoplasma infection actually influenced the spontaneous course. A unique feature in the present case is the simultaneous onset of both rhabdomyolysis and transverse myelitis in a single patient subsequent to M. pneumoniae infection. Respiratory infection did not precede his rhabdomyolysis and extensive myelitis. Rothstein and Kenny [15] described a similar case, an adult patient with cranial neuropathy, myeloradiculopathy, and myositis as the complications of M. pneumoniae infection. In their report, the diagnosis of neurological disturbance was based on the clinical presentation, without confirmation from neuroimaging. The maximal
130 PEDIATRIC NEUROLOGY Vol. 40 No. 2
creatine kinase in their patient was >40,000 units, and the muscle biopsy disclosed lymphocytic infiltration and neurogenic atrophy. No other serum electrolyte derangement was mentioned, however, so the diagnosis was of acute myositis rather than rhabdomyolysis. The present patient had significant signal abnormalities and spinal cord swelling in spinal MRI, compatible with the diagnosis of transverse myelitis. Furthermore, the laboratory data, including evidence of hyperuricemia and hypocalcemia, implied the destruction of muscle cells and supported the diagnosis of rhabdomyolysis. In the present case, with the unique finding in this young child of concomitant rhabdomyolysis and transverse myelitis in association with M. pneumoniae infection, the failure to yield M. pneumoniae from cerebrospinal fluid via cultures and polymerase chain reaction supported the evidence of direct toxic or immune-mediated mechanism. Experience with this patient suggests that, in cases of concurrent acute transverse myelitis and rhabdomyolysis, an association with M. pneumoniae should be considered even without antecedent respiratory infection. References [1] Cassell GH, Cole BC. Mycoplasmas as agents of human disease. N Engl J Med 1981;304:80-9. [2] Koskiniemi M. CNS manifestations associated with Mycoplasma pneumoniae infections: summary of cases at the University of Helsinki and review. Clin Infect Dis 1993;17(Suppl. 1):S52-7. [3] Ponka A. Central nervous system manifestations associated with serologically verified Mycoplasma pneumoniae infection. Scand J Infect Dis 1980;12:175-84. [4] Decaux G, Szyper M, Ectors M, Cornil A, Franken L. Central nervous system complications of Mycoplasma pneumoniae. J Neurol Neurosurg Psychiatry 1980;43:883-7. [5] Berger RP, Wadowsky RM. Rhabdomyolysis associated with infection by Mycoplasma pneumoniae: a case report. Pediatrics 2000;105:433-6. [6] Daxbo¨ck F, Brunner G, Popper H, et al. A case of lung transplantation following Mycoplasma pneumoniae infection. Eur J Clin Microbiol Infect Dis 2002;21:318-22. [7] Minami K, Maeda H, Yanagawa T, Suzuki H, Izumi G, Yoshikawa N. Rhabdomyolysis associated with Mycoplasma pneumoniae infection. Pediatr Infect Dis J 2003;22:291-3. [8] Gupta R, Gupta A, Goyal V, Guleria R, Kumar A. Mycoplasma pneumonia associated with rhabdomyolysis and the Guillain-Barre syndrome. Indian J Chest Dis Allied Sci 2005;47:305-8. [9] Poels PJP, Gabree¨ls FJM. Rhabdomyolysis: a review of the literature. Clin Neurol Neurosurg 1993;95:175-92. [10] Singh U, Scheld WM. Infectious etiologies of rhabdomyolysis: three case reports and review. Clin Infect Dis 1996;22:642-9. [11] Goebels N, Helmchen C, Abele-Horn M, Gasser T, Pfister HW. Extensive myelitis associated with Mycoplasma pneumoniae infection: magnetic resonance imaging and clinical long-term follow-up. J Neurol 2001;248:204-8. [12] Fernald GW. Immunologic mechanisms suggested in the association of M. pneumoniae infection and extrapulmonary disease: a review. Yale J Biol Med 1983;56:475-9. [13] Abele-Horn M, Franck W, Busch U, Nitschko H, Roos R, Heesemann J. Transverse myelitis associated with Mycoplasma pneumoniae infection. Clin Infect Dis 1998;26:909-12. [14] Ropper AH, Poskanzer DC. The prognosis of acute and subacute transverse myelopathy based on early signs and symptoms. Ann Neurol 1978;4:51-9. [15] Rothstein TL, Kenny GE. Cranial neuropathy, myeloradiculopathy, and myositis: complications of Mycoplasma pneumoniae infection. Arch Neurol 1979;36:476-7.