Brief Communication
Guillain-Barre´ Syndrome in a Boy With Lung Fluke Infection: Case Report and Literature Review
Journal of Child Neurology 2015, Vol. 30(9) 1208-1210 ª The Author(s) 2014 Reprints and permission: sagepub.com/journalsPermissions.nav DOI: 10.1177/0883073814546689 jcn.sagepub.com
Cui-Wei Yang, MM1, Feng Gao, MM1, and Zhe-Zhi Xia, MM1
Abstract Guillain-Barre´ syndrome is the most common acute peripheral neuropathy in children in most countries. The cause and pathogenesis of the disease have yet to be clarified. There have been only a few reports of Guillain-Barre´ syndrome resulting from parasite infections worldwide, no cases of Guillain-Barre´ syndrome after lung fluke infection have been reported. We report a case of an 8-year-old male patient with Guillain-Barre´ syndrome after lung fluke infection. The child had a history of consumption of undercooked crabs. He was diagnosed with paragonimiasis. The patient experienced paralysis of and pain in the lower limbs about 3 weeks after symptom onset. Neurologic and electrophysiologic examination findings supported the diagnosis of GuillainBarre´ syndrome. Parasitic infections should also be considered when determining which antecedent infection is associated with Guillain-Barre´ syndrome. Keywords Guillain-Barre´ syndrome, parasitic infections, paragonimiasis, children Received April 21, 2014. Received revised June 30, 2014. Accepted for publication July 01, 2014.
Guillain-Barre´ syndrome has become the most common acute peripheral neuropathy in children since the eradication of poliomyelitis in most areas of the world. The cause and pathogenesis of the disease have yet to be clarified; however, it is widely believed to be an autoimmune peripheral neuropathy.1 About two-thirds of the children with Guillain-Barre´ syndrome have a history of antecedent infections 1 to 3 weeks before Guillain-Barre´ syndrome onset. There are only a few reports of Guillain-Barre´ syndrome following parasitic infections worldwide.2,3 Paragonimiasis (lung fluke disease) is a type of zoonotic parasitic disease caused by paragonimus (commonly referred to as the lung fluke), which lives in human organs such as the lungs. There have not been any reports of Guillain-Barre´ syndrome following lung fluke infection to date. Therefore, this report is likely the first of Guillain-Barre´ syndrome caused by lung flukes or any other type of fluke.
of undercooked river crabs and unboiled stream water over the past 6 months. Cerebrospinal fluid testing showed an increased protein level and normal cell count. Electrophysiologic evidence of demyelination of the motor and sensory nerves was discovered (see Table 1). Slowing of motor nerve conduction velocity and prolongation of distal latency occurred in the left tibial and bilateral median nerves. Reduction in the compound muscle action potential amplitude occurred in the left tibial nerve. The sensory nerve action potential was absent following stimulation to the bilateral sural nerves. The motor nerve conduction velocity of the right common peroneal nerve was within the normal range, whereas the distal latency was prolonged. The F wave of the left common peroneal nerve was absent. The Fresponse frequency in the left medial nerve was reduced to 50%, and the latency was significantly prolonged. Based on these findings, the patient was diagnosed with acute inflammatory demyelinating polyneuropathy.
Case Report The patient was a boy aged 8 years 6 months. He was admitted to the hospital with the chief complaint of progressive weakness of and pain in the lower limbs for 2 weeks. Pain developed in the lower limbs approximately 3 weeks after symptom onset, followed by weakness in the lower limbs, unsteady gait, and the inability to stand up from squatting position unassisted, and the symptoms progressed. The patient had a history of consumption
1
The Children’s Hospital of Zhejiang University, School of Medicine Hangzhou, Hangzhou, China
Corresponding Author: Cui-Wei Yang, MM, The Children’s Hospital of Zhejiang University, School of Medicine Hangzhou, China, 57# Zhu Gan Lane, Hangzhou, 310003, China. Email: [email protected]
Downloaded from jcn.sagepub.com at University of Sussex Library on August 8, 2015
Yang et al
1209
Table 1. Nerve Conduction Findings. Median nerve Motor MCV (m/s) Patient 34.4 Normal value 57.2 + (mean + SD) 3.7
DL (ms) 5.9 2.64 + 0.4
Tibial nerve
Sural nerve
Motor
Sensory
Sensory CMAP (mV) 3.6 8.83 + 1.9
FL (ms)
SCV (m/s)
SNAP (mV)
MCV (m/s)
DL (ms)
CMAP (mV)
FL (ms)
SCV (m/s)
SNAP (mV)
34 20.1 + 1.2
39.6 43.7 + 3.4
5.4 20.5 + 3.5
34.0 48.2 + 2.7
4.8 3.64 + 0.8
1.6 15.7 + 1.8
NE 36.3 + 3.7
NE 40.6 + 4.7
NE 18.67 + 4.4
Abbreviations: CMAP, compound muscle action potential; DL, distal latency; FL, F-wave latency; MCV, motor nerve conduction velocity; NE, not elicited; SCV, sensory nerve conduction velocity; SD, standard deviation; SNAP, sensory nerve action potential.
The chest radiograph and ultrasonographic scan revealed right pleural effusion, the chest computed tomographic scan showed a right-sided inflammatory pulmonary lesion and moderate right pleural effusion, and the ultrasonography demonstrated a bright spot in the right posterior lobe of the liver, indicating calcification. Magnetic resonance imaging (MRI) scans of the brain and spinal cord were unremarkable. The eosinophil count was increased, and bone marrow examination results revealed that that the eosinophil percentage was increased. C-reactive protein level was 4 mg/L, and the erythrocyte sedimentation rate was normal. The pleural aspiration results showed a significantly increased cell count and protein level, with a karyocyte count of 9600 106/L and polykaryocyte percentage of 90%. Eosinophils accounted for the majority of the polykaryocytes. The protein level was 90 g/L and the glucose level was 0.1 mmol/L. Chyle test results were negative. Pleural fluid culture yielded Escherichia coli, and no eggs were found in the stool or pleural fluid. Purified protein derivative skin test results were negative. Vitamin B12 and folic acid levels were normal. Stool samples from the patient were negative for Campylobacter jejuni. Serologic studies were negative for all the following: cytomegalovirus, Epstein-Barr virus, influenza virus A and B, Mycoplasma pneumoniae, and hepatitis virus. The patient received 10 g (0.5 g/kg) intravenous immunoglobulin after the cerebrospinal fluid analysis and electrophysiologic examination results were obtained on the first day after admission. However, immunoglobulin was withdrawn as there was no evidence of paralysis of the respiratory muscles or the muscles innervated by the lower cranial nerves and no obvious progression of disease. The patient had no healthcare insurance and his family could not afford the high cost of treatment. The weakness of the lower limbs began to abate on day 4 after admission (18 days after the onset of neurologic symptoms). The patient could walk on his own at 3 weeks after admission and could walk up a flight of stairs without assistance (but with great effort) at 4 weeks after admission. The aforementioned laboratory test results indicated that there was a high probability that the patient was infected with a parasite, which was affecting the lungs and pleurae. Serum enzyme-linked immunosorbent assay showed the presence of antibodies against lung flukes. Therefore, the patient was diagnosed with paragonimiasis (lung fluke disease). Praziquantel was orally administered on day 10 after admission.
The serum cytomegalovirus and Epstein-Barr virus test results remained negative 1 month after hospitalization. The patient’s muscle strength normalized 3 months after hospitalization. The chest radiograph was unremarkable. The peripheral blood eosinophil percentage was reduced to 7%.
Discussion The diagnosis of Guillain-Barre´ syndrome is based on the following typical clinical features: rapid development of muscle paralysis, areflexia, and cerebrospinal fluid tests showing albuminocytologic dissociation. Commonly, the progression of symptoms occurs within 4 weeks.4 In this case, lower limb pain occurred first, followed by progressive weakness of the lower limbs, reduction of the patellar reflex, and loss of the Achilles tendon reflex, indicating a high probability of Guillain-Barre´ syndrome. Clinical and laboratory examination findings were consistent with the diagnosis of Guillain-Barre´ syndrome. The patient began to recover within 4 weeks after the onset of symptoms and completely recovered at the follow-up visit 3 months after hospitalization, further supporting the diagnosis of Guillain-Barre´ syndrome. Guillain-Barre´ syndrome is further classified into acute inflammatory demyelinating polyneuropathy, acute motor axonal neuropathy, acute motor sensory axonal neuropathy, and Miller Fisher syndrome, a clinical variant of Guillain-Barre´ syndrome. This case met the diagnostic criteria for the subtype acute inflammatory demyelinating polyneuropathy.5,6 Although the clinical manifestations and examination results indicated Guillain-Barre´ syndrome, some diseases associated with acute flaccid paralysis had to be excluded before the final diagnosis was made. Poliomyelitis was excluded because the patient did not have a fever at the onset of neuropathic symptoms, had not received an oral polio vaccine recently, and the laboratory test results were negative. Spinal cord diseases were excluded because spinal cord MRI was unremarkable, there was no sensory level, and there was no evidence of sphincter dysfunction or pathologic signs. Parasagittal cortical syndrome was excluded based on unremarkable brain MRI. Peripheral nerve diseases caused by poisons or metabolic disorders were excluded according to the medical history and laboratory tests.
Downloaded from jcn.sagepub.com at University of Sussex Library on August 8, 2015
1210
Journal of Child Neurology 30(9)
The question arose as to whether the onset of Guillain-Barre´ syndrome following lung fluke infection was mere coincidence. The most widely recognized pathogenetic mechanism for Guillain-Barre´ syndrome to date is ‘‘molecular mimicry.’’ This theory posits that some components of the pathogen (foreign antigens) resemble certain structural components of the peripheral nerve tissues (self-antigens); thus, mistaken immune recognition may occur. Then, autoimmune T cells and autoantibodies begin to attack the components of the peripheral nerve tissue. Such inflammatory T-cell and macrophage infiltration causes demyelination of the peripheral nerves, and subsequent axonal degeneration may occur through direct cytotoxic effects and the release of inflammatory mediators, such as cytokines and nitric oxide.7 It is estimated that Guillain-Barre´ syndrome is associated with a history of antecedent infection in twothirds of patients.7 These antecedent infections are primarily respiratory tract and gastrointestinal infections. The pathogens causing such infections mainly include C jejuni (4%-66%), cytomegalovirus (5%-15%), Epstein Barr virus (2%-10%), and pneumonic mycoplasma (1%-5%); in addition, influenza virus A or B and hepatitis virus infections are also associated with Guillain-Barre´ syndrome.5,8 C jejuni infection is the most common antecedent infection in Guillain-Barre´ syndrome, particularly in some areas of East Asia and North China. The epidemic seasons are summer and autumn, and acute motor axonal neuropathy is the most common subtype.7 The patient showed no symptoms of gastroenteritis before the onset of the disorder. No C jejuni was detected, and the boy was not from a C jejuni– endemic area; therefore, this infection was excluded. Cytomegalovirus, Epstein Barr virus, pneumonic mycoplasma, and respiratory tract virus infections were also excluded. Vaccination was not considered as a possible cause of Guillain-Barre´ syndrome for this patient. Serum enzyme-linked immunosorbent assay indicated the presence of antibodies against lung flukes. The purified protein derivative skin test results were negative. The patient achieved a clinical response to praziquantel. Therefore, the diagnosis of paragonimiasis was established. In this case, paragonimiasis did not affect the patient’s brain or spinal cord according to the available data. Peripheral neuropathies occurring after paragonimiasis are rare, and there have been no reports of Guillain-Barre´ syndrome following paragonimiasis. To our knowledge, there are only a few reports of Guillain-Barre´ syndrome resulting from parasitic infections worldwide. In 1998, Richardson et al described a case of Guillain-Barre´ syndrome after Cyclospora infection.9 There are no reports of Guillain-Barre´ syndrome following lung fluke infection. To our knowledge, this report might be the
first on Guillain-Barre´ syndrome caused by lung fluke or any other flukes. Although the pathogenic mechanism remains unclear, there was no doubt that the patient had Guillain-Barre´ syndrome following lung fluke infection. More studies are needed to clarify whether Guillain-Barre´ syndrome can be caused by lung fluke infection and the mechanisms underlying its pathogenesis. We propose that paragonimiasis should be considered when physicians attempt to determine the antecedent infection in Guillain-Barre´ syndrome. Acknowledgments The author gratefully acknowledges the neurophysiological assistance of Drs Jing Chen and Jun Yao.
Declaration of Conflicting Interests The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The authors received no financial support for the research, authorship, and/or publication of this article.
References 1. Kieseier BC, Hartung HP. Therapeutic strategies in the GuillainBarre syndrome. Semin Neurol. 2003;23:159-168. 2. Kanjalkar M, Karnad DR, Narayana RV, Shah PU. Guillain-Barre syndrome following malaria. J Infect. 1999;38:48-50. 3. Sithinamsuwan P, Sinsawaiwong S, Limapichart K. GuillainBarre’s syndrome associated with Plasmodium falciparum malaria: role of plasma exchange. J Med Assoc Thai. 2001;84:1212-1216. 4. Guillain G, Barre´ J, Strohl A. Sur un syndrome de radiculone´vrite avec hyperalbuminose du liquide ce´phalo-rachidien sans re´action cellulaire. Remarques sur les caracte`res cliniques et graphiques des re´flexes tendineux. Bull Soc Med Hop Paris. 1916;40:1462-1470. 5. Hughes RA, Cornblath DR. Guillain-Barre syndrome. Lancet. 2005;366:1653-1666. 6. Asbury AK, Cornblath DR. Assessment of current diagnostic criteria for Guillain-Barre syndrome. Ann Neurol. 1990;27(suppl): S21-S24. 7. Carre JC, Houmdaophet S. [Paragonimiasis]. Rev Pneumol Clin. 1998;54:359-364. 8. Hadden RD, Karch H, Hartung HP, et al. Preceding infections, immune factors, and outcome in Guillain-Barre syndrome. Neurology. 2001;56:758-765. 9. Richardson RF, Jr., Remler BF, Katirji B, Murad MH. GuillainBarre syndrome after Cyclospora infection. Muscle Nerve. 1998; 21:669-671.
Downloaded from jcn.sagepub.com at University of Sussex Library on August 8, 2015
Guillain-Barre´ Syndrome in a Boy With Lung Fluke Infection: Case Report and Literature Review
Journal of Child Neurology 2015, Vol. 30(9) 1208-1210 ª The Author(s) 2014 Reprints and permission: sagepub.com/journalsPermissions.nav DOI: 10.1177/0883073814546689 jcn.sagepub.com
Cui-Wei Yang, MM1, Feng Gao, MM1, and Zhe-Zhi Xia, MM1
Abstract Guillain-Barre´ syndrome is the most common acute peripheral neuropathy in children in most countries. The cause and pathogenesis of the disease have yet to be clarified. There have been only a few reports of Guillain-Barre´ syndrome resulting from parasite infections worldwide, no cases of Guillain-Barre´ syndrome after lung fluke infection have been reported. We report a case of an 8-year-old male patient with Guillain-Barre´ syndrome after lung fluke infection. The child had a history of consumption of undercooked crabs. He was diagnosed with paragonimiasis. The patient experienced paralysis of and pain in the lower limbs about 3 weeks after symptom onset. Neurologic and electrophysiologic examination findings supported the diagnosis of GuillainBarre´ syndrome. Parasitic infections should also be considered when determining which antecedent infection is associated with Guillain-Barre´ syndrome. Keywords Guillain-Barre´ syndrome, parasitic infections, paragonimiasis, children Received April 21, 2014. Received revised June 30, 2014. Accepted for publication July 01, 2014.
Guillain-Barre´ syndrome has become the most common acute peripheral neuropathy in children since the eradication of poliomyelitis in most areas of the world. The cause and pathogenesis of the disease have yet to be clarified; however, it is widely believed to be an autoimmune peripheral neuropathy.1 About two-thirds of the children with Guillain-Barre´ syndrome have a history of antecedent infections 1 to 3 weeks before Guillain-Barre´ syndrome onset. There are only a few reports of Guillain-Barre´ syndrome following parasitic infections worldwide.2,3 Paragonimiasis (lung fluke disease) is a type of zoonotic parasitic disease caused by paragonimus (commonly referred to as the lung fluke), which lives in human organs such as the lungs. There have not been any reports of Guillain-Barre´ syndrome following lung fluke infection to date. Therefore, this report is likely the first of Guillain-Barre´ syndrome caused by lung flukes or any other type of fluke.
of undercooked river crabs and unboiled stream water over the past 6 months. Cerebrospinal fluid testing showed an increased protein level and normal cell count. Electrophysiologic evidence of demyelination of the motor and sensory nerves was discovered (see Table 1). Slowing of motor nerve conduction velocity and prolongation of distal latency occurred in the left tibial and bilateral median nerves. Reduction in the compound muscle action potential amplitude occurred in the left tibial nerve. The sensory nerve action potential was absent following stimulation to the bilateral sural nerves. The motor nerve conduction velocity of the right common peroneal nerve was within the normal range, whereas the distal latency was prolonged. The F wave of the left common peroneal nerve was absent. The Fresponse frequency in the left medial nerve was reduced to 50%, and the latency was significantly prolonged. Based on these findings, the patient was diagnosed with acute inflammatory demyelinating polyneuropathy.
Case Report The patient was a boy aged 8 years 6 months. He was admitted to the hospital with the chief complaint of progressive weakness of and pain in the lower limbs for 2 weeks. Pain developed in the lower limbs approximately 3 weeks after symptom onset, followed by weakness in the lower limbs, unsteady gait, and the inability to stand up from squatting position unassisted, and the symptoms progressed. The patient had a history of consumption
1
The Children’s Hospital of Zhejiang University, School of Medicine Hangzhou, Hangzhou, China
Corresponding Author: Cui-Wei Yang, MM, The Children’s Hospital of Zhejiang University, School of Medicine Hangzhou, China, 57# Zhu Gan Lane, Hangzhou, 310003, China. Email: [email protected]
Downloaded from jcn.sagepub.com at University of Sussex Library on August 8, 2015
Yang et al
1209
Table 1. Nerve Conduction Findings. Median nerve Motor MCV (m/s) Patient 34.4 Normal value 57.2 + (mean + SD) 3.7
DL (ms) 5.9 2.64 + 0.4
Tibial nerve
Sural nerve
Motor
Sensory
Sensory CMAP (mV) 3.6 8.83 + 1.9
FL (ms)
SCV (m/s)
SNAP (mV)
MCV (m/s)
DL (ms)
CMAP (mV)
FL (ms)
SCV (m/s)
SNAP (mV)
34 20.1 + 1.2
39.6 43.7 + 3.4
5.4 20.5 + 3.5
34.0 48.2 + 2.7
4.8 3.64 + 0.8
1.6 15.7 + 1.8
NE 36.3 + 3.7
NE 40.6 + 4.7
NE 18.67 + 4.4
Abbreviations: CMAP, compound muscle action potential; DL, distal latency; FL, F-wave latency; MCV, motor nerve conduction velocity; NE, not elicited; SCV, sensory nerve conduction velocity; SD, standard deviation; SNAP, sensory nerve action potential.
The chest radiograph and ultrasonographic scan revealed right pleural effusion, the chest computed tomographic scan showed a right-sided inflammatory pulmonary lesion and moderate right pleural effusion, and the ultrasonography demonstrated a bright spot in the right posterior lobe of the liver, indicating calcification. Magnetic resonance imaging (MRI) scans of the brain and spinal cord were unremarkable. The eosinophil count was increased, and bone marrow examination results revealed that that the eosinophil percentage was increased. C-reactive protein level was 4 mg/L, and the erythrocyte sedimentation rate was normal. The pleural aspiration results showed a significantly increased cell count and protein level, with a karyocyte count of 9600 106/L and polykaryocyte percentage of 90%. Eosinophils accounted for the majority of the polykaryocytes. The protein level was 90 g/L and the glucose level was 0.1 mmol/L. Chyle test results were negative. Pleural fluid culture yielded Escherichia coli, and no eggs were found in the stool or pleural fluid. Purified protein derivative skin test results were negative. Vitamin B12 and folic acid levels were normal. Stool samples from the patient were negative for Campylobacter jejuni. Serologic studies were negative for all the following: cytomegalovirus, Epstein-Barr virus, influenza virus A and B, Mycoplasma pneumoniae, and hepatitis virus. The patient received 10 g (0.5 g/kg) intravenous immunoglobulin after the cerebrospinal fluid analysis and electrophysiologic examination results were obtained on the first day after admission. However, immunoglobulin was withdrawn as there was no evidence of paralysis of the respiratory muscles or the muscles innervated by the lower cranial nerves and no obvious progression of disease. The patient had no healthcare insurance and his family could not afford the high cost of treatment. The weakness of the lower limbs began to abate on day 4 after admission (18 days after the onset of neurologic symptoms). The patient could walk on his own at 3 weeks after admission and could walk up a flight of stairs without assistance (but with great effort) at 4 weeks after admission. The aforementioned laboratory test results indicated that there was a high probability that the patient was infected with a parasite, which was affecting the lungs and pleurae. Serum enzyme-linked immunosorbent assay showed the presence of antibodies against lung flukes. Therefore, the patient was diagnosed with paragonimiasis (lung fluke disease). Praziquantel was orally administered on day 10 after admission.
The serum cytomegalovirus and Epstein-Barr virus test results remained negative 1 month after hospitalization. The patient’s muscle strength normalized 3 months after hospitalization. The chest radiograph was unremarkable. The peripheral blood eosinophil percentage was reduced to 7%.
Discussion The diagnosis of Guillain-Barre´ syndrome is based on the following typical clinical features: rapid development of muscle paralysis, areflexia, and cerebrospinal fluid tests showing albuminocytologic dissociation. Commonly, the progression of symptoms occurs within 4 weeks.4 In this case, lower limb pain occurred first, followed by progressive weakness of the lower limbs, reduction of the patellar reflex, and loss of the Achilles tendon reflex, indicating a high probability of Guillain-Barre´ syndrome. Clinical and laboratory examination findings were consistent with the diagnosis of Guillain-Barre´ syndrome. The patient began to recover within 4 weeks after the onset of symptoms and completely recovered at the follow-up visit 3 months after hospitalization, further supporting the diagnosis of Guillain-Barre´ syndrome. Guillain-Barre´ syndrome is further classified into acute inflammatory demyelinating polyneuropathy, acute motor axonal neuropathy, acute motor sensory axonal neuropathy, and Miller Fisher syndrome, a clinical variant of Guillain-Barre´ syndrome. This case met the diagnostic criteria for the subtype acute inflammatory demyelinating polyneuropathy.5,6 Although the clinical manifestations and examination results indicated Guillain-Barre´ syndrome, some diseases associated with acute flaccid paralysis had to be excluded before the final diagnosis was made. Poliomyelitis was excluded because the patient did not have a fever at the onset of neuropathic symptoms, had not received an oral polio vaccine recently, and the laboratory test results were negative. Spinal cord diseases were excluded because spinal cord MRI was unremarkable, there was no sensory level, and there was no evidence of sphincter dysfunction or pathologic signs. Parasagittal cortical syndrome was excluded based on unremarkable brain MRI. Peripheral nerve diseases caused by poisons or metabolic disorders were excluded according to the medical history and laboratory tests.
Downloaded from jcn.sagepub.com at University of Sussex Library on August 8, 2015
1210
Journal of Child Neurology 30(9)
The question arose as to whether the onset of Guillain-Barre´ syndrome following lung fluke infection was mere coincidence. The most widely recognized pathogenetic mechanism for Guillain-Barre´ syndrome to date is ‘‘molecular mimicry.’’ This theory posits that some components of the pathogen (foreign antigens) resemble certain structural components of the peripheral nerve tissues (self-antigens); thus, mistaken immune recognition may occur. Then, autoimmune T cells and autoantibodies begin to attack the components of the peripheral nerve tissue. Such inflammatory T-cell and macrophage infiltration causes demyelination of the peripheral nerves, and subsequent axonal degeneration may occur through direct cytotoxic effects and the release of inflammatory mediators, such as cytokines and nitric oxide.7 It is estimated that Guillain-Barre´ syndrome is associated with a history of antecedent infection in twothirds of patients.7 These antecedent infections are primarily respiratory tract and gastrointestinal infections. The pathogens causing such infections mainly include C jejuni (4%-66%), cytomegalovirus (5%-15%), Epstein Barr virus (2%-10%), and pneumonic mycoplasma (1%-5%); in addition, influenza virus A or B and hepatitis virus infections are also associated with Guillain-Barre´ syndrome.5,8 C jejuni infection is the most common antecedent infection in Guillain-Barre´ syndrome, particularly in some areas of East Asia and North China. The epidemic seasons are summer and autumn, and acute motor axonal neuropathy is the most common subtype.7 The patient showed no symptoms of gastroenteritis before the onset of the disorder. No C jejuni was detected, and the boy was not from a C jejuni– endemic area; therefore, this infection was excluded. Cytomegalovirus, Epstein Barr virus, pneumonic mycoplasma, and respiratory tract virus infections were also excluded. Vaccination was not considered as a possible cause of Guillain-Barre´ syndrome for this patient. Serum enzyme-linked immunosorbent assay indicated the presence of antibodies against lung flukes. The purified protein derivative skin test results were negative. The patient achieved a clinical response to praziquantel. Therefore, the diagnosis of paragonimiasis was established. In this case, paragonimiasis did not affect the patient’s brain or spinal cord according to the available data. Peripheral neuropathies occurring after paragonimiasis are rare, and there have been no reports of Guillain-Barre´ syndrome following paragonimiasis. To our knowledge, there are only a few reports of Guillain-Barre´ syndrome resulting from parasitic infections worldwide. In 1998, Richardson et al described a case of Guillain-Barre´ syndrome after Cyclospora infection.9 There are no reports of Guillain-Barre´ syndrome following lung fluke infection. To our knowledge, this report might be the
first on Guillain-Barre´ syndrome caused by lung fluke or any other flukes. Although the pathogenic mechanism remains unclear, there was no doubt that the patient had Guillain-Barre´ syndrome following lung fluke infection. More studies are needed to clarify whether Guillain-Barre´ syndrome can be caused by lung fluke infection and the mechanisms underlying its pathogenesis. We propose that paragonimiasis should be considered when physicians attempt to determine the antecedent infection in Guillain-Barre´ syndrome. Acknowledgments The author gratefully acknowledges the neurophysiological assistance of Drs Jing Chen and Jun Yao.
Declaration of Conflicting Interests The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The authors received no financial support for the research, authorship, and/or publication of this article.
References 1. Kieseier BC, Hartung HP. Therapeutic strategies in the GuillainBarre syndrome. Semin Neurol. 2003;23:159-168. 2. Kanjalkar M, Karnad DR, Narayana RV, Shah PU. Guillain-Barre syndrome following malaria. J Infect. 1999;38:48-50. 3. Sithinamsuwan P, Sinsawaiwong S, Limapichart K. GuillainBarre’s syndrome associated with Plasmodium falciparum malaria: role of plasma exchange. J Med Assoc Thai. 2001;84:1212-1216. 4. Guillain G, Barre´ J, Strohl A. Sur un syndrome de radiculone´vrite avec hyperalbuminose du liquide ce´phalo-rachidien sans re´action cellulaire. Remarques sur les caracte`res cliniques et graphiques des re´flexes tendineux. Bull Soc Med Hop Paris. 1916;40:1462-1470. 5. Hughes RA, Cornblath DR. Guillain-Barre syndrome. Lancet. 2005;366:1653-1666. 6. Asbury AK, Cornblath DR. Assessment of current diagnostic criteria for Guillain-Barre syndrome. Ann Neurol. 1990;27(suppl): S21-S24. 7. Carre JC, Houmdaophet S. [Paragonimiasis]. Rev Pneumol Clin. 1998;54:359-364. 8. Hadden RD, Karch H, Hartung HP, et al. Preceding infections, immune factors, and outcome in Guillain-Barre syndrome. Neurology. 2001;56:758-765. 9. Richardson RF, Jr., Remler BF, Katirji B, Murad MH. GuillainBarre syndrome after Cyclospora infection. Muscle Nerve. 1998; 21:669-671.
Downloaded from jcn.sagepub.com at University of Sussex Library on August 8, 2015
