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Angiostrongylus cantonensis (A. cantonensis) is a nematode worm that is the most common cause of eosinophilic meningitis (see Figure 1). It is principally found in Southeast Asia, Australia and the Pacific.1–3 Recent media attention regarding the difficulties in diagnosing A. cantonensis meningitis highlights the need for medical practitioners to be aware of the disease.4 Figure 1. Angiostrongylus cantonensis Source: Wikimedia Commons. Lindo JF, Waugh C, Hall J, et al. Enzootic Angiostrongylus cantonensis in rats and snails after an outbreak of human eosinophilic meningitis, Jamaica. Emerging Infectious Diseases 2002;8(3):324–326. Case reportA 51-year-old man of Tongan ethnicity presented to the Emergency Department with a 3-week history of right-sided headache and two episodes of nausea and vomiting on the day of presentation. The headache was constant with variable severity and exacerbations to 9 out of 10 primarily experienced in the right peri-auricular occipital and temporal areas. There was no history of trauma, hearing loss, ear discharge, photophobia, or rash.Two weeks before presentation he had returned from Tuvalu where he had been living for the preceding 3 months. He had seen his family doctor three times for this illness and had been treated for a presumed viral illness with paracetamol.His past medical history includes obesity, hypertension, type 2 diabetes mellitus, hyperlipidaemia and gout. His regular medications are metformin 1 g BD, Quinapril 20 mg BD, simvastatin 40 mg nocte and felodipine ER 10 mg mane.On examination he was afebrile and other vital signs were normal. He was alert and orientated. Examination of the cardiovascular, respiratory and abdominal systems was normal. His neurological exam was normal including a normal cranial nerve exam and there were no signs of meningism. He had no skin lesions or rashes. There was no lymphadenopathy.A CT of the head was performed to exclude an intracranial haemorrhage in the emergency department. There was no haematoma present but fluid in the right mastoid cavity was noted. He was referred to otorhinolaryngology (ORL) for presumed mastoiditis.On ENT review his left ear appeared normal but the right tympanic membrane was moderately retracted with evidence of effusion. There was no erythema overlying the mastoid and no mastoid tenderness. He was treated with antibiotics for presumed acute otitis media. However he then proceeded to have a seizure-like episode and was referred to the general medicine department.Relevant blood tests that were performed are shown in Table 1. Table 1. Blood test results Blood test Result Reference range White blood count Neutrophils Eosinophils CRP ESR HbA1c 14.53 10.61 0.78 16 5 41 4–11 (E+9/L) 1.9–7.5 (E+9/L) 0–0.5 (E+9/L) 0–5 (mg/L) 0–20 (mm/hour) 20–40 mmol/mol A lumbar puncture was performed with an opening pressure of 54cm (n 10–20cm) and the CSF was clear and colourless. The CSF contained 270 WBC × 106/L (7% polymorphs, 70% lymphocytes, 5% monocytes, 18% eosinophils) and a glucose of 3.2 mmol/L (normal 2.8–4.4 mmol/L) and protein of 0.73 g/L (normal 0.15–0.45 g/L).No organisms were seen on Gram stain and there was no growth after 5 days incubation.CSF histology and cytology revealed a lymphocytosis and eosinophilia with no evidence of malignant cells. Mycobacterium tuberculosis DNA was not detected on nucleic acid amplification assay nor on Ziehl-Neelsen staining.The CSF was negative for Streptococcus pneumoniae on immunochromatographic test. The CSF was also negative for Enterovirus and Cryptococcal antigen. A. cantonensis serology is pending.An LP was performed 7 days later. The CSF contained 140 WBC × 106/L (1% polymorphs, 60% lymphocytes, 4% monocytes, 35% eosinophils) and a glucose of 2.6 mmol/L (normal 2.8–4.4 mmol/L) and protein of 0.6 g/L (normal 0.15–0.45 g/L).His symptoms improved immediately following both lumbar punctures. MRI showed no evidence of dural venous sinus thrombosis.Based on the history, the elevated WBC with eosinophilia, the CSF showing a high WBC with eosinophilia and increased protein, a diagnosis of Angiostrongylus cantonensis eosinophilic meningitis was made.Unfortunately he presented 3 days following discharge with decreased GCS and right arm weakness. CT and MRI revealed a 7 × 2.5 × 3cm strip of haemorrhage within the left temporal lobe. There was intraventricular blood with mild hydrocephalus and midline shift to the right of around 12 mm. There was no mass lesion, vascular malformation, or venous thrombosis identified as a cause for the haemorrhage (see Figure 2). Figure 2. CT of patient's head showing acute left temporal haemorrhage with intraventricular blood DiscussionThis is the first reported case of A. cantonensis meningitis complicated by an intraparenchymal cerebral haemorrhage. In 1982, Kliks et al. reported one case of subarachnoid haemorrhage presumed to be due to Angiostrongylus meningitis, but case reports and reviews of Angiostrongylus meningitis have not revealed any other cases complicated by intracranial haemorrhage.5,6Diagnosis of Angiostrongylus meningitis is based on a history of possible exposure e.g. consumption of unwashed lettuce in an endemic region, clinical findings and CSF eosinophilia.1 Definitive diagnosis, such as serologic tests, are available but are rarely used due to price and poor specificity. Direct identification of the Angiostrongylus parasite in humans has not been described in the literature.1The main differential diagnosis of parasitic eosinophilic meningitis is Gnathostoma meningitis. This usually presents with more severe disease and may affect the viscera and skin along with the CNS, elevated opening pressures are less common and imaging may reveal nodular lesions, CNS haemorrhage or hydrocephalus.1,6–8 However Gnathostoma meningitis is not found in the Pacific and therefore it would be very unlikely to be the cause of this patient's haemorrhage.1Another possibility is that consequences of the metabolic syndrome caused this patient's intracranial haemorrhage, however he does not have evidence of ischaemic heart disease or cerebrovascular disease.This case highlights the difficulty of diagnosing this condition. The patient was reviewed a number of times prior to presentation and treated for a presumed viral illness. Furthermore, incidental findings on the first set of imaging distracted the consulting physician from the diagnosis. Therefore it is important that medical practitioners in the primary and hospital sectors have a broad differential diagnosis for any unwell returned traveller.Author information: Nikola Lilic, Otorhinolaryngology Registrar, Department of Otolaryngology Head and Neck Surgery, Counties Manukau District Health Board, Otahuhu, Auckland; Ben Addison, General Surgery Registrar, Department of General Surgery, North Shore Hospital, Takapuna, Auckland & Clinical Medical Education Fellow, University of AucklandCorrespondence: Nikola Lilic, Module 3, Manukau Super Clinic, 901 Great South Road, Manurewa, Auckland, New Zealand. Fax: +64 (0)9 3757038; email: nikola.z.lilic@gmail.comReferences:1.Ramirez-Avila L, et al. Eosinophilic meningitis due to Angiostrongylus and Gnathostoma species. Clin infect Dis 2009;48:322–327.2.Graeff-Teixeira C, Da Silva ACA, Yoshimura K. Update on eosinophilic meningoencephalitis and its clinical relevance. Clin Microbiol Rev 2009;22:322–348.3.Prociv P, Carlisle MS. The spread of Angiostrongylus cantonensis in Australia. Southeast Asian J Trop Med Public Health 2001;32:126–128.4.Tait M. Salad bug from Fiji nearly kills NZ tourist. The New Zealand Herald; 20 July 2013. http://www.nzherald.co.nz/nz/news/article.cfm?c_id=1&objectid=109005155.Kliks MM, Kroenke K, Hardman JM. Eosinophilic radiculomyelo-encephalitis: an angiostrongyliasis outbreak in American Samoa related to ingestion of Achatinafulica snails. Am J Trop Med Hyg 1982;31:1114–22.6.Koo J, Pien F, Kliks MM. Angiostrongylus (Parastrongylus) eosinophilic meningitis. Rev Infect Dis 1988;10:1155–1162.7.Boongird P, Phuapradit P, Siridej N, et al. Neurological manifestations of gnathostomiasis. J Neurol Sci 1977;31:279–91.8.Rusnak JM, Lucey DR. Clinical gnathostomiasis: case report and review of the English-language literature. Clin Infect Dis 1993;16:33–50.

Summary

Abstract

Angiostrongylus cantonensis (A. cantonensis) is a nematode parasite found in Southeast Asia, Australia and the Pacific that is the most common cause of eosinophilic meningitis. -We report a case of intraparenchymal cerebral haemorrhage associated with A. cantonensis meningitis. This complication has not previously been reported in the literature.

Aim

Method

Results

Conclusion

Author Information

Acknowledgements

Correspondence

Correspondence Email

Competing Interests

For the PDF of this article,
contact nzmj@nzma.org.nz

View Article PDF

Angiostrongylus cantonensis (A. cantonensis) is a nematode worm that is the most common cause of eosinophilic meningitis (see Figure 1). It is principally found in Southeast Asia, Australia and the Pacific.1–3 Recent media attention regarding the difficulties in diagnosing A. cantonensis meningitis highlights the need for medical practitioners to be aware of the disease.4 Figure 1. Angiostrongylus cantonensis Source: Wikimedia Commons. Lindo JF, Waugh C, Hall J, et al. Enzootic Angiostrongylus cantonensis in rats and snails after an outbreak of human eosinophilic meningitis, Jamaica. Emerging Infectious Diseases 2002;8(3):324–326. Case reportA 51-year-old man of Tongan ethnicity presented to the Emergency Department with a 3-week history of right-sided headache and two episodes of nausea and vomiting on the day of presentation. The headache was constant with variable severity and exacerbations to 9 out of 10 primarily experienced in the right peri-auricular occipital and temporal areas. There was no history of trauma, hearing loss, ear discharge, photophobia, or rash.Two weeks before presentation he had returned from Tuvalu where he had been living for the preceding 3 months. He had seen his family doctor three times for this illness and had been treated for a presumed viral illness with paracetamol.His past medical history includes obesity, hypertension, type 2 diabetes mellitus, hyperlipidaemia and gout. His regular medications are metformin 1 g BD, Quinapril 20 mg BD, simvastatin 40 mg nocte and felodipine ER 10 mg mane.On examination he was afebrile and other vital signs were normal. He was alert and orientated. Examination of the cardiovascular, respiratory and abdominal systems was normal. His neurological exam was normal including a normal cranial nerve exam and there were no signs of meningism. He had no skin lesions or rashes. There was no lymphadenopathy.A CT of the head was performed to exclude an intracranial haemorrhage in the emergency department. There was no haematoma present but fluid in the right mastoid cavity was noted. He was referred to otorhinolaryngology (ORL) for presumed mastoiditis.On ENT review his left ear appeared normal but the right tympanic membrane was moderately retracted with evidence of effusion. There was no erythema overlying the mastoid and no mastoid tenderness. He was treated with antibiotics for presumed acute otitis media. However he then proceeded to have a seizure-like episode and was referred to the general medicine department.Relevant blood tests that were performed are shown in Table 1. Table 1. Blood test results Blood test Result Reference range White blood count Neutrophils Eosinophils CRP ESR HbA1c 14.53 10.61 0.78 16 5 41 4–11 (E+9/L) 1.9–7.5 (E+9/L) 0–0.5 (E+9/L) 0–5 (mg/L) 0–20 (mm/hour) 20–40 mmol/mol A lumbar puncture was performed with an opening pressure of 54cm (n 10–20cm) and the CSF was clear and colourless. The CSF contained 270 WBC × 106/L (7% polymorphs, 70% lymphocytes, 5% monocytes, 18% eosinophils) and a glucose of 3.2 mmol/L (normal 2.8–4.4 mmol/L) and protein of 0.73 g/L (normal 0.15–0.45 g/L).No organisms were seen on Gram stain and there was no growth after 5 days incubation.CSF histology and cytology revealed a lymphocytosis and eosinophilia with no evidence of malignant cells. Mycobacterium tuberculosis DNA was not detected on nucleic acid amplification assay nor on Ziehl-Neelsen staining.The CSF was negative for Streptococcus pneumoniae on immunochromatographic test. The CSF was also negative for Enterovirus and Cryptococcal antigen. A. cantonensis serology is pending.An LP was performed 7 days later. The CSF contained 140 WBC × 106/L (1% polymorphs, 60% lymphocytes, 4% monocytes, 35% eosinophils) and a glucose of 2.6 mmol/L (normal 2.8–4.4 mmol/L) and protein of 0.6 g/L (normal 0.15–0.45 g/L).His symptoms improved immediately following both lumbar punctures. MRI showed no evidence of dural venous sinus thrombosis.Based on the history, the elevated WBC with eosinophilia, the CSF showing a high WBC with eosinophilia and increased protein, a diagnosis of Angiostrongylus cantonensis eosinophilic meningitis was made.Unfortunately he presented 3 days following discharge with decreased GCS and right arm weakness. CT and MRI revealed a 7 × 2.5 × 3cm strip of haemorrhage within the left temporal lobe. There was intraventricular blood with mild hydrocephalus and midline shift to the right of around 12 mm. There was no mass lesion, vascular malformation, or venous thrombosis identified as a cause for the haemorrhage (see Figure 2). Figure 2. CT of patient's head showing acute left temporal haemorrhage with intraventricular blood DiscussionThis is the first reported case of A. cantonensis meningitis complicated by an intraparenchymal cerebral haemorrhage. In 1982, Kliks et al. reported one case of subarachnoid haemorrhage presumed to be due to Angiostrongylus meningitis, but case reports and reviews of Angiostrongylus meningitis have not revealed any other cases complicated by intracranial haemorrhage.5,6Diagnosis of Angiostrongylus meningitis is based on a history of possible exposure e.g. consumption of unwashed lettuce in an endemic region, clinical findings and CSF eosinophilia.1 Definitive diagnosis, such as serologic tests, are available but are rarely used due to price and poor specificity. Direct identification of the Angiostrongylus parasite in humans has not been described in the literature.1The main differential diagnosis of parasitic eosinophilic meningitis is Gnathostoma meningitis. This usually presents with more severe disease and may affect the viscera and skin along with the CNS, elevated opening pressures are less common and imaging may reveal nodular lesions, CNS haemorrhage or hydrocephalus.1,6–8 However Gnathostoma meningitis is not found in the Pacific and therefore it would be very unlikely to be the cause of this patient's haemorrhage.1Another possibility is that consequences of the metabolic syndrome caused this patient's intracranial haemorrhage, however he does not have evidence of ischaemic heart disease or cerebrovascular disease.This case highlights the difficulty of diagnosing this condition. The patient was reviewed a number of times prior to presentation and treated for a presumed viral illness. Furthermore, incidental findings on the first set of imaging distracted the consulting physician from the diagnosis. Therefore it is important that medical practitioners in the primary and hospital sectors have a broad differential diagnosis for any unwell returned traveller.Author information: Nikola Lilic, Otorhinolaryngology Registrar, Department of Otolaryngology Head and Neck Surgery, Counties Manukau District Health Board, Otahuhu, Auckland; Ben Addison, General Surgery Registrar, Department of General Surgery, North Shore Hospital, Takapuna, Auckland & Clinical Medical Education Fellow, University of AucklandCorrespondence: Nikola Lilic, Module 3, Manukau Super Clinic, 901 Great South Road, Manurewa, Auckland, New Zealand. Fax: +64 (0)9 3757038; email: nikola.z.lilic@gmail.comReferences:1.Ramirez-Avila L, et al. Eosinophilic meningitis due to Angiostrongylus and Gnathostoma species. Clin infect Dis 2009;48:322–327.2.Graeff-Teixeira C, Da Silva ACA, Yoshimura K. Update on eosinophilic meningoencephalitis and its clinical relevance. Clin Microbiol Rev 2009;22:322–348.3.Prociv P, Carlisle MS. The spread of Angiostrongylus cantonensis in Australia. Southeast Asian J Trop Med Public Health 2001;32:126–128.4.Tait M. Salad bug from Fiji nearly kills NZ tourist. The New Zealand Herald; 20 July 2013. http://www.nzherald.co.nz/nz/news/article.cfm?c_id=1&objectid=109005155.Kliks MM, Kroenke K, Hardman JM. Eosinophilic radiculomyelo-encephalitis: an angiostrongyliasis outbreak in American Samoa related to ingestion of Achatinafulica snails. Am J Trop Med Hyg 1982;31:1114–22.6.Koo J, Pien F, Kliks MM. Angiostrongylus (Parastrongylus) eosinophilic meningitis. Rev Infect Dis 1988;10:1155–1162.7.Boongird P, Phuapradit P, Siridej N, et al. Neurological manifestations of gnathostomiasis. J Neurol Sci 1977;31:279–91.8.Rusnak JM, Lucey DR. Clinical gnathostomiasis: case report and review of the English-language literature. Clin Infect Dis 1993;16:33–50.

Summary

Abstract

Angiostrongylus cantonensis (A. cantonensis) is a nematode parasite found in Southeast Asia, Australia and the Pacific that is the most common cause of eosinophilic meningitis. -We report a case of intraparenchymal cerebral haemorrhage associated with A. cantonensis meningitis. This complication has not previously been reported in the literature.

Aim

Method

Results

Conclusion

Author Information

Acknowledgements

Correspondence

Correspondence Email

Competing Interests

For the PDF of this article,
contact nzmj@nzma.org.nz

View Article PDF

Angiostrongylus cantonensis (A. cantonensis) is a nematode worm that is the most common cause of eosinophilic meningitis (see Figure 1). It is principally found in Southeast Asia, Australia and the Pacific.1–3 Recent media attention regarding the difficulties in diagnosing A. cantonensis meningitis highlights the need for medical practitioners to be aware of the disease.4 Figure 1. Angiostrongylus cantonensis Source: Wikimedia Commons. Lindo JF, Waugh C, Hall J, et al. Enzootic Angiostrongylus cantonensis in rats and snails after an outbreak of human eosinophilic meningitis, Jamaica. Emerging Infectious Diseases 2002;8(3):324–326. Case reportA 51-year-old man of Tongan ethnicity presented to the Emergency Department with a 3-week history of right-sided headache and two episodes of nausea and vomiting on the day of presentation. The headache was constant with variable severity and exacerbations to 9 out of 10 primarily experienced in the right peri-auricular occipital and temporal areas. There was no history of trauma, hearing loss, ear discharge, photophobia, or rash.Two weeks before presentation he had returned from Tuvalu where he had been living for the preceding 3 months. He had seen his family doctor three times for this illness and had been treated for a presumed viral illness with paracetamol.His past medical history includes obesity, hypertension, type 2 diabetes mellitus, hyperlipidaemia and gout. His regular medications are metformin 1 g BD, Quinapril 20 mg BD, simvastatin 40 mg nocte and felodipine ER 10 mg mane.On examination he was afebrile and other vital signs were normal. He was alert and orientated. Examination of the cardiovascular, respiratory and abdominal systems was normal. His neurological exam was normal including a normal cranial nerve exam and there were no signs of meningism. He had no skin lesions or rashes. There was no lymphadenopathy.A CT of the head was performed to exclude an intracranial haemorrhage in the emergency department. There was no haematoma present but fluid in the right mastoid cavity was noted. He was referred to otorhinolaryngology (ORL) for presumed mastoiditis.On ENT review his left ear appeared normal but the right tympanic membrane was moderately retracted with evidence of effusion. There was no erythema overlying the mastoid and no mastoid tenderness. He was treated with antibiotics for presumed acute otitis media. However he then proceeded to have a seizure-like episode and was referred to the general medicine department.Relevant blood tests that were performed are shown in Table 1. Table 1. Blood test results Blood test Result Reference range White blood count Neutrophils Eosinophils CRP ESR HbA1c 14.53 10.61 0.78 16 5 41 4–11 (E+9/L) 1.9–7.5 (E+9/L) 0–0.5 (E+9/L) 0–5 (mg/L) 0–20 (mm/hour) 20–40 mmol/mol A lumbar puncture was performed with an opening pressure of 54cm (n 10–20cm) and the CSF was clear and colourless. The CSF contained 270 WBC × 106/L (7% polymorphs, 70% lymphocytes, 5% monocytes, 18% eosinophils) and a glucose of 3.2 mmol/L (normal 2.8–4.4 mmol/L) and protein of 0.73 g/L (normal 0.15–0.45 g/L).No organisms were seen on Gram stain and there was no growth after 5 days incubation.CSF histology and cytology revealed a lymphocytosis and eosinophilia with no evidence of malignant cells. Mycobacterium tuberculosis DNA was not detected on nucleic acid amplification assay nor on Ziehl-Neelsen staining.The CSF was negative for Streptococcus pneumoniae on immunochromatographic test. The CSF was also negative for Enterovirus and Cryptococcal antigen. A. cantonensis serology is pending.An LP was performed 7 days later. The CSF contained 140 WBC × 106/L (1% polymorphs, 60% lymphocytes, 4% monocytes, 35% eosinophils) and a glucose of 2.6 mmol/L (normal 2.8–4.4 mmol/L) and protein of 0.6 g/L (normal 0.15–0.45 g/L).His symptoms improved immediately following both lumbar punctures. MRI showed no evidence of dural venous sinus thrombosis.Based on the history, the elevated WBC with eosinophilia, the CSF showing a high WBC with eosinophilia and increased protein, a diagnosis of Angiostrongylus cantonensis eosinophilic meningitis was made.Unfortunately he presented 3 days following discharge with decreased GCS and right arm weakness. CT and MRI revealed a 7 × 2.5 × 3cm strip of haemorrhage within the left temporal lobe. There was intraventricular blood with mild hydrocephalus and midline shift to the right of around 12 mm. There was no mass lesion, vascular malformation, or venous thrombosis identified as a cause for the haemorrhage (see Figure 2). Figure 2. CT of patient's head showing acute left temporal haemorrhage with intraventricular blood DiscussionThis is the first reported case of A. cantonensis meningitis complicated by an intraparenchymal cerebral haemorrhage. In 1982, Kliks et al. reported one case of subarachnoid haemorrhage presumed to be due to Angiostrongylus meningitis, but case reports and reviews of Angiostrongylus meningitis have not revealed any other cases complicated by intracranial haemorrhage.5,6Diagnosis of Angiostrongylus meningitis is based on a history of possible exposure e.g. consumption of unwashed lettuce in an endemic region, clinical findings and CSF eosinophilia.1 Definitive diagnosis, such as serologic tests, are available but are rarely used due to price and poor specificity. Direct identification of the Angiostrongylus parasite in humans has not been described in the literature.1The main differential diagnosis of parasitic eosinophilic meningitis is Gnathostoma meningitis. This usually presents with more severe disease and may affect the viscera and skin along with the CNS, elevated opening pressures are less common and imaging may reveal nodular lesions, CNS haemorrhage or hydrocephalus.1,6–8 However Gnathostoma meningitis is not found in the Pacific and therefore it would be very unlikely to be the cause of this patient's haemorrhage.1Another possibility is that consequences of the metabolic syndrome caused this patient's intracranial haemorrhage, however he does not have evidence of ischaemic heart disease or cerebrovascular disease.This case highlights the difficulty of diagnosing this condition. The patient was reviewed a number of times prior to presentation and treated for a presumed viral illness. Furthermore, incidental findings on the first set of imaging distracted the consulting physician from the diagnosis. Therefore it is important that medical practitioners in the primary and hospital sectors have a broad differential diagnosis for any unwell returned traveller.Author information: Nikola Lilic, Otorhinolaryngology Registrar, Department of Otolaryngology Head and Neck Surgery, Counties Manukau District Health Board, Otahuhu, Auckland; Ben Addison, General Surgery Registrar, Department of General Surgery, North Shore Hospital, Takapuna, Auckland & Clinical Medical Education Fellow, University of AucklandCorrespondence: Nikola Lilic, Module 3, Manukau Super Clinic, 901 Great South Road, Manurewa, Auckland, New Zealand. Fax: +64 (0)9 3757038; email: nikola.z.lilic@gmail.comReferences:1.Ramirez-Avila L, et al. Eosinophilic meningitis due to Angiostrongylus and Gnathostoma species. Clin infect Dis 2009;48:322–327.2.Graeff-Teixeira C, Da Silva ACA, Yoshimura K. Update on eosinophilic meningoencephalitis and its clinical relevance. Clin Microbiol Rev 2009;22:322–348.3.Prociv P, Carlisle MS. The spread of Angiostrongylus cantonensis in Australia. Southeast Asian J Trop Med Public Health 2001;32:126–128.4.Tait M. Salad bug from Fiji nearly kills NZ tourist. The New Zealand Herald; 20 July 2013. http://www.nzherald.co.nz/nz/news/article.cfm?c_id=1&objectid=109005155.Kliks MM, Kroenke K, Hardman JM. Eosinophilic radiculomyelo-encephalitis: an angiostrongyliasis outbreak in American Samoa related to ingestion of Achatinafulica snails. Am J Trop Med Hyg 1982;31:1114–22.6.Koo J, Pien F, Kliks MM. Angiostrongylus (Parastrongylus) eosinophilic meningitis. Rev Infect Dis 1988;10:1155–1162.7.Boongird P, Phuapradit P, Siridej N, et al. Neurological manifestations of gnathostomiasis. J Neurol Sci 1977;31:279–91.8.Rusnak JM, Lucey DR. Clinical gnathostomiasis: case report and review of the English-language literature. Clin Infect Dis 1993;16:33–50.

Summary

Abstract

Angiostrongylus cantonensis (A. cantonensis) is a nematode parasite found in Southeast Asia, Australia and the Pacific that is the most common cause of eosinophilic meningitis. -We report a case of intraparenchymal cerebral haemorrhage associated with A. cantonensis meningitis. This complication has not previously been reported in the literature.

Aim

Method

Results

Conclusion

Author Information

Acknowledgements

Correspondence

Correspondence Email

Competing Interests

Contact diana@nzma.org.nz
for the PDF of this article

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