- Email: [email protected]
Neurological involvement during Katayama syndrome
Reflection and Reaction
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Senior K. Dengue fever: what hope for control? Lancet Infect Dis 2007; 7: 636. Farrar J, Focks D, Gubler D, et al. Towards a global dengue research agenda. Trop Med Int Health 2007; 12: 695–99. Focks D, Alexander N. Multicountry study of Aedes aegypti pupal productivity survey methodology: findings and recommendations. Geneva: World Health Organization, 2007. TDR/IDM/Den/06.1. Kay BH, Nam VS. New strategy against Aedes aegypti in Vietnam. Lancet 2005; 365: 613–17. Sihuincha M, Zamora-Perea E, Orellana-Rios W, et al. Potential use of pyriproxyfen for control of Aedes aegypti (Diptera: Culicidae) in Iquitos, Peru. J Med Entomol 2005; 42: 620–30.
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McCall PJ, Kittayapong P. Control of dengue vectors: tools and strategies. WHO Scientific Working Group meeting on dengue; Geneva: Switzerland; Oct 1–5, 2006. http://www.who.int/tdr/publications/publications/swg_ dengue_2.htm (accessed Nov 15, 2007). Kroeger A, Lenhart A, Ochoa M, et al. Effective control of dengue vectors with curtains and water container covers treated with insecticide in Mexico and Venezuela: cluster randomised trials. BMJ 2006; 332: 1247–50. Kroeger A, Nathan MB. Dengue: setting the global research agenda. Lancet 2006; 368: 2193–95.
Neurological involvement during Katayama syndrome We read with interest the Review on acute schistosomiasis (ie, invasive schistososomiasis, Katayama syndrome) by Allen Ross and colleagues.1 The neurological involvement that is sometimes observed during this phase of schistosomiasis calls for specific comments regarding its clinical presentation, pathophysiology, and treatment. Neurological manifestations rarely occur during the invasive phase of schistosomiasis. Indeed, in the largest series to date, during the Philippines campaign (1944–45) of World War II, neurological manifestations were observed in only about 2% of cases during the invasive phase.2 Of the 1200 American soldiers infected with Schistosoma japonicum, 27 presented with a neurological involvement during this phase. Headache, disturbances of sensorium, and weakness were all present, and about 84% of patients were febrile at one time or another; 44% presented with a transient hemiplegia or tetraplegia, 60% complained of visual impairment, and 50% reported incontinence, speech impairment, and ataxia. Neurological manifestations have also been described in case reports of the acute phase of S japonicum, Schistosoma mansoni, and Schistosoma haematobium infections in travellers, contributing to a better understanding of the clinical manifestations during this stage. For example, the brain involvement during the acute phase of schistosomiasis may be revealed by headache, confusion, seizures, loss of consciousness, focal deficiencies, visual impairment, ataxia, urinary incontinence, and motor paralysis.2–8 This neurological involvement differs from that observed during the chronic phase of the disease.3 Clinical manifestations occur within 6 weeks after infection, as reported in small outbreaks in exposed travellers.9,10 http://infection.thelancet.com Vol 8 January 2008
During this phase of the disease cycle, schistosomulae have not reached their adult stage. Therefore, egg laying—which usually starts at least 2 months after the infestation—is not possible.11 Consequently, eggs cannot be responsible for the neurological manifestations. Nevertheless, these life-threatening neurological manifestations are always associated with marked eosinophilia, which reaches a peak during the invasive phase.9,10,12 The most likely pathophysiological mechanism to explain such manifestations is, therefore, eosinophil-mediated toxicity leading to vasculitis and small vessel thrombosis.6,7 By contrast with what is recommended by Ross and colleagues,1 praziquantel should be contraindicated during the acute phase. First, praziquantel is not efficient, as shown by studies in travellers.7,10 Second, the drug may lead to complications (paradoxical reactions), as described in four (40%) of ten treated patients in a recent outbreak in French travellers.7,10 Instead, corticosteroids are the recommended treatment, especially in emergency situations.12 It is therefore important to distinguish the two pathophysiological mechanisms of neurological involvement during schistosomiasis.3 Whereas the neurological involvement seen during the acute phase is caused by vasculitis and calls for corticosteroids, that observed during the chronic phase is caused by granuloma developing around eggs that migrated accidentally in the brain and calls for specific treatment with praziquantel and sometimes surgery. *Stéphane Jauréguiberry, Eric Caumes Department of Infectious and Tropical Disease and ParasitologyMycology, Hôpital Pitié Salpêtrière, Assistance Publique des Hôpitaux de Paris, Paris, France
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Reflection and Reaction
[email protected]
7
We declare that we have no conflicts of interest. 1 2 3 4
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Ross AG, Vickers D, Olds GR, Shah SM, McManus DP. Katayama syndrome. Lancet Infect Dis 2007; 7: 218–24. Kane C, Most H. Schistosomiasis of the central nervous system. Arch Neurol Psychiatry 1948; 59: 141–83. Pittella JE. Neuroschistosomiasis. Brain Pathol 1997; 7: 649–62. Vachon F, Jebrak G, Boulu P, Coulaud JP. Severe manifestations during acute schistosomiasis due to S mansoni. A case with praziquantel failure. Med Mal Infect 1984; 14: 102–06 (in French). Kirchhoff LV, Nash TE. A case of schistosomiasis japonica: resolution of CAT-scan detected cerebral abnormalities without specific therapy. Am J Trop Med Hyg 1984; 33: 1155–58. Granier H, Potard M, Diraison P, Nicolas X, Laborde JP, Talarmin F. Acute encephalitis concurrent with primary infection by Schistosoma mansoni. Med Trop (Mars) 2003; 63: 60–63.
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11 12
Jauréguiberry S, Ansart S, Perez L, Danis M, Bricaire F, Caumes E. Acute neuroschistosomiasis: two cases associated with cerebral vasculitis. Am J Trop Med Hyg 2007; 76: 964–66. Pittella JE. The relation between involvement of the central nervous system in schistosomiasis mansoni and the clinical forms of the parasitosis. A review. J Trop Med Hyg 1991; 94: 15–21. Jaureguiberry S, Perez L, Paris L, Bricaire F, Danis M, Caumes E. Invasive schistosomiases. Presse Med 2005; 34: 1641–45. Grandiere-Perez L, Ansart S, Paris L, et al. Efficacy of praziquantel during the incubation and invasive phase of Schistosoma haematobium schistosomiasis in 18 travelers. Am J Trop Med Hyg 2006; 74: 814–18. Davis A. Schistosomiasis. Cook GC, Zumla AI, ed. Manson’s tropical diseases. London: Saunders, 2002. Sarazin M, Caumes E, Cohen A, Amarenco P. Multiple microembolic borderzone brain infarctions and endomyocardial fibrosis in idiopathic hypereosinophilic syndrome and in Schistosoma mansoni infestation. J Neurol Neurosurg Psychiatry 2004; 75: 305–07.
On this year’s cover
Sydney Couldridge
For 2008 Sydney Couldridge replaces Martin Haake as the journal’s cover illustrator. We thank Martin for his eye-catching work throughout 2007. Sydney is originally from South Africa, where he trained as a graphic artist. He has been based in London for 12 years where he lives with his wife and two sons. As a freelance illustrator Sydney has worked with leading advertising agencies on brands such as Coca Cola, British Airways, Kellogg’s, Cadburys, BMW, and
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Alfa Romeo. He has also produced cover and editorial illustrations for publications including New Scientist, Arena, Marketing Week, and The Lancet Oncology. An original illustration, Hussar, by Sydney is shown on the left. John McConnell The Lancet Infectious Diseases, 32 Jamestown Road, London NW1 7BY, UK
http://infection.thelancet.com Vol 8 January 2008
1 2 3
4 5
Senior K. Dengue fever: what hope for control? Lancet Infect Dis 2007; 7: 636. Farrar J, Focks D, Gubler D, et al. Towards a global dengue research agenda. Trop Med Int Health 2007; 12: 695–99. Focks D, Alexander N. Multicountry study of Aedes aegypti pupal productivity survey methodology: findings and recommendations. Geneva: World Health Organization, 2007. TDR/IDM/Den/06.1. Kay BH, Nam VS. New strategy against Aedes aegypti in Vietnam. Lancet 2005; 365: 613–17. Sihuincha M, Zamora-Perea E, Orellana-Rios W, et al. Potential use of pyriproxyfen for control of Aedes aegypti (Diptera: Culicidae) in Iquitos, Peru. J Med Entomol 2005; 42: 620–30.
6
7
8
McCall PJ, Kittayapong P. Control of dengue vectors: tools and strategies. WHO Scientific Working Group meeting on dengue; Geneva: Switzerland; Oct 1–5, 2006. http://www.who.int/tdr/publications/publications/swg_ dengue_2.htm (accessed Nov 15, 2007). Kroeger A, Lenhart A, Ochoa M, et al. Effective control of dengue vectors with curtains and water container covers treated with insecticide in Mexico and Venezuela: cluster randomised trials. BMJ 2006; 332: 1247–50. Kroeger A, Nathan MB. Dengue: setting the global research agenda. Lancet 2006; 368: 2193–95.
Neurological involvement during Katayama syndrome We read with interest the Review on acute schistosomiasis (ie, invasive schistososomiasis, Katayama syndrome) by Allen Ross and colleagues.1 The neurological involvement that is sometimes observed during this phase of schistosomiasis calls for specific comments regarding its clinical presentation, pathophysiology, and treatment. Neurological manifestations rarely occur during the invasive phase of schistosomiasis. Indeed, in the largest series to date, during the Philippines campaign (1944–45) of World War II, neurological manifestations were observed in only about 2% of cases during the invasive phase.2 Of the 1200 American soldiers infected with Schistosoma japonicum, 27 presented with a neurological involvement during this phase. Headache, disturbances of sensorium, and weakness were all present, and about 84% of patients were febrile at one time or another; 44% presented with a transient hemiplegia or tetraplegia, 60% complained of visual impairment, and 50% reported incontinence, speech impairment, and ataxia. Neurological manifestations have also been described in case reports of the acute phase of S japonicum, Schistosoma mansoni, and Schistosoma haematobium infections in travellers, contributing to a better understanding of the clinical manifestations during this stage. For example, the brain involvement during the acute phase of schistosomiasis may be revealed by headache, confusion, seizures, loss of consciousness, focal deficiencies, visual impairment, ataxia, urinary incontinence, and motor paralysis.2–8 This neurological involvement differs from that observed during the chronic phase of the disease.3 Clinical manifestations occur within 6 weeks after infection, as reported in small outbreaks in exposed travellers.9,10 http://infection.thelancet.com Vol 8 January 2008
During this phase of the disease cycle, schistosomulae have not reached their adult stage. Therefore, egg laying—which usually starts at least 2 months after the infestation—is not possible.11 Consequently, eggs cannot be responsible for the neurological manifestations. Nevertheless, these life-threatening neurological manifestations are always associated with marked eosinophilia, which reaches a peak during the invasive phase.9,10,12 The most likely pathophysiological mechanism to explain such manifestations is, therefore, eosinophil-mediated toxicity leading to vasculitis and small vessel thrombosis.6,7 By contrast with what is recommended by Ross and colleagues,1 praziquantel should be contraindicated during the acute phase. First, praziquantel is not efficient, as shown by studies in travellers.7,10 Second, the drug may lead to complications (paradoxical reactions), as described in four (40%) of ten treated patients in a recent outbreak in French travellers.7,10 Instead, corticosteroids are the recommended treatment, especially in emergency situations.12 It is therefore important to distinguish the two pathophysiological mechanisms of neurological involvement during schistosomiasis.3 Whereas the neurological involvement seen during the acute phase is caused by vasculitis and calls for corticosteroids, that observed during the chronic phase is caused by granuloma developing around eggs that migrated accidentally in the brain and calls for specific treatment with praziquantel and sometimes surgery. *Stéphane Jauréguiberry, Eric Caumes Department of Infectious and Tropical Disease and ParasitologyMycology, Hôpital Pitié Salpêtrière, Assistance Publique des Hôpitaux de Paris, Paris, France
9
Reflection and Reaction
[email protected]
7
We declare that we have no conflicts of interest. 1 2 3 4
5
6
Ross AG, Vickers D, Olds GR, Shah SM, McManus DP. Katayama syndrome. Lancet Infect Dis 2007; 7: 218–24. Kane C, Most H. Schistosomiasis of the central nervous system. Arch Neurol Psychiatry 1948; 59: 141–83. Pittella JE. Neuroschistosomiasis. Brain Pathol 1997; 7: 649–62. Vachon F, Jebrak G, Boulu P, Coulaud JP. Severe manifestations during acute schistosomiasis due to S mansoni. A case with praziquantel failure. Med Mal Infect 1984; 14: 102–06 (in French). Kirchhoff LV, Nash TE. A case of schistosomiasis japonica: resolution of CAT-scan detected cerebral abnormalities without specific therapy. Am J Trop Med Hyg 1984; 33: 1155–58. Granier H, Potard M, Diraison P, Nicolas X, Laborde JP, Talarmin F. Acute encephalitis concurrent with primary infection by Schistosoma mansoni. Med Trop (Mars) 2003; 63: 60–63.
8
9 10
11 12
Jauréguiberry S, Ansart S, Perez L, Danis M, Bricaire F, Caumes E. Acute neuroschistosomiasis: two cases associated with cerebral vasculitis. Am J Trop Med Hyg 2007; 76: 964–66. Pittella JE. The relation between involvement of the central nervous system in schistosomiasis mansoni and the clinical forms of the parasitosis. A review. J Trop Med Hyg 1991; 94: 15–21. Jaureguiberry S, Perez L, Paris L, Bricaire F, Danis M, Caumes E. Invasive schistosomiases. Presse Med 2005; 34: 1641–45. Grandiere-Perez L, Ansart S, Paris L, et al. Efficacy of praziquantel during the incubation and invasive phase of Schistosoma haematobium schistosomiasis in 18 travelers. Am J Trop Med Hyg 2006; 74: 814–18. Davis A. Schistosomiasis. Cook GC, Zumla AI, ed. Manson’s tropical diseases. London: Saunders, 2002. Sarazin M, Caumes E, Cohen A, Amarenco P. Multiple microembolic borderzone brain infarctions and endomyocardial fibrosis in idiopathic hypereosinophilic syndrome and in Schistosoma mansoni infestation. J Neurol Neurosurg Psychiatry 2004; 75: 305–07.
On this year’s cover
Sydney Couldridge
For 2008 Sydney Couldridge replaces Martin Haake as the journal’s cover illustrator. We thank Martin for his eye-catching work throughout 2007. Sydney is originally from South Africa, where he trained as a graphic artist. He has been based in London for 12 years where he lives with his wife and two sons. As a freelance illustrator Sydney has worked with leading advertising agencies on brands such as Coca Cola, British Airways, Kellogg’s, Cadburys, BMW, and
10
Alfa Romeo. He has also produced cover and editorial illustrations for publications including New Scientist, Arena, Marketing Week, and The Lancet Oncology. An original illustration, Hussar, by Sydney is shown on the left. John McConnell The Lancet Infectious Diseases, 32 Jamestown Road, London NW1 7BY, UK
http://infection.thelancet.com Vol 8 January 2008