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Encephalitis and dengue
CORRESPONDENCE
Encephalitis and dengue Sir—Richard Whitley and John Gnann (Feb 9, p 507)1 review common and emerging pathogens associated with viral central nervous system (CNS) infections. Nevertheless, they do not mention dengue, an acute viral disease transmitted by Aedes mosquitoes, and highly endemic in many tropical and subtropical areas of the world. Indirect effects of dengue infection on the CNS may be an explanation for encephalopathy, but the presence of IgM antibody to dengue in the cerebrospinal fluid (CSF) and reports of virus isolation from brain tissue and CSF of patients with neurological symptoms suggest direct virus invasion of the CNS.2 Three types of neurological manifestations have been associated with confirmed dengue infection: non-specific symptoms of headache, dizziness, delirium, drowsiness, sleeplessness, and restlessness; severe syndromes of depressed sensorium, lethargy, confusion, seizures, meningismus, paresis, and coma that are sometimes clinically indistinguishable from encephalitis; and delayed syndromes of paralysis of lower or upper extremities or larynx, seizures, tremors, amnesia, loss of sensation, manic psychosis, depression, dementia, and Guillain-Barré syndrome. Neurological complications associated with dengue infection can arise in dengue fever and dengue haemorrhagic fever. Any virus serotype may be involved, but DEN-2 and DEN-3 are most frequently reported as the cause of severe neurological disease. Most reported cases of dengue encephalopathy or encephalitis recover without neurological sequelae.3 The frequency of neurological changes as the presenting sign in dengue is unknown, but neurological complications associated with dengue infection have been recognised since the beginning of the 20th century and reported in almost every country in Asia and in many countries in the Americas.3 In one study in Vietnam, 4% of patients admitted to a neurology ward with suspected CNS infections were infected with dengue virus,4 and in Thailand, 18% of children admitted to a hospital with encephalitis-like illness were confirmed as having dengue infection.5 In Indonesia, 70% of virologically confirmed fatal dengue infections (n=30) presented with one or more neurological signs, and 7% were admitted for viral encephalitis, which was listed as the cause of death.3 The re-emergence of dengue as an important pathogen justifies its inclusion in the differential diagnosis of
patients with acute onset of encephalitis in endemic countries or with a travel history suggestive of dengue exposure. *Enid J García-Rivera, José G Rigau-Pérez Dengue Branch, Division of Vector-Borne Infectious Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, 1324 Calle Cañada, San Juan, PR 00920, USA (e-mail: [email protected]) 1
2
3
4
5
Whitley RJ, Gnann W. Viral encephalitis: familiar and emerging pathogens. Lancet 2002; 359: 507–14. Lum LC, Lam SK, Choy YS, George R, Harun F. Dengue encephalitis: a true entity? Am J Trop Med Hyg 1996; 54: 256–59. Gubler DJ, Kuno G, Waterman SH. Neurologic disorders associated with dengue infection: proceedings of the International Conference on Dengue/Dengue Hemorrhagic Fever, Kuala Lumpur, Malaysia, September 1983: 290–301. Solomon T, Dung NM, Vaughn DW, et al. Neurologic manifestations of dengue infection. Lancet 2000; 344: 1053–59. Kankirawatana P, Chokephaibulkit K, Puthavathana P, et al. Dengue infection presenting with central nervous system manifestation. J Child Neurol 2000; 15: 544–47.
Effects of biological attack on US food supplies Sir—In their discussion on the preparedness and response of US agencies to a terrorist attack on the country’s food supply, Jeremy Sobel and colleagues (March 9, p 874)1 do not mention vulnerabilities existing in the current system used for recognition and investigation of food poisoning outbreaks. While researching outbreak investigation techniques in different cities and counties in New York State, I identified several issues that might compound the investigation of an intentional or unintentional food poisoning outbreak. The investigation of an outbreak depends on its detection, and under the current system, there are difficulties associated with detection of outbreaks. Clinicians are poor reporters of foodpoisoning cases, especially when patients are examined in hospital accident and emergency rooms. Merely providing clinicians with a list of Health Department officials, as Sobel and colleagues suggest, will not improve reporting rates, since various studies have shown that there are many reasons why clinicians do not report. These include unawareness of statutory obligations,2 concerns of violating doctor-patient privilege,3 and a lack of understanding of the purpose of notification.4 Furthermore, food poisoning cases are reported to different divisions in the
THE LANCET • Vol 360 • July 20, 2002 • www.thelancet.com
same health department; it is not uncommon for the communicable disease programme to receive information about confirmed cases from laboratories or medical professionals, whereas the food safety programme gathers information from the public and other agencies. There is no central database that collates this information. Consequently, even if there are epidemiological commonalities between cases they will not come to light because the information is inadequately shared between the different divisions. In fact, information sharing is an issue that also arises when local officials have to work with federal agencies during investigations. Indeed, the involvement of federal agencies during investigations is fraught with difficulties. There is substantial jurisdictional overlap between products regulated by federal agencies. For example, closed meat sandwiches are regulated by the US Food and Drug Administration, whereas open meat sandwiches are regulated by the US Department of Agriculture.5 Consequently, it can be challenging for local officials to correctly identify the agency in charge. Moreover, bureaucratically run public-health organisations may abdicate responsibility when jurisdictional responsibility is unclear. Unfortunately, even when the correct agency is approached they seem to hesitate to get involved unless there is conclusive evidence to prove that the food in question was the cause of the illness. This type of evidence is unavailable in most investigations. Therefore, trace-back investigations by federal agencies to identify the source of the food may not be done because of lack of evidence. An intentionally or unintentionally contaminated food source can, therefore, continue unabated. Protocols and simulated exercises do not obviate the weaknesses inherent in the system; most of which are solvable. Detection of outbreaks and the thoroughness of investigations needs to be improved. Azarmeen Jamasji Department of Public Health and Policy, London School of Hygiene and Tropical Medicine, Health Services Research Unit, London WC1E 7HT, UK (e-mail: [email protected]) 1
2
3 4
Sobel J, Khan AS, Swerdlow DL. Threat of biological terrorist attack on the US food supply: the CDC perspective. Lancet 2002; 359: 874–80. Durrheim DN, Thomas J. General practice awareness of notifiable infectious diseases. Public Health 1994; 108: 273–78. Hume J. On reports and rapport from VD control. Am J Public Health 1980; 70: 164–66. Voss S. How much do doctors know about the notification of infectious diseases? BMJ 1992; 304: 755.
261
For personal use. Only reproduce with permission from The Lancet Publishing Group.
Encephalitis and dengue Sir—Richard Whitley and John Gnann (Feb 9, p 507)1 review common and emerging pathogens associated with viral central nervous system (CNS) infections. Nevertheless, they do not mention dengue, an acute viral disease transmitted by Aedes mosquitoes, and highly endemic in many tropical and subtropical areas of the world. Indirect effects of dengue infection on the CNS may be an explanation for encephalopathy, but the presence of IgM antibody to dengue in the cerebrospinal fluid (CSF) and reports of virus isolation from brain tissue and CSF of patients with neurological symptoms suggest direct virus invasion of the CNS.2 Three types of neurological manifestations have been associated with confirmed dengue infection: non-specific symptoms of headache, dizziness, delirium, drowsiness, sleeplessness, and restlessness; severe syndromes of depressed sensorium, lethargy, confusion, seizures, meningismus, paresis, and coma that are sometimes clinically indistinguishable from encephalitis; and delayed syndromes of paralysis of lower or upper extremities or larynx, seizures, tremors, amnesia, loss of sensation, manic psychosis, depression, dementia, and Guillain-Barré syndrome. Neurological complications associated with dengue infection can arise in dengue fever and dengue haemorrhagic fever. Any virus serotype may be involved, but DEN-2 and DEN-3 are most frequently reported as the cause of severe neurological disease. Most reported cases of dengue encephalopathy or encephalitis recover without neurological sequelae.3 The frequency of neurological changes as the presenting sign in dengue is unknown, but neurological complications associated with dengue infection have been recognised since the beginning of the 20th century and reported in almost every country in Asia and in many countries in the Americas.3 In one study in Vietnam, 4% of patients admitted to a neurology ward with suspected CNS infections were infected with dengue virus,4 and in Thailand, 18% of children admitted to a hospital with encephalitis-like illness were confirmed as having dengue infection.5 In Indonesia, 70% of virologically confirmed fatal dengue infections (n=30) presented with one or more neurological signs, and 7% were admitted for viral encephalitis, which was listed as the cause of death.3 The re-emergence of dengue as an important pathogen justifies its inclusion in the differential diagnosis of
patients with acute onset of encephalitis in endemic countries or with a travel history suggestive of dengue exposure. *Enid J García-Rivera, José G Rigau-Pérez Dengue Branch, Division of Vector-Borne Infectious Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, 1324 Calle Cañada, San Juan, PR 00920, USA (e-mail: [email protected]) 1
2
3
4
5
Whitley RJ, Gnann W. Viral encephalitis: familiar and emerging pathogens. Lancet 2002; 359: 507–14. Lum LC, Lam SK, Choy YS, George R, Harun F. Dengue encephalitis: a true entity? Am J Trop Med Hyg 1996; 54: 256–59. Gubler DJ, Kuno G, Waterman SH. Neurologic disorders associated with dengue infection: proceedings of the International Conference on Dengue/Dengue Hemorrhagic Fever, Kuala Lumpur, Malaysia, September 1983: 290–301. Solomon T, Dung NM, Vaughn DW, et al. Neurologic manifestations of dengue infection. Lancet 2000; 344: 1053–59. Kankirawatana P, Chokephaibulkit K, Puthavathana P, et al. Dengue infection presenting with central nervous system manifestation. J Child Neurol 2000; 15: 544–47.
Effects of biological attack on US food supplies Sir—In their discussion on the preparedness and response of US agencies to a terrorist attack on the country’s food supply, Jeremy Sobel and colleagues (March 9, p 874)1 do not mention vulnerabilities existing in the current system used for recognition and investigation of food poisoning outbreaks. While researching outbreak investigation techniques in different cities and counties in New York State, I identified several issues that might compound the investigation of an intentional or unintentional food poisoning outbreak. The investigation of an outbreak depends on its detection, and under the current system, there are difficulties associated with detection of outbreaks. Clinicians are poor reporters of foodpoisoning cases, especially when patients are examined in hospital accident and emergency rooms. Merely providing clinicians with a list of Health Department officials, as Sobel and colleagues suggest, will not improve reporting rates, since various studies have shown that there are many reasons why clinicians do not report. These include unawareness of statutory obligations,2 concerns of violating doctor-patient privilege,3 and a lack of understanding of the purpose of notification.4 Furthermore, food poisoning cases are reported to different divisions in the
THE LANCET • Vol 360 • July 20, 2002 • www.thelancet.com
same health department; it is not uncommon for the communicable disease programme to receive information about confirmed cases from laboratories or medical professionals, whereas the food safety programme gathers information from the public and other agencies. There is no central database that collates this information. Consequently, even if there are epidemiological commonalities between cases they will not come to light because the information is inadequately shared between the different divisions. In fact, information sharing is an issue that also arises when local officials have to work with federal agencies during investigations. Indeed, the involvement of federal agencies during investigations is fraught with difficulties. There is substantial jurisdictional overlap between products regulated by federal agencies. For example, closed meat sandwiches are regulated by the US Food and Drug Administration, whereas open meat sandwiches are regulated by the US Department of Agriculture.5 Consequently, it can be challenging for local officials to correctly identify the agency in charge. Moreover, bureaucratically run public-health organisations may abdicate responsibility when jurisdictional responsibility is unclear. Unfortunately, even when the correct agency is approached they seem to hesitate to get involved unless there is conclusive evidence to prove that the food in question was the cause of the illness. This type of evidence is unavailable in most investigations. Therefore, trace-back investigations by federal agencies to identify the source of the food may not be done because of lack of evidence. An intentionally or unintentionally contaminated food source can, therefore, continue unabated. Protocols and simulated exercises do not obviate the weaknesses inherent in the system; most of which are solvable. Detection of outbreaks and the thoroughness of investigations needs to be improved. Azarmeen Jamasji Department of Public Health and Policy, London School of Hygiene and Tropical Medicine, Health Services Research Unit, London WC1E 7HT, UK (e-mail: [email protected]) 1
2
3 4
Sobel J, Khan AS, Swerdlow DL. Threat of biological terrorist attack on the US food supply: the CDC perspective. Lancet 2002; 359: 874–80. Durrheim DN, Thomas J. General practice awareness of notifiable infectious diseases. Public Health 1994; 108: 273–78. Hume J. On reports and rapport from VD control. Am J Public Health 1980; 70: 164–66. Voss S. How much do doctors know about the notification of infectious diseases? BMJ 1992; 304: 755.
261
For personal use. Only reproduce with permission from The Lancet Publishing Group.