Click for next page ( 278


The National Academies | 500 Fifth St. N.W. | Washington, D.C. 20001
Copyright © National Academy of Sciences. All rights reserved.
Terms of Use and Privacy Statement



Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.

Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.

OCR for page 277
Appendix B Surveillance and Response of Select Zoonotic Disease Outbreaks WILDLIFE TRADE AND THE HUMAN MONKEYPOX OUTBREAK IN THE UNITED STATES Multistate Epidemiological Investigation The first U.S. outbreak of human monkeypox was reported in May 2003 and initially included cases in Wisconsin, Indiana, and Illinois. By the end of the outbreak in June 2003, there were reports of cases in Missouri, Kansas, and Ohio (CDC, 2003a). As of July 31, 2003, there were 72 re- ported cases, of which 37 were laboratory confirmed (CDC, 2003b). Epi- demiological and trace-back investigation by local, state, and federal public health authorities found that patients acquired the disease from prairie dogs in contact with human monkeypox-infected African rodents (CDC, 2003b). These prairie dogs were housed together with infected African rodents in an Illinois wholesale pet store. Approximately 200 prairie dogs were in this facility and possibly exposed to human monkeypox in the period between when the Illinois animal distributor purchased the African rodents and the first reported human case of human monkeypox. A Texan animal distribu- tor legally imported the infected rodents (762 rodents that included rope squirrels, tree squirrels, Gambian giant rats, brush-tailed porcupines, dor- mice, and striped mice) from Accra, Ghana (CDC, 2003a). These rodents were not screened for disease before or after they entered the United States. Of this shipment, 23 percent of the imported rodents could not be traced beyond the port of entry because records were not available. Before labo- ratory confirmation, trace-forward investigations suspected these rodents 

OCR for page 277
 GLOBAL SURVEILLANCE AND RESPONSE TO zOONOTIC DISEASES were the source of human monkeypox. This investigation determined that no other U.S. animals besides prairie dogs were infected with human mon- keypox (CDC, 2003b). Finally, clinical studies concluded that respiratory and direct mucocutaneous exposures were important routes of transmis- sions between infected prairie dogs and humans (Guarner et al., 2004). CDC and FDA Restrictions of Rodents from Africa On June 11, 2003, the Centers for Disease Control and Prevention (CDC) and Food and Drug Administration (FDA) jointly issued an order pursuant to 42 C.F.R. 70.2 and 21 C.F.R. 120.30, respectively, to restrict the “transportation or offering for transportation in interstate commerce, or the sale, offering for sale, or offering for any other type of commercial or public distribution, including the release into the environment of” prairie dogs, tree squirrels, rope squirrels, Gambian giant rats, dormice, brush-tailed porcupines, and striped mice (CDC, 2003a; FDA, 2008). In addition, pursuant to 42 C.F.R. 71.32(b), CDC implemented an immediate embargo on the importation of all rodents from Africa. Because the ac- tions taken by state health authorities were insufficient to prevent the spread of human monkeypox, CDC and FDA issued an interim final rule (42 C.F.R. 71.56 and 21 C.F.R. 1240.63 respectively) under section 361 of the Public Health Service (PHS) Act that was intended to prevent future introduction, establishment, and spread of the human monkeypox virus in the United States. Based on risk-assessment of the further transmission of the human monkeypox virus, FDA removed its regulation in 21 C.F.R. 1240.63 in 2008 and concluded that CDC’s interim final rule and routine state disease surveillance and preventive measures were sufficient to pre- vent new human and animal cases of human monkeypox. Under section 368(a) of the PHS Act, any person who violates a regulation prescribed under the Act may be punished by imprisonment for up to 1 year or fined up to $100,000 per violation if death has not resulted from the violation or up to $250,000 per violation if death has resulted. Organizations may be fined up to $200,000 per violation not resulting in death and $500,000 per violation resulting in death (FDA, 2008). Reemergence of Human Monkeypox in Africa The virus that causes human monkeypox was first isolated in 1958 from monkeys and recognized as a new virus of the genus Orthopoxvirus (same genus as the smallpox virus although different epidemiologically and biologically) (Guarner et al., 2004). Human monkeypox, however, was first identified in humans in 1970 in the tropical areas of the Democratic Repub- lic of the Congo (DRC) (Breman, 2000; CDC, 2003a). The first outbreaks

OCR for page 277
 APPENDIX B of human monkeypox occurred in the period of 1970–1980 in the DRC, Côte d’Ivoire, Liberia, Nigeria, and Sierra Leone. Active disease surveillance was implemented with the assistance of the World Health Organization (WHO) in 1981–1986 in the DRC, where most of the human cases during this period occurred. Reporting of human monkeypox decreased, and after 1992 no new cases were reported to WHO. Failure to maintain disease surveillance of human monkeypox contributed to the reemergence of the disease in the DRC in 1996. Epidemiological and laboratory investigation of the DRC outbreak concluded that the disease was mild but highly trans- missible (Heymann et al., 1998). UK GOVERNMENT REGULATORY RESPONSE TO CONTROL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE)1 In 1986, when BSE was identified as a new disease, the Ministry of Agriculture, Fisheries and Food (MAFF) was the government agency re- sponsible for overseeing state veterinary services under the State Veterinary Service for Great Britain, composed of the Veterinary Investigation Ser- vice (VI Service), the Veterinary Field Service, and the Central Veterinary Laboratory (CVL). The VI Service implemented surveillance and provided expert advice for veterinary surgeons in private practice about unknown animal diseases. Employees of the VI Service reported to the assistant chief veterinarian and the chief veterinary officer at MAFF. MAFF and its agencies, prior to the identification of BSE, relied on a passive surveillance system for the identification of new diseases in animals. The surveillance of nonnotifiable diseases was based on the ob- servations of an astute farmer and veterinarian, who would voluntarily notify one of the many Veterinary Investigation Centers (VICs) of the VI Service. December 22, 1984—David Bee, a local private veterinarian, was called to examine Cow 133, owned by Peter Stent of Pitsham Farm in Sussex. Cow 133 developed a head tremor and a lack of coordination before dying on February 11, 1985. Bee sought assistance from J. M. Watkin-Jones, a vet- erinarian at the Winchester VIC, one of the branches of the VI Service. September 13, 1985—Carol Richardson, the pathologist on duty at the CVL, received samples of brain, spinal cord, and kidney of Cow 142 and examined them. Cow 142 was also owned by Stent and was showing ner- vous clinical signs similar to Cow 133. Richardson shared the sample with her colleagues at the CVL Pathology Department. Initially, the pathologi- cal examination suggested that the cause of the disease was not acute, but chronic bacteremia or endotoxemia. 1 The BSE Inquiry (2000).

OCR for page 277
0 GLOBAL SURVEILLANCE AND RESPONSE TO zOONOTIC DISEASES April 1985—Colin Whitaker, a private veterinarian, was called to Plurenden Manor Farm in Kent to look at a cow. He sent the cow to the University of Bristol Veterinary School at Langford, and postmortem examination showed “progressive nervous signs, hyperesthesia, tremors, mania and hind leg ataxia.” November 1986—Whitaker consulted Dr. Carl Johnson, veterinary officer of the Wye VIC, who referred the brains of the three animals to the CVL in November and December 1986. December 11, 1986—The CVL also received brain samples from a cow that was referred by Langford VIC, in Bristol. In December 1986, after the identification of BSE as a novel disease by CVL scientists, Dr. Watson, CVL director, informed William Rees, chief veterinary officer at MAFF, about BSE. In June 1987, new knowledge regarding the pathology and epidemiology of the disease led to the notification of this new disease to other ministers and government officials. After the preponderance of the evidence at the time regarding the risks posed by this novel disease to hu- man health, the government implemented a series of regulations aimed at the animal feed and rendering industry as well as slaughterhouses. Because it was initially understood that BSE was spread through ani- mal feed, in June 1988, the Bovine Spongiform Encephalopathy Order 1988 introduced a ban of ruminant feed in addition to the compulsory notification of BSE. The Order, which came into effect on July 18 and only applied to Great Britain, required farmers or their veterinarians to notify the local Divisional Veterinary Officer if they suspected an animal was affected by BSE. At this point, MAFF would send one of its own veterinarians to investigate. The ruminant feed ban included the follow- ing provisions: (1) No person shall knowingly sell or supply for feeding to animals any feedstuff in which he knows or has reason to suspect any animal protein has been incorporated. (2) No person shall feed to an animal any feedstuff in which he knows or has reason to suspect that any animal protein has been incorporated. On August 8, 1988, two further Orders came into effect: The Bovine Spongiform Encephalopathy (Amendment) Order 1988 and The Bovine Spongiform Encephalopathy Compensation Order 1988. They introduced a policy of compulsory slaughter of BSE-infected animals and payment of compensation to the owner of the slaughtered animal. On November 13, 1989, the Bovine Offal (Prohibition) Regulations 1989 came into effect in England and Wales. This regulation prohibited

OCR for page 277
 APPENDIX B the use of specified bovine offal (SBO) in the preparation of food for hu- man consumption after findings showed that particular cattle organs were most likely to carry the infective agent. SBO included the brain, spinal cord, thymus, spleen, tonsils, and intestines from a bovine animal more than 6 months of age. One of the unintended consequences of this ban was that renderers (rendering is the process of converting animal byproducts into more useful materials, e.g., purifying fatty tissue into lard or tallow) demanded that mechanically recovered bovine meat (MRM) should not contain SBO, and thus no longer welcomed cow heads containing the brain. As a result, a practice rapidly developed at many slaughterhouses of split- ting the skull and removing the brain. This practice gave rise to problems of contamination. Later on, review of the SBO ban revealed a concern about the risk that slaughterhouse practices would result in the contamination of MRM. MAFF officials assumed that the regulations up to 1989 would have reduced the scale of infection to a fraction of that at the height of the epidemic. However, many more animals born after the ban (BAB) were diag- nosed with BSE, which showed proof of the limitation and problems in the implementation of the BSE legislation up to 1989. The first case of BSE in an animal born after the introduction of the ruminant feed ban was not confirmed until March 1991. By September 1992, the number of BABs had risen to 220. By September 1994, the total number of BABs had reached 12,860. It was concluded that BABs had been fed contaminated feed. Based on the finding, more aggressive regulatory measures followed in the period 1994–1996 to prevent the spread of the disease and to protect human health. The UK BSE epidemic forced changes in different sectors of the animal and food production industry. First, regulations of the rendering industry changed the rendering processes, and, as a result of BSE, meat and bone meal is no longer used in the United Kingdom in animal feed or as fertilizer. Second, the introduction of regulations of the animal feed industry affected the industry but was an essential part of control of the disease. Third, it was considered essential that slaughterhouses separated SBO from those parts of the carcass that were going to enter the human food chain. All these in- terventions underscore that the risk of disease or contamination was in the processing of animal materials, which put humans at risk at many different points of this process.

OCR for page 277
 GLOBAL SURVEILLANCE AND RESPONSE TO zOONOTIC DISEASES February 23, 2003: CDC February 27, 2003: and WHO experts arrive in Chinese Ministry of Health Beijing. Chinese authorities declares the epidemic is November 16, 2002: First do not authorize the team of contained. Government case of SARS is recorded experts to travel to officials in Beijing order that in Foshan, Guangdong Guangdong Province and information about the Province, China. Chinese limit their access to official disease spread should not authorities initially data. The active efforts of be disclosed, treating this characterize the first SARS government officials in information as “top secret.” cases as an atypical Beijing to suppress Attempts to suppress pneumonia and suspect knowledge of the outbreak information fail when on that the causative agent is and the spread of the April 4, the health director an influenza virus. In disease within China of China’s Center for January 2003, Guangdong compromise the Disease Control apologizes health authorities release a international response, to China’s citizens about report with details of the especially the investigations the agency’s failure to outbreak, but official on the magnitude and risk inform the public about the confirmation to WHO is of an international spread of threat of this new disease. provided on February 14. the disease. February 21, 2002: The February 26, 2003: A man first known SARS case is with respiratory symptoms reported in Hong Kong. A who had stayed at the medical doctor who had Metropole Hotel in Hong treated patients in Kong before arriving in Guangzhou in the Vietnam is admitted to a Guangdong Province hospital in Hanoi. After an arrives at the Metropole increase in the reports to Hotel in Hong Kong where WHO about the spread of he infects 16 individuals. the atypical pneumonia in hospital personnel in Hong Kong and Vietnam, WHO sends an emergency alert to Global Outbreak Alert and Response Network partners on March 12. FIGURE B-1 National and international response to the SARS outbreak.

OCR for page 277
 APPENDIX B March 15, 2003: WHO issues Global Travel Advisory. Before the identification of the April 3, 2003: WHO expert causative agent, the virus team finally arrives in spreads within 6 months to Guangdong Province. The 30 countries and next day, U.S. President administrative regions. The George W. Bush signs virus transmission along executive order adding five major airline routes by SARS to the list of the symptomatic individuals quarantinable traveling from Hong Kong to communicable diseases, Beijing, Hanoi, Singapore, which provides CDC July 5, 2003: WHO Taiwan, and Toronto with legal authority to announces the global accelerates the global implement isolation and containment of the SARS spread of SARS. quarantine measures. outbreak. March 27, 2003: WHO April 16, 2003: WHO issues recommendation of laboratory network exit screening of announces conclusive passengers at airports. identification of new coronavirus as the causative agent for SARS. The Chinese government increases transparency through the release of number of cases in each Province, in addition to daily updates. Moreover, based on media reports, more than 120 officials were dismissed, including the health minister and Beijing’s mayor, or penalized for ineffective response to the outbreak.

OCR for page 277
 GLOBAL SURVEILLANCE AND RESPONSE TO zOONOTIC DISEASES HIGHLY PATHOGENIC AVIAN INFLUENZA H5N1 SURVEILLANCE IN HONG KONG AND VIETNAM H5N1 Virus Evolution Highly pathogenic avian influenza (HPAI) H5N1 virus is the causative agent for millions of bird deaths in Southeast Asia, the Middle East, Eu- rope, and Africa. The natural reservoir of the influenza type A virus is wild waterfowl, but the virus can also infect domestic poultry and humans and cause illness and death, thus the high pathogenicity of the virus (Nguyen et al., 2005). Virus typing and serological identification tests have indicated that different strains of type A influenza H5N1 are responsible for illness and death in humans in Southeast Asia since the Hong Kong outbreak in 1997 (Wan et al., 2008). This outbreak was characterized by a 10 percent incidence of HPAI H5N1 infection in live-bird market poultry workers exposed to infected domestic birds housed in close contact with wild wa- terfowl (Nguyen et al., 2005). After the Hong Kong outbreak, the virus spread to other countries in the region more likely through the poultry trade. Although the H5N1 virus has reassorted many times, all these viruses carry the same H5 hemagglutinin (HA) gene, which has a central role in antigenic drift. In Vietnam, isolation of the H5N1 virus shows six different HA clades, thus suggesting that the virus has been introduced at least six times since the first isolation in poultry in 2001 (Wan et al., 2008). Response to HPAI H5N1 Outbreak in Hong Kong In 1997, Hong Kong health authorities quickly instituted strong con- trol measures in poultry to minimize or stop human exposures (Webster, 2004). These measures included slaughter of 1.6 million chickens present in wholesale facilities or vendors within Hong Kong; banning importation of chickens from neighboring areas; instituting serological monitoring of chickens in Hong Kong; marketing chickens separately from other avian species; separating chickens and ducks for transport to market; slaughtering chickens and ducks separately; changing the operation and management of the live market system such that aquatic birds were no longer housed and sold in Hong Kong live bird markets, rather they were made available for sale only as killed, chilled poultry; serologically screening all poultry imported for sale in Hong Kong for avian influenza virus H5 subtype anti- body prior to release for sale; and instituting measures to improve hygiene in the markets. Further interventions were instituted that included estab- lishing surveillance in live poultry markets and in poultry at the Chinese border at which each arriving flock was quarantined, tested, and held for 2 days, flocks with one or more sick birds were rejected, and clean flocks

OCR for page 277
 APPENDIX B were moved to a central wholesale warehouse and held for 2 or more days. Culling was carried out on an ongoing basis as necessary; monthly rest days in live bird markets were instituted where unsold poultry in retail markets were killed, markets were left empty a whole day, cleaned, and restocked with fresh poultry the next day; and birds were vaccinated in outbreak situations. Transmission of the virus and further outbreaks in poultry were controlled and stopped. During 1998–2003, isolated outbreaks of HPAI H5N1 in poultry oc- curred in Southeast Asia; however, it was not until mid-2003, when more widespread outbreaks in poultry occurred in South Korea. There were significant delays in international reporting, and weaker response measures were instituted and the virus began to spread across Southeast Asia. Addi- tional outbreaks in poultry and human cases of HPAI were next identified in Vietnam in 2003. HPAI H5N1 Outbreaks in Humans and Animals in Vietnam HPAI infection in humans was first officially reported in Vietnam in January 2004; subsequently the country has endured six waves of epi- zootics of HPAI H5N1 in poultry (Vu, 2009). In 2003–2004, two waves of outbreaks in poultry affected many provinces (56 provinces reported outbreaks during the first wave and 17 provinces during the second wave), which resulted in the death by infection or culling of more than 44 mil- lion birds (Sims, 2007; Vu, 2009). During the third wave from December 2004 to April 2005, outbreaks were reported in 36 provinces, with about 2 million birds killed. At this time, the government implemented a pilot vaccination campaign and was recommending a nationwide vaccination (Vu, 2009). During the fourth wave from October to December 2005, 21 provinces reported outbreaks in poultry, which resulted in a loss of 4 mil- lion birds. In 2006, the virus activity was low mainly due to mass vaccina- tion of poultry in the previous year; however, new reassorted viruses were still circulating at low levels (Wan et al., 2008). From December 2006 to November 2007, the reemergence of virus was reported in poultry in more than 20 provinces and resulted in a loss of 270,000 birds. Recent reports indicate that a sixth wave of outbreaks occurred from December 2007 to March 2008 (Vu, 2009). In March 2009, the government reported eight outbreaks in six more provinces. Vaccination of Poultry in 2005 In October 6, 2005, the government of Vietnam launched the vaccina- tion campaign nationwide (Vu, 2009). The goal of vaccination was to re- duce the number of susceptible poultry, raise the immunological resistance

OCR for page 277
 GLOBAL SURVEILLANCE AND RESPONSE TO zOONOTIC DISEASES to virus, and reduce the amount of the virus that immune-infected poultry can excrete (Sims, 2007). In mid-2005, the government also introduced a number of control measures such as banning of duck breeding, public awareness campaigns, and the closure of urban markets in addition to restricting culling to known infected flocks in order to reduce the risk of infection to HPAI H5N1 viruses (Van Nam, 2007). The next year, in 2006, scientists suggested that the lower activity of virus was due to vaccination. Postvaccination disease surveillance provided evidence that the mass vac- cination program and other control measures were successful in control- ling transmission to humans, as there were no reported cases of disease in humans in 2006. On the other hand, vaccination activities resulted in a shift to passive disease surveillance of the virus, which assumed the eradication of the virus in Vietnam and bordering countries. However, the emergence of the virus in 2007 and later years demonstrates the systematic failure to detect the new variants circulating in Vietnam, although at lower levels, previous to the 2007 outbreak. Although vaccination was important in reducing the virus genetic reservoir, the experience in Vietnam demonstrates that strengthening disease surveillance in poultry is an essential component of the strategy to be able to prevent and control the introduction of new HPAI H5N1 strains into the country (Wan et al., 2008). Response Measures and Impacts on Human and Animal Morbidity and Mortality Although Vietnam is one of the countries most affected by HPAI H5N1, the response measures have been successful in controling new infections in poultry and preventing transmission to humans. Additionally, there was a cost benefit of implementing vaccination in poultry versus mass culling of poultry. However, the World Organization for Animal Health has recently emphasized the need for an exit strategy in places where vaccination is be- ing used as a control measure that have been able to improve veterinary services and biosecurity measures (OIE, 2009). Some experts believe eradi- cation of HPAI H5N1 would be difficult to achieve and thus many countries will continue to use vaccination for many years (Sims, 2007). This means that a mass vaccination program may be unsustainable, especially due to the high costs and the limited number of field staff as in the case of Viet- nam. However, Vietnam has taken steps to review their current vaccination policies and explore the option of more targeted vaccination of poultry. It has also recognized the importance of postvaccination disease surveil- lance, especially in monitoring the effects of vaccination on emergence of virus variants. As of July 1, 2009, 436 human cases of HPAI H5N1 and 262 deaths have been reported from 15 countries (WHO, 2009a). Despite further surveillance and response efforts instituted in poultry by human

OCR for page 277
 APPENDIX B and health authorities of affected countries, poultry outbreaks and human cases continue to occur. WEST NILE VIRUS OUTBREAK IN NEW YORK CITY2 West Nile virus (WNV) first appeared in birds around mid-June of 1999 when veterinarians at Bayside veterinary clinic in the Flushing neigh- borhood of Queens identified neurological disorders in crows. By mid- August, dead crows were sent to the state Department of Environmental Conservation (DEC), which had jurisdiction over wildlife, for necropsy examinations. Parallel to the bird deaths in Queens, numerous crows and other birds were dying in and around the Bronx Zoo, prompting veterinar- ians at the zoo to send dead birds to the DEC for examination. The chief pathologist at the Bronx Zoo, however, believed that the DEC wildlife pathologist’s determination of the cause of deaths of bird specimens from Queens was not correct since it was not based on histopathology, and therefore decided to initiate her own necropsy on zoo birds, which showed possible encephalitis. Only days later, a separate epidemiological investiga- tion of suspected human cases of viral encephalitis was initiated by the New York City Department of Health (DOH) Bureau of Communicable Disease. An initial investigation by city public health officials revealed a cluster of human cases with the same symptoms; subsequently the city DOH noti- fied the state health department and CDC for additional assistance. After conversations with CDC and the state health department, city health of- ficials sent patient specimens to the state virology laboratory for examina- tion. Field investigations revealed the presence of Culex pipiens mosquito breeding sites and larvae in many of the patients’ homes and in the Queens neighborhood, reinforcing the theory of viral encephalitis. In early September 1999, public health and veterinary authorities con- tinued to conduct two separate investigations. The human outbreak inves- tigations involved multiple laboratory facilities (state and federal), public health officials at the local, state, and federal level, and city government officials. On the animal side, mainly state wildlife scientists and Bronx Zoo veterinarians conducted investigations of the deaths in birds. On September 2, 1999, state laboratory tests were positive for a flavivirus; specifically the test showed a strong serological reaction to St. Louis Encephalitis (SLE) virus, results that were confirmed the next day by the CDC Division of Vector-Borne Infectious Disease laboratory in Fort Collins, Colorado. The same day, city officials announced CDC’s confirmation of an SLE outbreak in New York City and the decision to initiate mosquito control activities. At this point of the human outbreak investigation, communications 2 GAO (2000); Fine and Layton (2001); Scott (2002).

OCR for page 277
 GLOBAL SURVEILLANCE AND RESPONSE TO zOONOTIC DISEASES between federal, state, and local public health officials were consistent. However, key public health officials were not aware of the early events in birds, especially the neurological disorders identified by local veterinarians and the increased deaths of birds in the Bronx Zoo. City public health of- ficials first became aware of the bird deaths after news report on the SLE outbreak resulted in calls to the bureau hotline. On the other hand, after lis- tening to news reports of an SLE outbreak in Queens, the Bronx Zoo chief pathologist began to suspect a possible link between the bird deaths and human cases of SLE and decided to send specimens directly to the National Veterinary Services Laboratory (NVSL), a U.S. Department of Agriculture (USDA) reference laboratory located in Ames, Iowa. After multiple efforts by the Bronx Zoo chief pathologist to send zoo specimens to the CDC laboratory in Fort Collins, the laboratory scientists accepted to examine the bird specimens from the Bronx Zoo. Still the pri- ority of the CDC laboratory in Fort Collins was to not only process thou- sands of samples from hospitals but also confirm the initial SLE diagnosis through lengthy viral neutralization tests, which required isolation of the virus and polymerase chain reaction (PCR). Although some of these tests reveal questions on the accuracy of the diagnostic tools, the CDC labora- tory did not reconsider the SLE diagnosis until the NVSL notified them that they had successfully isolated a flavivirus from one of the Bronx speci- mens and other specimens received from the state DEC. At the same time, independent analyses of human specimens by the New York State (NYS) DOH virology laboratory resulted in a negative PCR reaction for SLE. In addition, in a meeting between state and city health officials and CDC the participants raised questions about the accuracy of the results from serologic tests performed on specimens of suspected and confirmed cases. The issue of test accuracy was again raised in a meeting of an independent working group studying encephalitis from unknown origin in which NYS health officials and CDC participated. By the end of the meeting, it was agreed that the NYS DOH would share specimens of human brain tissue with Dr. Ian Lipkin, an academic researcher from University of California at Irvine attending the meeting. Around the same time, independent efforts by the Bronx Zoo chief pathologist resulted in the involvement of the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID). Parallel to the independent investigations by Dr. Lipkin and USAMRIID, a Fort Collins scientist began PCR testing on human specimens after PCR tests on bird specimens received from NVSL resulted in high reactivity to West Nile virus. Almost simultaneously to the CDC laboratory’s confirma- tion of WNV in birds, Dr. Lipkin informed the NYS DOH that the identity of the flavivirus could be either WNV or Kunjin virus. Finally, on September 27, 1999, CDC announced that the human outbreaks in New York City were due to West Nile virus.

OCR for page 277
 APPENDIX B Although the delay in diagnosis of WNV did not have an effect on the response to the human outbreak, especially since mosquito control activi- ties had been implemented, some experts suggest that the failure of public health and veterinary authorities to recognize the unexpected increase of neurological disorders and deaths in birds as potential index cases of a new outbreak in that animal population lead to the establishment of WNV in the area and ultimately its spread. Moreover, the need for laboratory facilities able to test for animal diseases and the insistence of the Bronx Zoo pathologist in the linkage between the deaths in birds and the SLE outbreak resulted in the convergence of these parallel investigations. The lack of communication linkages between the animal and human health sec- tors at the time was an additional barrier. After the WNV outbreak, many steps have been taken to close this gap and to integrate animal and human health surveillance in New York City. In December 2001, the New York City Health Code added to the Communicable Disease Control Section new animal disease reporting requirements, which established new procedures for reporting and controling of animal diseases that are transmittable to humans or any animal disease of public health importance. In addition, an invitation to join the Health Alert Network (HAN), an e-mail-based alert system, was extended to veterinarians and other animal or wildlife specialists who wish to receive veterinary alerts from the New York City DOH. Furthermore, the NYS DOH has sponsored several meetings, jointly with the Veterinary Medical Association, on animal disease surveillance as part of the efforts to enhance relations with the animal health community (practicing veterinarians, wildlife specialists, zoo veterinarians, agriculture agencies, etc.). INFLUENZA A(H1N1) PANDEMIC, 2009 In the United States, seasonal influenza infections result in high mor- bidity and mortality in humans, resulting in approximately 36,000 excess deaths annually. For the most part, these deaths occur in older and younger people having less developed or compromised immune systems. Pandemic influenza events have occurred every 40–50 years over the past several hundred years. During the 20th century, pandemic influenza has occurred in 1918, 1957, and 1968. The 1918 influenza pandemic caused extremely high rates of morbidity and mortality, especially in healthy adults between 20–40 years of age. Since 2003, continuing human influenza infections from HPAI H5N1 have caused great concern over the potential of this virus to result in the next pandemic. With the high mortality rate observed among infected patients, human health officials have been worried that should this virus become easily transmissible, a pandemic with this virus would also be accompanied by severe illness, morbidity, and mortality.

OCR for page 277
0 GLOBAL SURVEILLANCE AND RESPONSE TO zOONOTIC DISEASES Detection and Identification of Risk Factors In March and April 2009, influenza caused by a novel influenza A(H1N1) virus was detected in human populations in Mexico and the United States (Brownstein et al., 2009). Early results from phylogenetic studies aimed at determining the genetic composition of the virus (Smith et al., 2009) found that the virus is derived from combinations of swine viruses that have been circulating over the past 20 years. Because of this, the virus was quickly referred to as the “swine flu” by human health authorities and the media, even though to date, there has been only one known occur- rence of an outbreak caused by this virus in pigs. The specifics of when and how this virus emerged, in what populations, how long its circulation has gone undetected, as well as the source of exposure for the outbreak in pigs remain the focus of ongoing investigations. This outbreak highlights a need for more strategic and systematic surveillance of influenza in pigs. Response As the new virus was detected and began to spread, health officials in Mexico quickly decided to close schools and take other actions to limit opportunities for large groups of people to come together where person- to-person spread could easily occur. Health officials in Mexico and the United States quickly launched outbreak investigations to learn more about the virus, routes of and risk factors for transmission, and the potential for severe morbidity and mortality. In the United States, local health authorities based decisions for school closures on information that CDC was provid- ing in daily updates. As increased numbers of cases were detected, it was determined that this new virus was spread the same way that seasonal influenza is transmitted, and although morbidity rates among the exposed were high, mortality was relatively low. Unfortunately, the name used to refer to the disease as “swine flu” was not based on actual detection of the virus in pigs or from human cases resulting from contact with sick pigs. And despite a joint press release from OIE/FAO and WHO, many people quickly associated wrongly that they could become infected by eating pork. The negative impact of the inappropriate naming of the virus on the pork industry was significant and is described below. However, once this impact became known to human health authorities, they quickly responding by changing the name of the virus and infection to novel influenza A(H1N1) 2009, which was greatly appreciated by animal health authorities and the swine industry. The media, however, continued to inappropriately refer to the virus as the “swine flu,” causing public confusion about the actual risk factors for exposure and therefore leading policymakers to base their responses on factors other than evidence. For example, despite the lack of

OCR for page 277
 APPENDIX B evidence of any swine infections, Egypt responded to the outbreak by cull- ing more than 250,000 pigs in the country. Outcome and Impact Human infections are being monitored globally. On June 11, 2009, WHO declared an influenza pandemic caused by this virus. As of July 6, 2009, pandemic A(H1N1) 2009 virus had been officially reported in 94,512 human cases, caused 429 deaths, and had been found in 99 countries, terri- tories, and areas (WHO, 2009b). Those under the age of 50 years appeared to be at increased risk of infection. Work has begun to develop a vaccine that would be available by the 2009–2010 winter season in North America. By incorrectly naming a virus transmitted between humans as swine flu, this has resulted in trade bans and reductions in pork consumption, ultimately causing losses of approximately $28 million per week to the swine indus- try (Snelson, 2009; TVMDL, 2009). Given the importance of encouraging disease surveillance, reporting, and response by the livestock industry in an effective emerging zoonotic disease surveillance system, these losses based on misinformation are unfortunate and serve to discourage future coopera- tion in an integrated surveillance and response effort. The accurate naming of influenza viruses is significant in reporting and response and critical in effectively conveying information to protect public health. REFERENCES Breman, J. G. 2000. Monkeypox: An emerging infection for humans. In Emerging infections , edited by M. Scheld, W. A. Craig, and J. M. Hughes. Washington, DC: ASM Press. Brownstein, J. S., C. C. Freifeld, and L. C. Madoff. 2009. Influenza A (H1N1) virus, 2009— Online monitoring. N Engl J Med 360(21):2156. CDC (Centers for Disease Control and Prevention). 2003a. Multistate outbreak of monkeypox— Illinois, Indiana, and Wisconsin, 2003. MMWR 52(23):537–540. CDC. 2003b. Update: Multistate outbreak of monkeypox—Illinois, Indiana, Kansas, Mis- souri, Ohio, and Wisconsin, 2003. MMWR 52(27):642–646. FDA (Food and Drug Administration). 2008. Control of communicable diseases; restrictions on African rodents, prairie dogs, and certain other animals, final rule. Federal Register 73(174):51912–51919. Fine, A., and M. Layton. 2001. Lessons from the West Nile viral encephalitis outbreak in New York City, 1999: Implications for bioterrorism preparedness. Clin Infect Dis 32(2):277–282. GAO (U.S. General Accountability Office). 2000. West Nile virus outbreak: Lessons for public health preparedness. Washington, DC: U.S. Government Printing Office. GAO. 2004. Emerging infectious diseases: International Asian SARS outbreak challenged na- tional and international responses. Washington, DC: U.S. Government Printing Office. Guarner, J., B. J. Johnson, C. D. Paddock, W. J. Shieh, C. S. Goldsmith, M. G. Reynolds, I. K. Damon, R. L. Regnery, and S. R. Zaki. 2004. Monkeypox transmission and pathogenesis in prairie dogs. Emerg Infect Dis 10(3):426–431.

OCR for page 277
 GLOBAL SURVEILLANCE AND RESPONSE TO zOONOTIC DISEASES Heymann, D. L., M. Szczeniowski, and K. Esteves. 1998. Re-emergence of monkeypox in Africa: A review of the past six years. Br Med Bull 54(3):693–702. Nguyen, D. C., T. M. Uyeki, S. Jadhao, T. Maines, M. Shaw, Y. Matsuoka, C. Smith, T. Rowe, X. Lu, H. Hall, X. Xu, A. Balish, A. Klimov, T. M. Tumpey, D. E. Swayne, L. P. Huynh, H. K. Nghiem, H. H. Nguyen, L. T. Hoang, N. J. Cox, and J. M. Katz. 2005. Isolation and characterization of avian influenza viruses, including highly pathogenic H5N1, from poultry in live bird markets in Hanoi, Vietnam, in 2001. J Virol 79(7):4201–4212. OIE (World Organization for Animal Health). 2009. Avian influenza and vaccination: What is the scientific recommendation?—The OIE repeats critical requisites for best use of vac- cination in birds and for a systematic exit strategy, OIE Press Release, March, 4. Price-Smith, A. T. 2009. Contagion and chaos: Disease ecology and national security in the era of globalization. Cambridge, Massachusetts: MIT Press. Scott, E. 2002. The West Nile virus outbreak in New York City (a): On the trail of a killer virus. Document C16-02-1645.0, Kennedy School of Government Case Program. Boston, MA: Harvard University. Sims, L. D. 2007. Lessons learned from Asian H5N1 outbreak control. Avian Diseases 50:174–181. Smith, G. J., D. Vijaykrishna, J. Bahl, S. J. Lycett, M. Worobey, O. G. Pybus, S. K. Ma, C. L. Cheung, J. Raghwani, S. Bhatt, J. S. Peiris, Y. Guan, and A. Rambaut. 2009. Origins and evolutionary genomics of the 2009 swine-origin H1N1 influenza A epidemic. Nature 459(7250):1122–1125. Snelson, H. 2009. HN update and economic impact. http://www.aasv.org/news/story.php ?id=3562 (accessed July 13, 2009). The BSE Inquiry. 2000. The BSE Inquiry: The inquiry into BSE and variant CJD in the United Kingdom. London, UK: Stationery Office. http://www.bseinquiry.gov.uk (accessed Janu- ary 14, 2009). TVMDL (Texas Veterinary Medical Diagnostics Laboratory). 2009. HN economic impact May , 00—Price and value impact since April . http://tvmdl.tamu.edu/content/ main/articles/h1n1/h1n1_impact.php (accessed July 13, 2009). Van Nam, H. 2007. Vaccination for control of HN avian influenza in Viet Nam. Presenta- tion, International Ministerial Conference on Avian and Pandemic Influenza, New Delhi, December 4–6. http://www.fao.org/docs/eims/upload//237239/ah706e.pdf (accessed Au- gust 11, 2009). Vu, T. 2009. The political economy of avian influenza response and control in Vietnam. Work- ing Paper 19. Brighton, UK: STEPS Centre. Wan, X. F., T. Nguyen, C. T. Davis, C. B. Smith, Z. M. Zhao, M. Carrel, K. Inui, H. T. Do, D. T. Mai, S. Jadhao, A. Balish, B. Shu, F. Luo, M. Emch, Y. Matsuoka, S. E. Lindstrom, N. J. Cox, C. V. Nguyen, A. Klimov, and R. O. Donis. 2008. Evolution of highly patho- genic H5N1 avian influenza viruses in Vietnam between 2001 and 2007. PLoS ONE 3(10):e3462. Webster, R. G. 2004. Wet markets—A continuing source of severe acute respiratory syndrome and influenza? Lancet 363(9404):234–236. WHO (World Health Organization). 2003a. Update —SARS: Chronology of a serial killer. http://www.who.int/csr/don/2003_07_04/en/ (accessed on October 17, 2008). WHO. 2003b. Consensus document on the epidemiology of severe acute respiratory syndrome (SARS). WHO/CDS/CSR/GAR/2003.11. Geneva, Switzerland: WHO. WHO. 2009a. Cumulative number of confirmed human cases of avian influenza A/(HN) reported to WHO. http://www.who.int/csr/disease/avian_influenza/country/cases_table_ 2009_07_01/en/index.html (accessed August 11, 2009). WHO. 2009b. Pandemic (HN) 00—Update . http://www.who.int/csr/don/2009_07_ 06/en/index.html (accessed July 22, 2009).