Showing papers on "Outbreak published in 2000"
Journal Article•
TL;DR: Current methods to detect FBDOs are improving, and several changes to improve the ease and timeliness of reporting FBDO data are occurring (e.g., a revised form to simplify FBDO reporting by state health departments and electronic reporting methods).
Abstract: Problem/condition Since 1973, CDC has maintained a collaborative surveillance program for collection and periodic reporting of data on the occurrence and causes of foodborne-disease outbreaks (FBDOs) in the United States. Reporting period covered This summary reviews data from January 1993 through December 1997. Description of system The Foodborne-Disease Outbreak Surveillance System reviews data concerning FBDOs, defined as the occurrence of two or more cases of a similar illness resulting from the ingestion of a common food. State and local public health departments have primary responsibility for identifying and investigating FBDOs. State, local, and territorial health departments use a standard form to report these outbreaks to CDC. Results During 1993-1997, a total of 2,751 outbreaks of foodborne disease were reported (489 in 1993, 653 in 1994, 628 in 1995, 477 in 1996, and 504 in 1997). These outbreaks caused a reported 86,058 persons to become ill. Among outbreaks for which the etiology was determined, bacterial pathogens caused the largest percentage of outbreaks (75%) and the largest percentage of cases (86%). Salmonella serotype Enteritidis accounted for the largest number of outbreaks, cases, and deaths; most of these outbreaks were attributed to eating eggs. Chemical agents caused 17% of outbreaks and 1% of cases; viruses, 6% of outbreaks and 8% of cases; and parasites, 2% of outbreaks and 5% of cases. Interpretation The annual number of FBDOs reported to CDC did not change substantially during this period or from previous years. During this reporting period, S. Enteritidis continued to be a major cause of illness and death. In addition, multistate outbreaks caused by contaminated produce and outbreaks caused by Escherichia coli O157:H7 remained prominent. Actions taken Current methods to detect FBDOs are improving, and several changes to improve the ease and timeliness of reporting FBDO data are occurring (e.g., a revised form to simplify FBDO reporting by state health departments and electronic reporting methods). State and local health departments continue to investigate and report FBDOs as part of efforts to better understand and define the epidemiology of foodborne disease in the United States. At the regional and national levels, surveillance data provide an indication of the etiologic agents, vehicles of transmission, and contributing factors associated with FBDOs and help direct public health actions to reduce illness and death caused by FBDOs.
1,810 citations
TL;DR: Control programmes, which imply allowing a low incidence of infection, are not an acceptable method for managing HPAI, but have been used during some outbreaks of MPAI.
Abstract: Highly pathogenic (HP) avian influenza (AI) (HPAI) is an extremely contagious, multi-organ systemic disease of poultry leading to high mortality, and caused by some H5 and H7 subtypes of type A influenza virus, family Orthomyxoviridae. However, most AI virus strains are mildly pathogenic (MP) and produce either subclinical infections or respiratory and/or reproductive diseases in a variety of domestic and wild bird species. Highly pathogenic avian influenza is a List A disease of the Office International des Epizooties, while MPAI is neither a List A nor List B disease. Eighteen outbreaks of HPAI have been documented since the identification of AI virus as the cause of fowl plague in 1955. Mildly pathogenic avian influenza viruses are maintained in wild aquatic bird reservoirs, occasionally crossing over to domestic poultry and causing outbreaks of mild disease. Highly pathogenic avian influenza viruses do not have a recognised wild bird reservoir, but can occasionally be isolated from wild birds during outbreaks in domestic poultry. Highly pathogenic avian influenza viruses have been documented to arise from MPAI viruses through mutations in the haemagglutinin surface protein. Prevention of exposure to the virus and eradication are the accepted methods for dealing with HPAI. Control programmes, which imply allowing a low incidence of infection, are not an acceptable method for managing HPAI, but have been used during some outbreaks of MPAI. The components of a strategy to deal with MPAI or HPAI include surveillance and diagnosis, biosecurity, education, quarantine and depopulation. Vaccination has been used in some control and eradication programmes for AI.
677 citations
TL;DR: Genotypes 1 and 2 were significantly more common in patients infected during the late-summer–autumn peak and in those with a history of foreign travel, and among the sporadic cases, there were distinct geographical and temporal variations in the distribution of the genotypes.
Abstract: Cryptosporidium present in 1,705 fecal samples from humans and 105 from livestock animals were analyzed by PCR-restriction fragment length polymorphism of the Cryptosporidium oocyst wall protein. Overall, genotype 1 (human exclusive type) was detected in 37.8% of the samples from humans, genotype 2 (broad host range) was detected in 61.5%, a third genotype designated genotype 3 (Cryptosporidium meleagridis) was detected in 0.3%, and both genotypes 1 and 2 were recovered from 0.4%. All samples from livestock yielded genotype 2. Among 469 patients infected during eight drinking water-related outbreaks, five outbreaks were predominantly due to genotype 1, and three were due to genotype 2. Fifty-four samples were collected from patients involved with five swimming pool-associated outbreaks: two outbreaks were due to genotype 1, one was due to genotype 2, and the remaining two involved both genotypes 1 and 2. Among 26 family outbreaks and 1 children's nursery outbreak (2 to 3 members per group), the same genotype was recovered from the different members of each outbreak: 13 were due to genotype 1, and 14 were due to genotype 2. In eighteen patients reporting contact with animals and/or farms, genotype 1 was recovered from one patient and genotype 2 was recovered from the remaining 17. Among the sporadic cases, there were distinct geographical and temporal variations in the distribution of the genotypes. The spring peak in cases was due to genotype 2. Genotype 1 was significantly more common in patients infected during the late-summer-autumn peak and in those with a history of foreign travel.
356 citations
TL;DR: The foodborne and waterborne outbreaks of cyclosporiasis that were documented from 1990 through 1999 are reviewed, highlighting the need for health care personnel to consider that seemingly isolated cases of infection could be part of widespread outbreaks and should be reported to public health officials.
Abstract: Cyclospora cayetanensis, a coccidian parasite that causes protracted, relapsing gastroenteritis, has a short recorded history. In retrospect, the first 3 documented human cases of Cyclospora infection were diagnosed in 1977 and 1978. However, not much was published about the organism until the 1990s. One of the surprises has been the fact that a parasite that likely requires days to weeks outside the host to become infectious has repeatedly caused foodborne outbreaks, including large multistate outbreaks in the United States and Canada. In this review, I discuss what has been learned about this enigmatic parasite since its discovery and what some of the remaining questions are. My focus is the foodborne and waterborne outbreaks of cyclosporiasis that were documented from 1990 through 1999. The occurrence of the outbreaks highlights the need for health care personnel to consider that seemingly isolated cases of infection could be part of widespread outbreaks and should be reported to public health officials. Health care personnel should also be aware that stool specimens examined for ova and parasites usually are not examined for Cyclospora unless such testing is specifically requested and that Cyclospora infection is treatable with trimethoprim-sulfamethoxazole.
301 citations
TL;DR: Direct, close contact with pigs was the primary source of human Nipah infection, but other sources, such as infected dogs and cats, cannot be excluded.
Abstract: P= .001 and were more likely than case-farm controls to perform activities requiring direct contact with pigs (86% vs. 50%, ). Only 8% of case patients reported no contact with pigs. P= .005 The outbreak stopped after pigs in the affected areas were slaughtered and buried. Direct, close contact with pigs was the primary source of human Nipah infection, but other sources, such as infected dogs and cats, cannot be excluded.
270 citations
26 May 2000
TL;DR: This surveillance summary probably underestimate the true incidence of waterborne disease associated with drinking water because not all WBDOs are recognized, investigated, and reported to CDC or EPA.
Abstract: Problem/condition Since 1971, CDC and the U.S. Environmental Protection Agency (EPA) have maintained a collaborative surveillance system for collecting and periodically reporting data relating to occurrences and causes of waterborne-disease outbreaks (WBDOs). Reporting period covered This summary includes data from January 1997 through December 1998 and a previously unreported outbreak in 1996. Description of the system The surveillance system includes data regarding outbreaks associated with drinking water and recreational water. State, territorial, and local public health departments are primarily responsible for detecting and investigating WBDOs and voluntarily reporting them to CDC on a standard form. Results During 1997-1998, a total of 13 states reported 17 outbreaks associated with drinking water. These outbreaks caused an estimated 2,038 persons to become ill. No deaths were reported. The microbe or chemical that caused the outbreak was identified for 12 (70.6%) of the 17 outbreaks; 15 (88.2%) were linked to groundwater sources. Thirty-two outbreaks from 18 states were attributed to recreational water exposure and affected an estimated 2,128 persons. Eighteen (56.3%) of the 32 were outbreaks of gastroenteritis, and 4 (12.5%) were single cases of primary amebic meningoencephalitis caused by Naegleria fowleri, all of which were fatal. The etiologic agent was identified for 29 (90.6%) of the 32 outbreaks, with one death associated with an Escherichia coli O157:H7 outbreak. Ten (55.6%) of the 18 gastroenteritis outbreaks were associated with treated pools or ornamental fountains. Of the eight outbreaks of dermatitis, seven (87.5%) were associated with hot tubs, pools, or springs. Interpretation Drinking water outbreaks associated with surface water decreased from 31.8% during 1995-1996 to 11.8% during 1997-1998. This reduction could be caused by efforts by the drinking water industry (e.g., Partnership for Safe Water), efforts by public health officials to improve drinking water quality, and improved water treatment after the implementation of EPA's Surface Water Treatment Rule. In contrast, the proportion of outbreaks associated with systems supplied by a groundwater source increased from 59.1% (i.e., 13) during 1995-1996 to 88.2% (i.e., 15) during 1997-1998. Outbreaks caused by parasites increased for both drinking and recreational water. All outbreaks of gastroenteritis attributed to parasites in recreational water were caused by Cryptosporidium, 90% occurred in treated water venues (e.g., swimming pools and decorative fountains), and fecal accidents were usually suspected. The data in this surveillance summary probably underestimate the true incidence of WBDOs because not all WBDOs are recognized, investigated, and reported to CDC or EPA. Actions taken To estimate the national prevalence of waterborne disease associated with drinking water, CDC and EPA are conducting a series of epidemiologic studies to better quantify the level of waterborne disease associated with drinking water in nonoutbreak conditions. The Information Collection Rule implemented by EPA in collaboration with the drinking water industry helped quantifythe level of pathogens in surface water. Efforts by CDC to address recreational water outbreaks have included meetings with the recreational water industry, focus groups to educate parents on prevention of waterborne disease transmission in recreational water settings, and publications with guidelines for parents and pool operators.
264 citations
TL;DR: Pneumonia was the commonest presentation in both groups and, in addition, eight patients (two deaths) presented with melioidosis encephalomyelitis, the commonmost cause of fatal community-acquired septicemic pneumonia.
260 citations
TL;DR: Characterisation of isolates showed them to be of clonal origin (ET-37) and closely related to other meningococci with an established propensity to cause disease clusters and a reappraisal of vaccination strategies for travellers is required.
257 citations
TL;DR: The authors describe the new disease and provide the epidemiological findings recorded among infected pigs, and the control programmes which were instituted to contain the virus in the national swine herd are outlined.
Abstract: Between late 1998 and 1999, the spread of a new disease of pigs, characterized by a pronounced respiratory and neurological syndrome, sometimes accompanied by the sudden death of sows and boars, was recorded in pig farms in peninsular Malaysia. The disease appeared to have a close association with an epidemic of viral encephalitis among workers on pig farms. A previously unrecognised paramyxovirus was later identified from this outbreak; this virus was related to, but distinct from, the Hendra virus discovered in Australia in 1994. The new virus was named 'Nipah' and was confirmed by molecular characterization to be the agent responsible for the disease in both humans and pigs. The name proposed for the new pig disease was 'porcine respiratory and neurological syndrome' (also known as 'porcine respiratory and encephalitis syndrome'), or, in peninsular Malaysia, 'barking pig syndrome'. The authors describe the new disease and provide the epidemiological findings recorded among infected pigs. In addition, the control programmes which were instituted to contain the virus in the national swine herd are outlined.
256 citations
Journal Article•
TL;DR: In this paper, the authors linked 29 cases of listeriosis to eating deli turkey meat and found that the Listeria isolates from these cases were indistinguishable by pulsed-field gel electrophoresis (PulseNet pattern numbers GX6A16.0014 by Asc1) and ribotyping.
Abstract: Since May 2000, 29 illnesses caused by a strain of Listeria monocytogenes (LM) have been identified in 10 states: New York (15 cases); Georgia (three); Connecticut, Ohio, and Michigan (two each); and California, Pennsylvania, Tennessee, Utah, and Wisconsin (one each). Dates of LM isolation ranged from May 17 through November 26 with 26 (90%) infections occurring since July 15. When subtyped, the LM isolates from these cases were indistinguishable by pulsed-field gel electrophoresis (PulseNet pattern numbers GX6A16.0014 by Asc1 and GX6A12.0017 by Apa1) and ribotyping (DUP-1053). This report summarizes the investigation, which linked these cases of listeriosis to eating deli turkey meat.
253 citations
TL;DR: The extent of environmental contamination that may occur during a large NLV outbreak is demonstrated for the first time in a large hotel in North-West England.
Abstract: A protracted outbreak of Norwalk-like virus (NLV)-associated gastroenteritis occurred in a large hotel in North-West England between January and May 1996. We investigated the pattern of environmental contamination with NLV in the hotel during and after the outbreak. In the ninth week, 144 environmental swabs taken from around the hotel were tested for NLV by nested RT-PCR. The sites were categorized according to the likelihood of direct contamination with vomit/faeces. The highest proportion of positive samples were detected in directly contaminated carpets, but amplicons were detected in sites above 1.5 m which are unlikely to have been contaminated directly. The trend in positivity of different sites paralleled the diminishing likelihood of direct contamination. A second environmental investigation of the same sites 5 months after the outbreak had finished were all negative by RT-PCR. This study demonstrates for the first time the extent of environmental contamination that may occur during a large NLV outbreak.
TL;DR: An investigation found the outbreak strain of listeriosis caused by Listeria monocytogenes serotype 3a in packaged butter served at the TCH and at the source dairy and recall of the product ended the outbreak.
Abstract: In February 1999, an outbreak of listeriosis caused by Listeria monocytogenes serotype 3a occurred in Finland. All isolates were identical. The outbreak strain was first isolated in 1997 in dairy butter. This dairy began delivery to a tertiary care hospital (TCH) in June 1998. From June 1998 to April 1999, 25 case patients were identified (20 with sepsis, 4 with meningitis, and 1 with abscess; 6 patients died). Patients with the outbreak strain were more likely to have been admitted to the TCH than were patients with other strains of L. monocytogenes (60% vs. 8%; odds ratio, 17.3; 95% confidence interval, 2.8-136.8). Case patients admitted to the TCH had been hospitalized longer before cultures tested positive than had matched controls (median, 31 vs. 10 days; P = .008). An investigation found the outbreak strain in packaged butter served at the TCH and at the source dairy. Recall of the product ended the outbreak.
TL;DR: In Germany, tracing of contact herds and clinical examination combined with carefully targeted virological testing of suspicious animals is likely to be the most important measure to immediately uncover secondary outbreaks of CSF.
TL;DR: Initial analysis of the HA gene from two USA sources indicates a virus related to swine and human influenza with no base insertion at the HA1‐HA2 cleavage junction which, at least in avian influenza A, characterises high virulence.
Abstract: Influenza A virus initiated worldwide epidemics (pandemics) in 1918, 1957, 1968 and 1977. A revised calculation of the 1918-1919 pandemic estimates that 40 million persons died and 500 million were infected. The mortalities in 1957 and 1968 were nearly 6 million. Biological and genetic characteristics of the causative agents of the more recent pandemics, have been well studied but little is known about the causative agent of the Great Pandemic in 1918. Genetic characterisation of the 1918 virus has been achieved by sourcing virus RNA from formalin fixed lung samples or by exhuming frozen victims of the outbreak from Arctic regions. Initial analysis of the HA gene from two USA sources indicates a virus related to swine and human influenza with no base insertion at the HA1-HA2 cleavage junction which, at least in avian influenza A, characterises high virulence. Important unanswered questions are whether the 1918 virus spread pantropically perhaps to include the brain and hence cause encephalitis including the later lethargic forms, or whether infection was confined to the respiratory tract. Re-examination of reports of respiratory disease in England and France in 1916-1917 may indicate a non-Spanish origin of the pandemic and a period of 2 years for the virus to be seeded worldwide. In contrast the other two pandemic viruses in 1957 and 1968 appeared to originate in Asia. New anti-neuraminidase drugs in conjunction with amantadine and novel developments with influenza vaccines would be expected to ameliorate the disease in a future pandemic.
TL;DR: Hantavirus cardiopulmonary syndrome, a rodent-borne zoonosis, has been endemic in the Americas for at least several decades and it is hypothesized that the 1991-1992 El Niño-southern oscillation caused increased precipitation that allowed an increase in rodent population densities, thereby increasing the possibility of transmission to humans.
Abstract: Hantavirus cardiopulmonary syndrome (HCPS), a rodent-borne zoonosis, has been endemic in the Americas for at least several decades. It is hypothesized that the 1991-1992 El Nino-southern oscillation (ENSO) caused increased precipitation that allowed an increase in rodent population densities, thereby increasing the possibility of transmission to humans. The result was a 1993-1994 outbreak of the disease in the Four Corners states of the southwestern United States. A second strong ENSO occurred in 1997-1998, after a period of considerable public education about the risks of hantavirus infection that began during the 1993-1994 outbreak. The caseload of HCPS increased 5-fold above baseline in the Four Corners states in 1998-1999. Regions that had received increased rainfall in 1998 were especially affected. A large majority of the 1998-1999 case patients reported indoor exposure to deer mice. Hantavirus outbreaks can occur in response to abiotic events, even in the face of extensive public education and awareness.
TL;DR: Screening high-risk patients during outbreaks and reducing the use of third-generation cephalosporins and aminoglycosides contribute to the control of these epidemics.
Abstract: An observational study was undertaken to describe a nosocomial outbreak caused by multiresistant Klebsiella pneumoniae (MRKP). Ten patients in the pediatric intensive care unit (ICU) at a hospital in Madrid were colonized by or infected with MRKP from October 1997 to April 1998. Thirty-two patients with MRKP-negative surveillance cultures who were admitted to the ICU during the outbreak period were selected as control patients. Random amplified polymorphic DNA analysis of MRKP isolates revealed patterns that were indistinguishable from each other. After identification of colonized patients by surveillance cultures and implementation of standard and contact precautions, the outbreak was controlled. An age <12 weeks (odds ratio [OR], 13.1) and previous treatment with third-generation cephalosporins and aminoglycosides (OR, 31.2) were independently associated with MRKP colonization and/or infection. Individual exposure to antibiotics, irrespective of other clinical determinants, is a risk factor for MRKP acquisition. Screening high-risk patients during outbreaks and reducing the use of third-generation cephalosporins and aminoglycosides contribute to the control of these epidemics.
TL;DR: Basic information is reviewed, recent developments in the epidemiology and epizootiology of WNV are summarized and current threats to public and animal health are summarized.
Abstract: West Nile virus (WNV) has emerged in recent years in temperate regions of Europe and North America, presenting a threat to both public and animal health The most serious manifestation of infection is fatal encephalitis in humans and horses, as well as mortality in certain domestic and wild birds A recent development in the epizootiology of this mosquito-borne flavivirus was the occurrence of a severe outbreak in New York City and surrounding areas During this outbreak, mortality was observed in humans, horses, a cat and numerous species of wild birds, particularly members of the family Corvidae (crows) The author reviews basic information and summarises recent developments in the epidemiology and epizootiology of WNV
TL;DR: The authors describe the size and duration of outbreaks caused by imported infections after indigenous transmission has been eliminated and show that the status of the elimination process can be monitored by assessing the proportion of cases imported and the distribution of outbreak sizes.
Abstract: Elimination of an infectious disease is often understood to mean the total absence of cases in a population. This situation can occur only if the entire population is immune as a result of either natural disease or vaccination. However, this costly and unrealistic scenario is not necessary to ensure elimination, more appropriately defined as a situation in which sustained transmission cannot occur and secondary spread from importations of disease will end naturally, without intervention. The authors describe the size and duration of outbreaks caused by imported infections after indigenous transmission has been eliminated. They show that the status of the elimination process can be monitored by assessing the proportion of cases imported and the distribution of outbreak sizes. Measles in Canada, the United States, and the United Kingdom provides a good example of the relevance of these criteria. Surveillance of the size and duration of these outbreaks enables maintenance of elimination to be monitored.
TL;DR: The environmental survival patterns of the five MRSA strains showed qualitative and quantitative differences between the two outbreak and three sporadic strains, and a gradual decline was noted for all strains.
TL;DR: There has been a shift from high to medium endemicity of HAV infection throughout Latin America, which may result in more clinical cases in adolescents and adults and a greater potential for outbreaks, and the vaccination strategy for hepatitis A should be reviewed.
TL;DR: The experience demonstrated that the EV71 isolated in Taiwan had strong dermatotropic as well as neurotropic tendencies, and early detecting CNS involvement and commencing aggressive therapy may reduce the mortality.
TL;DR: A VRE outbreak in a BICU over 13 months was caused by a single clone and application of barrier isolation and an aggressive environmental decontamination program can eradicate VRE from a burn population.
Abstract: Objective: To investigate and control an outbreak of colonization and infection caused by vancomycin-resistant enterococci (VRE) in a burn intensive care unit (BICU). Design: Epidemiological investigation, including multiple point-prevalence culture surveys of patients and environment, cultures from hands of healthcare workers (HCWs), pulsed-field gel electrophoresis (PFGE) typing of patient and environmental isolates, case-control study, and institution and monitoring of control measures. Setting: BICU in an 800-bed university medical center in Galveston, Texas. Results: Between June 6, 1996, and July 14, 1997, 21 patients were colonized by VRE, and 4 of these patients developed bacteremia. Of 2,844 environmental cultures, 338 (11.9%) were positive, but all hand cultures from HCWs were negative. PFGE typing indicated that the outbreak was clonal, with VRE isolates from patients differing by ≤4 bands from the index case. Thirteen of 14 environmental isolates varied by ≤4 bands from the pattern of the index case. A case-control study analyzed by exact logistic regression identified diarrhea (odds ratio [OR], 43.9; 95% confidence interval [CI95], 5.5-infinity; P=.0001) and administration of an antacid (OR, 24.2; CI95,2.9-infinity; P=.002) as independent risk factors for acquisition of VRE. During a 5-week period in October and November 1996, all patient and 317 environmental cultures were negative for VRE. The outbreak recurred from a contaminated electrocardiogram lead that had not been identified during the prior 5 weeks. VRE were finally eradicated from the BICU in July 1997, using barrier isolation and a very aggressive environmental decontamination program. Conclusions: A VRE outbreak in a BICU over 13 months was caused by a single clone. After apparent eradication of VRE from a BICU, recrudescence of the outbreak occurred, evidently from a small inapparent source of environmental contamination. Changes in gastrointestinal (GI) tract function (motility) and administration of medications, other than antibiotics, that have an effect on the GI tract may increase the risk of GI tract colonization by VRE in burn patients. Application of barrier isolation and an aggressive environmental decontamination program can eradicate VRE from a burn population.
TL;DR: Bovine viral diarrhea virus (BVDV) infection continues to have a significant impact upon US cattle producers despite the availability of more than 140 federally licensed vaccines, andylogenetic analysis and differences in virulence suggest that BVDV2 are heterogeneous.
TL;DR: The epidemiology of outbreaks of infection due to SRSVs is reviewed, recommendations for their management in the hospital setting are made and the basic principles which underpin these recommendations will be applicable to the management of some community-based institutional outbreaks.
TL;DR: Most nonbacterial gastroenteritis outbreaks were related to SRSV infection, and >60% of the outbreaks were caused by contaminated food.
Abstract: Surveillance results from pediatric cases and outbreaks of viral gastroenteritis in Japan are presented. In winter, both small round structured virus (SRSV, or Norwalk-like viruses) and rotavirus were detected from infants with gastroenteritis; however, in recent years, the prevailing time of SRSV infection has preceded that of rotavirus infection. Most nonbacterial gastroenteritis outbreaks were related to SRSV infection, and >60% of the outbreaks were caused by contaminated food. In small-sized outbreaks, raw oysters were the primary source of transmission. In large-sized outbreaks, school lunches and catered meals that were served at schools, banquet halls, and hospitals were most often implicated in the transmission of foodborne gastroenteritis.
TL;DR: In this paper, a series of dengue outbreaks in a Brazilian city was correlated with the intensity of its anti-vector source-reduction activities, and the proportion of houses infested by vector mosquitoes correlated inversely with intensity of anti-mosquito interventions.
Abstract: To identify the critical vector density that potentiates dengue outbreaks in an endemic site and to identify obstacles to anti-dengue activities, we correlated a series of dengue outbreaks in a Brazilian city with the intensity of its anti-vector source-reduction activities. The proportion of houses infested by vector mosquitoes correlated inversely with intensity of anti-mosquito interventions, and the vector population developed independently of rainfall. Local periods of drought promoted vector abundance in two ways: residents stored water in which vector mosquitoes could breed, and cholera outbreaks due to contaminated water diverted local health workers from routine anti-vector activities. One dengue outbreak became apparent to authorities more than two months after it commenced but would have been identified almost immediately had dengue-like disease in indicator hospitals been monitored. Active surveillance, therefore, offers a window of opportunity for promptly executed anti-dengue interventions. Source-reduction measures that suppress vector infestations to less than 1% of houses effectively avert outbreaks of dengue.
Journal Article•
TL;DR: The transmission of EV 71 was related to number of siblings in a household, rural residence and contact with cases of HFMD, and genotype analyses show that genotypes have changed with time in the United States and Japan.
Abstract: Enterovirus 71 (EV71) was first recognized in 1974. Since then it has been implicated in 13 small and large outbreaks world-wide. Large outbreaks of hand, foot and mouth disease (HFMD), mostly benign, occurred in Japan in 1973 and 1978. Four outbreaks with brain stem encephalitis and significant numbers of deaths occurred in Bulgaria and Hungary in the late 1970's and in Malaysia and Taiwan in 1997 and 1998 respectively. During the latter two epidemics, pulmonary edema and hemorrhage often leading to quick deaths in children aged from 0.5 to 3 years old was first recognized. In Taiwan 78 deaths and over 100,000 cases of HFMD occurred. Coxsackie A16 cocirculated with EV 71, without however, causing any severe illnesses. The transmission of EV 71 was related to number of siblings in a household, rural residence and contact with cases of HFMD. Genotype analyses show that genotypes have changed with time in the United States and Japan. Recent isolates from Japan are similar to the isolates from Malaysia and Taiwan in 1997 and 1998, respectively. Even though genotype analysis has not identified specific sequences responsible for neurovirulence, the strains causing brain stem encephalitis and pulmonary edema in the Far East are similar and have arisen since 1997. Seroepidemiological studies in Taiwan suggest that children aged from 0.5 to 4 years old are most susceptible while the rest of the population are over 50% immune. Theoretically there is a pool of such susceptible subjects every few years. In prevention for another major outbreak, a simple, inactivated Salk type vaccine should be immediately prepared and made available.
TL;DR: The potential for epidemic forecasting is examined and the issues associated with the development of global networks for surveillance and prediction are discussed, along with issues relating to further development.
Abstract: Emerging infectious diseases pose a growing threat to human populations. Many of the world's epidemic diseases (particularly those transmitted by intermediate hosts) are known to be highly sensitive to long-term changes in climate and short-term fluctuations in the weather. The application of environmental data to the study of disease offers the capability to demonstrate vector-environment relationships and potentially forecast the risk of disease outbreaks or epidemics. Accurate disease forecasting models would markedly improve epidemic prevention and control capabilities. This chapter examines the potential for epidemic forecasting and discusses the issues associated with the development of global networks for surveillance and prediction. Existing global systems for epidemic preparedness focus on disease surveillance using either expert knowledge or statistical modelling of disease activity and thresholds to identify times and areas of risk. Predictive health information systems would use monitored environmental variables, linked to a disease system, to be observed and provide prior information of outbreaks. The components and varieties of forecasting systems are discussed with selected examples, along with issues relating to further development.
TL;DR: These models suggest that pathogen‐driven outbreaks in forest defoliators occur partly because newly hatched insect larvae have higher average susceptibility than do older larvae, and show that a combination of seasonality and delays between infection and death can lead to unstable cycles in the absence of a stabilizing mechanism.
Abstract: Models of outbreaks in forest‐defoliating insects are typically built from a priori considerations and tested only with long time series of abundances. We instead present a model built from experimental data on the gypsy moth and its nuclear polyhedrosis virus, which has been extensively tested with epidemic data. These data have identified key details of the gypsy moth–virus interaction that are missing from earlier models, including seasonality in host reproduction, delays between host infection and death, and heterogeneity among hosts in their susceptibility to the virus. Allowing for these details produces models in which annual epidemics are followed by bouts of reproduction among surviving hosts and leads to quite different conclusions than earlier models. First, these models suggest that pathogen‐driven outbreaks in forest defoliators occur partly because newly hatched insect larvae have higher average susceptibility than do older larvae. Second, the models show that a combination of seas...
01 Jan 2000
TL;DR: To identify the critical vector density that potentiates dengue outbreaks in an endemic site and to identify obstacles to anti-dengue activities, a series of denguing outbreaks in a Brazilian city were correlated with the intensity of its anti-vector source-reduction activities.
Abstract: To identify the critical vector density that potentiates dengue outbreaks in an endemic site and to identify obstacles to anti-dengue activities, we correlated a series of dengue outbreaks in a Brazilian city with the intensity of its anti-vector source-reduction activities. The proportion of houses infested by vector mosquitoes correlated in- versely with intensity of anti-mosquito interventions, and the vector population developed independently of rainfall. Local periods of drought promoted vector abundance in two ways: residents stored water in which vector mosquitoes could breed, and cholera outbreaks due to contaminated water diverted local health workers from routine anti-vector activities. One dengue outbreak became apparent to authorities more than two months after it commenced but would have been identified almost immediately had dengue-like disease in indicator hospitals been monitored. Active sur- veillance, therefore, offers a window of opportunity for promptly executed anti-dengue interventions. Source-reduction measures that suppress vector infestations to less than 1% of houses effectively avert outbreaks of dengue.