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Evaluation of the molecular epidemiology of an outbreak of multiply resistant Shigella sonnei in a day-care center by using pulsed-field gel electrophoresis and plasmid DNA analysis.

Outbreaks of diarrhea in child day-care centers (DCC) are common. This study was undertaken to evaluate the molecular epidemiology of an outbreak of diarrhea due to Shigella sonnei. This outbreak involved 25 of 52 (48%) DCC children and 14 of 132 (11%) teachers and household contacts. S. sonnei isolates from nine children and five contacts were characterized by antimicrobial susceptibility, plasmid content, plasmid DNA restriction fragment pattern, and pulsed-field gel electrophoresis (PFGE) of total genomic DNA; 33 isolates from Houston, Tex., Chicago, Ill., and Mexico City, Mexico, also were studied. All outbreak isolates were resistant to ampicillin and trimethoprim-sulfamethoxazole and shared five to six plasmids ranging from 3.3 to 70 MDa. A total of 8 of 12 temporally associated nonoutbreak Houston isolates had plasmid profiles and restriction fragment patterns similar to those of the outbreak strain, despite possessing different antibiotic susceptibility patterns. PFGE demonstrated identical DNA patterns among outbreak isolates and similar or identical patterns among temporally associated sporadic Houston isolates with plasmid profiles similar to that of the outbreak strain. All other nonoutbreak strains from Houston, Chicago, and Mexico had plasmid profiles, restriction fragment patterns, and PFGE patterns different from those of the outbreak strain. DCC outbreak isolates could be distinguished from most sporadic isolates by antimicrobial susceptibility testing, but plasmid analysis and PFGE could not differentiate common-source isolates from sporadic isolates in the same location during the same time period, indicating that isolates present in the community were genetically similar to those producing outbreaks in the DCC.

Child Day Care Centers↗

Food-initiated outbreak of methicillin-resistant Staphylococcus aureus analyzed by pheno- and genotyping.

An outbreak of methicillin-resistant Staphylococcus aureus (MRSA) involving 27 patients and 14 health-care workers (HCW) was studied. The outbreak started in the hematology unit of the University Hospital Rotterdam, Dijkzigt, The Netherlands, and spread to the surgical unit. Twenty-one patients (77.8%) developed clinical disease, and five died. Subsequently, MRSA was detected in food and in the throat of one of the HCW who prepared food for hematology patients. Food contaminated by an HCW most likely caused the first case of MRSA septicemia. This route of transmission has not been described before. The outbreak strain was probably transmitted to the surgical unit by a colonized nurse, where it caused an explosive outbreak. Airborne probably transmitted to the surgical unit by a colonized nurse, where it caused an explosive outbreak. Airborne MRSA transmission played an important role in disseminating the organism. The outbreak was controlled within 6 months by intensifying surveillance, temporarily closing the affected wards, treating carriers, and instituting an MRSA ward outside the hospital. Phage typing, insertion sequence probing, protein A gene typing, and DNA fingerprinting by PCR revealed that all outbreak-related isolates were identical. By pulsed-field gel electrophoresis, all but one of the outbreak-related isolates were determined to be identical. Protein A gene typing identified numerous (11) repeat units in all outbreak-related isolates, which supports the suggestion that the outbreak strain may have been more virulent and more transmissible than other MRSA strains. Pheno- and genotyping studies underlined the value of DNA fingerprinting methods for investigation of MRSA epidemiology. Optimal discriminatory power was achieved by combining the results of four genotyping methods.

Base Sequence↗

Patterns of resistance associated with integrons, the extended-spectrum beta-lactamase SHV-5 gene, and a multidrug efflux pump of Klebsiella pneumoniae causing a nosocomial outbreak.

Multiresistant Klebsiella pneumoniae caused a nosocomial outbreak. Resistance patterns of the presumed outbreak isolates varied among and within patients. In order to control the outbreak, screening for extended-spectrum beta-lactamase (ESBL)-producing K. pneumoniae was commenced. A number of susceptible K. pneumoniae strains were stored to serve as controls in genetic strain typing. Typing by pulsed-field gel electrophoresis proved the clonality of the strains in the recognized outbreak patients. Typing of the control strains by pulsed-field gel electrophoresis showed that at least one patient had been missed by the ESBL screening procedure. Further genetic typing confirmed the presence of the SHV-5 ESBL gene in all but one of the outbreak strains. Variable presence of integrons that carried the aminoglycoside resistance genes aadB and aadA2 was found. A gyrA mutation in codon 83 was present in all outbreak strains tested, despite considerable differences in ciprofloxacin MICs. The MICs of ciprofloxacin and the chemically unrelated drug cefoxitin were correlated (r = 0.86, P < 0.01) and were compatible with the overexpression of an efflux pump in a subset of the outbreak strains. We conclude that outbreak strains that express an ESBL gene only at a low level may pass unnoticed in a screening procedure, when the laboratory is unaware of variable ESBL expression. In this particular outbreak, screening for strains for which ciprofloxacin MICs were > or =0.25 micro g/ml would in retrospect have been the most sensitive method for detection of the K. pneumoniae outbreak strain.

ATP Binding Cassette Transporter, Subfamily B↗

Antigenic and genetic characterisation of Newcastle disease viruses isolated from outbreaks in domestic fowl and turkeys in Great Britain during 1997.

Antigenic and genetic analyses of viruses from the 11 outbreaks of Newcastle disease in Great Britain, 12 of the outbreaks in Northern Ireland and the single outbreak in the Republic of Ireland which occurred in 1997, indicated that they were all essentially similar. In addition, the viruses from the British Isles were very similar to viruses isolated from three outbreaks in pheasants in Denmark between August and November 1996, from a goosander in Finland in September 1996, from an outbreak in chickens in Norway in February 1997, and from an outbreak in chickens in Sweden in November 1997. Viruses from outbreaks in other countries during 1995 to 1997 could be distinguished antigenically and/or genetically from the 1996 to 1997 Scandinavian/British Isles isolates, as could viruses responsible for two separate outbreaks in caged birds in quarantine premises in Great Britain in March 1997. Minor nucleotide differences in the 413-base region of the fusion gene and the 187-base region of the haemagglutinin-neuraminidase gene sequenced in this study allowed the 1996 to 1997 Scandinavian/British Isles isolates to be divided into groups. These groups broadly corresponded to the clusters of disease outbreaks, but suggested that the discrete outbreak in Scotland was probably the result of virus spread from Northern Ireland. Overall, the antigenic and genetic analyses of these viruses were consistent with the theory that the virus was introduced into the British Isles by migratory birds moving from north-east Europe. However, it was not possible to rule out other sources, such as the movement of pheasants from Denmark.

Animals↗

The epidemiology and clinical analysis of several outbreaks of herpes gladiatorum.

UNLABELLED: PURPOSE The purpose of this analysis was to determine whether present National Federation of State High School Associations (NFHS) guidelines adequately prevent and control outbreaks of primary herpes gladiatorum (HG) in high-school wrestlers. METHODS: Using telephone interviews, direct physical examinations, and review of medical charts, data were collected on HG outbreaks among participating teams in the 1999 Minnesota State High School League (MSHSL) wrestling season and on HG outbreaks for 3 yr at a 28-d summer wrestling camp. RESULTS: The outbreak during the 1999 MSHSL wrestling season involved 61 wrestlers and three coaches on 19 teams over 42 d, with a 32.7% probability of transmission to sparring partners. Typical length of time from exposure to outbreak varied from 4 to 11 d with an average of 6.80 +/- 1.70 d. Analysis of data from three outbreaks at a 28-d wrestling camp showed that most outbreaks (96%) occurred on the ventral surface of the body, with 71.9% on the head, face, and neck, areas in direct contact when wrestlers are engaged in the lock-up position. Analysis of data from the 2001 camp outbreak showed that the locations of the lesions reflected the handedness of the wrestler. CONCLUSION: The NFHS guidelines are inadequate to prevent and control outbreaks of HG. The focus of preventive efforts needs to change from mat cleanliness to more rapid detection of outbreaks by requiring culture results and appropriate therapy for all suspected bacterial and herpes lesions before allowing return to contact. To minimize and control spread of HG, treatment and isolation should be implemented based not only on vesicle formation but also on systemic signs and symptoms.

2-Aminopurine↗

A deep learning approach to real-time HIV outbreak detection using genetic data.

Pathogen genomic sequence data are increasingly made available for epidemiological monitoring. A main interest is to identify and assess the potential of infectious disease outbreaks. While popular methods to analyze sequence data often involve phylogenetic tree inference, they are vulnerable to errors from recombination and impose a high computational cost, making it difficult to obtain real-time results when the number of sequences is in or above the thousands. Here, we propose an alternative strategy to outbreak detection using genomic data based on deep learning methods developed for image classification. The key idea is to use a pairwise genetic distance matrix calculated from viral sequences as an image, and develop convolutional neutral network (CNN) models to classify areas of the images that show signatures of active outbreak, leading to identification of subsets of sequences taken from an active outbreak. We showed that our method is efficient in finding HIV-1 outbreaks with R0 &#x2265; 2.5, and overall a specificity exceeding 98% and sensitivity better than 92%. We validated our approach using data from HIV-1 CRF01 in Europe, containing both endemic sequences and a well-known dual outbreak in intravenous drug users. Our model accurately identified known outbreak sequences in the background of slower spreading HIV. Importantly, we detected both outbreaks early on, before they were over, implying that had this method been applied in real-time as data became available, one would have been able to intervene and possibly prevent the extent of these outbreaks. This approach is scalable to processing hundreds of thousands of sequences, making it useful for current and future real-time epidemiological investigations, including public health monitoring using large databases and especially for rapid outbreak identification.

Humans↗

Cheese-associated outbreaks of human illness in the United States, 1973 to 1992: sanitary manufacturing practices protect consumers.

To identify contributing factors for cheese-associated outbreaks, we reviewed all cheese-associated outbreaks of human illness reported to the Centers for Disease Control and Prevention (CDC) with onsets during 1973 to 1992. The infrequency of large, cheese-associated outbreaks was notable because such outbreaks had been a frequent public health problem before the mid-20th century. Of 32 reported cheese-associated outbreaks, 11 attributed to manufacturing errors caused most of the illnesses and hospitalizations and all 58 deaths. Important factors in these 11 outbreaks were manufacturing cheese with raw or improperly pasteurized milk and postpasteurization contamination. If current Food and Drug Administration sanitary requirements for cheesemaking had been met, these outbreaks would have been preventable. In two outbreaks of Salmonella infections, fewer than 10 Salmonella per 100 g of cheese were detected. In two outbreaks of Brucella infections, efforts to recover the pathogen from the implicated cheese were unsuccessful, emphasizing the inadequacy of end product testing for assuring consumer safety. Curing cheeses kills most bacteria present in cheeses; however, evidence from sources other than the CDC Foodborne Disease Outbreak Surveillance System suggests that curing alone may not be a sufficient pathogen control step to eliminate Salmonella, Listeria, and E. coli O157:H7 from cheese.

Bacterial Infections↗

Fresh produce: a growing cause of outbreaks of foodborne illness in the United States, 1973 through 1997.

Fresh produce is an important part of a healthy diet. During the last three decades, the number of outbreaks caused by foodborne pathogens associated with fresh produce consumption reported to the Centers for Disease Control and Prevention has increased. To identify trends, we analyzed data for 1973 through 1997 from the Foodborne Outbreak Surveillance System. We defined a produce-associated outbreak as the occurrence of two or more cases of the same illness in which epidemiologic investigation implicated the same uncooked fruit, vegetable, salad, or juice. A total of 190 produce-associated outbreaks were reported, associated with 16,058 illnesses, 598 hospitalizations, and eight deaths. Produce-associated outbreaks accounted for an increasing proportion of all reported foodborne outbreaks with a known food item, rising from 0.7% in the 1970s to 6% in the 1990s. Among produce-associated outbreaks, the food items most frequently implicated included salad, lettuce, juice, melon, sprouts, and berries. Among 103 (54%) produce-associated outbreaks with a known pathogen, 62 (60%) were caused by bacterial pathogens, of which 30 (48%) were caused by Salmonella. During the study period, Cyclospora and Escherichia coli O157:H7 were newly recognized as causes of foodborne illness. Foodborne outbreaks associated with fresh produce in the United States have increased in absolute numbers and as a proportion of all reported foodborne outbreaks. Fruit and vegetables are major components of a healthy diet, but eating fresh uncooked produce is not risk free. Further efforts are needed to better understand the complex interactions between microbes and produce and the mechanisms by which contamination occurs from farm to table.

Consumer Product Safety↗

[Noroviruses are the most common pathogens causing nosocomial gastroenteritis outbreaks in Hungarian hospitals].

INTRODUCTION: Norovirus (genera; previously "Norwalk-like viruses") of the family Caliciviridae are an important cause of acute gastroenteritis outbreaks. Epidemics commonly occur in crowded community and spread by fecal-oral route through contaminated food, water and direct contact. AIMS: To determine the incidence and epidemiological role of caliciviruses in nosocomial gastroenteritis outbreaks in hospitals in Hungary. METHODS: Between November 1998 and April 2002, 277 stool samples of 39 nonbacterial hospital outbreaks reported as "enteritis infectiosa" with unknown etiology from 13 of 19 counties in Hungary were examined by reverse transcription-polymerase chain reaction (RT-PCR) for Norovirus and Sapovirus and by a new recombinant enzyme immune assay (rEIA) for Norovirus only. RESULTS: 99 (36%) of 277 stool specimens were positive by RT-PCR and 29 (74%) and 38 (97%) of 39 outbreaks were positive by RT-PCR and RT-PCR and/or rEIA for Norovirus, respectively. Norovirus were the most frequently detected agents in the registered nosocomial enteric hospital outbreaks in years 2000 (n = 4; 31%) and 2001 (n = 7; 23%). In the first 4 months of 2002, 25 (66%) of 38 nosocomial outbreaks was caused by Norovirus. Seventeen (44%) outbreaks occurred in single internal wards and eight (21%) in more than one (2-8) ward. An average of 32% (0-80%) of the sick persons, were member of the hospital staff. Twenty four (63%) Norovirus-associated outbreaks occurred between January and March 2002. CONCLUSIONS: This is the first comprehensive country-wide surveillance of nosocomial gastroenteritis outbreaks in hospitals associated with Norovirus. Data showed that Norovirus were the most important cause of these outbreaks in Hungary but the epidemiological role of this virus is probably further underestimated.

Caliciviridae Infections↗

[Impact of guidelines in investigating foodborne disease outbreaks services in Lazio region, Italy].

Epidemiological investigation of foodborne disease outbreaks helps us to better define the risks, hazards and vehicles involved. In 1997 guidelines on epidemiological methods for investigating these outbreaks were implemented in the Lazio Region. Methods used in investigating the 410 foodborne disease outbreaks reported in the 1996-2000 period were analysed to evaluate the impact of the guide lines on health services. Specific food attack-rates (epidemiological methods) were calculated more frequently in outbreaks with setting of mass catering with many exposed people (46% of these outbreaks) than in outbreaks in home setting with few exposed people (13% of these cases). Inversely, in smaller outbreaks the proportion of cases with detected aetiology (microbiological method) was higher (66%) than in larger ones (43%). For foodborne disease outbreaks with at least 30 people exposed epidemiological methods of investigating showed temporal trend in the period 1996-2000: the epidemics in which attack rates were calculated increased from 50% to 83%, those in which epidemic curve was drawn increased from 17% to 79%, and those in which food specific attack rates were calculated increased from 33% to 58%. The hazard analysis of critical control points (HACCP) was performed only in 18.3% of the cases. In conclusion, the guide lines resulted in a wider application of epidemiological methods in large outbreaks with a well defined exposure resulting in an improved detection of vehicles of foodborne diseases. Epidemiological methods possibly are not adequate to investigate smaller foodborne outbreaks.

Cohort Studies↗

Benchmark data and power calculations for evaluating disease outbreak detection methods.

INTRODUCTION: Early detection of disease outbreaks enables public health officials to implement immediate disease control and prevention measures. Computer-based syndromic surveillance systems are being implemented to complement reporting by physicians and other health-care professionals to improve the timeliness of disease-outbreak detection. Space-time disease-surveillance methods have been proposed as a supplement to purely temporal statistical methods for outbreak detection to detect localized outbreaks before they spread to larger regions. OBJECTIVE: The aims of this study were twofold: 1) to design and make available benchmark data sets for evaluating the statistical power of space-time early detection methods and 2) to evaluate the power of the prospective purely temporal and space-time scan statistics by applying them to the benchmark data sets at different parameter settings. METHODS: Simulated data sets based on the geography and population of New York City were created, including effects of outbreaks of varying size and location. Data sets with no outbreak effects were also created. Scan statistics were then run on these data sets, and the resulting power performances were analyzed and compared. RESULTS: The prospective space-time scan statistic performs well for a spectrum of outbreak models. By comparison, the prospective purely temporal scan statistic has higher power for detecting citywide outbreaks but lower power for detecting geographically localized outbreaks. CONCLUSIONS: The benchmark data sets created for this study can be used successfully for formal statistical power evaluations and comparisons. If an anomaly caused by an outbreak is local, purely temporal surveillance methods might be unable to detect it, in which case space-time methods would be necessary for early detection.

Benchmarking↗

Infectious disease outbreaks related to drinking water in Canada, 1974-2001.

BACKGROUND: Recent public attention on drinking water supplies in the aftermath of waterborne infection outbreaks in Walkerton and North Battleford raises questions about safety. We analyzed information on waterborne outbreaks occurring between 1974 and 2001 in order to identify apparent trends, review the current status of monitoring and reporting, and gain a better understanding of the impact of drinking water quality on public health and disease burden. METHODS: Data from outbreak investigations, published and unpublished, were categorized by the type of drinking water provider and were assessed to be definitely, probably or possibly waterborne in nature. RESULTS: The final data set consisted of 288 outbreaks of disease linked to a drinking water source. There were 99 outbreaks in public water systems, 138 outbreaks in semi-public systems and 51 outbreaks in private systems. The main known causative agents of waterborne disease outbreaks were (in descending frequency of occurrence) Giardia, Campylobacter, Cryptosporidium, Norwalk-like viruses, Salmonella and hepatitis A virus. SUMMARY: We found that severe weather, close proximity to animal populations, treatment system malfunctions, poor maintenance and treatment practices were associated with the reported disease outbreaks resulting from drinking water supplies. However, issues related to the accuracy, co-ordination, compatibility and detail of data exist. A systematic and coordinated national surveillance system for comparison purposes, trend identification and policy development is needed so that future waterborne disease outbreaks can be avoided.

Agriculture↗

Food poisoning outbreaks associated with manufactured foods in England and Wales: 1980-1989.

In the ten-year period, 1980-89, 294 reported outbreaks of food poisoning were associated with eating pre-cooked sliced meats, meat products and other manufactured foods in England and Wales, including 65 outbreaks in which the product was imported. Salmonellas were the most commonly reported agent, causing 132 (45%) of the outbreaks; other bacteria caused a further 51 (17%) outbreaks. The remainder were due to viruses (five outbreaks), scombrotoxin (60 outbreaks), or were of unknown cause (46 outbreaks). The number of outbreaks associated with manufactured foods accounted for only a small proportion (less than 5%) of food poisoning outbreaks reported to CDSC during this period and needs to be set against the huge amounts of manufactured foods consumed. However, because of the quantities made and the widespread distribution of particular products, such outbreaks may affect many individuals who are geographically widespread.

Cross-Sectional Studies↗

The combined effects of pathogens and predators on insect outbreaks.

The economic damage caused by episodic outbreaks of forest-defoliating insects has spurred much research, yet why such outbreaks occur remains unclear. Theoretical biologists argue that outbreaks are driven by specialist pathogens or parasitoids, because host-pathogen and host-parasitoid models show large-amplitude, long-period cycles resembling time series of outbreaks. Field biologists counter that outbreaks occur when generalist predators fail, because predation in low-density defoliator populations is usually high enough to prevent outbreaks. Neither explanation is sufficient, however, because the time between outbreaks in the data is far more variable than in host-pathogen and host-parasitoid models, and far shorter than in generalist-predator models. Here we show that insect outbreaks can be explained by a model that includes both a generalist predator and a specialist pathogen. In this host-pathogen-predator model, stochasticity causes defoliator densities to fluctuate erratically between an equilibrium maintained by the predator, and cycles driven by the pathogen. Outbreaks in this model occur at long but irregular intervals, matching the data. Our results suggest that explanations of insect outbreaks must go beyond classical models to consider interactions among multiple species.

Animals↗

A large community outbreak of salmonellosis caused by intentional contamination of restaurant salad bars.

CONTEXT: This large outbreak of foodborne disease highlights the challenge of investigating outbreaks caused by intentional contamination and demonstrates the vulnerability of self-service foods to intentional contamination. OBJECTIVE: To investigate a large community outbreak of Salmonella Typhimurium infections. DESIGN: Epidemiologic investigation of patients with Salmonella gastroenteritis and possible exposures in The Dalles, Oregon. Cohort and case-control investigations were conducted among groups of restaurant patrons and employees to identify exposures associated with illness. SETTING: A community in Oregon. Outbreak period was September and October 1984. PATIENTS: A total of 751 persons with Salmonella gastroenteritis associated with eating or working at area restaurants. Most patients were identified through passive surveillance; active surveillance was conducted for selected groups. A case was defined either by clinical criteria or by a stool culture yielding S Typhimurium. RESULTS: The outbreak occurred in 2 waves, September 9 through 18 and September 19 through October 10. Most cases were associated with 10 restaurants, and epidemiologic studies of customers at 4 restaurants and of employees at all 10 restaurants implicated eating from salad bars as the major risk factor for infection. Eight (80%) of 10 affected restaurants compared with only 3 (11%) of the 28 other restaurants in The Dalles operated salad bars (relative risk, 7.5; 95% confidence interval, 2.4-22.7; P<.001). The implicated food items on the salad bars differed from one restaurant to another. The investigation did not identify any water supply, food item, supplier, or distributor common to all affected restaurants, nor were employees exposed to any single common source. In some instances, infected employees may have contributed to the spread of illness by inadvertently contaminating foods. However, no evidence was found linking ill employees to initiation of the outbreak. Errors in food rotation and inadequate refrigeration on ice-chilled salad bars may have facilitated growth of the S Typhimurium but could not have caused the outbreak. A subsequent criminal investigation revealed that members of a religious commune had deliberately contaminated the salad bars. An S Typhimurium strain found in a laboratory at the commune was indistinguishable from the outbreak strain. CONCLUSIONS: This outbreak of salmonellosis was caused by intentional contamination of restaurant salad bars by members of a religious commune.

Contact Tracing↗

Polymerase chain reaction detection of small round-structured viruses from two related hospital outbreaks of gastroenteritis using inosine-containing primers.

Two outbreaks of gastroenteritis in the UK which occurred nine days apart at Lymington and Southampton hospitals were investigated. The clinical and epidemiological features of both outbreaks were characteristic of small round-structured virus (SRSV) infection with rapid onset of diarrhoea and/or nausea and vomiting and propagation of the outbreaks by secondary spread. SRSV particles were observed by immune electron microscopy (EM) in 60% of faecal samples from both outbreaks and no other pathogens were detected. The index case for the second outbreak was a patient who was admitted with diarrhoea and vomiting after being discharged from Lymington hospital during the first outbreak. The possibility that the two outbreaks were caused by the same strain of SRSV was investigated by the polymerase chain reaction (PCR). New inosine-containing PCR primers were designed to amplify the RNA polymerase region of SRSV cDNA from genetic groups I and II. The PCR using the group II primers achieved a higher detection rate for SRSVs in faecal samples (68% of samples positive from both outbreaks) than immune EM. SRSVs were not detected using the group I primers or using conventional degenerate PCR primers. The nucleotide sequences of PCR amplicons from both outbreaks were identical providing molecular epidemiological evidence for the involvement of a single SRSV strain. Comparison of the RNA polymerase region of this virus with the equivalent regions of genetic group I (69.4-75.0% amino acid identify) and genetic group II (88.9-100% amino acid and 77.1-88.1% nucleotide identity) SRSVs revealed that the causative SRSV was a distinct member of genetic group II.

Amino Acid Sequence↗

Co-circulation of genotype IA and new variant IB hepatitis A virus in outbreaks of acute hepatitis in Hungary--2003/2004.

Hepatitis A virus (HAV) is one of the most important causes of acute infectious hepatitis worldwide. In Hungary, the reported number of HAV infections has been decreasing in the last four decades, nevertheless, still, each year 500-800 new cases and multiple outbreaks occur, particularly in the northeast region of Hungary. In Hungary, serology is used routinely to establish the diagnosis of HAV infection without genetic analysis of HAV strains for molecular epidemiology. In this study, serum samples collected from symptomatic patients were tested by enzyme-immunoassay (anti-HAV-IgM ELISA) to establish the cause of three acute hepatitis A outbreaks (outbreak 1--from low prevalence region in Southwest Hungary in 2003 and outbreaks 2 and 3 from the endemic region in Northeast Hungary in 2004). Outbreak strains were characterized by reverse transcription-polymerase chain reaction (RT-PCR) amplification of a 360 bp viral VP1/2A region, amplicon sequencing and phylogenetic analysis. Four, seven, and three sera from outbreaks 1, 2, and 3, respectively, were investigated by RT-PCR for HAV genome and HAV RNA was detected in 4 (100%), 4 (57%), and 2 (67%) samples. All strains belonged to genotype I HAV. Outbreak 1 was caused by the new variant subtype IB and outbreaks 2 and 3 caused by genetically identical subtype IA strains. The Hungarian IA and IB hepatitis A viruses had the highest nucleotide identity, 98.4% and 99.0%, to IT-SCH-00 and IT-MAR-02 strains, respectively, detected in year 2000 and 2002 in Italy. Endemic subtype IA and probably imported new variant subtype IB HAV viruses was detected in outbreaks of hepatitis in Hungary that are closely related genetically to HAV strains in Italy.

Acute Disease↗

[Principles of an outbreak investigation in public health practice].

An outbreak (or epidemic) is a higher number of cases of a given disease in a given population and time interval. A timely investigation has for aim to identify the source and vehicle of the outbreak and provides unique opportunities to better understand its occurrence and the role of contributing risk factors to implement the most appropriate measures to control it and prevent further recurrences. The investigation of an outbreak is based on a multidisciplinary approach (clinical, epidemiological, environmental, and microbiological) with a descriptive and analytical (hypothesis testing) phase. In this article, we describe the methodological approach of a field outbreak investigation illustrated by examples taken from our experience. The investigation includes the following steps: establishing the existence of the outbreak; defining the disease; finding cases; describing cases by time, place, and person characteristics; establishing a hypothesis related to the mode of occurrence; testing the hypotheses; conducting an environmental investigation; conducting a microbiological investigation; controlling the outbreak, preventing further occurrences, and writing an investigation report to share experience with the public health and scientific community. The investigation of an outbreak is an evolving process: information gathered or conclusions made at a given stage must be fully used for following steps. The social, institutional, and political background associated with outbreaks usually makes their investigation complex and should be taken into account. The earlier the outbreak is detected and investigated in close relation with public health authorities, the greater will be the potential preventive impact of control measures.

Adult↗