SEARCH · PubMed Health

Results for “outbreak response”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources

PubMed1998

Demonstration that Australian Pasteurella multocida isolates from sporadic outbreaks of porcine pneumonia are non-toxigenic (toxA-) and display heterogeneous DNA restriction endonuclease profiles compared with toxigenic isolates from herds with progressive atrophic rhinitis.

Capsular types A and D of Pasteurella multocida cause economic losses in swine because of their association with progressive atrophic rhinitis (PAR) and enzootic pneumonia. There have been no studies comparing whole-cell DNA profiles of isolates associated with these two porcine respiratory diseases. Twenty-two isolates of P. multocida from diseased pigs in different geographic localities within Australia were characterised genotypically by restriction endonuclease analysis (REA) with the enzyme CfoI. Seven of 12 P. multocida isolates from nasal swabs from pigs in herds where PAR was either present or suspected displayed a capsular type D phenotype. These were shown to possess the toxA gene by polymerase chain reaction (PCR) and Southern hybridisation, and further substantiated by production of cytotoxin in vitro. The CfoI profile of one of these seven isolates, which was from the initial outbreak of PAR in Australia (in Western Australia, WA), was identical with profiles of all six other toxigenic isolates from sporadic episodes in New South Wales (NSW). The evidence suggests that the strain involved in the initial outbreak was responsible for the spread of PAR to the eastern states of Australia. Another 10 isolates, representing both capsular types A and D, were isolated exclusively from porcine lung lesions after sporadic outbreaks of enzootic pneumonia in NSW and WA. CfoI restriction endonuclease profiles of these isolates revealed considerable genomic heterogeneity. Furthermore, none of these possessed the toxA gene. This suggests that P. multocida strains with the toxA gene do not have a competitive survival advantage in the lower respiratory tract or that toxin production does not play a role in the pathology of pneumonic lesions, or both. REA with polyacrylamide gel electrophoresis and silver staining was found to be a practical and discriminatory tool for epidemiological tracing of P. multocida outbreaks associated with PAR or pneumonia in pigs.

Animals↗

PubMed2000

Meningococcal disease in South African goldmines--epidemiology and strategies for control.

OBJECTIVES: To describe the epidemiology of meningococcal disease in South African goldmines and to suggest strategies for the prevention and control of further outbreaks. DESIGN: We prospectively investigated a meningococcal outbreak that occurred in 1996 and describe the control measures that were implemented. In addition, we conducted a retrospective analysis of routinely collected data on meningococcal disease in these mines from 1972 to 1996. SETTING: Four goldmines in Gauteng, employing 30,000 workers who live in hostels. SUBJECTS: All cases of meningococcal disease at the mine hospital. RESULTS: Between 1972 and 1976, 588 cases were diagnosed, with peaks in 1972 (203 cases, 727/100,000) and 1975 (147 cases, 564/100,000). Since 1978 less than 5 cases have been reported in most years, but smaller outbreaks occurred in 1990 (30 cases, 89/100,000) and 1996 (14 cases, 50/100,000). The 1996 outbreak (group A, clone I-1) was part of a larger outbreak in Gauteng that originated in Mozambique and began in one mine in July 1996, after which a mass vaccination campaign was implemented. This was followed by a smaller outbreak among non-vaccinated workers at an adjacent mine. Five patients were new recruits. CONCLUSIONS: Despite a dramatic reduction in meningococcal disease over the last 25 years due mainly to changes in the work force, there are still outbreaks in this community. Those most at risk are young men who are new to the industry. Suggestions for prevention include effective surveillance, routine vaccination of new recruits and a rapid response to outbreaks, with mass vaccination and provision of chemoprophylaxis to close contacts.

Adolescent↗

PubMed2001

Coexistence of SHV-4- and TEM-24-producing Enterobacter aerogenes strains before a large outbreak of TEM-24-producing strains in a French hospital.

In 1996, a monitoring program was initiated at the teaching hospital of Amiens, France, and carried out for 3 years. All extended-spectrum beta-lactamase (ESBL)-producing Enterobacter aerogenes isolates recovered from clinical specimens were collected for investigation of their epidemiological relatedness by pulsed-field gel electrophoresis and enterobacterial repetitive intergenic consensus PCR (ERIC-PCR) and determination of the type of ESBL harbored by isoelectric focusing and DNA sequencing. Molecular typing revealed the endemic coexistence, during the first 2 years, of two clones expressing, respectively, SHV-4 and TEM-24 ESBLs, while an outbreak of the TEM-24-producing strain raged in the hospital during the third year, causing the infection or colonization of 165 patients. Furthermore, this strain was identified as the prevalent clone responsible for outbreaks in many French hospitals since 1996. This study shows that TEM-24-producing E. aerogenes is an epidemic clone that is well established in the hospital's ecology and able to spread throughout wards. The management of the outbreak at the teaching hospital of Amiens, which included the reinforcement of infection control measures, failed to obtain complete eradication of the clone, which has become an endemic pathogen.

Bacterial Proteins↗

PubMed2005

How parasitism affects critical patch-size in a host-parasitoid model: application to the forest tent caterpillar.

Habitat structure has broad impacts on many biological systems. In particular, habitat fragmentation can increase the probability of species extinction and on the other hand it can lead to population outbreaks in response to a decline in natural enemies. An extreme consequence of fragmentation is the isolation of small regions of suitable habitat surrounded by a large region of hostile matrix. This scenario can be interpreted as a critical patch-size problem, well studied in a continuous time framework, but relatively new to discrete time models. In this paper we present an integrodifference host-parasitoid model, discrete in time and continuous in space, to study how the critical habitat-size necessary for parasitoid survival changes in response to parasitoid life history traits, such as emergence time. We show that early emerging parasitoids may be able to persist in smaller habitats than late emerging species. The model predicts that these early emerging parasitoids lead to more severe host outbreaks. We hypothesise that promoting efficient late emerging parasitoids may be key in reducing outbreak severity, an approach requiring large continuous regions of suitable habitat. We parameterise the model for the host species of the forest tent caterpillar Malacosoma disstria Hbn., a pest insect for which fragmented landscape increases the severity of outbreaks. This host is known to have several parasitoids, due to paucity of data and as a first step in the modelling we consider a single generic parasitoid. The model findings are related to observations of the forest tent caterpillar offering insight into this host-parasitoid response to habitat structure.

Animals↗

PubMed2000

Adenovirus 7a: a community-acquired outbreak in a children's hospital.

BACKGROUND: Adenoviruses produce many illnesses in children, particularly respiratory and gastrointestinal disease. The most common adenoviral respiratory infections in children are caused by types 1, 2, 3 and 5. Adenoviruses spread rapidly in closed environments often causing epidemic disease. Serotype 7a has been responsible for outbreaks of respiratory disease in children living in close proximity with one another. This report describes a large community-acquired adenovirus 7a epidemic in hospitalized children. METHODS: Evaluation of all patients with cultures positive for adenovirus from a children's hospital-based virology laboratory during a recognized adenovirus outbreak. All such adenovirus isolates were typed, and patients with adenovirus 7a are described by review of medical records. RESULTS: Between March 1 and July 26, 1997, 47 children admitted to the hospital were identified as infected with adenovirus. Of these 47 patients 26 (55%) were infected with adenovirus 7a. Twenty-four (92%) infections were community-acquired. The age range was 11 days to 10 years with a median of 9.5 months. Twenty-two patients (84%) had respiratory symptoms, and 21 (8%) had fever, making these the most common symptoms. The mean durations of fever and hospitalization were 5.5 and 7 days, respectively. One of 26 patients died. CONCLUSIONS: Adenovirus 7a can cause large community epidemics affecting children. The disease produced by adenovirus 7a in children is almost exclusively of the respiratory tract, and in some individuals it may be very severe and possibly fatal.

Adenovirus Infections, Human↗

PubMed2001

The outbreak of West Nile virus infection in the New York City area in 1999.

BACKGROUND: In late August 1999, an unusual cluster of cases of meningoencephalitis associated with muscle weakness was reported to the New York City Department of Health. The initial epidemiologic and environmental investigations suggested an arboviral cause. METHODS: Active surveillance was implemented to identify patients hospitalized with viral encephalitis and meningitis. Cerebrospinal fluid, serum, and tissue specimens from patients with suspected cases underwent serologic and viral testing for evidence of arboviral infection. RESULTS: Outbreak surveillance identified 59 patients who were hospitalized with West Nile virus infection in the New York City area during August and September of 1999. The median age of these patients was 71 years (range, 5 to 95). The overall attack rate of clinical West Nile virus infection was at least 6.5 cases per million population, and it increased sharply with age. Most of the patients (63 percent) had clinical signs of encephalitis; seven patients died (12 percent). Muscle weakness was documented in 27 percent of the patients and flaccid paralysis in 10 percent; in all of the latter, nerve conduction studies indicated an axonal polyneuropathy in 14 percent. An age of 75 years or older was an independent risk factor for death (relative risk adjusted for the presence or absence of diabetes mellitus, 8.5; 95 percent confidence interval, 1.2 to 59.1), as was the presence of diabetes mellitus (age-adjusted relative risk, 5.1; 95 percent confidence interval, 1.5 to 17.3). CONCLUSIONS: This outbreak of West Nile meningoencephalitis in the New York City metropolitan area represents the first time this virus has been detected in the Western Hemisphere. Given the subsequent rapid spread of the virus, physicians along the eastern seaboard of the United States should consider West Nile virus infection in the differential diagnosis of encephalitis and viral meningitis during the summer months, especially in older patients and in those with muscle weakness.

Adolescent↗

PubMed2004

Private sector hospital response to the 2003 dengue outbreak in the Indian capital metropolis of Delhi.

During 2003, the Indian capital metropolis of Delhi was afflicted with an outbreak of dengue. A private-sector tertiary care hospital responded instantly to the sudden influx of 162 patients during an 8-week interval. That was an unusual challenge because, until 1997, the hospital had exclusively managed patients with ophthalmic disorders. Dengue patients received fiscal concessions and several free services. A multidisciplinary cell was commissioned for case management. Apart from a diagnosis of patients with dengue and their clinical management, suspected or confirmed dengue episodes were instantly reported to health authorities. Anti-mosquito measures in the hospital premises including residential areas for the nursing personnel prevented any local virus transmission. The integrated therapeutic and public health response was associated with a 1.23% case fatality rate. The protocol developed during the dengue outbreak would address every locally reportable disease in the future.

Adolescent↗

PubMed1977

Foodborne disease outbreaks of chemical etiology in the United States, 1970-1974.

In the United States between 1970 and 1974 there was an increase each year both in the absolute number of foodborne diseases outbreaks of chemical etiology reported to the Center for Disease Control and in the proportion of these outbreaks in the total reported foodborne disease outbreaks. Nearly half (48.9%) of these foodborne disease outbreaks of chemical origin were caused by toxic fish or shellfish. Of the rest, 16.5% were caused by poisonous mushrooms, 10.9% by heavy metal poisoning, 7.2% by excessive use in food of monosodium glutamate (the etiologic agent of Chinese Restaurant Syndrome) and 16.5% by miscellaneous chemicals. Practices that contributed to the occurrence of these outbreaks included the inadvertent selection for consumption of toxic fish, shellfish, or mushrooms, storage of fish at improper temperatures, storage of acidic liquids in metal containers, and addition of excessive amounts of monosodium glutamate to foods. Commercially-processed foods were responsible for outbreaks of scombroid fish poisoning, shellfish poisoning, and heavy metal poisoning. Because outbreaks of chemical etiology due to contaminated commercial products do occur, prompt recognition and reporting of outbreaks to public health personnel are essential so that epidemiologic investigations can be conducted and effective control measures promptly initiated.

Animals↗

PubMed1993

Profile of Escherichia coli O157:H7 pathogen responsible for hamburger-borne outbreak of hemorrhagic colitis and hemolytic uremic syndrome in Washington.

We analyzed Escherichia coli O157:H7 isolates from stool samples of five patients who had bloody diarrhea and were infected during a large food-borne outbreak of hemorrhagic colitis in Washington state. The isolates were assessed for Shiga-like toxin profile, adherence and plasmid traits, mouse virulence, capsule, and enterohemolysin production. The profiles of the five isolates were indistinguishable from each other and similar to that of E. coli O157:H7 strain EDL933, an organism responsible for a similar hamburger-associated food poisoning episode in 1982.

Adolescent↗

PubMed2004

Concurrent summer influenza and pertussis outbreaks in a nursing home in Sydney, Australia.

OBJECTIVE: To report on the investigation of a summer outbreak of acute respiratory illness among residents of a Sydney nursing home. DESIGN: An epidemiologic and microbiological investigation of the resident cohort at the time of the outbreak and medical record review 5 months later. SETTING: A nursing home located in Sydney, Australia, during February to July 1999. PATIENTS: The cohort of residents present in the nursing home at the time of the outbreak. INTERVENTIONS: Public health interventions included recommendations regarding hygiene, cohorting of residents and staff, closure to further admissions, and prompt reporting of illness; and virologic and serologic studies of residents. RESULTS: Of the 69 residents (mean age, 85.1 years), 35 fulfilled the case definition of acute respiratory illness. Influenza A infection was confirmed in 19 residents, and phylogenetic analysis of the resulting isolate, designated H3N2 A/Sydney/203/99, showed that it differed from strains isolated in eastern Australia during the same period. Serologic evidence of Bordetella infection was also found in 10 residents; however, stratified epidemiologic analysis pointed to influenza A as the cause of illness. CONCLUSIONS: The investigation revealed an unusual summer outbreak of influenza A concurrent with subclinical pertussis infection. Surveillance of acute respiratory illness in nursing homes throughout the year, rather than solely during epidemic periods, in combination with appropriate public health laboratory support, would allow initiation of a timely public health response to outbreaks of acute respiratory illness in this setting.

Aged↗

PubMed2000

Measles outbreak in young adults in Victoria, 1999.

OBJECTIVES: To describe an outbreak of measles in Victoria. DESIGN: Case series with cases identified through enhanced passive surveillance and outbreak-related active surveillance. SETTING: State of Victoria, 1999. MAIN OUTCOME MEASURES: Number of cases; epidemiological links and patterns of transmission; patient demographic features and vaccination status; complications. RESULTS: 75 cases were identified (74 laboratory-confirmed; and one epidemiologically linked to a laboratory-confirmed case), with onset between 11 February and 2 May 1999. The first case was in a 21-year-old woman who had recently holidayed in Bali and worked at a large cinema complex in Melbourne. Sixteen cases occurred in people who had contact with the index case at the cinema on one evening. The outbreak spread to regional Victoria and South Australia. Median age of patients was 22 years; 64 (85%) were born between 1968 and 1981, with only one patient in the age group targeted by the primary school component of the 1998 Australian Measles Control Campaign; this child had not been vaccinated. More than a third of patients (28) were hospitalised (total, 97 inpatient days), and five were healthcare workers. CONCLUSIONS: This outbreak was caused by international importation of measles virus. It highlights the change in epidemiology of measles in Australia, from a disease of childhood to one predominantly affecting young adults. A strong two-dose childhood vaccination program, vigilant surveillance, and rapid response to outbreaks will continue to be the basis of measles control, but better protection for young adults should be considered.

Adolescent↗

PubMedDate not supplied

[Brazilian purpuric fever. Fast characterization of invasive strains of Haemophilus aegyptius].

Strains of H. aegyptius isolated during outbreak of Brazilian Purpuric Fever (BPF) in Brazil were characterized antigenically by slide agglutination test utilizing antiserum produced with a H. aegyptius strain isolated from blood culture from a patient with BPF. By means of this method, it were identified H. aegyptius strains responsible for outbreaks of conjunctivitis with identical antigenic characteristics to strains isolated from BPF. The sensitivity and specificity of slide seroagglutination test was 97.7% and 89.6% respectively; therefore this assay was efficient to be used as a screening method in the studies of purulent conjunctivitis for detecting high risk populations for BPF, and to implement measures that will increase the efficiency of epidemiologic surveillance.

Acute Disease↗

PubMed2006

[Two patients with mumps].

Two patients, men aged 17 and 19 years respectively, were admitted with parotitis epidemica and orchitis caused by mumps. The second patient also had meningitis. PCR analysis revealed that, in both cases, the causative agentwas a mumps virus that was genetically related to a wild-type virus responsible for an outbreak in Singapore. This viral strain was also responsible for a mumps outbreak at Hotel School The Hague in September 2004. Both patients were not fully vaccinated. Both patients were from regions in which clustering of patients with clinical signs of mumps has been seen. Interestingly, a number of patients with confirmed mumps had been fully vaccinated. Possible explanations for the increase in mumps cases include low vaccination and immunity levels, primary and secondary vaccine failure and the emergence of genetically disparate mumps viruses.

Adolescent↗

PubMed1989

Prevalence of enterotoxigenic Escherichia coli strains in outbreaks and sporadic cases of diarrhoea in Spain.

Escherichia coli strains isolated 1985-1988 in Spain from patients with diarrhoea were examined; 1170 strains were isolated from 582 sporadic cases of diarrhoea in children, and seven strains were associated with seven outbreaks of diarrhoea. Strains positive for STa enterotoxin production in the infant mouse test were also assayed for production of LT enterotoxin on Vero cells and by a coagglutination test. Thirty-one strains were STa positive: 28 were isolated from 16 (2.7%) sporadic cases of diarrhoea and three were responsible for outbreaks. The majority of STa+LT- strains from both outbreaks and sporadic cases were serotype O153:H45 and expressed the CFA/I colonization factor antigen. Enterotoxigenic STa+LT- strains of serotype O27:H7 and STa+LT+ CFA/II+ strains of serotype O6:K15:H16 were also isolated frequently from sporadic cases.

Antigens, Bacterial↗

PubMed1999

A method to detect low levels of enteric viruses in contaminated oysters.

Direct isolation and identification of pathogenic viruses from oysters implicated in gastroenteritis outbreaks are hampered by inefficient methods for recovering viruses, naturally occurring PCR inhibitors, and low levels of virus contamination. In this study we focused on developing rapid and efficient oyster-processing procedures that can be used for sensitive PCR detection of viruses in raw oysters. Poliovirus type 3 (PV3) Sabin strain was used to evaluate the efficacy of virus recovery and the removal of PCR inhibitors during oyster-processing procedures. These procedures included elution, polyethylene glycol precipitation, solvent extraction, and RNA extraction. Acid adsorption-elution in which glycine buffer (pH 7.5) was used was found to retain fewer inhibitors than direct elution in which glycine buffer (pH 9.5) was used. RNA extraction in which a silica gel membrane was used was more effective than single-step RNA precipitation for removing additional nonspecific PCR inhibitors. The final 10-microl volume of RNA concentrates obtained from 2 g of oyster tissue (concentration factor, 200-fold) was satisfactory for efficient reverse transcription-PCR detection of virus. The overall detection sensitivity of our method was 1 PFU/g of oyster tissue initially seeded with PV3. The method was utilized to investigate a 1998 gastroenteritis outbreak in California in which contaminated oysters were the suspected disease transmission vehicle. A genogroup II Norwalk-like virus was found in two of three recalled oyster samples linked by tags to the harvest dates and areas associated with the majority of cases. The method described here improves the response to outbreaks and can be used for rapid and sensitive detection of viral agents in outbreak-implicated oysters.

Animals↗

PubMed1993

Bordetella pertussis and Bordetella parapertussis: two immunologically distinct species.

Bordetella pertussis and Bordetella parapertussis are closely related species. Both are responsible for outbreaks of whooping cough in humans and produce similar virulence factors, with the exception of pertussis toxin, specific to B. pertussis. Current pertussis whole-cell vaccine will soon be replaced by acellular vaccines containing major adhesins (filamentous hemagglutinin and pertactin) and major toxin (pertussis toxin). All of these factors are antigens that stimulate a protective immune response in the murine respiratory model and in clinical assays. In the present study, we examined the protective efficacies of these factors, and that of adenylate cyclase-hemolysin, another B. pertussis toxin, against B. parapertussis infection in a murine respiratory model. As expected, pertussis toxin did not protect against B. parapertussis infection, since this bacterium did not express this protein, but the surprising result was that none of the other factors were protective against B. parapertussis infection. Furthermore, B. parapertussis adenylate cyclase-hemolysin, although it protected against B. parapertussis infection, did not protect against B. pertussis infection. Despite a high degree of homology between both B. pertussis and B. parapertussis species, no cross-protection was observed. Our results outline the fact that, as in other gram-negative bacteria, Bordetella surface proteins vary immunologically.

Adenylate Cyclase Toxin↗

PubMed1996

An outbreak of horseshoe crab poisoning in Chon Buri, Thailand: clinical, toxicologic and therapeutic considerations.

In 1994-1996, an outbreak of horseshoe crab poisoning by eating toxic eggs of the horseshoe crab Carcinoscorpius rotundicauda affected over 100 persons in Chon Buri which located on the eastern coast of Thailand. We discuss clinical description and management of this first major outbreak. The responsible toxin has been partially purified by means of ultrafiltration and high performance liquid chromatography. The horseshoe crab toxin is identified as tetrodotoxin (TTX) and anhydro TTX.

Animals↗

PubMedDate not supplied

Shortage of vaccines during a yellow fever outbreak in Guinea.

A yellow fever epidemic erupted in Guinea in September, 2000. From Sept 4, 2000, to Jan 7, 2001, 688 instances of the disease and 225 deaths were reported. The diagnosis was laboratory confirmed by IgM detection in more than 40 patients. A mass vaccination campaign was limited by insufficient international stocks. After the epidemic in Guinea, the International Coordinating Group on Vaccine Provision for Epidemic Meningitis Control decided that 2 million doses of 17D yellow fever vaccine, being stored as part of a UNICEF stockpile, should be used only in response to outbreaks.

Disease Outbreaks↗