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[Chronicle of an announced pandemic?].

In the last years our country has been affected by several outbreaks of infectious diseases such as Cholera and Hanta virus and recently, by pathogens associated to red tide. Chile was able to manage those emergencies using the local health system. The new threat that may emerge and could eventually overcome that capacity, is the possible H5N1 influenza virus outbreak. Influenza is responsible for the most destructive pandemic, the Spanish influenza, that killed over 40 million individuals in 1918. The new influenza strain (H5N1) is at present endemic in poultry in Asia and has been associated to human fatal cases in Hong Kong and Vietnam. Even though this strain is not able yet to be transmitted among humans, evidence has accumulated that such ability could be reached by the new strain, since it was already detected in pigs. That particular evidence may indicate that the virus could adapt to infect humans, since a similar situation was observed in several of the influenza pandemics. The World Health Organization set a "task force" to develop a strategy that may help to control the virus spread. Several countries are already stocking anti-flu drugs and others are developing new vaccine that are currently been assayed in human volunteers. It is possible that we may have a vaccine before the outbreak; this development is even faster than for SARS. The mayor question to be addressed for developing countries is: what will be done if we do not have the vaccine on time?

Animals↗

An outbreak of Q fever probably due to contact with a parturient cat.

Thirty-three cases (24 definite, nine probable) of Q fever were diagnosed in Victoria County, Cape Breton, Nova Scotia from May to August, 1985. Twenty-six of the cases occurred in residents of Baddeck (population 900, attack rate 2.8 percent), and 21 of the cases occurred during the month of June. There was geographic clustering of the cases: 14 of the 33 (42 percent) lived or worked in four buildings located side by side in the center of town. A case control study revealed that 25 of 29 cases were exposed to a cat that gave birth to stillborn kittens on June 8, 1985 and had bled per vaginum for three weeks prior to delivery. The cat lived in one of the buildings where geographic clustering occurred and frequently visited the other buildings. None of the 40 control subjects was so exposed (p less than 0.001). This cat had an antibody titer of 1:512 to Coxiella burnetii phase 1 antigen and a titer of 1:1024 to phase 2 antigen. Exposure to cattle, sheep and goats, the traditional reservoirs of Q fever, was uncommon among patients and control subjects and none of eight cattle tested had antibodies to C burnetii phase I antigen. We conclude that the infected parturient cat was probably responsible for this outbreak of Q fever affecting 2.8 percent of the population of the town of Baddeck.

Adolescent↗

Vitamin D toxicosis in cats: natural outbreak and experimental study.

A pathological study on 5 of 21 cats affected naturally with systemic calcinosis was performed. The animals ranged in age from 1 to 9 years. Hematology and serum chemistry analyses showed the elevated values of phosphorus, blood urea nitrogen and serum creatinine. X-ray examination disclosed the increased density of systemic bones. Histologically, marked calcification was present at the vascular walls of almost all the organs including the lungs, trachea, kidneys, heart, aorta, alimentary tracts, choroid plexus and bones. In the lungs, kidneys and stomach, the calcified lesions were associated with deposition of oxalate crystals. Serum chemistry showed more elevated values of 25-hydroxycholecalciferol (vitamin D) of the affected cats than the normal level. Retrospective examination revealed that these cats had been fed the commercial pet foods containing a large amount of vitamin D (6,370 IU/100 g diet) from their young age, and its value was about ten times as much as that of the control food (680 IU/100 g diet). Pathological changes found in the cats from the experimental vitamin D3 toxicosis were similar to those in the natural cases. In addition, tissue levels of calcium, phosphorous and zinc in the lungs and kidneys were markedly elevated in both natural and vitamin D-intoxicated cases. These findings suggest that long-term feeding of the pet food containing excessive vitamin D was responsible for the outbreak of the systemic calcinosis in the cats.

Animals↗

A predominantly clonal multi-institutional outbreak of Clostridium difficile-associated diarrhea with high morbidity and mortality.

BACKGROUND: In March 2003, several hospitals in Quebec, Canada, noted a marked increase in the incidence of Clostridium difficile-associated diarrhea. METHODS: In 2004 we conducted a prospective study at 12 Quebec hospitals to determine the incidence of nosocomial C. difficile-associated diarrhea and its complications and a case-control study to identify risk factors for the disease. Isolates of C. difficile were typed by pulsed-field gel electrophoresis and analyzed for binary toxin genes and partial deletions in the toxin A and B repressor gene tcdC. Antimicrobial susceptibility was evaluated in a subgroup of isolates. RESULTS: A total of 1703 patients with 1719 episodes of nosocomial C. difficile-associated diarrhea were identified. The incidence was 22.5 per 1000 admissions. The 30-day attributable mortality rate was 6.9 percent. Case patients were more likely than matched controls to have received fluoroquinolones (odds ratio, 3.9; 95 percent confidence interval, 2.3 to 6.6) or cephalosporins (odds ratio, 3.8; 95 percent confidence interval, 2.2 to 6.6). A predominant strain, resistant to fluoroquinolones, was found in 129 of 157 isolates (82.2 percent), and the binary toxin genes and partial deletions in the tcdC gene were present in 132 isolates (84.1 percent). CONCLUSIONS: A strain of C. difficile that was resistant to fluoroquinolones and had binary toxin and a partial deletion of the tcdC gene was responsible for this outbreak of C. difficile-associated diarrhea. Exposure to fluoroquinolones or cephalosporins was a risk factor.

Aged↗

Pathotypical and genotypical characterization of strains of Newcastle disease virus isolated from outbreaks in chicken and goose flocks in some regions of China during 1985-2001.

Twenty-nine strains of Newcastle disease virus (NDV) isolated from outbreaks in chicken and goose flocks in several regions of China during 1985-2001 were characterized pathotypically and genotypically. All except one of these strains were velogenic. For genotyping, phylogenetic tree analysis (nt 47-420), restriction site mapping (nt 334-1682) and residue substitution analysis (residues 4-124) of the F gene were performed using sequences of our isolates and sequences of selected NDV strains from GenBank. The results revealed that most of these newly characterized strains belonged to six novel genetic groups that were designated as VIf, VIg, VIIc, VIId, VIIe and IX. The genotype IX viruses, to which the China challenge strain F48E8 used for vaccine evaluation belonged, were found only in China and still induced sporadic infections in certain areas. Isolates belonging to group VIf and VIg were distinct from previously reported members of genotype VI, with genetic distance from 2.5 to 12.1%. Subgenotype VIIc, VIId and VIIe viruses, which were distributed in clusters in the phylogenetic tree distinct from members of subgenotypes VIIa and VIIb, were responsible for disease outbreaks in chicken and goose flocks and circulated predominantly in southern China in recent years. Finally, cross-protective testing showed that specific-pathogen free (SPF) chickens vaccinated with La Sota vaccines can be fully protected against challenge by strains from genetic groups VIb, VIg, VIId and IX, indicating that the antigenic differences between strains of various genotypes are insufficient to change the cross-protection conferred by the commonly used vaccine.

Amino Acid Sequence↗

A canine distemper outbreak in Alaska: diagnosis and strain characterization using sequence analysis.

Vaccination with modified-live vaccines has been very effective in reducing the incidence of canine distemper, a disease that can be devastating in unvaccinated populations. A diagnostic submission to the Animal Health Diagnostic Laboratory at Michigan State University, East Lansing, Michigan, involved a case in which several hundred dogs in an Alaskan town died in a suspected canine distemper outbreak. Cytoplasmic and intranuclear eosinophilic inclusion bodies, consistent with canine distemper virus (CDV) infection, were found in urinary bladder, spleen, lung, and salivary gland. Direct fluorescent antibody test gave results that could be considered positive for canine distemper. Because of the condition of the tissues received, the histopathology and fluorescent antibody-staining results were suggestive but not conclusive of CDV. In this study, immunohistochemistry, reverse transcriptase-polymerase chain reaction (RT-PCR), and DNA sequencing were used to confirm the presence of canine distemper virus in these tissues and to perform molecular characterization of the virus. Immunohistochemistry showed the presence of the virus in spleen, lung, and salivary gland. Viral RNA was detected by RT-PCR in brain, spleen, liver, lung, and kidney, both with nucleoprotein and phosphoprotein (P)-gene-specific primers. Sequence alignment and phylogenetic analysis of a 540-bp P-gene fragment of the Alaskan strain with corresponding sequences of 2 vaccine and 7 wild-type CDV strains showed that the virus responsible for the outbreak was closely related to a virulent strain of distemper virus from Siberia.

Alaska↗

Vibrio cholerae O1 outbreak isolates in Mozambique and South Africa in 1998 are multiple-drug resistant, contain the SXT element and the aadA2 gene located on class 1 integrons.

The characteristics of Vibrio cholerae O1 biotype El Tor, serotype Ogawa isolates from outbreaks of cholera in 1998 amongst migrant workers in the South African provinces of Gauteng and Mpumalanga, on the border of Mozambique, are reported. The isolates seem to have originated from the same clone since they are of two closely related BglI ribotypes. These ribotypes had a high similarity to ribotypes of V. cholerae O1 recently found in three South-east Asian countries. Isolates were resistant to furazolidone, streptomycin, sulfamethoxazole, trimethoprim and tetracycline. Only two isolates contained plasmids of 54 and 63 kb in size. PCR and DNA sequencing revealed that the chromosomally located resistance determinants present included an aadA2 gene cassette contained in a class 1 integron; the SXT element, which is a transposon-like element containing resistance genes; and the tetA gene. A co-transfer of chromosomal closely located genes encoding the SXT element and tetA was shown by mating experiments, PCR and pulsed-field gel electrophoresis analyses. Our study shows for the first time that multiple-resistant V. cholerae O1 isolates containing class 1 integrons and the SXT element were responsible for cholera outbreaks in Southern Africa. Studies are needed to determine the spread of this multiple-resistant O1 strain and further genetic details of the association of the SXT element, tetA and class 1 integrons, including their means of transfer.

Anti-Bacterial Agents↗

[Outbreak of gastroenteritis caused by Norwalk virus at a senior citizens assisted living facility in Granada, Spain].

BACKGROUND: The outbreaks of acute gastroenteritis caused by a virus are currently one of the health problems having the greatest impact on those living in senior citizen facilities. The objective of this study is that of investigating the causes of the start and contagion of an outbreak of acute gastroenteritis caused by a Norwalk-Like virus. METHOD: At a senior citizen living facility with 141 residents and 71 employees exposed, the relations between the disease in question and different independent variables: personal traits, features of location, date of onset of symptoms, clinical pattern of the disease and causal factors (food and drinking water intake). A descriptive study, a contingency table and a hypothesis ?2 test, design of cases and controls with the calculation of the unprocessed and subsequently adjusted Odds Ratio (IC 95%) were carried out using logic regression. RESULTS: No significant differences were found in the personal trait and features of location variables. The attack rate among the residents was 30.1%, being 21.12% among the employees. In the adjusted Odds Ratio calculation, solely the whipped cream mousse showed causal relationship values (adjusted Odds Ratio = 4.66; IC-95% 1.15-18.91; p = 0.031). Ten patient stool samples were sent for analysis, no disease-causing bacteria having been detected, Norwalk-Like virus however having been isolated in three samples. CONCLUSIONS: The whipped cream mousse having been found to possibly have been responsible for the outbreak is a first involving Norwalk virus, but this result is subject to limitations, such as the possible bias of classification due to failing to recall having eaten foods. Even so, this is an element to be taken into account in the control of acute viral gastroenteritis.

Acute Disease↗

Prolonged outbreak of infection due to TEM-21-producing strains of Pseudomonas aeruginosa and enterobacteria in a nursing home.

Over a 6-year period, 24 extended-spectrum beta-lactamase (ESBL)-producing isolates of Pseudomonas aeruginosa were collected from 18 patients living in a nursing home. These isolates had a delayed development of a red pigment and exhibited a similar antibiotype (resistance to all beta-lactams except for imipenem and to gentamicin, tobramycin, netilmicin, ciprofloxacin, and rifampin) associated with the production of the TEM-21 beta-lactamase and a type II 3'-N-aminoglycoside acetyltransferase [AAC(3)-II] enzyme. Surprisingly, serotyping showed that these isolates belonged to four successive serotypes (P2, P16, P1, and PME), although molecular typing by PCR methods and pulsed-field gel electrophoresis yielded identical or similar profiles. Moreover, in all isolates the bla(TEM-21) gene was part of a chromosomally located Tn801 transposon truncated by an IS6100 element inserted within the resolvase gene, and the aac(3)-II gene was adjacent to this structure. During the same period, 17 ESBL-producing isolates of enterobacteria were also collected from 10 of these patients. These isolates harbored a similar large plasmid that contained the bla(TEM-21) and the aac(3)-II genes and that conferred additional resistance to sulfonamides and chloramphenicol, as well as to kanamycin, tobramycin, netilmicin, and amikacin, conveyed by an AAC(6')-I enzyme. The bla(TEM-21) gene was part of the Tn801 transposon disrupted by IS4321. Thus, a single clone of P. aeruginosa that had undergone a progressive genetic drift associated with a change in serotype appeared to be responsible for an outbreak of nosocomial infections in a nursing home. This strain has probably acquired the bla(TEM-21)-encoding plasmid that was epidemic among the enterobacteria at the institution, followed by chromosomal integration and genomic reorganization.

Aged↗

Principles of measles control.

WHO's Expanded Programme on Immunization has significantly helped to reduce global morbidity and mortality from measles. Recently, some African countries with high vaccine coverage levels have reported measles outbreaks in children above the current target age group for immunization. Outbreaks such as these are to be expected, unless close to 100% of the population are immunized with a vaccine which is 100% effective. Success of an immunization programme requires identification of the distribution and ages of susceptible children and reduction of their concentration throughout the community. Priority should be given to urban and densely populated rural areas. In large urban areas, high coverage of infants must be achieved soon after the age at which they lose their maternal antibodies and become susceptible. This will be facilitated by the introduction of high-dose measles vaccines which can be given at 6 months of age. Where measles incidence is increasing among children aged over 2 years, immunization of older children may be considered during contacts with the health care system, or at primary school entry, if this does not divert resources from immunization of younger children. Health workers should be informed of the predicted changes in measles epidemiology following immunization. The collection, analysis and use of data on measles (vaccine coverage, morbidity and mortality) should be improved at all levels of the health care system in order to monitor the immunization programme's overall impact, identify pockets of low coverage, and allow early detection of and response to measles outbreaks.

Africa↗

Epidemics of diarrhea caused by a clindamycin-resistant strain of Clostridium difficile in four hospitals.

BACKGROUND: Large outbreaks of diarrhea caused by a newly recognized strain of Clostridium difficile occurred in four hospitals located in different parts of the United States between 1989 and 1992. Since frequent use of clindamycin was associated with the outbreak in one of the hospitals, we examined the resistance genes of the epidemic-strain isolates and studied the role of clindamycin use in these outbreaks. METHODS: Case-control studies were performed at three of the four hospitals to assess the relation of the use of clindamycin to C. difficile-associated diarrhea. All isolates of the epidemic strain and representative isolates of other strains identified during each outbreak were tested for susceptibility to clindamycin. Chromosomal DNA from these representative isolates was also analyzed by dot blot hybridization and amplification with the polymerase chain reaction (PCR) with the use of probes and primers from a previously described determinant of erythromycin resistance - the erythromycin ribosomal methylase B (ermB) gene - found in C. perfringens and C. difficile. RESULTS: In a stratified analysis of the case-control studies with pooling of the results according to the Mantel-Haenszel method, we found that the use of clindamycin was significantly increased among patients with diarrhea due to the epidemic strain of C. difficile, as compared with patients whose diarrhea was due to nonepidemic strains (pooled odds ratio, 4.35; 95 percent confidence interval, 2.02 to 9.38; P<0.001). Exposure to other types of antibiotics or hospitalization in a surgical ward was not significantly associated with the risk of C. difficile-associated diarrhea due to the epidemic strain. All epidemic-strain isolates were highly resistant to clindamycin (minimal inhibitory concentration, >256 microg per milliliter). DNA hybridization and PCR analysis showed that all these isolates had an ermB gene, which encodes a 23S ribosomal RNA methylase that mediates resistance to macrolide, lincosamide, and streptogramin antibiotics. Only 15 percent of the nonepidemic strains were resistant to clindamycin. CONCLUSIONS: A strain of C. difficile that is highly resistant to clindamycin was responsible for large outbreaks of diarrhea in four hospitals in different states. The use of clindamycin is a specific risk factor for diarrhea due to this strain. Resistance to clindamycin further increases the risk of C. difficile-associated diarrhea, an established complication of antimicrobial use.

Anti-Bacterial Agents↗

Synergy between nisin and select lactates against Listeria monocytogenes is due to the metal cations.

Listeria monocytogenes, a major foodborne pathogen, has been responsible for many outbreaks and recalls. Organic acids and antimicrobial peptides (bacteriocins) such as nisin are produced by lactic acid bacteria and are commercially used to control pathogens in some foods. This study examined the effects of lactic acid (LA) and its salts in combination with a commercial nisin preparation on the growth of L. monocytogenes Scott A and its nisin-resistant mutant. Because of an increase in its activity at a lower pH, nisin was more active against L. monocytogenes when used in combination with LA. Most of the salts of LA, including potassium lactate, at up to 5% partially inhibited the growth of L. monocytogenes and had no synergy with nisin. Zinc and aluminum lactate, as well as zinc and aluminum chloride (0.1%), worked synergistically with 100 IU of nisin per ml to control the growth of L. monocytogenes Scott A. No synergy was observed when zinc or aluminum lactate was used with nisin against nisin-resistant L. monocytogenes. The nisin-resistant strain was more sensitive to Zn lactate than was wild-type L. monocytogenes Scott A; however, the cellular ATP levels of the nisin-resistant strain were not significantly affected. Changes in the intracellular ATP levels of the wild-type strain support our hypothesis that pretreatment with zinc lactate sensitizes cells to nisin. The similar effects of thesalts of hydrochloric and lactic acids support the hypothesis that metal cations are responsible for synergy with nisin.

Aluminum↗

Emergence and rapid spread of carbapenem resistance during a large and sustained hospital outbreak of multiresistant Acinetobacter baumannii.

Beginning in 1992, a sustained outbreak of multiresistant Acinetobacter baumannii infections was noted in our 1,000-bed hospital in Barcelona, Spain, resulting in considerable overuse of imipenem, to which the organisms were uniformly susceptible. In January 1997, carbapenem-resistant (CR) A. baumannii strains emerged and rapidly disseminated in the intensive care units (ICUs), prompting us to conduct a prospective investigation. It was an 18-month longitudinal intervention study aimed at the identification of the clinical and microbiological epidemiology of the outbreak and its response to a multicomponent infection control strategy. From January 1997 to June 1998, clinical samples from 153 (8%) of 1,836 consecutive ICU patients were found to contain CR A. baumannii. Isolates were verified to be A. baumannii by restriction analysis of the 16S-23S ribosomal genes and the intergenic spacer region. Molecular typing by repetitive extragenic palindromic sequence-based PCR and pulsed-field gel electrophoresis showed that the emergence of carbapenem resistance was not by the selection of resistant mutants but was by the introduction of two new epidemic clones that were different from those responsible for the endemic. Multivariate regression analysis selected those patients with previous carriage of CR A. baumannii (relative risk [RR], 35.3; 95% confidence interval [CI], 7.2 to 173.1), those patients who had previously received therapy with carbapenems (RR, 4.6; 95% CI, 1.3 to 15.6), or those who were admitted into a ward with a high density of patients infected with CR A. baumannii (RR, 1.7; 95% CI, 1.2 to 2.5) to be at a significantly greater risk for the development of clinical colonization or infection with CR A. baumannii strains. In accordance, a combined infection control strategy was designed and implemented, including the sequential closure of all ICUs for decontamination, strict compliance with cross-transmission prevention protocols, and a program that restricted the use of carbapenem. Subsequently, a sharp reduction in the incidence rates of infection or colonization with A. baumannii, whether resistant or susceptible to carbapenems, was shown, although an alarming dominance of the carbapenem-resistant clones was shown at the end of the study.

Acinetobacter↗

Measles eradication: recommendations from a meeting cosponsored by the World Health Organization, the Pan American Health Organization, and CDC.

Recent successes in interrupting indigenous transmission of measles virus in the Americas and in the United Kingdom prompted the World Health Organization (WHO), Pan American Health Organization (PAHO), and CDC to convene a meeting in July, 1996 to consider the feasibility of global measles eradication. Presentations at the meeting included an overview of global measles control and elimination efforts; detailed reviews of successful measles elimination efforts in Latin America, the English-speaking Caribbean, Canada, and the United States; surveillance for clinical disease; laboratory tools for antibody detection and virus identification; and other factors that might influence the feasibility of disease eradication. With this background information, meeting organizers asked participants to address five questions: 1) Is global measles eradication feasible? 2) Is measles eradication feasible with current vaccines? 3) What are the appropriate vaccination strategies for measles eradication? 4) How should surveillance for measles be carried out? 5) What role should outbreak control play in the strategy to eliminate measles? Participants agreed that measles eradication is technically feasible with available vaccines and recommended adoption of the goal of global eradication with a target date during 2005-2010, with the proviso that measles eradication efforts should not interfere with poliomyelitis eradication but should build on the successes of the global Poliomyelitis Eradication Initiative. Although existing vaccines are adequate for eradication, vaccination strategies that rely on administration of a single dose of vaccine are not. In the Americas, sustained interruption of indigenous measles virus transmission has been achieved through a three-tiered vaccination strategy that includes a) "catch-up" vaccination of all persons aged 1-14 years, regardless of disease history or vaccination status; b) "keep-up" vaccination of > or = 90% of children in each successive birth cohort at age 12 months and c) "follow-up" campaigns designed to vaccinate all persons within a specific age range whenever the number of susceptible persons in the preschool-aged population approximates the size of a typical birth cohort (in practice, every 3-5 years). In other regions, different strategies may be optimal. Surveillance, a critical component of any strategy to eliminate or eradicate measles, has two functions: to assess the effectiveness of the measles elimination strategy and to detect circulation of measles virus in a population. Systematic surveillance based on clinical diagnosis should be implemented early in any measles elimination program. In countries attempting to eliminate indigenous measles, all isolated cases of measles and at least one case in each chain of transmission should be confirmed by laboratory tests. Specimens for virus isolation (e.g., urine, nasopharyngeal swabs, or blood) should be collected in conjunction with field investigations. Vaccination campaigns generally have not proved to be effective responses to measles outbreaks. Outbreaks should be treated as opportunities to reinforce surveillance and to identify measures to prevent future outbreaks. The major obstacles to measles eradication are not technical but perceptual, political, and financial. Measles is often mistakenly perceived as a mild illness. This misperception, which is particularly prevalent in industrialized countries, can inhibit the development of public and political support for the allocation of resources required for an effective elimination effort. The disease burden imposed by measles should be documented, particularly in industrialized countries, so that this information can be used to educate parents, medical practitioners, public health workers, and political leaders about the benefits of measles eradication.

Disease Outbreaks↗

Neurotoxin domoic acid produces cytotoxicity via kainate- and AMPA-sensitive receptors in cultured cortical neurones.

Domoic acid, a naturally occurring kainoid, has been responsible for several outbreaks of fatal poisoning after shellfish ingestion, and we examined its neurotoxic mechanism in cultured murine cortical neurones. Using observations of neuronal viability and morphology, exposure to domoic acid for 24 h was found to induce substantial concentration-dependent neuronal cell death. Domoic acid-mediated neuronal death was attenuated by the non-N-methyl-D-aspartate receptor antagonist 6-cyano-7-nitro-quinoxaline-2,3-dione and the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptor-selective antagonist LY293558 ((3S,4aR,6R,8aR)-6-[2-(1H-tetrazol-5-yl)-ethyl]-1,2,3, 4,4a,5,6,7,8,8a-decahydroisoquinoline-3-carboxylic acid), but unaffected by NS-102 (5-nitro-6,7,8,9-tetrahydrobenzo[g]indole-2, 3-dione-3-oxime)--a low-affinity kainate receptor antagonist. Domoic acid was equipotent with (S)-AMPA (EC50 values 3.8 and 3.4 microM respectively); however, (S)-AMPA induced only 50% cell death compared to > 80% cell death induced by domoic acid. Kainate also killed > 80% of cortical neurones; however, domoic acid was about 19 times more potent than kainate (EC50 75 microM). We show the potent neurotoxicity of domoic acid for the first time in a pure neuronal model and indicate that domoic acid acts via high-affinity AMPA- and kainate-sensitive glutamate receptors to produce excitotoxic cell death.

Animals↗

Implementing a public web based GIS service for feedback of surveillance data on communicable diseases in Sweden.

BACKGROUND: Surveillance data allow for analysis, providing public health officials and policy-makers with a basis for long-term priorities and timely information on possible outbreaks for rapid response (data for action). In this article we describe the considerations and technology behind a newly introduced public web tool in Sweden for easy retrieval of county and national surveillance data on communicable diseases. METHODS: The web service was designed to automatically present updated surveillance statistics of some 50 statutory notifiable diseases notified to the Swedish Institute for Infectious Disease Control (SMI). The surveillance data is based on clinical notifications from the physician having treated the patient and laboratory notifications, merged into cases using a unique personal identification number issued to all Swedish residents. The web service use notification data from 1997 onwards, stored in a relational database at the SMI. RESULTS: The web service presents surveillance data to the user in various ways; tabulated data containing yearly and monthly disease data per county, age and sex distribution, interactive maps illustrating the total number of cases and the incidence per county and time period, graphs showing the total number of cases per week and graphs illustrating trends in the disease data. The system design encompasses the database (storing the data), the web server (holding the web service) and an in-the-middle computer (to ensure good security standards). CONCLUSIONS: The web service has provided the health community, the media, and the public with easy access to both timely and detailed surveillance data presented in various forms. Since it was introduced in May 2003, the system has been accessed more than 1,000,000 times, by more than 10,000 different viewers (over 12.600 unique IP-numbers).

Age Distribution↗

Two contiguous outbreaks of dengue type 2 in north Queensland.

OBJECTIVES: To investigate two outbreaks of dengue type 2 in north Queensland, one in the Torres Strait beginning in late 1996, the other in a Cairns suburb in early 1997. DESIGN: Epidemiological investigation of all laboratory-confirmed cases of dengue, entomological investigation of the local environment, and laboratory analysis of the isolated dengue viruses. MAIN OUTCOME MEASURES: Numbers of confirmed and of locally acquired cases; virus serotype; comparison of nucleotide sequences between viruses isolated from the two outbreaks; and Breteau Index (BI = number of containers with larvae of the mosquito vector Aedes aegypti found per 100 houses investigated) on the affected islands and in the Cairns suburb. RESULTS: There were 201 confirmed cases of dengue in the Torres Strait outbreak, which lasted nearly seven months, and seven confirmed cases in the Cairns outbreak, which lasted about nearly 11 weeks. Most (190) were confirmed as dengue type 2. Nucleotide sequencing of viruses isolated from the two outbreaks showed they were identical. Ae. aegypti breeding sites were very common on the five Torres Strait islands surveyed (BIs, 73-219--high risk), but less so in the Cairns suburb (BI, 23). The most common breeding sites were water storage reservoirs, particularly rainwater tanks, on the outer Torres Strait islands, discarded containers (such as plastic containers, buckets and tyres) on Thursday Island, and garden items (such as flowerpot bases and jars) in Cairns. CONCLUSIONS: The virus responsible for the Cairns outbreak was most probably introduced from the Torres Strait, whereas the virus responsible for the Torres Strait outbreak was imported from Papua New Guinea. Preventive strategies tailored to specific locations are needed to reduce breeding of Ae. aegypti in north Queensland, and the consequent risk of future outbreaks of dengue.

Adolescent↗

Bats are natural reservoirs of SARS-like coronaviruses.

Severe acute respiratory syndrome (SARS) emerged in 2002 to 2003 in southern China. The origin of its etiological agent, the SARS coronavirus (SARS-CoV), remains elusive. Here we report that species of bats are a natural host of coronaviruses closely related to those responsible for the SARS outbreak. These viruses, termed SARS-like coronaviruses (SL-CoVs), display greater genetic variation than SARS-CoV isolated from humans or from civets. The human and civet isolates of SARS-CoV nestle phylogenetically within the spectrum of SL-CoVs, indicating that the virus responsible for the SARS outbreak was a member of this coronavirus group.

Amino Acid Sequence↗