Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The genus Yersinia is composed of 11 species, three of which are pathogenic in humans. The three pathogens, Y. pestis, Y. enterocolitica, and Y. pseudotuberculosis, cause a broad spectrum of disease ranging from pneumonic plague to acute gastroenteritis. Each of the three requires a large, well-defined plasmid for full virulence, as well as many chromosomally encoded virulence factors (CEVF). This review will describe these CEVF and their roles in virulence. In addition, a possible model for key events in Y. enterocolitica pathogenesis is described based on information revealed by analysis of several of the CEVF.
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PMID:Yersinia virulence: more than a plasmid. 1175 Jul 96

A prospective study was carried out on 210 cases of children under 10 years of age with fever. Cases of gastroenteritis, respiratory tract infections, and suspected sepsis in children seen or admitted to the pediatric hospital were studied. Clinical and microbiological data were recorded in a questionnaire or obtained from patient medical records. Most of the children with septicemia (71.3 per cent) were less than 1 year old. Focal source of bacteremia was gastroenteritis (40.4 per cent), pneumonia or bronchopneumonia (20 per cent), meningitis (7.4 per cent), and urinary tract infections (7.4 per cent). The predominant pathogens isolated from blood or stool specimens were gram-positive bacteria (53.3 per cent), mainly Streptococcus pneumoniae and coagulase-negative Staphylococcus spp. The gram-negative bacteria (45.6 per cent) were mainly Escherichia coli, Klebsiella pneumoniae, Haemophilus influenzae, Neisseria meningitidis, and Yersinia spp. One case of Candida albicans (1.1 per cent) was reported. Pasteurella pneumotropica was reported in two cases for the first time. The mortality rate was 4 per cent, mostly from septicemia cases. Long duration of hospitalization (> 10 days) and parenteral feeding were identified as risk factors. Resistance of the isolated pathogens to several commonly used antibiotics was observed. Empirical treatment with antibiotics is recommended only in life-threatening cases.
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PMID:Bacteremia in children: etiologic agents, focal sites, and risk factors. 1182 4

A prospective study of 62 chemotherapy-induced neutropenic episodes in patients with acute leukaemia was conducted to determine the incidence and causes of abdominal infections, and to assess the diagnostic value of the combined use of ultrasonography (US) and microbiology. Each patient underwent US of liver, gallbladder and complete bowel before chemotherapy, on days 2-4 after the end of chemotherapy and in cases of fever, diarrhoea or abdominal pain. US was combined with a standardized clinical examination and a broad spectrum of microbiological investigations. From January to August 2001, 243 US examinations were performed. The overall incidence of abdominal infectious diseases was 17.7% (11 out of 62, 95% confidence interval (CI): 9-29%). Four patients (6.5%) developed neutropenic enterocolitis; two of them died, two survived. Bowel wall thickening (BWT) > 4 mm in these four patients ranged from 5.8 to 23.6 mm and was detected only in one patient with mucositis. In three other patients (4.8%) Clostridium difficile, and in one patient (1.6%) Campylobacter jejuni, caused enterocolitis without BWT. Cholecystitis was diagnosed in three patients (4.8%) and hepatic candidiasis was strongly suspected in one patient. Abdominal infections caused by gastroenteritis viruses, cytomegalovirus (CMV) or Cryptosporidium were not observed. We conclude that in neutropenic patients with acute leukaemia receiving chemotherapy: (i) BWT is not a feature of chemotherapy-induced mucositis and should therefore be considered as sign of infectious enterocolitis; (ii) viruses, classic bacterial enteric pathogens (Salmonella, Shigella, Yersinia, Campylobacter, Aeromonas, Vibrio subsp., enterohaemorrhagic Escherichia coli) and Cryptosporidium have a very low incidence; and (iii) abdominal infections may be underestimated when US is not used in every patient with abdominal pain.
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PMID:Abdominal infections in patients with acute leukaemia: a prospective study applying ultrasonography and microbiology. 1197 17

In 2000, the OzFoodNet network was established to enhance surveillance of foodborne diseases across Australia. OzFoodNet consists of 7 sites and covers 68 per cent of Australia's population. During 2001, sites reported 15,815 cases of campylobacteriosis, 6,607 cases of salmonellosis, 326 cases of shigellosis, 71 cases of yersiniosis, 61 cases of listeriosis, 47 cases of shiga-toxin producing E. coli and 5 cases of haemolytic uraemic syndrome. Sites reported 86 foodborne outbreaks affecting 1,768 people, of whom 4.0 per cent (70/1,768) were hospitalised and one person died. There was a wide range of foods implicated in these outbreaks and the most common agent was S. Typhimurium. Sites reported two international outbreaks; one of multi-drug resistant S. Typhimurium Definitive Type 104 due to helva imported from Turkey, and one of S. Stanley associated with dried peanuts from China. The National Centre for Epidemiology and Population Health conducted a national survey of gastroenteritis. Preliminary data from interviews of 2,417 people suggests that the incidence of foodborne illness is significantly higher than previously thought. OzFoodNet initiated case control studies into risk factors for Campylobacter, Salmonella, Listeria, and shiga-toxin producing E. coli. OzFoodNet developed a foodborne disease outbreak register for Australia; established a network of laboratories to type Campylobacter; prepared a survey of pathology laboratories; reviewed Australian data on listeriosis; and assessed the usefulness of sentinel surveillance for gastroenteritis. This program of enhanced surveillance has demonstrated its capacity to nationally investigate and determine the causes of foodborne disease.
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PMID:Enhancing foodborne disease surveillance across Australia in 2001: the OzFoodNet Working Group. 1241 2

The aim of this article is to define the currently accepted role of antibacterials in the treatment of acute gastroenteritis in children. Most cases of acute gastroenteritis in children are viral, self-limited, and need only supportive treatment. Appropriate fluid and electrolyte therapy, with close attention to nutrition, remain central to therapy.Antibacterial therapy serves as an adjunct, to shorten the clinical course, eradicate causative organisms, reduce transmission, and prevent invasive complications. Selection of antibacterials to use in acute bacterial gastroenteritis is based on clinical diagnosis of the likely pathogen prior to definitive laboratory results. Antibacterial therapy should be restricted to specific bacterial pathogens and disease presentations. In general, infections with Shigella spp. and Vibrio cholera should usually be treated with antibacterials, while antibacterials are only used in severe unresponsive infections with Salmonella, Yersinia, Aeromonas, Campylobacter, Plesiomonas spp., and Clostridium difficile. Antibacterials should be avoided in enterohemorrhagic Escherichia coli infection. However, empiric therapy may be appropriate in the presence of a severe illness with bloody diarrhea and stool leucocytes, particularly in infancy and the immunocompromised. The benefits and risks of adverse drug reactions should be weighed before prescribing antibacterials. Moreover, a major concern is the emergence of antibacterial-resistant strains due to the widespread use of antibacterial agents.
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PMID:Acute gastroenteritis in children : what role for antibacterials? 1271 15

Results of the Dutch laboratory surveillance of bacterial gastroenteritis between 1991 and 2001 are presented and compared with recent findings in general practices and in the community. Between 1996 and 2000 the mean annual number of stools screened by sentinel laboratories was about 1000 samples/100,000 inhabitants, which is 4% of the estimated annual incidence of gastroenteritis in the Dutch population. Campylobacter (36/100,000 inhabitants) and salmonella (24/100,000 inhabitants) were the main pathogens isolated. Since 1996, the incidence of laboratory confirmed salmonellosis decreased by 30%, predominantly among young children. The incidence of campylobacter was highest in urban areas and Salmonella Enteritidis emerged as the predominant serotype in urban areas. Between 1991 and 2001, multi-resistant Salmonella Typhimurium DT104 emerged to comprise up to 15% of all salmonella isolates in 2001. Reported rates of Shigella spp. and Yersinia spp. varied little, with average annual incidences of 3.2 and 1.2 cases/100,000 inhabitants, respectively. Escherichia coli O157 (90% STEC) was scarcely found (0.26/100,000).
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PMID:Laboratory surveillance of bacterial gastroenteric pathogens in The Netherlands, 1991-2001. 1282 27

In 2002, OzFoodNet continued to enhance surveillance of foodborne diseases across Australia. The OzFoodNet network expanded to cover all Australian states and territories in 2002. The National Centre for Epidemiology and Population Health together with OzFoodNet concluded a national survey of gastroenteritis, which found that there were 17.2 (95% C.I. 14.5-19.9) million cases of gastroenteritis each year in Australia. The credible range of gastroenteritis that may be due to food each year is between 4.0-6.9 million cases with a mid-point of 5.4 million. During 2002, there were 23,434 notifications of eight bacterial diseases that may have been foodborne, which was a 7.7 per cent increase over the mean of the previous four years. There were 14,716 cases of campylobacteriosis, 7,917 cases of salmonellosis, 505 cases of shigellosis, 99 cases of yersiniosis, 64 cases of typhoid, 62 cases of listeriosis, 58 cases of shiga toxin producing E. coli and 13 cases of haemolytic uraemic syndrome. OzFoodNet sites reported 92 foodborne disease outbreaks affecting 1,819 persons, of whom 5.6 per cent (103/1,819) were hospitalised and two people died. There was a wide range of foods implicated in these outbreaks and the most common agent was Salmonella Typhimurium. Sites reported two outbreaks with potential for international spread involving contaminated tahini from Egypt resulting in an outbreak of Salmonella Montevideo infection and an outbreak of suspected norovirus infection associated with imported Japanese oysters. In addition, there were three outbreaks associated with animal petting zoos or poultry hatching programs and 318 outbreaks of suspected person-to-person transmission. Sites conducted 100 investigations into clusters of gastrointestinal illness where a source could not be identified, including three multi-state outbreaks of salmonellosis. OzFoodNet identified important risk factors for foodborne disease infection, including: Salmonella infections due to chicken and egg consumption, bakeries as a source of Salmonella infection, and problems associated with spit roast meals served by mobile caterers. There were marked improvements in surveillance during 2002, with all jurisdictions contributing to national cluster reports, increasing use of analytical studies to investigate outbreaks and 96.9 per cent of Salmonella notifications on state and territory surveillance databases recording complete information about serotype and phage type. During 2002, there were several investigations that showed the benefits of national collaboration to control foodborne disease. Sharing surveillance data from animals, humans and foods and rapid sharing of molecular typing information for human isolates of potentially foodborne organisms could further improve surveillance of foodborne disease in Australia.
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PMID:Foodborne disease in Australia: incidence, notifications and outbreaks. Annual report of the OzFoodNet network, 2002. 1292 36

During December 2002-January 2003, the Chicago Department of Public Health (CDPH) investigated a cluster of Yersinia enterocolitica infections reported during a 10-week period among nine Chicago infants aged < or =1 year. This report summarizes the investigation of these cases and underscores the continuing risks for enteric infection among infants exposed to chitterlings (i.e., pork intestines), and the need for health-care providers to be aware of Y. enterocolitica as a cause of gastroenteritis, particularly in black children during traditional winter holiday celebrations.
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PMID:Yersinia enterocolitica gastroenteritis among infants exposed to chitterlings--Chicago, Illinois, 2002. 1453 10

Yersinia pestis, the causative agent of plague, seems to have evolved from a gastrointestinal pathogen, Yersinia pseudotuberculosis, in just 1,500-20,000 years--an 'eye blink' in evolutionary time. The third pathogenic Yersinia, Yersinia enterocolitica, also causes gastroenteritis but is distantly related to Y. pestis and Y. pseudotuberculosis. Why do the two closely related species cause remarkably different diseases, whereas the distantly related enteropathogens cause similar symptoms? The recent availability of whole-genome sequences and information on the biology of the pathogenic yersiniae have shed light on this paradox, and revealed ways in which new, highly virulent pathogens can evolve.
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PMID:The yersiniae--a model genus to study the rapid evolution of bacterial pathogens. 1504 Jan 80

Active surveillance for laboratory-confirmed Yersinia enterocolitica (YE) infections was conducted at 5 Foodborne Diseases Active Surveillance Network (FoodNet) sites in the United States during 1996-1999. The annual incidence averaged 0.9 cases/100,000 population. After adjusting for missing data, the average annual incidence by race/ethnicity was 3.2 cases/100,000 population among black persons, 1.5 cases/100,000 population among Asian persons, 0.6 cases/100,000 population among Hispanic persons, and 0.4 cases/100,000 population among white persons. Incidence increased with decreasing age in all race/ethnicity groups. Black infants had the highest incidence (141.9 cases/100,000 population; range, 8.7 cases/100,000 population in Minnesota to 207.0 cases/100,000 population in Georgia). Seasonal variations in incidence, with a marked peak in December, were noted only among black persons. YE infections should be suspected in black children with gastroenteritis, particularly during November-February. Culturing for YE should be part of routine testing of stool specimens by clinical laboratories serving populations at risk, especially during the winter months.
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PMID:Population-based surveillance for Yersinia enterocolitica infections in FoodNet sites, 1996-1999: higher risk of disease in infants and minority populations. 1509 88


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