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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The fecal mucus obtained from 110 samples in 50 children with diarrhea was studied. Leukocytes were present in 44 cases and 66 samples were negative. Patients with E. coli 0111 did not show fecal leukocytes in contrast with those with E. coli 0119. Patients with shigellosis showed fecal leukocytes of polymorphonuclear predominance, the same as patients with non-thyphoid salmonellosis. But when septicemia was present, either from salmonella or from other enterobacteria, there was a striking increase in percentage of mononuclears. Several patients with negative stool cultures showed fecal leukocytes of polymorphonuclear predominance which suggested residual inflammatory reaction or presence of bacteriologically unidentified invasive E. coli. The index of diagnostic prediction for this test was 73%. Its routine use is recommended in any child with acute or protracted diarrhea, before the initiation of antimicrobial treatment.
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PMID:[Analysis of fecal mucus in children with prolonged and acute diarrhea]. 76 31

This report describes a case of septicemia and meningitis secondary to dog bites by two different dogs on two consecutive days. The case is noteworthy because of the unusual characteristics of the etiologic agent and the inability to place the etiologic agent into any currently defined genus or to identify it by the existing systems of classification. The organism is a small, thin, Gram-negative bacillus after 24 hours of incubation on blood agar; after prolonged incubation, it becomes filamentous. The organism is catalase- and oxidase-positive, hydrolyzes esculin, and forms acid in glucose, xylose, and maltose after 21 days' incubation. The organism does not manifest lysis on sheep blood agar, and does not grow on MacConkey, Salmonella-Shigella, Centrimide, nutrient, or Kligler iron agars. The tests for urea, nitrate reduction, and indol are negative. The unidentified Gram-negative bacillus showed susceptibility to all antimicrobials tested except gentamicin.
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PMID:A previously undescribed gram-negative bacillus causing septicemia and meningitis. 126 16

Certain DNA probes derived from accessory genes of cloned K88 and F41 determinants hybridize with Escherichia coli strains that express K88 or F41 and with certain other E. coli strains that do not express these antigens. We found that these probes hybridized with human enteroinvasive E. coli, and with bovine E. coli isolates which produced a fatal septicemia in experimentally infected piglets. These strains did not hybridize with probes derived from the structural subunit genes encoding the K88 and F41 antigens. E. coli strains isolated from turkeys with septicemia, Shigella and Salmonella strains did not hybridize to the K88 and F41 accessory gene probes. The K88 and F41 accessory genes probes hybridized with a 200 kb plasmid which is required for invasion by human enteroinvasive E. coli. The K88 and F41 accessory gene homology in the bovine isolates was located on a 150 kb transmissible plasmid but was unrelated to plasmids encoding aerobactin, Vir, or colicin V, which are suspected virulence factors in septicemic E. coli. A common plasmid-encoded antigen was associated with bovine isolates that hybridized with the K88 and F41 accessory gene probes. This included strains which express CS31A, a surface antigen associated with bovine septicemic E. coli, which also hybridized with the K88 and F4 accessory gene probes. The results suggest that the K88 and F41 accessory gene probes hybridized with sequences that may be associated with a common mechanism of pilus expression in distinct groups of E. coli pathogens.
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PMID:Characterization of bovine septicemic, bovine diarrheal, and human enteroinvasive Escherichia coli that hybridize with K88 and F41 accessory gene probes but do not express these adhesins. 198 1

The bacteria constituting the species Escherichia coli are commonly found in the intestinal flora of man and animals, and were until late 1950s recognized as non-pathogenic normal cohabitants. However, certain strains might induce disease, and E. coli should therefore be regarded as a potential pathogenic organism. The pathogenic strains can cause distinct disease syndrome as different diarrheal diseases, wound infections, meningitis, septicemia, artherosclerosis, hemolytic uremic syndrome and immunological diseases such as reactive and rheumatoid arthritis. Several different groups of diarrhea-inducing strains are known. The enterotoxigenic E. coli (ETEC) strains produce one or more of toxins from the heat-labile and the heat-stable enterotoxin families. These strains possess specific adhesion fimbria for intestinal attachment and colonization. Some enteropathogenic E. coli strains (EPEC) produce one or more of the cytotoxins, but adhere also to intestinal cells interfering with the electrolyte transport system. The group of strains possessing invasive properties are designated enteroinvasive E. coli (EIEC). Recently, the enterohemorrhagic E. coli (EHEC) strains have been identified and shown to produce one or more of the cytotoxins (vero-cytotoxins, shiga-like toxins). Food originating from warm-blooded animals may be contaminated with E. coli, but contamination from human sources are more common for food involved in outbreak of disease. In general, strains causing disease in animals do possess other colonization factors than those found on human pathogenic strains. EIEC strains are, like Shigella, only known to induce disease in man. However, both healthy and sick cattle are suspected to be a major reservoir for EHEC strains, and several outbreaks have been associated with consumption of meat or meat products. Cheeses have been the source of outbreaks of both ETEC and EIEC in Europe and the USA, while water seems to be a major source for the different diarrheic E. coli strains affecting children and tourists in the 3rd world. Strains causing non-enteric disease are less known as being transmitted to humans with food as a vector, but the importance of some of these diseases, should implicate further research on what role food plays in spreading these organisms. The recipient of the potential pathogenic E. coli through food, the humans, are also of different risk of contracting diseases.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pathogenic Escherichia coli found in food. 201 3

Complications that can lead to death during shigellosis include intestinal as well as systemic manifestations. The former include intestinal perforation, toxic megacolon, and dehydration, and the latter include sepsis, hyponatremia, hypoglycemia, seizures and encephalopathy, hemolyticuremic syndrome, pneumonia, and malnutrition. Data on the frequency of these complications come primarily from hospital-based studies, in which sepsis-either with Shigella or with other Enterobacteriaceae-and hypoglycemia are the most common causes of death. Management of these two complications requires broad-spectrum empiric antibiotic treatment of all severely ill, malnourished patients with shigellosis as well as frequent feedings to prevent hypoglycemia. Unfortunately, in developing countries, access to parenteral broad-spectrum antimicrobial agents is often limited, and frequent feedings are often precluded by the severe anorexia that is characteristic of shigellosis. Realistic approaches to the reduction of mortality from shigellosis must continue to focus on prevention and early antimicrobial therapy rather than on treatment of established complications.
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PMID:Potentially lethal complications of shigellosis. 204 57

During an outbreak of dysentery in the Northeastern part of Thailand, eight cases of HUS were admitted to Srinagarind Hospital from April to September 1987. Their ages ranged from 6 months to 6 years (mean age = 2.4 years). All patients had prodromal symptoms of mucous bloody diarrhea. The stool culture was positive for Shigella dysentery type I in one case. The treatment included blood transfusion, peritoneal dialysis, exchange transfusion and supportive treatment. One patient died from nosocomial septicemia. For the survivors, platelets count returned to normal after 7 to 19 days (mean 12.8 days). The duration of azotemia ranged from 12 to 36 days (mean = 20 days). One patient was azotemic during 40 days of hospitalization.
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PMID:Hemolytic uremic syndrome associated with Shigellosis: a report of 8 cases. 224 28

To determine the role of bacterial and host factors in the pathogenesis of shigellemia, blood and fecal Shigella isolates were compared for serum resistance and siderophore production, and shigellemic patients were examined for decreased serum bactericidal activity or increased serum transferrin saturation compared to control patients with non-bacteremic shigellosis. The majority of both blood (36/38) and fecal (36/48) Shigella isolates were sensitive to normal serum (greater than 2 log kill/60 min). Shigella dysenteriae type 1 strains were the most sensitive, and Shigella sonnei strains were the most resistant. Siderophore production was species- and serotype-dependent. Shigella dysenteriae type 1 produced only enterochelin; most Shigella flexneri expressed only aerobactin, and Shigella sonnei secreted both types of siderophores. No difference in siderophores was noted between blood and fecal strains within a given serotype. In contrast, shigellemic patients exhibited a 43-fold decrease in serum bactericidal activity and a two-fold increase in transferrin saturation compared to well-nourished control patients. These results indicate that the pathogenesis of Shigella septicemia is not related to serum resistance or siderophore production but may involve serum abnormalities associated with malnutrition.
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PMID:Role of bacterial and host factors in the pathogenesis of Shigella septicemia. 237 88

To focus attention on the problem of infant mortality in Lebanon, data were compiled on infant mortality from 1978 to 1986 at the American University of Beirut Medical Center. Causes of death are analyzed for 602 males and 398 females. 54.9% deaths occurred at 1 month of age and 77.4% died within the 1st year. Autopsies were performed on .7%. 37.7% of all neonatal deaths were due to neonatal diseases such as hyaline membrane disease, asphyxia neonatorum, immaturity, necrotizing enterocolitis, hemorrhage, hemolysis, meconium aspiration, and kernicterus. Better prenatal care would reduce this group, or the administration of corticosteroids to the mother 24-48 hours prior to delivery, as well as rapid resuscitation at birth and prevention of the 5 curses: hypoxemia, hypoglycemia, hypothermia, hypotension, and acidosis. Although unavailable in Lebanon, administration of surfactants through an endotracheal tube would also help. Infections constitute 25.1% of deaths; many are preventable through adequate public health measures and strict personal hygiene, i.e., diseases such as sepsis, pneumonia, meningitis, gastroenteritis, hepatitis, encephalitis, and 1-2 cases of the following: diphtheria, measles, peritonitis, tetanus, tuberculosis, cytomegalis inclusion, herpes, parathyphoid, pertussis, poliomyelitis, and shigellosis. Congenital diseases were 21.6%. In utero diagnosis could prevent some diseases and in utero treatment is possible for hydrocephalus and hydronephrosis. Screening programs postnatally could lead to treatment. 5.9% were malignancies such as leukemia, lymphoma, brain tumors, histocytosis, Wilm's tumor, Ewing sarcoma, and Hodgkin's disease. Early diagnosis is critical if mortality is to be reduced in this group, but medical advances are still needed. 2.9% are miscellaneous diseases such as poisoning, rheumatic diseases, marasmus, Reye's syndrome, nephrosis, rickets, and epilepsy. Most of these diseases are preventable, except for rheumatic inflammation of the heart. Recommended necessary steps to reduce infant mortality are: prenatal care, diagnosis and screening, intrauterine surgery; resuscitation and intensive care centers with modern equipment and trained personnel; national vaccination and screening programs; adequate public health measures and hygiene; parental education; and well-equipped hospitals to serve all regardless of income level.
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PMID:Pediatric mortality: an avoidable tragedy. 251 28

Thirty-seven children (median age, 2 years) with shigellosis in Bangladesh were subjected to postmortem examination to determine causes of death and the spectrum of intestinal histopathology. Infecting species were: Shigella dysenteriae 1, 7 cases; S. dysenteriae 2, 2 cases; Shigella flexneri, 23 cases; Shigella boydii, 4 cases; and mixed infection with Shigella boydii and Shigella sonnei, 1 case. Complicating conditions detected before death included malnutrition in 25 cases, pneumonia in 11 cases and septicemia in 8 cases. In all 37 cases the colon showed gross colitis, consisting of mucosal erythema and edema; superficial ulcerations were visible in 15 cases. Microscopically in the colon the lamina propria showed inflammatory cellular infiltration in 27 cases and crypt abscesses were present in 22 cases. In 9 cases each there were colonic glands in the submucosa and branching of colonic crypts, indicating increased regenerative activity of crypt cells. Severe lesions were mucosal denudation and deep ulceration in 15 cases with a pseudomembrane in 7 and pseudopolyposis in 2 of these patients. The most common underlying cause of death was colitis, whereas the most common immediate and associated causes were, respectively, septicemia and pneumonia. These results indicated that fatal childhood shigellosis results from severe colitis, often complicated by septicemia and concomitant malnutrition and pneumonia.
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PMID:Causes of death and the histopathologic findings in fatal shigellosis. 259 52

We have treated 42 episodes of pediatric infections with sulbactam/ampicillin since 1987. Included were 9 cellulitis, 9 urinary tract infections, 5 cervical lymphadenitis, 4 meningitis, 2 thoracic empyema, 2 osteomyelitis, 2 sepsis, 1 furuncle, 1 perianal abscess, 1 dental abscess, 1 peritonsillitis, 1 salmonellosis, 1 shigellosis, 1 peritonitis, 1 suppurative thyroiditis, 1 infective endocarditis. Responsible pathogens were Escherichia coli in 8, Staphylococcus aureus in 6, Hemophilus influenzae in 2, Streptococcus pneumoniae in 3, Streptococcus viridans in 2, Staphylococcus epidermidis in 1, Bacteroides fragilis in 1, Salmonella D1 in 1, Shigella sonnei in 1, Klebsiella pneumoniae in 1, Enterobacter agglomerans in 1, Acinetobacter calcoaceticus in 1, Enterobacter cloacae in 1, group A beta-hemolytic streptococcus in 1, and polymicrobial infection in 4 cases. Thirty-nine out of 41 (95%) clinically evaluable patients cured and all (34/34) bacteriologically evaluable patients eradicated their pathogens after treatment with sulbactam/ampicillin. Side reactions were seen in five patients; one maculopapular skin rash, one hemolytic anemia, two diarrhea, and one liver function impairment plus leukopenia. All these reactions were transient and did not require interruption of therapy. These results indicate that sulbactam/ampicillin is safe and effective in the treatment of common pediatric infections beyond the neonatal period.
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PMID:A clinical evaluation of sulbactam/ampicillin in the treatment of pediatric infections. 263 93


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