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

Most of 82 F165-positive Escherichia coli isolated from calves and piglets with diarrhea or septicemia and possessing pap related sequences caused mannose-resistant, neuraminidase-resistant hemagglutination of human and bovine erythrocytes. Less than half of these isolates demonstrated binding specificity for the alpha-D-galactosyl-(1-4)-beta-D-galactopyranose or galactose-N-acetyl-alpha-(1-3) galactose-N-acetyl moieties recognized by P and F (or Prs) adhesins respectively. Binding specificity for the galactose-N-acetyl-alpha-(1-3) galactose-N-acetyl moiety was associated with isolates causing septicemia in newborn piglets.
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PMID:Receptor binding specificity and pathogenicity of Escherichia coli F165-positive strains isolated from piglets and calves and possessing pap related sequences. 809 16

During a study of the nutritional requirements of clinical isolates of Escherichia coli, we found that 21 (7.0%) of 301 strains required nicotinamide to grow in minimal medium. The nicotinamide-requiring strains were present in 16 (15.8%) of 101 cultures of urine from young women with acute cystitis, in 5 (5.0%) of 100 stool specimens from healthy adults, and in none of 100 blood samples from adult patients with bacteremia. Most of the strains belonged to serogroup O18:K1:H7, were hemolytic, possessed type 1 fimbriae, and exhibited similar patterns of antibiotic susceptibility. Two of the urinary isolates expressed S fimbriae, and all 16 urinary isolates contained the sfaS homologue gene on their chromosomes. One of the stool isolates contained the sfaS gene. The urinary isolates closely resembled a large clone of E. coli that is reportedly associated with neonatal meningitis and sepsis. It may be possible to detect this and related clones by their requirement for nicotinamide and to screen strains for S fimbriae by relatively inexpensive hemagglutination methods, including the use of avian P1 antigens to detect mannose-resistant, non-P-fimbriated E. coli; the agglutination of bovine erythrocytes; and the use of bovine mucin to detect sialyl galactosides in S fimbriae.
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PMID:Isolation of a nicotinamide-requiring clone of Escherichia coli O18:K1:H7 from women with acute cystitis: resemblance to strains found in neonatal meningitis. 809 16

A total of 159 Escherichia coli colonies isolated from the stools of 23 healthy cats were studied for production of alpha-haemolysin (Hly), enterohaemolysin (EntHly), cytotoxic necrotizing factors (CNF1 and CNF2), verotoxins (VT) and heat-labile enterotoxin (LT). Hly+CNF1+, Hly+CNF2+, Hly+VT+ and Hly+ E. coli colonies were isolated from 12 (48%), 1 (4%), 1 (4%) and 2 (8%) respectively of the cats sampled. None of the 159 E. coli colonies produced LT or EntHly. Nine of 12 Hly+CNF1+ strains from the cats belonged to serogroup O6 and eleven to serotypes (O4:K?:H5 or H-, O6:K13:H1, O6:K53:H-, O6:K53:H1, O6:K53:H7 and O6:K14:H31) found among Hly+CNF1+ E. coli that cause urinary tract infections and sepsis in humans. Furthermore, 10 Hly+CNF1+ strains from the cats expressed the mannose-resistant haemagglutination (MRHA) type III. By contrast, the majority of nontoxigenic E. coli strains were MRHA negative and belonged to different O groups. We conclude that cats are a important reservoir of Hly+CNF1+ E. coli strains that possess similar characteristics to strains that can cause extraintestinal infections in humans and that Hly+ E. coli from cats usually do not produce shiga-like toxins with cytotoxic activity on Vero cells.
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PMID:Haemolytic Escherichia coli strains isolated from stools of healthy cats produce cytotoxic necrotizing factor type 1 (CNF1). 812 97

A multivariate analysis of 3334 Escherichia coli strains originating from different clinical materials revealed that 50.2% of isolates belonged to the most common 12 (O1, O2, O4, O6, O7, O8, O15, O18, O45, O75, O78, O83) out of 133 serogroups. Haemolysin (Hly) production, mannose resistant haemagglutinating activity for human erythrocytes (MRHA) and colicinogenicity (Col) were recorded in 30, 30 and 36%, respectively. Antigens K1 and K5 were present in 11% and 6.6%, respectively. Association were found among certain serotypes and virulence markers (O1, H-, H7, K1, MRHA, Col; O2, H-, Kl, Col; O4, H-, H5, MRHA, Hly; O6, H-, H1, MRHA, Hly; O6, K5, MRHA, Col; O7, H-, H4, K1, MRHA, Col; O18ac, H7, K1, Col; O18ac, H-, K5, MRHA, Hly; O78, H-, Col (V-type); O83, H-, K1, Col). There were associations among clinical specimens, age of patients, nosocomial group of diseases, serogroups and virulence markers, too (cerebrospinal fluid-CSF-O7, O18ac, O45, O83-K1-newborn meningitis; O78-ColV-meningitis, sepsis, inflammations diseases of premature babies; CFS-O6, MRHA, Hly-adult-meningitis, sepsis, urinary tract infection-UTI-, pneumonia, other inflammatory diseases; blood-O2, O4, O6, O18ac, ONT, K5, MRHA, Hly-sepsis, UTI, hepatic diseases; urine-O1, O2, O4, O6, O18ac, O75, virulence markers fall to differ among upper and lower UTI; faeces-O1, O4, O6, O18ac, O78, virulence markers rare). Associations were also found among animal pathogenicity tests, specimens, serogroups and virulence factors: highly virulent group strains (i.e. LD50 below 10(6)) belonged to serogroups O2, O6, O18ac, possessed antigen K1 (less frequently the presence of MRHA, Hly, K5) and originated mainly from CSF. With mouse lung toxicity test correlations of serogroups (O4, O6, O18ac), antigen K5, MRHA, Hly and specimens (blood) were also shown. However, association was found between the lack of virulence factors and phage insensitivity and also between K5 positivity and sensitivity to phages 16, 17, there were no correlations between serogroups and phage patterns. On the basis of the above-described associations one can find correlations among virulence markers, serotype, and nosological group of diseases. Animal pathogenicity tests give additional data in understanding the pathomechanism of diseases. Correlations between phage patterns and serogroups reveal certain epidemiological relatedness and also virulence of strains.
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PMID:Computerized complex typing of Escherichia coli strains from different clinical materials. 819 67

Twenty isolates of Pasteurella (Moraxella) anatipestifer from ducks with serositis and septicemia in Thailand between 1988 and 1989 were characterized by various tests. Eighteen isolates fermented glucose and maltose, 3 fructose and 1 each mannose, arabinose, trehalose or sorbitol. All isolates produced gelatinase but not urease, while 2, 3, 5 and 6 produced indole, were CAMP positive, and were proteolytic for milk and coagulated serum respectively. Seven enzymes, phosphatase alkaline, esterase (C4), esterase lipase (C8), leucine arylamidase, valine arylamidase, phosphatase acid and phosphoamidase were detected from all the isolates. The isolates were highly susceptible to ampicillin, erythromycin, penicillin G and tylosin. Gel-diffusion precipitin tests demonstrated that serotype 1 was most prevalent (60%) and serotype 6 followed (5%). Seven isolates (35%) were untypable. These results indicated that P. anatipestifer of serotype 1 played an important role in recent outbreaks of the disease in Thailand.
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PMID:Physiological characteristics, antimicrobial susceptibility and serotypes of Pasteurella anatipestifer isolated from ducks in Thailand. 820 23

Seventeen children aged 3 weeks to 19 months with severe Protracted Diarrhea (PD), and who were deteriorating on our standard management protocol (including special diets) were given Parenteral Nutrition (PN) for 4 to 19 days with crystalline aminoacid solution (Vamin N) in 10% dextrose and lipid emulsion (Intralipid 10%). Peripheral lines were used in majority (84%). Enteral feeds were started early and rebuilt as per tolerance. The mean daily protein and caloric intake achieved by hyperalimentation was 2.2 +/- 0.7 g/kg and 106 +/- 41 K cal/kg respectively. Diarrheal control and improvement in nutritional status was achieved in all but 4 who died (2 of refractory diarrhea and 2 of sepsis, 1 of which was probably PN related). Other PN related, treatable complications included thrombophlebitis (11.8%), sepsis (17.6%), and metabolic imbalance (17.6%). PN solutions and accessories alone cost an approximate average of Rs. 280/day, with extras for biochemical monitoring (Rs. 70/day) and special nursing (Rs. 200/day). Only 5 of the 13 survivors had a significant relapse of PD, within 5 to 80 days of discharge, necessitating further PN in 2. There were no further deaths. PN was therefore, found to be of life saving value in 13 of 17 children with severe protracted diarrhea and therefore, must be available in specialised units caring for such children.
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PMID:Parenteral nutrition in the management of severe protracted diarrhea. 824 81

We showed previously that a mutant strain of group B Streptococcus (GBS) defective in capsule production was avirulent. This study describes the derivation of an unencapsulated mutant from a highly encapsulated wild-type strain of type III GBS, COH1, by transposon mutagenesis with Tn916 delta E. The mutant, COH1-13, was sensitive to phagocytic killing by human leukocytes in vitro and was relatively avirulent in a neonatal rat sepsis model compared with the wild-type strain. No capsular polysaccharide was evident in the cytoplasm or on the cell surface of the mutant strain. The Tn916 delta E insertion site in COH1-13 was mapped to the same chromosomal location as the Tn916 insertion site in the unencapsulated type III mutant COH31-15 reported previously. Nucleotide sequencing of DNA flanking the insertion site in COH1-13 revealed an open reading frame, designated cpsD, with significant homology to the rfbP gene of Salmonella typhimurium. RfbP encodes a galactosyl transferase enzyme that catalyses the transfer of galactose to undecaprenol phosphate, the initial step in O-polysaccharide synthesis. A particulate fraction of a lysate of wild-type strain GBS COH1 mediated the transfer of galactose from UDP-galactose to an endogenous acceptor. The galactose-acceptor complex partitioned into organic solvents, suggesting it is lipid in nature or membrane-associated. Galactosyl transferase activity was significantly reduced in the unencapsulated mutant strain COH1-13. These results, together with the similarity in deduced amino acid sequence between cpsD and rfbP suggest that cpsD encodes a galactosyl transferase essential for assembly of the GBS type III capsular polysaccharide.
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PMID:Identification of cpsD, a gene essential for type III capsule expression in group B streptococci. 835 11

Streptococcus suis causes sepsis, meningitis, and other serious infections in piglets, and meningitis in humans. Hemagglutination inhibition experiments with mono- and oligosaccharides and glycoproteins indicated that galactose-binding strains of S. suis recognized the Gal alpha 1-4Gal sequence present in the P1 and Pk blood group antigen structures. In thin-layer chromatography overlay assays the bacteria bound to trihexosylceramide (GbO3) but not to globoside (GbO4) or Forssman glycolipid (GbO5), in contrast to P-fimbriated Escherichia coli, which bound only to the latter two. The S. suis adhesin also differed from that of E. coli in that some of the hydrogen bonds formed with the receptor, as determined with chemically modified receptor analogues, were different. In agreement with the binding specificity, the S. suis bacteria agglutinated best among P blood group erythrocytes those of the P1k and P2k type, and from different animal erythrocytes those from rabbit, which express GbO3 as the predominant glycolipid. Binding to frozen sections of pig pharyngeal tissue was decreased by the free GbO3 oligosaccharide and its protein conjugate, which indicated that the corresponding glycolipid may function as receptor for galactose-binding strains of S. suis in pig pharyngeal epithelium.
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PMID:Characterization of a novel bacterial adhesion specificity of Streptococcus suis recognizing blood group P receptor oligosaccharides. 844 Jul 15

A case of hyponatremia and then hypernatremia in a hospitalized patient receiving total parenteral nutrition (TPN) is described, and the etiologies, diagnoses, and treatments of hyponatremia and hypernatremia are reviewed. A 23-year-old man whose left leg had been amputated after a motorcycle accident required parenteral nutrition because of an ileus. After developing sepsis, he was given antimicrobials administered in standard dilutions of 5% dextrose injection, contributing 3 L of free water a day to his fluid intake. The patient subsequently became hyponatremic, and the sodium content of the TPN solution was increased to 140 meq/L. Multiple doses of furosemide and albumin were administered because of weight gain and edema of the lower extremity. After 14 days, all antimicrobial therapy was discontinued, and 2 days later the patient became hypernatremic. The sodium content of the TPN solution was decreased and then eliminated. Because of a 16-kg weight loss, diuretic therapy was stopped. This patient's hyponatremia was caused by administration of large amounts of sodium-free fluids (i.e., antimicrobials in 5% dextrose injection). The most appropriate management would have been to change the fluids in which the antimicrobials were diluted, with no change in the sodium content of the TPN solution. The patient's subsequent hypernatremia is best explained by a loss of free water. To manage this condition, it would have been appropriate to administer 5% dextrose injection to replace the free-water loss. Once the patient had reached baseline weight and therapy with the diuretic had been discontinued, maintenance therapy with 0.45% sodium chloride injection would have been beneficial. No change in the TPN sodium content should have been required. It is important to recognize all factors that predispose patients receiving TPN to hyponatremia and hypernatremia. Although the focus is often on the sodium content of the TPN solution, sodium and fluid can be administered by other means, including medication admixtures and maintenance intravenous fluids.
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PMID:Sodium imbalance in a patient receiving total parenteral nutrition. 845 63

Classical galactosemia, which is caused by deficiency of galactose-1-phosphate uridyltransferase, is characterized by acute problems of hepatocellular dysfunction, sepsis, cataracts and failure to thrive. Galactose limitation reverses these symptoms immediately; however, the long-term complications, such as mental retardation and ovarian failures are major problems in most of these patients. In order to investigate the molecular basis for phenotype variation in galactosemia, we have screened the most common mutation in the GALT gene, Q188R. We have further examined those patients who are heterozygous for Q188R or negative for this mutation by SSCP analysis and direct sequencing. In three male patients, we have identified, for the first time, two stop-codon mutations in the GALT gene, G212X (exon 7) and E340X (exon 10). Two patients of 8 and 28 years of age, respectively, who are compound heterozygotes for Q188R and G212X, have severe mental retardation and their general clinical condition is more severe than that of patients with missense mutations. The third patient, who is 8 years of age and who is homozygous for E340X, the N314D polymorphism and a silent substitution L218L, presents with a relatively normal physical and mental condition to date.
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PMID:Characterization of two stop codon mutations in the galactose-1-phosphate uridyltransferase gene of three male galactosemic patients with severe clinical manifestation. 852 34


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