Serratia Marcescens Infection of the Urinary Tract: A Nosocomial Infection

Allen, Samuel D.; Conger, Kyril B.

doi:10.1016/s0022-5347(17)62391-7

Cited by 40 publications

(12 citation statements)

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“…Notwithstanding these difficulties, it is certainly possible to gain a reasonably accurate idea of what is happening elsewhere, and the veritable spate of publications from the USA in recent years naming Serratia marcescens as a pathogen (Atlas and Belding, 1968;Dodson, 1968;Nelms et al, 1968;Ringrose et al, 1968;Allen and Conger, 1969;Alexander etal, 1969;Altemeier et al, 1969;Cabrera, 1969;Quintiliani and Gifford, 1969) would certainly indicate that the organism is a fairly common cause of disease in that country. Our own impression, however, which incidentally was shared by all of the British bacteriologists with whom we had discussed this topic, was that Serratia marcescens is an uncommon, if not rare, clinically significant isolate in the bacteriology laboratory in this country.…”

Section: Discussionmentioning

confidence: 99%

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Hodgson

1971

J Clin Pathol

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During a four-month period an intensive effort was made to isolate and identify everySerratia marcescensstrain present in the clinical material received for bacteriological assessment in the laboratory. Ten strains were isolated from eight patients, the organism possibly being responsible for infection in five of these patients.Serratia marcescensis thus commoner than expected and it is difficult to explain the fact that there are so few references to it as a pathogen in the British literature.

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Section: Discussionmentioning

confidence: 99%

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Hodgson

1971

J Clin Pathol

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“…In 1962, Ewing, Johnson & Davis reported that most serratia infections originated in hospital; later papers described the characteristics of serratia infection in the urinary tract (Taylor & Keane, 1962;Lancaster, 1962;Clayton & Von Graevenitz, 1966;Allen & Conger, 1969), in the respiratory tract (Cabrera, 1969) and at several different sites (McCracken & Lipscomb, 1965;Stenderup, Faergeman & Ingerslev, 1966;Stamm et al 1976; 3-2 Mutton, Brady & Markness, 1981;Anagnostakis et al 1981). Interest in such organisms stimulated several studies on their antigenic composition and on the possibilities of serological, biochemical and bacteriocin typing (Traub, Raymond & Startsman, 1971;Farmer, 1972;Edwards & Ewing, 1972;Grimont & Grimont, 1978;Branca et al 1979).…”

Section: Introductionmentioning

confidence: 99%

Epidemiological and bacteriological investigation ofSerratia marcescensepidemic in a nursery and in a neonatal intensive care unit

Montanaro

Grasso

Annino

et al. 1984

J. Hyg.

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SUMMARYAn epidemic caused by Serratia marcescens that involved 26 infants admitted to the Neonatal Intensive Care Unit (NICU) and 82 infants admitted to the Nursery of the 2nd Medical School of Naples is reported. Two different biotypes of S. marcescens with two completely different epidemiological patterns were identified. The prevalent biotype (A8b trigonelline-) was isolated in the delivery room, in the operating room, in the Nursery and in the NICU from items, healthy infant exereters and affected infants; the second biotype (A3a) was isolated only in the NICU from staff, two healthy infant exereters and two affected infants. Colonization of the throat and the gastrointestinal tract was frequent. Infected and colonized infants were the most important reservoir for serratia in the Nursery and in the NICU particularly for the type strain A3a. A mucus aspiration apparatus contaminated in the delivery room and the contamination of several instruments and items probably had a major role in the initiation and maintenance of the spread of the A8b strain. Mass contamination of the nursery has been related to overcrowding and a lack of the control measures; the transfer of high-risk colonized infants caused spread in the NICU.In the NICU the attack rate was 26 0; 69 % of infants became ill; the case fatality ratio was 19 0. Epidemiological investigation of the infants at risk showed some factors predisposing to infection with serratia. The hygienic measures failed to control the spread of serratia and it was necessary to refuse new admissions to pregnant women in order to decontaminate and re-organize the wards.

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“…The nucleotide sequence of smfA, the gene encoding the major structural component of MR fimbriae, revealed that this gene encodes a 174-amino-acid polypeptide with a typical procaryotic signal peptide. The primary structure of the smfA product showed significant homology with the primary structure of the E. coli fimbrial subunit.Serratia marcescens is a bacterial species causing nosocomial infection in the urinary and respiratory tracts (3,16,17,30). Gram-negative bacteria isolated from patients with an urinary tract infection adhere to uroepithelial surfaces by bacterial surface appendages known as pili or fimbriae (13,15,43).…”

mentioning

confidence: 99%

“…Serratia marcescens is a bacterial species causing nosocomial infection in the urinary and respiratory tracts (3,16,17,30). Gram-negative bacteria isolated from patients with an urinary tract infection adhere to uroepithelial surfaces by bacterial surface appendages known as pili or fimbriae (13,15,43).…”

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Cloning and sequence of the gene encoding the major structural component of mannose-resistant fimbriae of Serratia marcescens

et al. 1988

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Serratia marcescens US46, a human urinary tract isolate, exhibits mannose-resistant hemagglutination and agglutinates yeast cells, thereby indicating that it has two types of adhesins. We constructed a cosmid library for the DNA of this organism and isolated DNA clones carrying genes for mannose-sensitive (MS) and mannose-resistant (MR) fimbriae. On introduction of the cloned genes into Escherichia coli K-12, MS and MR fimbriae were formed. These fimbriae were functionally and morphologically indistinguishable from those of S. marcescens. Subcloning of these gene clusters revealed that the genes encoding MS fimbriae reside on a 9-kilobase (kb) DNA fragment, while those encoding MR fimbriae are present on a 12-kb fragment. Transposon insertion and maxicell analyses revealed thgt formation of MR fimbriae is controlled by several genes which reside on the 9-kb fragment. The nucleotide sequence of smfA, the gene encoding the major structural component of MR fimbriae, revealed that this gene encodes a 174-amino-acid polypeptide with a typical procaryotic signal peptide. The primary structure of the smfA product showed significant homology with the primary structure of the E. coli fimbrial subunit.Serratia marcescens is a bacterial species causing nosocomial infection in the urinary and respiratory tracts (3,16,17,30). Gram-negative bacteria isolated from patients with an urinary tract infection adhere to uroepithelial surfaces by bacterial surface appendages known as pili or fimbriae (13,15,43). S. marcescens isolated from such patients also possesses fimbriae and adheres to uroepithelial cells (47).There are at least two classes of adhesins in S. marcescens (1,26,27). One class, designated MRHA, agglutinates chicken erythrocytes in the presence of D-mannose and is associated with thick rigid fimbriae. The other, named MSHA, exhibits mannose-sensitive hemagglutination of guinea pig and chicken erythrocytes and is associated with thin flexible fimbriae. The latter adhesin is also responsible for agglutinating yeast cells. S. marcescens US46, isolated from a patient with a urinary tract infection, exhibits mannose-resistant hemagglutination and agglutinates yeast cells, thereby indicating that this strain possesses two classes of adhesins (26).To elucidate mechanisms related to the genetic control of formation of mannose-resistant (MR) and mannose-sensitive (MS) fimbriae of S. marcescens, we attempted to clone the DNA fragments carrying these genes. We placed fragments of the chromosomal DNA of strain US46 on appropriate vectors and introduced them into the nonfimbriated strain E. coli K-12. Thus, we were able to clone the chromosomal determinants for MR and MS fimbriae of S. marcescens US46. We determined the nucleotide sequence of the smfA (for S. marcescens fimbria A) gene, which encodes the major structural component (major fimbrial subunit) of MR fimbriae of S. marcescens US46. MATERIALS AND METHODSBacterial strains and growth conditions. The bacterial strains used are listed in Table 1. E. coli K-12, strain * Cor...

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Serratia Marcescens Infection of the Urinary Tract: A Nosocomial Infection

Cited by 40 publications

References 5 publications

Search for Serratia

Search for Serratia

Epidemiological and bacteriological investigation ofSerratia marcescensepidemic in a nursery and in a neonatal intensive care unit

Cloning and sequence of the gene encoding the major structural component of mannose-resistant fimbriae of Serratia marcescens

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