M. Ann Melly

Nursery epidemic due to multiply-resistant Klebsiella pneumoniae: epidemiologic setting and impact on perinatal health care delivery.

Gram-negative bacilli frequently cause epidemics in high-risk newborn intensive care units. Recently, an epidemic caused by a multiply-resistant K. pneumoniae, serotype 21, occurred in the Vanderbilt University intensive care nursery. The background of this outbreak included an increasing endemic nosocomial sepsis rate, operation of the facility in excess of rated capacity, and increasingly inadequate nurse-to-patient staffing ratios. The epidemic lasted 11 weeks; 26 (12%) of the 232 infants at risk in the unit became colonized. Five infants developed systemic illness and one died. Cohorting, reinforcement of strict handwashing and isolation procedures, and closure of the unit to outborn admissions resulted in rapid termination of the outbreak. Followup studies performed on infants colonized with the epidemic bacterium demonstrated persistent fecal shedding up to 13 months following discharge from the hospital. This epidemic had a detrimental influence on high-risk newborn and obstetric health care delivery in an area encompassing portions of three states. Under a system of progressively more sophisticated referral units, nosocomial infections occurring at a tertiary center can have an impact on other hospitals within the network.

The repeating sequence of the capsular polysaccharide of Staphylococcus aureus M

The anomeric configuration of the sugar residues of the capsular polysaccharide antigen of Staphylococcus aureus M were established by 13C-n.m.r. spectroscopy, and the linkage positions by g.l.c.-m.s. after methylation, indicating a leads to 4)-O-(2-acetamido-2-deoxy-alpha-D-galactopyranosyluronic acid)-(1 leads to 4)-O-(2-acetamido-2-deoxy-alpha-D-galactopyranosyluronic acid)-(1 leads to 3)-O-(2-acetamido-2-deoxy-alpha-D-fucopyranosyl)-(1 leads to repeating unit. A taurine residue is linked by an amide bond, on the average, to every fourth 2-acetamido-2-deoxy-D-galactopyranosyluronic acid residue.

SEPSIS CAUSED BY CONTAMINATED INTRAVENOUS FLUIDS

Abstract Thirty-one cases of nosocomial sepsis that occurred from July 1970 through May 1971 in a 500-bed hospital were related to bacterial contamination of intravenous fluid bottles produced by o...

THE IMPORTANCE OF SURFACE ANTIGENS IN STAPHYLOCOCCAL VIRULENCE

While certain biological characteristics of staphylococci such as coagulase and hemolysin production correlate reasonably well with “pathogenicity,” the precise factors which define staphylococcal virulence remain obscure. Although Gilbert in 1931 suggested that the possession of a capsule might be a determinant of staphylococcal virulence,’ until recently i t has generally been thought that surface or capsular antigens played no role in determining pathogenicity of staphylococci. Since 1961, however, the virulence of an unusual group of staphylococcal strains has been shown to be directly related to the presence of surface or capsular antigens which retard phagocytosis. I t is the purpose of this paper to summarize the work we have done with these strains and to indicate how these microorganisms may relate to the problem of human staphylococcal disease. In 1958 Hunt and Moses‘ observed that the Smith strain of Staphylococcus aureus produced two colonial variants in serum or plasma soft agar which differed markedly in their virulence for mice. The diffuse colonial variant (see FIGURE 1) consistantly killed mice when injected intraperitoneally, while similar numbers of the compact colonial variant failed to produce fatal disease. Because this appeared to be a unique model in which to study factors correlating with virulence among staphylococci, the biologic characteristics and the experimental infections produced by these two colonial variants of the Smith strain have been closely scrutinized in our lab~ora tory .~ The observation of Hunt and Moses was readily confirmed. Marked differences in mortality were noted after the intraperitoneal administration of the Smith diffuse and compact variants. Injection of approximately 5 x 10’ or more diffuse variant staphylococci resulted in the death of most animals 5.5 to 12 hours later; while injection of similar numbers of compact variant staphylococci failed to kill mice. The results of such an experiment are shown in TABLE 1. The majority of the biologic characteristics of the two variants were found to be identical. Both strains produced similar amounts of alpha hemolysin; both produced delta hemoIysin; both produced simiIar quantities of free coagulase; the antibiotic sensitivities of both strains were almost identical; and neither strain could be typed by the standard typing phages either at

Attachment of pathogenic Neisseria to human mucosal surfaces: Role in pathogenesis

Studies of the interaction betweenNeisseria gonorrhoeae and human fallopian tube mucosa in organ culture suggest that attachment of gonococci is important, not only to secure the organism in the host, but also to initiate the disease process. The steps observed in gonococcal infection of fallopian tube organ cultures are: 1) attachment of gonococci to microvilli of nonciliated cells; 2) release from gonococci of lipopolysaccharide and possibly other toxic moities to cause mucosa damage; 3) engulfment or phagocytosis of gonococci by nonciliated cells; 4) transport of phagocytic vacuoles containing gonococci to the base of the nonciliated cells; and 5) exocytosis of gonococci within phagocytic vacuoles into the subepithelial tissues.In vivo, these steps might result in extensive local disease (e. g. salpingitis) or in the invasion of blood vessels to cause disseminated disease. Preliminary studies of human nasopharyngeal tissue in organ culture infected withNeisseria meningitidis indicate that meningococci attach to microvilli of nonciliated cells and are phagocytized by these cells. Meningococci subsequently appear in subepithelial tissues, though the route they take is not yet certain. These observations suggest at least some of the ways in which attachment may play a role in disease caused byN. gonorrhoeae andN. meningitidis. Mechanisms to block this attachment may provide new approaches to the prevention of infections caused by the pathogenicNeisseria. Untersuchungen zur Wechselwirkung zwischenNeisseria gonorrhoeae und menschlicher Tubenschleimhaut in Organkultur lassen annehmen, daß das Anheften der Gonokokken den Erreger im Wirtsorganismus schützt und außerdem den Krankheitsprozeß in Gang setzt. In Organkulturen von Tubengewebe lassen sich folgende Schritte der Gonokokkeninfektion beobachten: 1) Die Gonokokken lagern sich an die Microvilli zilienfreier Zellen an; 2) Gonokokken setzen Lipopolysaccharide und möglicherweise auch andere toxische Verbindungen frei, die die Schleimhaut schädigen; 3) zilienfreie Zellen verschlingen oder phagozytieren Gonokokken; 4) phagozytäre Vakuolen mit Gonokokken werden an die Basis der zilienfreien Zellen transportiert; 5) Gonokokken in den phagozytären Vakuolen treten in das subepitheliale Gewebe aus.In vivo könnten diese Vorgänge zu einem ausgedehnten, lokalisierten Krankheitsprozeß (beispielsweise einer Salpingitis) führen oder zur Invasion in Blutgefäße mit disseminierter Erkrankung. Frühere Untersuchungen anN. meningitidis-infiziertem menschlichen Nasopharyngealgewebe zeigen, daß Meningokokken sich an Microvilli nichtzilientragender Zellen anheften und von diesen Zellen phagozytiert werden. Anschließend erscheinen Meningokokken im subepithelialen Gewebe; der Weg der Ausbreitung ist allerdings noch ungewiß. Aus diesen Beobachtungen lassen sich zumindest einige der Vorgänge ableiten, über die Adhäsion in der Pathogenese von Gonokokken- und Meningokokkenerkrankungen eine Rolle spielt. Mechanismen, die das Anheften der Bakterien verhindern, bieten möglicherweise neue Ansätze für die Prävention von Erkrankungen, die durch pathogene Neisserien verursacht werden.