Complete Genome Sequence ofStaphylococcus aureusMCRF184, a Necrotizing Fasciitis-Causing Methicillin-Sensitive Sequence Type 45StaphylococcusStrain

We report here the complete genome sequence of a highly virulent methicillin-sensitiveStaphylococcus aureusstrain,MCRF184, belonging to sequence type 45. This staphylococcal strain was isolated from a surgical biopsy specimen from a patient with necrotizing fasciitis.

Efficacy of Telavancin against Penicillin-Resistant Pneumococci and Staphylococcus aureus in a Rabbit Meningitis Model and Determination of Kinetic Parameters

ABSTRACT The penetration of telavancin was 2% into inflamed meninges and ca. 1‰ into noninflamed meninges after two intravenous injections (30 mg/kg of body weight). In experimental meningitis, telavancin was significantly superior to vancomycin combined with ceftriaxone against a penicillin-resistant pneumococcal strain. Against a methicillin-sensitive staphylococcal strain, telavancin was slightly but not significantly superior to vancomycin.

Enterotoxin H in Staphylococcal Food Poisoning

Seven members of one family became ill with vomiting and diarrhea 4 h after eating a type of cheese produced in the state of Minas Gerais, Brazil. Staphylococcus aureus (2.9 × 108 CFU/g) that produced enterotoxin H (SEH) was isolated from the cheese. A low level of this enterotoxin was detected in the cheese extract before and after concentration 20-fold by copper chelate chromatography. The amount of SEH produced by the staphylococcal strain was 180 ng/ml of culture supernatant with production by the sac culture method. If only the ELISA ball kit had been used, it would have been concluded that enterotoxin D was the cause of the food poisoning.

Ampicillin-sulbactam is effective in prevention and therapy of experimental endocarditis caused by beta-lactamase-producing coagulase-negative staphylococci.

Optimal strategies for the prophylaxis and therapy of endocarditis caused by oxacillin-resistant, coagulase-negative staphylococci in patients with native or prosthetic valvular heart disease are not well defined. We compared the in vivo efficacies of ampicillin-sulbactam-based regimens with those of vancomycin-based oxacillin-resistant, beta-lactamase-producing coagulase-negative staphylococcal isolate (Staphylococcus haemolyticus SE220). Ampicillin-sulbactam (100 and 20 mg/kg of body weight, respectively, given intramuscularly in a two-dose regimen) was equivalent to vancomycin (30 mg/kg given intravenously in a two-dose regimen) in its prophylactic efficacy against the coagulase-negative staphylococcal strain (93 and 80%, respectively). The combination of ampicillin-sulbactam plus either rifampin or vancomycin did not enhance the prophylactic efficacy compared with that of ampicillin-sulbactam or vancomycin alone. In the therapy of established aortic valve endocarditis in rabbits caused by this same coagulase-negative staphylococcal strain, animals received 7-day ampicillin-sulbactam-based or vancomycin-based regimens with or without rifampin. All treatment regimens were effective at lowering intravegetation coagulase-negative staphylococcal densities and rendering vegetations culture negative compared with the coagulase-negative staphylococcal densities and vegetations of untreated controls, with ampicillin-sulbactam in combination with rifampin or vancomycin being the most active regimen. However, only the regimen of ampicillin-sulbactam in combination with vancomycin effectively prevented relapse of endocarditis posttherapy after a 5-day antibiotic-free period. For animals receiving rifampin-containing regimens, relapses of endocarditis were associated with the in vivo development of rifampin resistance among coagulase-negative staphylococcal isolates in the vegetation. Ampicillin-sulbactam was highly effective in the prevention of experimental endocarditis caused by a beta-lactamase-producing, oxacillin-resistant coagulase-negative staphylococcal strain. Ampicillin-sulbactam was also efficacious for the therapy of coagulase-negative staphylococcal endocarditis, especially when it was combined with vancomycin to prevent posttherapeutic relapses.

STAPHYLOCOCCI SHED IN MILK OF FRESHENED HEIFERS FOLLOWING THE USE OF MILKING MACHINES

The transmission of staphylococcal strains prevalent in the milk of 3 dairy herds to their respective, freshened heifers following the use of the milking machine was traced by phage typing. The introduction of new cows to 1 herd provided 1 staphylococcal strain that predominated in the herd. Some heifers acquired staphylococcal strains identical to those found in the herd within 1 wk following the use of the milking machine.

Evolution of the phenomenon of drug-resistance III. The origin of the development of resistance to sulphathiazole in Escherichia coli and Staphylococcus aureus

This study deals with the hourly determination of metabolic differences during growth with sulphathiazole (ST) between the ST-sensitive and ST-resistant strains of Escherichia coli and Staphylococcus aureus for the timing of the onset of resistance mechanism. The amounts of the extracellularly accumulated p-aminobenzoic acid (PAB), folic acid (FA) and citrovorum factor (CF) in the culture fluids and the growth rates are determined. As described in the preceding paper, the sequence of metabolic events with these strains is of the same pattern. The PAB curve in the resistant cell system with ST rises perpendicularly to a peak and then declines sharply followed by the rise of the growth curve. In contrast, in the sensitive cell system with ST, the PAB curve, after reaching a peak, forms a longlasting plateau or a dome-like plateau. During these plateau periods growth is absent. The decline in the plateau is followed by growth. In both the sensitive and resistant strains (E. coli ), the extracellularly accumulated PAB are quantitatively alike. Nevertheless, the PAB in the sensitive system is incapable of antagonizing ST which is of from 10- to 20-fold smaller amount than in the resistant system. As the antagonism of PAB to ST takes place the PAB curve declines and growth is initiated. These events are coincidental with the acquisition of resistance to ST during the PAB plateau period. The similar events in the ST-sensitive staphylococcal strain are associated with the development of the satellism .phenomenon. This phenomenon is manifested on the agar plates with ST until resistance is acquired. The resistant staphylococcal strain does not manifest the phenomenon of satellism. The data presented here and elsewhere are extrapolated to formulate the thesis that a drug or toxic agent exercises two roles on a living system: One, the role of a negative catalyst , and two, the role of a positive catalyst . The latter neutralizes the former giving rise to the phenomenon of resistance, or the evolution of biochemical mechanisms by which a living cell survives the action of toxic agents. A toxin of bacterial or other origins functions in a manner similar to the actions of drugs on bacteria giving rise to the immunological defence mechanism.

THE STREPTOKINASE-PLASMINOGEN SYSTEM

Human plasminogen, plasma, or serum increased the pathogenicity of six streptokinase-positive streptococcal strains for mice. Combinations of commercial streptokinase and plasminogen or streptokinase and plasma did not usually increase mouse mortality to a greater degree than did plasminogen or plasma alone, suggesting that the maximal effective amount of streptokinase was produced by the organisms. The pathogenicity of Salmonella paratyphi (fibrinolysin variable) and a Group D streptococcus (streptokinase-negative) was not increased by plasminogen, plasma, or streptokinase, whereas a combination of streptokinase and plasminogen, or streptokinase and plasma did significantly increase mouse mortality resulting from these organisms. Combinations of certain concentrations of streptokinase and plasminogen increased the pathogenicity of a fibrinolysin-negative staphylococcal strain for mice to a greater extent than did either substance alone. The observed results provide evidence that streptokinase, by an interaction with plasminogen, contributes to the pathogenicity of streptokinase-positive streptococci.