Treatment with Ca(OH)2 for inactivation of Salmonella Typhimurium and Enterococcus faecalis in soil contaminated with infected horse manure.

AIM: To investigate the inactivation of Salmonella enterica serovar Typhimurium and the faecal indicator Enterococcus faecalis in horse manure:soil mixtures by application of hydrated lime (Ca(OH)(2)). METHODS AND RESULTS: In laboratory incubations, the inhibitory effect of different concentrations of Ca(OH)(2), as well as different application techniques, was tested. Other variables were horse manure:soil ratio, incubation temperature (6 and 14°C) and soil type (sand/clay). Bacterial enumeration by the plate count method in samples taken at increasing intervals revealed that Ca(OH)(2) effectively reduced Salmonella Typhimurium numbers. However, to achieve a sufficient reduction, the Ca(OH)(2) had to be applied at a sufficient rate, and the amount required varied because of manure:soil ratio and incubation temperature. The results showed that a pH above 11 was needed and that a high pH had to be maintained for up to 7 days. An appropriate application technique for the Ca(OH)(2) was also important, so that a high pH was obtained throughout the whole material to be treated. In addition, a high manure:soil ratio in combination with a higher incubation temperature was found to rapidly neutralize the pH and to increase the risk of Salmonella re-growth. CONCLUSIONS: Application of Ca(OH)(2) can be an efficient method for treating a Salmonella-contaminated horse paddock. A high pH is a key factor in Salmonella inactivation, and thus, monitoring the pH during the treatment period is necessary. To avoid re-growth excess manure should be removed for separate treatment elsewhere. SIGNIFICANCE AND IMPACT OF THE STUDY: Persistence of Salmonella in horse paddocks poses a risk of disease transmission to healthy animals and people who come into contact with these animals. An efficient method to de-contaminate a Salmonella-contaminated soil would be a valuable tool for animal welfare and for public health.

Ampicillin treatment of Neisseria gonorrhoeae in vivo. An experimental study in rabbits.

The effect of ampicillin on gonococci was investigated in chambers subcutaneously implanted in rabbits. An intramuscular injection of ampicillin resulted in a rapid increase of the ampicillin concentration in serum, whereas the diffusion of ampicillin into the fluid of a non-infected chamber was comparatively slow. The ampicillin concentration was, however, maintained in the chamber fluid during a prolonged period of time as compared to ampicillin in serum. The concentration profile of ampicillin in the infected chamber was similar to that of the non-infected chamber, though at a lower level. No viable gonococci were detected 120 minutes after the injection of ampicillin. In contrast, the same concentration of ampicillin in a liquid culture resulted in slower reduction in the viability of the gonococcal strain. Even after 300 minutes a small population of gonococci was viable. Thus, a difference in the activity of ampicillin could be observed between the in vitro and the in vivo test situation.

Cefuroxime treatment of urethritis caused by a beta-lactamase-producing strain of Neisseria gonorrhoeae.

A patient who contracted urethritis from a beta-lactamase-producing strain of Neisseria gonorrhoeae was successfully treated with the cephalosporin derivative cefuroxime. As expected, neither cefuroxime nor cefamandole was hydrolysed by plasmid-coded gonococcal beta-lactamase. Cefuroxime ought to be a valuable and efficacious substitute for penicillins in the treatment of gonhorrhoea due to beta-lactamase-producing gonococcal strains.

Effects of low ampicillin concentrations on penicillin sensitive and beta-lactamase producing strains of Neisseria gonorrhoeae.

The effects of therapeutic concentrations of ampicillin on non-beta-lactamase and beta-lactamase producing strains of Neisseria gonorrhoeae were studied. A small but significant fraction of bacteria in a gonococcal population was found to respond in a bacteriostatic rather than a bactericidal way upon ampicillin treatment. In agreement with this was the finding of morphologically unaltered cells in the scanning electron microscope after ampicillin exposure. Ampicillin treatment of beta-lactamase producing gonococci caused a significant release of the enzyme into the surrounding growth media. However, initially all beta-lactamase activity was cellbound. The rate of initial ampicillin hydrolysis was much higher in intact cells of N. gonorrhoeae (TEM-1) than in cells of Escherichia coli K-12 (TEM-1). This suggests that the diffusion rate of ampicillin is much higher in the former organism. The viability of gonococci (TEM-1) was unlike E. coli (TEM-1) affected by low concentrations of ampicillin. However, after complete hydrolysis of ampicillin, viable gonococci (probably bacteriostatic reacting cells) were able to initiate new growth. This heterogeneity of the cell population to penicillin killing is probably one reason why beta-lactamase producing gonococci despite a rather low MIC-value to ampicillin cause infections that are not susceptible to therapy by this agent.