https://mmbr.asm.org/content/mmbr/47/1/46.full.pdf

Bactericidal and bacteriolytic activity of serum against gram-negative bacteria.

The susceptibility of strains of Neisseria gonorrhoeae to the bactericidal action of normal human sera was determined for isolates from patients with disseminated gonococcal infection and uncomplicated gonorrhea. Serum susceptibility was correlated with penicillin susceptibility and auxotype. 38 of 39 strains (97%) of N. gonorrhoeae from Seattle patients with disseminated gonococcal infection were resistant to the complement-dependent bactericidal action of normal human sera. 36 of these were inhibited by less than or equal to mug/ml of penicillin G and required arginine, hypoxanthine, and uracil for growth on chemically defined medium (Arg-Hyx-Ura- auxotype). 12 of 43 isolates from patients with uncomplicated gonorrhea were also of the Arg-Hyx-Ura-auxotype, inhibited by less than or equal to 0.030 mug/ml of penicillin G, and serum resistant. Of the 31 remaining strains of other auxotypes isolated from patients with uncomplicated gonorrhea, 18 (58.1%) were sensitive to normal human sera in titers ranging from 2 to 2,048. The bactericidal action of normal human sera may prevent the dissemination of serum-sensitive gonococci. However, since only a small proportion of individuals infected by serum-resistant strains develop disseminated gonococcal infection, serum resistance appears to be a necessary but not a sufficient virulence factor for dissemination. Host factors such as menstruation and pharyngeal gonococcal infection may favor the dissemination of serum-resistant strains. Since serum-resistant Arg-Hyx-Ura strains are far more frequently isolated from patients with disseminated gonococcal infection than serum-resistant strains of other auxotypes, Arg-Hyx-Ura-strains may possess other virulence factors in addition to serum resistance.

/pdf/gonococci-causing-disseminated-gonococcal-infection-are-3zfvp847mv.pdf

Gonococci causing disseminated gonococcal infection are resistant to the bactericidal action of normal human sera.

/pdf/a-study-of-the-relationship-of-the-normal-bactericidal-4y6vq693cu.pdf

A study of the relationship of the normal bactericidal activity of human serum to bacterial infection

With the recognition of the paramount role of inflammatory mediators in the pathogenesis of sepsis, there has been a rapid profusion of new reagents and strategies for the treatment of bacterial sepsis. The dynamic nature of the pathophysiologc events and the complex array of mediators generated in the septic process preclude accurate prediction of the efficacy of novel therapeutic agents from in vitro studies alone. Experimental data derived from animal research have been and will continue to be indispensable in the development of new therapeutic strategies for sepsis. The use of animal models of sepsis can provide invaluable information on the safety, efficacy, and pharmacokinetics of immunotherapeutic agents. Endotoxin, or lipopolysaccharide (LPS), has a central role in the initiation of the septic process. Circulating endotoxin in the absence of bacteria or circulating endotoxin liberated from growing or antibiotic-killed bacteria has been measured in association with sepsis (5, 15, 55, 65). Consequently, putative modulators of the sepsis syndrome are often evaluated for their ability to attenuate the effects of LPS administration to animals (3, 28). Following the assessment of a modulator's effect after endotoxin administration, it often is next tested for its ability to alter the course of sepsis following the administration of live bacteria to the animals. The intent of such challenges with live microbes is to stimulate the conditions in which bacterial infection leads to sepsis (1, 22, 27, 29, 49, 57, 62). Thus, the literature on sepsis distinguishes between two types of animal models of sepsis: endotoxin challenge and infection. Examination of this literature further reveals that some of the animal models of sepsis following challenge with very high doses of live organisms may more appropriately reflect intoxications similar to those resulting from LPS challenge. Typically in such experiments, the animal host is only responsive to the microbe at very high doses and the pathogen does not colonize and replicate significantly following challenge. Hence, the cytokine responses by the animal host to such insult may not be typical of those measured during true sepsis in animals and humans that progresses from a focus of infection. Since animal species differ considerably in their cardiovascular physiology and susceptibility to bacterial endotoxin, investigators carefully consider the relative merits and limitations of each animal model before extrapolating animal data to clinical efficacy in septic patients. Having given such consideration, however, many investigators do not give sufficient thought to the choice of the bacterial strain for use

Choice of bacteria in animal models of sepsis

Strains of Escherichia coli with sufficient K antigen to resist killing by complement were poorly phagocytosed when injected intravenously into mice. Phagocytosis was markedly increased by anti-OK but not by anti-O sera. In contrast anti-K sera had little or no effect on the bactericidal reaction. This was not because K antigenic sites were scarce but may have been because their position was such that complement was activated at a distance from its substrate. Red cells coated with K antigen were poorly lysed by complement and anti-K serum, suggesting that the K antibody did not activate complement very effectively although again the sites may have been too superficial. The effect of K antigens on phagocytosis and complement killing or lysis could all be explained by their ability to impair protein binding.

Strains of E. coli rich in K antigen were resistant to phagocytosis and complement killing and were virulent for mice on intracerebral injection. The significance of K antigens in animal and human infections is discussed.

The virulence for mice of strains of Escherichia coli related to the effects of K antigens on their resistance to phagocytosis and killing by complement.

The virulence of strains of Bacterium coli for mice.

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The virulence of strains of Bacterium coli for mice.