Atypical behaviour and survival of Streptococcus pyogenes L forms during intraperitoneal infection in rats

Abstract

Groups of rats were injected intraperitoneally with cell wall-deficient (L) forms of Streptococcus pyogenes, with their parental (S) forms, as well as with a combined inoculum of both forms (S+L). Peritoneal exudate samples were harvested on days 1, 3, 7, 15 and 30 after challenge and were investigated by microbiological, electron microscopic, cytometric and biochemical methods. Parental S forms were isolated from peritoneal exudate samples up to day 15 post infection, while L form cultures were isolated until the end of the examined interval. Electron microscopic examination revealed continuous adhesion of L forms on the macrophage surface as well as intracellular persistence inside them. It was demonstrated that the intraperitoneal inflammatory response to L form infection was higher than to the other infections and the monocyte-macrophage populations were predominant. The established atypical behaviour and long survival of S. pyogenes L forms in the rat's peritoneum could explain some of the mechanisms of the pathogens' persistence as well as the reasons for chronic streptococcal infections.

Persistence ofStreptococcus pyogenesin Stationary-Phase Cultures

“…However, these phenotypically altered bacterial cells were able to revert to their original forms (41). In agreement with this, in vivo studies have shown that cell walldefective streptococci were able to persist in a rat model of infection at least twice as long as their parental forms (29). The relevance of these observations to the mechanism of chronic infection seems to be borne out by a direct association between intracellular S. pyogenes and patients suffering from recurrent tonsillitis (36,37).…”

The Mycobacterium tuberculosis iniA gene is essential for activity of an efflux pump that confers drug tolerance to both isoniazid and ethambutol

“…We found that tolerant BCG could not be cultured onto solid media, although the presence of tolerant cells could be easily detected in liquid media. These cells may be analogous to cell wall‐deficient ‘persistent’ cells that have been described in other bacteria (Chandrasekhar and Ratnam, 1992; Domingue et al ., 1993; Mattman, 1993; Domingue and Woody, 1997; Markova et al ., 1997; Michailova et al ., 2000). However, we have been unable to directly observe cell wall‐deficient forms that are specific to the iniA overexpression strain.…”

Cell Wall Deficiency in Mycobacteria: Latency and Persistence

“…Reports about detection and isolation of BCG bacilli from patients with AIDS many years after vaccination (Armbruster et al, 1990;Reynes et al, 1989;Smith et al, 1992) give rise to questions about the mechanisms by which BCG bacilli persist in vivo for a long time. As far as cell wall deficiency facilitates the bacterial survival under unfavorable conditions, L-forms of different bacterial species have been shown to survive and persist for an extended period inside macrophages due to the ineffectual phagocytosis, digestion and clearance (Markova et al, 1997;Michailova et al, 1993;Michailova et al, 2000b;Michailova et al, 2007). The finding that of all the bacteria, L-forms predominate and are crucial to the survival of mycobacteria in vivo (Mattman, 2001;Michailova et al, 2005) needs to be taken into account when developing and putting in use new viable mycobacterial vaccines, especially considering that L-forms of M. bovis BCG bacilli have been found in the blood of persons vaccinated against TB with BCG vaccine (Xalabarder, 1958).…”