Extracts of leaves from the tea plant Camellia sinensis contain polyphenolic components with activity against a wide spectrum of microbes. Studies conducted over the last 20 years have shown that the green tea polyphenolic catechins, in particular (-)-epigallocatechin gallate (EGCg) and (-)-epicatechin gallate (ECg), can inhibit the growth of a wide range of Gram-positive and Gram-negative bacterial species with moderate potency. Evidence is emerging that these molecules may be useful in the control of common oral infections, such as dental caries and periodontal disease. Sub-inhibitory concentrations of EGCg and ECg can suppress the expression of bacterial virulence factors and can reverse the resistance of the opportunistic pathogen Staphylococcus aureus to beta-lactam antibiotics. For example, relatively low concentrations of ECg can sensitize methicillin-resistant S. aureus (MRSA) clinical isolates to levels of oxacillin that can be readily achieved in clinical practice. Catechin gallates such as ECg intercalate into phopsholipid bilayers and it is likely that they affect both virulence and antibiotic resistance by perturbing the function of key processes associated with the bacterial cytoplasmic membrane.

Staphylococcus aureus is a major pathogen both within hospitals and in the community. Methicillin, a β-lactam antibiotic, acts by inhibiting penicillin-binding proteins (PBPs) that are involved in the synthesis of peptidoglycan, an essential mesh-like polymer that surrounds the cell. S. aureus can become resistant to methicillin and other β-lactam antibiotics through the expression of a foreign PBP, PBP2a, that is resistant to the action of methicillin but which can perform the functions of the host PBPs. Methicillin-resistant S. aureus isolates are often resistant to other classes of antibiotics (through different mechanisms) making treatment options limited, and this has led to the search for new compounds active against these strains. An understanding of the mechanism of methicillin resistance has led to the discovery of accessory factors that influence the level and nature of methicllin resistance. Accessory factors, such as Fem factors, provide possible new targets, while compounds that modulate methicillin resistance such as epicatechin gallate, derived from green tea, and corilagin, provide possible lead compounds for development of inhibitors.

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Manned space flight induces a reduction in immune competence among crew and is likely to cause deleterious changes to the composition of the gastrointestinal, nasal, and respiratory bacterial flora, leading to an increased risk of infection. The space flight environment may also affect the susceptibility of microorganisms within the spacecraft to antibiotics, key components of flown medical kits, and may modify the virulence characteristics of bacteria and other microorganisms that contaminate the fabric of the International Space Station and other flight platforms. This review will consider the impact of true and simulated microgravity and other characteristics of the space flight environment on bacterial cell behavior in relation to the potential for serious infections that may appear during missions to astronomical objects beyond low Earth orbit.

Escherichia coli is a common cause of meningitis and sepsis in the newborn infant, and the large majority of isolates from these infections produce a polysialic acid (PSA) capsular polysaccharide, the K1 antigen, that protects the bacterial cell from immune attack. We determined whether a capsule-depolymerizing enzyme, by removing this protective barrier, could alter the outcome of systemic infection in an animal model. Bacteriophage-derived endosialidase E (endoE) selectively degrades the PSA capsule on the surface of E. coli K1 strains. Intraperitoneal administration of small quantities of recombinant endoE (20 g) to 3-day-old rats, colonized with a virulent strain of K1, prevented bacteremia and death from systemic infection. The enzyme had no effect on the viability of E. coli strains but sensitized strains expressing PSA to killing by the complement system. This study demonstrates the potential therapeutic efficacy of agents that cure infections by modification of the bacterial phenotype rather than by killing or inhibition of growth of the pathogen.