This is of particular interest because PMNs are the primary leukocyte involved in clearing bacteria corneal infections. Interestingly, it was shown that Staphylococcus aureus cells coated with serratamolide were also protected from PMN phagocytosis. This leads us to speculate that the presence of S. marcescens-derived serratamolide in contact lens cases or on lenses may better enable other pathogenic bacteria to establish ocular infections. It was noted that swrW was found in,35% of the tested ocular clinical isolates, and 40% of the swrW containing isolates were hemolysis positive on blood agar plates, suggesting that hemolytic strains express swrW sufficiently to produce hemolysis. In support of this premise, mutation of swrW in three out of five hemolysis positive strains severely reduced or eliminated hemolysis zones on blood agar plates. Of the swrW negative strains, 42% were hemolysis positive, indicating that other mechanisms of hemolysis are present in ocular clinical isolates. Another gene, swrA, present in some strains of S. marcescens is necessary for production of serrawettin W2, may account for the hemolysis positive phenotype of swrW negative strains. There is genetic evidence that the swrA-dependent product serrawettin W2, a structurally distinct surfactant, can act as a hemolytic agent. Serrawettin W2, consisting of five amino acids with a single acyl chain, is detected by Caenorhabditis elegans as a chemical signal to avoid S. marcescens colonies. Transposon mutation of the swrA gene, in strain Db10, led to the loss of hemolysis zones on blood agar plates that was correlated with the loss of serrawettin W2. Whereas the hemolysis and cytotoxicity data presented here suggest that serratamolide may contribute to bacterial infections, the absence of the swrW gene in many pathogenic and contact lens associated strains indicate that SwrW is not a requirement for colonization of contact lenses or for causing ocular diseases. Serratamolide may be more relevant in environmental settings than for human infections, as the majority of pigmented strains tested had the swrW gene, and pigmentation is generally associated with environmental isolates, whereas clinical isolates are almost exclusively non-pigmented. In an environmental setting serratamolide could contribute to the competitiveness of S. marcescens as it is a broad spectrum antibiotic. Furthermore, it was shown that a surfactant produced by Serratia sp. ATCC 39006 facilitates the dispersal of the antibiotic pigment prodigiosin, and serratamolide may act in an analogous fashion. Serratamolide has shown promise as an anticancer agent for its proapoptotic effect upon breast cancer and B-cell chronic lymphocytic leukemia cells. Therefore, understanding the pathways that control serratamolide production may yield improved ways to generate this cyclodepsipeptide. Further studies will focus on determining the regulatory pathway by which CRP regulates serratamolide production, and characterizing the role this surfactant plays in host-pathogen interactions. The life cycle of Plasmodium takes place in a Torin 1 vertebrate and in an insect host. When the mosquito takes up a bloodmeal from an infected host, it ingests sexual stages of Plasmodium, the gametocytes. In the mosquito, the gametocytes develop into gametes which fertilise to form a zygote.