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After the era of plentiful antibiotics we are alarmed by the increasing number of antibiotic resistant strains. The genetic flexibility and adaptability of Escherichia coli to constantly changing environments allows to acquire a great number of antimicrobial resistance mechanisms. Commensal strains of E. coli as versatile residents of the lower intestine are also repeatedly challenged by antimicrobial pressures during the lifetime of their host. As a consequence, commensal strains acquire the respective resistance genes, and/or develop resistant mutants in order to survive and maintain microbial homeostasis in the lower intestinal tract. Thus, commensal E. coli strains are regarded as indicators of antimicrobial load on their hosts. This chapter provides a short historic background of the appearance and presumed origin and transfer of antimicrobial resistance genes in commensal intestinal E. coli of animals with comparative information on their pathogenic counterparts. The dynamics, development, and ways of evolution of resistance in the E. coli populations differ according to hosts, resistance mechanisms, and antimicrobial classes used. The most frequent tools of E. coli against a variety of antimicrobials are the efflux pumps and mobile resistance mechanisms carried by plasmids and/or other transferable elements. The emergence of hybrid plasmids (both resistance and virulence) among E. coli is of further concern. Co-existence and co-transfer of these “bad genes” in this huge and most versatile in vivo compartment may represent an increased public health risk in the future. Significance of multidrug resistant (MDR) commensal E. coli seem to be highest in the food animal industry, acting as reservoir for intra- and interspecific exchange and a source for spread of MDR determinants through contaminated food to humans. Thus, public health potential of MDR commensal E. coli of food animals can be a concern and needs monitoring and more molecular analysis in the future.

Placental Protein 13 (PP13) is a galectin expressed by the syncytiotrophoblast. Women who subsequently develop preterm preeclampsia have low first trimester maternal serum PP13 concentrations. This study revealed that third trimester maternal serum PP13 concentration increased with gestational age in normal pregnancies (p<0.0001), and it was significantly higher in women presenting with preterm preeclampsia (p=0.02) and HELLP syndrome (p=0.01) than in preterm controls. Conversely, placental PP13 mRNA (p=0.03) and protein, as well as cytoplasmic PP13 staining of the syncytiotrophoblast (p<0.05) was decreased in these pathological pregnancies compared to controls. No differences in placental expression and serum concentrations of PP13 were found at term between patients with preeclampsia and control women. In contrast, the immunoreactivity of the syncytiotrophoblast microvillous membrane was stronger in both term and preterm preeclampsia and HELLP syndrome than in controls. Moreover, large syncytial cytoplasm protrusions, membrane blebs and shed microparticles strongly stained for PP13 in preeclampsia and HELLP syndrome. In conclusion, parallel to its decreased placental expression, an augmented membrane shedding of PP13 contributes to the increased third trimester maternal serum PP13 concentrations in women with preterm preeclampsia and HELLP syndrome.

A recent European Union Directive required member states to put monitoring and control programmes in place, of which vaccination is a central component. Live Salmonella vaccines generally confer better protection than killed vaccines, because the former stimulate both cell-mediated and humoral immunity. Administering Salmonella bacteria orally to newly hatched chickens results in extensive gut colonization and a strong adaptive immune stimulus but broiler chickens are immunologically immature. However, colonization exerts a variety of rapid (within 24 h) protective effects. These include specific colonization-inhibition (competitive exclusion) in which the protective bacteria exert a profound resistance to establishment and colonization by other related bacteria. This is thought to be primarily a metabolic attribute of the vaccinating bacteria but may also involve competition for attachment sites. The presence of large numbers of bacteria originating from a live Salmonella vaccine in the intestine can also induce infiltration of polymorphonuclear cells into the intestinal wall, which confers resistance to invasion and systemic spread by virulent Salmonella strains. This opens new perspectives for vaccine usage in broilers, layers and breeding poultry but also in other animals which show increased susceptibility to infection because of their young age or for other reasons, such as oral chemoprophylaxis or chemotherapy, where the lack of established normal gut flora is an issue. We recommend that all live vaccines considered for oral administration should be tested for their ability to induce the two protective effects described above. Further developments in live Salmonella vaccines are, however, currently hindered by fears associated with the use and release of live vaccines which may be genetically modified.