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Nosocomial acquisition of influenza is known to occur but the risk after exposure to a known case and the outcomes after acquisition are poorly defined.Prospective observational study of patients exposed to influenza from another patient in a multi-site healthcare organisation, with follow-up of 7 days or until discharge, and PCR-confirmation of symptomatic disease. Multivariable analysis was used to investigate association of influenza acquisition with high dependency unit/intensive care unit (HDU/ITU) admission and in-hospital mortality.23/298 (7.7%) contacts of 11 cases were subsequently symptomatic and tested influenza-positive during follow-up. HDU/ITU admission was significantly higher in these secondary cases (6/23, 26%) compared to flu-negative contacts (20/275, 7.2%; p = 0.002). In-hospital mortality was significantly higher in secondary cases (5/23, 21.7%) compared to flu-negative contacts (11/275, 4%; p 0.001). In multivariable analysis, age (OR 1.25 95% CI: 1.01-1.54, p = 0.02) and being a secondary case (OR 4.77, 95% CI: 1.63-13.9, p = 0.008) were significantly associated with HDU/ITU admission in contacts. Age (OR 1.00, 95% CI: 0.93-1.00, p = 0.02), being a secondary case after exposure to influenza (OR 3.81, 95% CI 1.09-13.3, p = 0.049) and co-morbidity (OR 1.29 per unit increment in the Charlson score, 95% CI 1.02-1.61, p = 0.03) were significantly associated with in-hospital mortality in contacts.Nosocomial acquisition of influenza was significantly associated with increased risk of HDU/ITU admission and in-hospital mortality.

SUMMARY We have used a panel of MoAbs to investigate the phenotype of macrophages and other leucocytes infiltrating onchocercal nodules. Nodules were removed from individuals at the end of the second year of a community-based, placebo-controlled trial of annual ivermectin chemotherapy in northern Nigeria. No significant differences were seen in the distribution and phenotype of leucocytes in nodules from ivermectin- and placebo-treated individuals. Live adult worms were only seen in nine of the 21 nodules examined. Three regions were clearly discernible within nodules containing both live and dead worms; an outer fibrovascular capsule (zone A), an inner adult worm bundle with surrounding hyaline extracellular matrix interspersed with solitary cells (zone B), and a dense cellular infiltrate surrounding and in contact with a variable proportion of the worm (zone C). Macrophages were the predominant cell type in all zones of the nodule. Those in zone B were distinguished by their dendritic morphology and strong reactivity with MoAbs directed against class II molecules. FcRl (CD64) and CD68, whereas macrophages in zone C were larger, more heterogeneous in shape, and were distinguished by strong reactivity with MoAbs directed against CR4 (CDlIc, CD18) and MRP8/MRP14, and with MoAb 24. T cells were found primarily in zones A and C, whilst eosinophils were found in only six nodules. A unique staining pattern was seen using MoAbs reacting with the calcium-binding protein MRP8/MRPI4. Most macrophages in zones A and B were negative; however, where the occasional positive macrophage was seen in zone B, MRP8/MRP14 was also found around the cell and on the neighbouring worm surface, giving the impression that MRP8/ MRP14 was being secreted onto the adult worm. Macrophages in zone C were also MRP8/MRP14-positive, and often the whole infiltrate was surrounded with extracellular MRP8/MRP14, with greatest concentration seen adjacent to the worm. M RP8/MRP14 was not identified on the surface of microfilariae (MF) within the same nodules. Since MRP8/MRP14 was seen on the adult worm in the absence of a leucocytic infiltrate, it may have an early role to play in the immune response to Onchocerca volvulus.

The gastrointestinal tract has a particularly complex relationship with the bacterial world. On the one hand it has its own indigenous microflora composed of a vast number of different bacterial species that are most densely represented in the large bowel. These organisms generally live symbiotically with the host without causing enteric disease. Furthermore, many organisms in the environment are ingested in food and water, yet do not colonise the intestinal tract in the face of local host defence mechanisms and the resident microflora (see Chapters 1 and 2). However, a few bacterial species can establish infection and cause disease following ingestion. Interestingly, it is likely that most of them have evolved from the nonpathogenic intestinal microflora of animals through acquisition of one or more groups of virulence factors. The genetic organisation and biochemical mechanisms involved in the functions of these virulence factors share common themes, yet overall, the pathophysiological characteristics of the major enteric infections are distinct. In general, the first step in the infectious process requires adherence or contact with the surface epithelium. From there, bacteria either remain in the lumen and secrete toxins and factors that modulate epithelial cell function, or invade and survive in the mucosal tissue.