Occurrence of infected amoebae in cooling towers compared with natural aquatic environments: implications for emerging pathogens.

Many species of bacteria pathogenic to humans, such as Legionella, are thought to have evolved in association with amoebal hosts. Several novel unculturable bacteria related to Legionella have also been found in amoebae, a few of which have been thought to be causes of nosocomial infections in humans. Because amoebae can be found in cooling towers, we wanted to know whether cooling tower environments might enhance the association between amoebae and bacterial pathogens of amoebae in order to identify potential "hot spots" for emerging human pathogens. To compare occurrence of infected amoebae in natural environments with those in cooling towers, 40 natural aquatic environments and 40 cooling tower samples were examined. Logistic regression analysis determined variables that were significant predictors of the occurrence of infected amoebae, which were found in 22 of 40 cooling tower samples but in only 3 of the 40 natural samples. An odds ratio showed that it is over 16 times more likely to encounter infected amoebae in cooling towers than in natural environments. Environmental data from cooling towers and natural habitats combined revealed dissolved organic carbon (DOC) and pH were predictors of the occurrence of the pathogens, however, when cooling tower data alone were analyzed, no variables accounted for the occurrence. Several bacteria have novel rRNA sequences, and most strains were not culturable outside of amoebae. Such pathogens of amoebae may spread to the environment via aerosols from cooling towers. Studies of emerging infectious diseases should strongly consider cooling towers as a source of amoeba-associated pathogens.

Serotype-dependent induction of pulmonary neutrophilia and inflammatory cytokine gene expression by reovirus.

Reovirus type 3 Dearing (T3D) causes a prominent neutrophil influx, substantially greater than seen with reovirus type 1 Lang (T1L) in a rat model of viral pneumonia. We sought to measure reovirus-mediated increases in chemokine mRNA expression in pulmonary cells. We found that the neutrophilia induced by T1L and T3D infection in vivo correlated directly with increased levels of chemokine mRNA expression in T3D-infected compared with those of T1IL-infected lungs. In vitro, reovirus-infected normal alveolar macrophages (AMs) and the rat AM cell line NR8383 expressed greater levels of macrophage inflammatory protein 2, KC, and tumor necrosis factor alpha mRNA. A synergism between reovirus and lipopolysaccharide was also detected for macrophage inflammatory protein 2 and KC mRNA expression. Tumor necrosis factor protein secretion was also increased to a greater extent by T3D than by T1L in primary rat AMs and the NR8383 cells. We conclude that the virus-mediated inflammatory cytokine induction suggests a role for these cytokines in the neutrophil influx observed in the rat reovirus pneumonia model.