RESUMO
Background and Aim: Campylobacter spp. are Gram-negative bacilli that are widely recognized as a primary cause of bacterial gastroenteritis worldwide. Campylobacteriosis is the disease caused by this pathogen. Recently, greater attention has been given to the prevalence of campylobacteriosis in different animals, including pets. These animals are considered to be significant reservoirs for this zoonosis. In Lebanon, the occurrence of Campylobacter infection is high. Our first-of-its-kind pilot study in Lebanon aimed to estimate the fecal prevalence of Campylobacter species in house dogs. Materials and Methods: Thirty-five rectal swabs were collected from male and female house dogs of different ages, both with or without diarrhea. Samples obtained from the dogs were subjected to qualitative microbiological culture testing and molecular diagnosis by polymerase chain reaction assays after bacterial DNA extraction. Results: Fecal prevalence of Campylobacter spp. in house dogs in this study was 17%. There was a relatively higher prevalence among young females and a significant difference between healthy dogs and those suffering from diarrhea. Conclusion: Campylobacteriosis was found to be prevalent among house dogs in Lebanon, making them potential carriers of Campylobacter species.
RESUMO
The blue-green phenazine, Pyocyanin (PYO), is a well-known virulence factor produced by Pseudomonas aeruginosa, notably during cystic fibrosis lung infections. It is toxic to both eukaryotic and bacterial cells and several mechanisms, including the induction of oxidative stress, have been postulated. However, the mechanism of PYO toxicity under the physiological conditions of oxygen limitation that are encountered by P. aeruginosa and by target organisms in vivo remains unclear. In this study, wild-type and mutant strains of the yeast Saccharomyces cerevisiae were used as an effective eukaryotic model to determine the toxicity of PYO (100-500 µmol/L) under key growth conditions. Under respiro-fermentative conditions (with glucose as substrate), WT strains and certain H2 O2 -hypersensitive strains showed a low-toxic response to PYO. Under respiratory conditions (with glycerol as substrate) all the strains tested were significantly more sensitive to PYO. Four antioxidants were tested but only N-acetylcysteine was capable of partially counteracting PYO toxicity. PYO did not appear to affect short-term respiratory O2 uptake, but it did seem to interfere with cyanide-poisoned mitochondria through a complex III-dependent mechanism. Therefore, a combination of oxidative stress and respiration disturbance could partly explain aerobic PYO toxicity. Surprisingly, the toxic effects of PYO were more significant under anaerobic conditions. More pronounced effects were observed in several strains including a 'petite' strain lacking mitochondrial DNA, strains with increased or decreased levels of ABC transporters, and strains deficient in DNA damage repair. Therefore, even though PYO is toxic for actively respiring cells, O2 may indirectly protect the cells from the higher anaerobic-linked toxicity of PYO. The increased sensitivity to PYO under anaerobic conditions is not unique to S. cerevisiae and was also observed in another yeast, Candida albicans.
