The presence of spiral bacteria in the feline stomach has been recognized for over a century, but the identities and degrees of prevalence of such organisms in privately owned cats are still poorly documented. The aims of this study were (i) to adapt different diagnostic tools and evaluate their practicality for diagnosing feline gastric Helicobacter colonization, (ii) to determine the prevalence of gastric Helicobacter-like organisms in pet cats, (iii) to identify the feline species, and (iv) to correlate the presence of a Helicobacter infection with gastritis. Biopsy samples were taken gastroscopically from the antra and the corpora of clinically healthy pet cats. Helicobacter-like organisms were detected by Gram staining, Warthin-Starry staining, and rapid urease testing in biopsy specimens and by [13C]urea breath testing in 79, 77, 78, and 85% of cases, respectively. PCR analysis revealed that 78% of the cats (38 of 49) were infected byHelicobacter heilmannii; however, none of them was harboring Helicobacter pylori or Helicobacter felis. Culture was positive for one cat; the organism was identified as Helicobacter pametensis by dot blot DNA hybridization. By a combination of the detection methods, 91% of the pet cats were found to be Helicobacter positive. For 46 cats (79%) diagnostic tests were concordant. All cats showed mild to moderate gastritis in either the antrum or the corpus, regardless of the presence or density of gastric bacteria. In summary, pet cats are frequently colonized by H. heilmannii without a significant correlation between infection and degree of gastritis.

Summary Bacteria of the Bordetella genus cause respiratory tract infections. Both broad host range (e.g. Bordetella bronchiseptica) and human-adapted (e.g. Bordetella pertussis) strains produce a surface-exposed and secreted protein called filamentous haemagglutinin (FHA) that functions in adherence and immunomodulation. Previous studies using B. pertussis and cultured mammalian cells identified several FHA domains with potential roles in host cell interactions, including an Arg-Gly-Asp (RGD) triplet that was reported to bind integrins on epithelial cells and monocytes to activate host signalling pathways. We show here that, in contrast to our previous report, the fhaB genes of B. pertussis and B. bronchiseptica are functionally interchangeable, at least with regard to the various in vitro and in vivo assays investigated. This result is significant because it indicates that information obtained studying FHA using B. bronchiseptica and natural-host animal models should apply to B. pertussis FHA as well. We also show that the C-terminus of mature FHA, which we name the MCD, mediates adherence to epithelial and macrophage-like cells and is required for colonization of the rat respiratory tract and modulation of the inflammatory response in mouse lungs. We could not, however, detect a role for the RGD in any of these processes.

Vancomycin, one of few effective treatments against methicillin-resistant Staphylococcus aureus, is nephrotoxic. The goals of this study were to (1) gain insights into molecular mechanisms of nephrotoxicity at the genomic level, (2) evaluate gene markers of vancomycin-induced kidney injury, and (3) compare gene expression responses after iv and ip administration. Groups of six female BALB/c mice were treated with seven daily iv or ip doses of vancomycin (50, 200, and 400 mg/kg) or saline, and sacrificed on day 8. Clinical chemistry and histopathology demonstrated kidney injury at 400 mg/kg only. Hierarchical clustering analysis revealed that kidney gene expression profiles of all mice treated at 400 mg/kg clustered with those of mice administered 200 mg/kg iv. Transcriptional profiling might thus be more sensitive than current clinical markers for detecting kidney damage, though the profiles can differ with the route of administration. Analysis of transcripts whose expression was changed by at least twofold compared with vehicle saline after high iv and ip doses of vancomycin suggested the possibility of oxidative stress and mitochondrial damage in vancomycin-induced toxicity. In addition, our data showed changes in expression of several transcripts from the complement and inflammatory pathways. Such expression changes were confirmed by relative real-time reverse transcription–polymerase chain reaction. Finally, our results further substantiate the use of gene markers of kidney toxicity such as KIM-1/Havcr1, as indicators of renal injury.

To survive in a host environment, microbial pathogens must sense local conditions, including nutrient availability, and adjust their growth state and virulence functions accordingly. No comprehensive investigation of growth phase-related gene regulation in Bordetella pertussis has been reported previously. We characterized changes in genome-wide transcript abundance of B. pertussis as a function of growth phase and availability of glutamate, a key nutrient for this organism. Using a Bordetella DNA microarray, we discovered significant changes in transcript abundance for 861 array elements during the transition from log phase to stationary phase, including declining transcript levels of many virulence factor genes. The responses to glutamate depletion exhibited similarities to the responses induced by exit from log phase, including decreased virulence factor transcript levels. However, only 23% of array elements that showed at least a fourfold growth phaseassociated difference in transcript abundance also exhibited glutamate depletion-associated changes, suggesting that nutrient limitation may be one of several interacting factors affecting gene regulation during stationary phase. Transcript abundance patterns of a Bvg ؉ phase-locked mutant revealed that the BvgAS two-component regulatory system is a key determinant of growth phase-and nutrient limitation-related transcriptional control. Several adhesin genes exhibited lower transcript abundance during stationary phase and under glutamate restriction conditions. The predicted bacterial phenotype was confirmed: adherence to bronchoepithelial cells decreased 3.3-and 4.4-fold at stationary phase and with glutamate deprivation, respectively. Growth phase and nutrient availability may serve as cues by which B. pertussis regulates virulence according to the stage of infection or the location within the human airway.During the course of infection, bacterial pathogens encounter a variety of challenging conditions in the host, including scarcity of carbon, nitrogen, iron, and other nutrients; fluctuations in pH; oxidative stress; and adverse conditions produced by the host innate and adaptive immune responses. In order to succeed, microorganisms must be able to modify their physiological state and virulence phenotype in accordance with changing features within the host, in a reciprocal and dynamic fashion. Growth phase-associated regulation is inherently related to pathogenicity, for in order to survive, bacteria must alter their growth rate and metabolic activity appropriately, according to cues in the host environment. Entry into stationary phase, defined as the moment when the bacterial growth rate begins to decline, is accompanied by development of cross-resistance to multiple stressors, promoting survival (34). In addition, studies have identified correlations between bacterial virulence and growth phase (22,38).No comprehensive study of growth phase-associated regulation has been performed with the obligate human pathogen Bordetella pertussis, the causative agent of...

Circumstantial evidence suggests that “Helicobacter heilmannii” infection is an example of zoonosis. The presence of “H. heilmannii” strains in a human subject with acute gastric erosions, in his two cats, and in two unrelated cats was analyzed, and the genetic relatedness of the human and feline strains was assessed. A 580-bp, PCR-amplified sequence of “H. heilmannii” urease B gene (ureB) obtained from biopsies from the human subject and his two cats was restricted withAluI and cloned for sequencing. Analysis of the restriction fragment length polymorphism of the ureB-amplified product suggested the presence of different individual “H. heilmannii” strains in the cats and of three distinct strains in the human subject. One of the “H. heilmannii”ureB sequences amplified from the human subject’s biopsies was identical to that derived from one of his cats. The degree of similarity between the other “H. heilmannii” human and feline nucleotide sequences was higher than 97%. Most of the base substitutions were conservative. We conclude that human and animal “H. heilmannii” strains are closely related and that humans can be infected by more than one “H. heilmannii” strain, as has been observed for Helicobacter pylori.