Prevalence of yeast-like fungi and evaluation of several virulence factors from feral pigeons in Seoul, Korea.

AIMS: Studies of pigeon-borne yeasts have tended to focus on species, such as Cryptococcus neoformans and Candida albicans, with scant attention to feral pigeons in Korea. We studied the prevalence of yeasts from faecal samples of feral pigeons obtained in various public places in Seoul, Korea, and assessed their potential capacity as human pathogens. METHODS AND RESULTS: Three hundred and six pigeon faeces samples were collected at city squares and parks in 21 localities in Seoul and Seoul Grand Park and analysed for yeast with conventional methods. Of the 306 samples, 126 (41·2%) were positive for yeast. Seventeen species of yeast were identified. The most frequent species were Candida glabrata (34·1%), Candida famata (12·7%), Cryptococcus albidus (14·3%) and Cryptococcus laurentii (7·9%). The yeast isolates were tested for virulence. Of the 116 isolates (ten isolates missing), 70·7% (n = 82) grew at 37°C. All the Cryptococcus spp. isolates possessed a capsule, 16·4% (n = 19) produced melanin, and 33·6% (n = 39) produced proteinase. Two Ca. glabrata, a Ca. famata and Ca. albicans as well as three C. neoformans, a C. laurentii and Ca. albicans isolates had three virulence factors. Accordingly, 29·3% (n = 34) isolates possessed more than two virulence factors except capsule formation. CONCLUSIONS: These results of this study indicate that feral pigeons harbour a variety of yeasts and are a reservoir of human pathogenic fungi. SIGNIFICANCE AND IMPACT OF THE STUDY: This study is the first time about the microflora (fungi) presents in faecal samples collected from a variety of public areas throughout Seoul, Korea.

The rate of Salmonella spp. infection in zoo animals at Seoul Grand Park, Korea.

Salmonellosis is an important zoonotic disease that affects both people and animals. The incidence of reptile-associated salmonellosis has increased in Western countries due to the increasing popularity of reptiles as pets. In Korea, where reptiles are not popular as pets, many zoos offer programs in which people have contact with animals, including reptiles. So, we determined the rate of Salmonella spp. infection in animals by taking anal swabs from 294 animals at Seoul Grand Park. Salmonella spp. were isolated from 14 of 46 reptiles (30.4%), 1 of 15 birds (6.7%) and 2 of 233 mammals (0.9%). These findings indicate that vigilance is required for determining the presence of zoonotic pathogen infections in zoo animals and contamination of animal facilities to prevent human infection with zoonotic diseases from zoo facilities and animal exhibitions. In addition, prevention of human infection requires proper education about personal hygiene.

Hypersecretion of mucin in response to inflammatory mediators by guinea pig tracheal epithelial cells in vitro is blocked by inhibition of nitric oxide synthase.

Primary cultures of guinea pig tracheal epithelial cells in air/liquid interface were exposed to one of four agents associated with airway inflammation: the peptide histamine (100 microM), the lipid mediator platelet-activating factor (1 microM), the cytokine tumor necrosis factor-alpha (15 ng/ml; specific activity 2.86 x 10(7) U/mg), or enzymatically generated reactive oxygen species (purine [500 microM]+xanthine oxidase [20 mU/ml]). Effects of each of these substances on release of mucin by guinea pig tracheal epithelial (GPTE) cells were measured using a monoclonal antibody-based enzyme-linked immunosorbent assay (ELISA). Each secretagogue significantly enhanced release of mucin, but the stimulatory effect of each was inhibited by pre-(+)co-incubation of the cells with the competitive inhibitor of nitric oxide synthase, NG-monomethyl-L-arginine (L-NMA), but not by NG-monomethyl-D-arginine (D-NMA), the inactive stereoisomer that does not inhibit nitric oxide synthase. Neither L-NMA nor D-NMA affected mucin secretion by themselves. The results suggest that each of these inflammation-associated mediators provokes airway epithelial mucin secretion via a mechanism involving intracellular production of nitric oxide (NO) as a critical signaling molecule.

Histamine provokes turnover of inositol phospholipids in guinea pig and human airway epithelial cells via an H1-receptor/G protein-dependent mechanism.

Guinea pig tracheal epithelial cells in primary air/liquid interface culture (GPTE) and virally transformed human bronchial epithelial cells (BEAS-2B) were exposed to histamine at concentrations of 1 to 100 microM. At concentrations greater than 1 microM, histamine elicited a concentration-dependent increase in accumulation of inositol phosphates in both cell types, as assessed by anion exchange chromatography. The effects of histamine were most pronounced at 15 to 30 min and were attenuated by the H1-receptor antagonist, pyrilamine. The H2-receptor antagonist, ranitidine, was without effect. Sodium fluoride (25 mM), a non-receptor-associated activator of GTP binding (G) proteins, increased accumulation of inositol phosphates within GPTE and BEAS cells. In cells permeabilized with digitonin, the nonhydrolyzable GTP analog, guanosine-5'-O-(3-thiotriphosphate) (GTP gamma S; 10 microM) increased inositol phosphate accumulation. This GTP gamma S-induced increase was attenuated by exposure to 500 microM guanosine-5'-O-(2-thiodiphosphate) (GDP beta S). Additionally, histamine-induced increases in inositol phosphate accumulation were potentiated by GTP gamma S and attenuated by GDP beta S. These data indicate involvement of a G protein in the response to histamine. Preincubation with pertussis toxin (100 ng/ml for 4 h) did not significantly affect the response, suggesting that the associated G protein was not pertussis toxin-sensitive. The presence of the phosphatidylinositol-specific phospholipase C (PI-PLC)-associated G protein, G alpha q/11, and the presence of mRNA for the Gq family, were ascertained by immunoblotting and Northern hybridization, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)