Serotypes in Saccharomyces telluris: Their relation to source of isolation

H.F. Hasenclever; R. M. Kocan

doi:10.1128/iai.7.4.610-612.1973

Home/Archive/USGS

USGS · 5222232

Serotypes in Saccharomyces telluris: Their relation to source of isolation

H.F. Hasenclever·R. M. Kocan

View original source ↗Export metadata ↓

Abstract

Three serotypes have been characterized with three reference strains of Saccharomyces telluris and designated as A, B, and C. One reference strain of Torpulopsis bovina , the imperfect form of S. telluris , belonged to serotype B. Strains (141) of S. telluris isolated from four columbid species were serotyped. All 98 strains of this yeast isolated from Columba livia (feral pigeon) belonged to serotype B. Three other columbid species, C. leucocephala (white-crowned pigeon), C. fasciata (band-tailed pigeon), and Zenaidura macroura (mourning dove) harbored strains of serotype C only. Serotype A was not isolated from any of the avian species.

Explore related subjects

Infection and Immunity Article

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

H.F. Hasenclever, R. M. Kocan. 1973. Serotypes in Saccharomyces telluris: Their relation to source of isolation. https://doi.org/10.1128/iai.7.4.610-612.1973

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related USGS reports

USGS2021

Disruption of the Francisella noatunensis orientalis pdpA gene results in virulence attenuation and protection in zebrafish

Several Francisella spp. including F. noatunensis are regarded as important emerging pathogens of wild and farmed fish. However, very few studies have investigated the virulence factors that allow these bacterial species to be pathogenic in fish. The Francisella Pathogenicity Island (FPI) is a well-described, gene-dense region encoding major virulence factors for the genus Francisella. PdpA is a member of the pathogenicity determining protein genes encoded by the FPI that are implicated in the ability of the mammalian pathogen, F. tularensis , to escape and replicate in infected host cells. Using a sacB suicide approach, we generated pdpA knockouts to address the role of PdpA as a virulence factor for F. noatunensis . Because polarity can be an issue in gene-dense regions, we generated two different marker-based mutants in opposing polarity ( Fno Δ pdpA1 and Δ pdpA2 ). Both mutants were attenuated (p<0.0001) in zebrafish challenges and displayed impaired intracellular replication (p<0.05) and cytotoxicity (p<0.05), all of which could be restored to wild-type (WT) levels by complementation for Fno Δ pdpA 1. Importantly, differences were found for bacterial burden and induction of acute phase and pro-inflammatory genes for Fno Δ pdpA 1 and Δ pdpA 2 compared to WT during acute infection. In addition, neither mutant resulted in significant histopathological changes. Finally, immunization with Fno Δ pdpA1 led to protection (p<0.012) against an acute lethal-dose 40 challenge with WT Fno in the zebrafish model of infection. Taken together, this study further demonstrates physiological similarities within the genus Francisella relative to their phylogenetic relationships and the utility of zebrafish for addressing virulence factors for the genus.

Infection and Immunity↗

USGS2012

Roles of inflammatory caspases during processing of zebrafish interleukin-1β in Francisella noatunensis infection

The interleukin-1 family of cytokines are essential for the control of pathogenic microbes but are also responsible for devastating autoimmune pathologies. Consequently, tight regulation of inflammatory processes is essential for maintaining homeostasis. In mammals, interleukin-1 beta (IL-1β) is primarily regulated at two levels, transcription and processing. The main pathway for processing IL-1β is the inflammasome, a multiprotein complex that forms in the cytosol and which results in the activation of inflammatory caspase (caspase 1) and the subsequent cleavage and secretion of active IL-1β. Although zebrafish encode orthologs of IL-1β and inflammatory caspases, the processing of IL-1β by activated caspase(s) has never been examined. Here, we demonstrate that in response to infection with the fish-specific bacterial pathogen Francisella noatunensis , primary leukocytes from adult zebrafish display caspase-1-like activity that results in IL-1β processing. Addition of caspase 1 or pancaspase inhibitors considerably abrogates IL-1β processing. As in mammals, this processing event is concurrent with the secretion of cleaved IL-1β into the culture medium. Furthermore, two putative zebrafish inflammatory caspase orthologs, caspase A and caspase B, are both able to cleave IL-1β, but with different specificities. These results represent the first demonstration of processing and secretion of zebrafish IL-1β in response to a pathogen, contributing to our understanding of the evolutionary processes governing the regulation of inflammation.

Infection and Immunity↗

USGS1972

Location and description of spiral-shaped microorganisms in the normal rat cecum

Some indigenous microorganisms have been shown to localize in certain anatomical sites of the digestive tract of mammals. We studied the ceca of normal adult rats by light and electron microscopy to determine whether any specific bacterial population localizes in this area. All rats studied showed that the crypt was packed with organisms whose morphological character differs from those of the cecal lumen. Organisms localized in the crypt were often identified topographically close to the microvilli of the epithelial cells. These organisms could be differentiated into three types according to their characteristic ultrastructure. Type 1 was a thin spiral-shaped microbe that resembled a Borrelia. Type 2 possessed helically coiled fibers and flagella-like appendages. Type 3 was spiral-shaped but lacked axial fibers. Types 1 and 2 were both capable of penetrating through the crypt epithelium into the lamina propria where they were found in either phagocytes or extracellular locations. These observations are discussed in relation to other host-microflora localization patterns.

Infection and Immunity↗