PLoS One. 2010 Dec 31;5(12):e14472.
The CD40-Autophagy Pathway Is Needed for Host Protection Despite IFN-Γ-Dependent Immunity and CD40 Induces Autophagy via Control of P21 Levels
Portillo JA, Okenka G, Reed E, Subauste A, Van Grol J, Gentil K, Komatsu M, Tanaka K, Landreth G, Levine B, Subauste CS.
Department of Ophthalmology and Visual Sciences, Case Western Reserve University School of Medicine, Cleveland, Ohio, United States of America.
Abstract
Autophagy degrades pathogens in vitro. The autophagy gene Atg5 has been reported to be required for IFN-γ-dependent host protection in vivo. However, these protective effects occur independently of autophagosome formation. Thus, the in vivo role of classic autophagy in protection conferred by adaptive immunity and how adaptive immunity triggers autophagy are incompletely understood. Employing biochemical, genetic and morphological studies, we found that CD40 upregulates the autophagy molecule Beclin 1 in microglia and triggers killing of Toxoplasma gondii dependent on the autophagy machinery. Infected CD40(-/-) mice failed to upregulate Beclin 1 in microglia/macrophages in vivo. Autophagy-deficient Beclin 1(+/-) mice, mice with deficiency of the autophagy protein Atg7 targeted to microglia/macrophages as well as CD40(-/-) mice exhibited impaired killing of T. gondii and were susceptible to cerebral and ocular toxoplasmosis. Susceptibility to toxoplasmosis occurred despite upregulation of IFN-γ, TNF-α and NOS2, preservation of IFN-γ-induced microglia/macrophage anti-T. gondii activity and the generation of anti-T. gondii T cell immunity. CD40 upregulated Beclin 1 and triggered killing of T. gondii by decreasing protein levels of p21, a molecule that degrades Beclin 1. These studies identified CD40-p21-Beclin 1 as a pathway by which adaptive immunity stimulates autophagy. In addition, they support that autophagy is a mechanism through which CD40-dependent immunity mediates in vivo protection and that the CD40-autophagic machinery is needed for host resistance despite IFN-γ.
PMID: 21217818 [PubMed - in process]
Wednesday, January 12, 2011
Determination of the Viability of Toxoplasma gondii in Cured Ham Using Bioassay
J Food Prot. 2010 Dec;73(12):2239-43.
Determination of the Viability of Toxoplasma gondii in Cured Ham Using Bioassay: Influence of Technological Processing and Food Safety Implications
Bayarri S, Gracia MJ, Lázaro R, Pe Rez-Arquillué C, Barberán M, Herrera A.
Departamento de Producción Animal y Ciencia de los Alimentos;, Email: sbayarri@unizar.es.
Abstract
Toxoplasmosis is a zoonotic disease caused by the protozoan Toxoplasma gondii and distributed worldwide. Ingestion of viable cysts from infected raw or undercooked meat is an important route of horizontal transmission of the parasite to humans. Little information is available concerning the effect of commercial curing on cysts of T. gondii. This study is the first in which the influence of processing of cured ham on the viability of T. gondii has been evaluated, using bioassay to assess the risk of infection from eating this meat product. Naturally infected pigs were selected for the study, and a mouse concentration bioassay technique was used to demonstrate viable bradyzoites of T. gondii in porcine tissues and hams. No viable parasites were found in the final product (14 months of curing) based on results of the indirect immunofluorescence assay and histological and PCR analyses. Our results indicate that the consumption of hams cured as described here poses an insignificant risk of acquiring toxoplasmosis. However, additional studies are required to evaluate the safety of ham products cured under different conditions of curing time, salt, and nitrite concentration.
PMID: 21219742 [PubMed - in process]
Determination of the Viability of Toxoplasma gondii in Cured Ham Using Bioassay: Influence of Technological Processing and Food Safety Implications
Bayarri S, Gracia MJ, Lázaro R, Pe Rez-Arquillué C, Barberán M, Herrera A.
Departamento de Producción Animal y Ciencia de los Alimentos;, Email: sbayarri@unizar.es.
Abstract
Toxoplasmosis is a zoonotic disease caused by the protozoan Toxoplasma gondii and distributed worldwide. Ingestion of viable cysts from infected raw or undercooked meat is an important route of horizontal transmission of the parasite to humans. Little information is available concerning the effect of commercial curing on cysts of T. gondii. This study is the first in which the influence of processing of cured ham on the viability of T. gondii has been evaluated, using bioassay to assess the risk of infection from eating this meat product. Naturally infected pigs were selected for the study, and a mouse concentration bioassay technique was used to demonstrate viable bradyzoites of T. gondii in porcine tissues and hams. No viable parasites were found in the final product (14 months of curing) based on results of the indirect immunofluorescence assay and histological and PCR analyses. Our results indicate that the consumption of hams cured as described here poses an insignificant risk of acquiring toxoplasmosis. However, additional studies are required to evaluate the safety of ham products cured under different conditions of curing time, salt, and nitrite concentration.
PMID: 21219742 [PubMed - in process]
Friday, January 07, 2011
Genomic Data Reveal Toxoplasma gondii Differentiation Mutants Are Also Impaired with Respect to Switching into a Novel Extracellular Tachyzoite State
PLoS One. 2010 Dec 30;5(12):e14463.
Genomic Data Reveal Toxoplasma gondii Differentiation Mutants Are Also Impaired with Respect to Switching into a Novel Extracellular Tachyzoite State
Lescault PJ, Thompson AB, Patil V, Lirussi D, Burton A, Margarit J, Bond J, Matrajt M.
Department of Microbiology and Molecular Genetics, University of Vermont, Burlington, Vermont, United States of America.
Abstract
Toxoplasma gondii pathogenesis includes the invasion of host cells by extracellular parasites, replication of intracellular tachyzoites, and differentiation to a latent bradyzoite stage. We present the analysis of seven novel T. gondii insertional mutants that do not undergo normal differentiation to bradyzoites. Microarray quantification of the variation in genome-wide RNA levels for each parasite line and times after induction allowed us to describe states in the normal differentiation process, to analyze mutant lines in the context of these states, and to identify genes that may have roles in initiating the transition from tachyzoite to bradyzoite. Gene expression patterns in wild-type parasites undergoing differentiation suggest a novel extracellular state within the tachyzoite stage. All mutant lines exhibit aberrant regulation of bradyzoite gene expression and notably some of the mutant lines appear to exhibit high proportions of the intracellular tachyzoite state regardless of whether they are intracellular or extracellular. In addition to the genes identified by the insertional mutagenesis screen, mixture model analysis allowed us to identify a small number of genes, in mutants, for which expression patterns could not be accounted for using the three parasite states - genes that may play a mechanistic role in switching from the tachyzoite to bradyzoite stage.
PMID: 21209930 [PubMed - in process]
Genomic Data Reveal Toxoplasma gondii Differentiation Mutants Are Also Impaired with Respect to Switching into a Novel Extracellular Tachyzoite State
Lescault PJ, Thompson AB, Patil V, Lirussi D, Burton A, Margarit J, Bond J, Matrajt M.
Department of Microbiology and Molecular Genetics, University of Vermont, Burlington, Vermont, United States of America.
Abstract
Toxoplasma gondii pathogenesis includes the invasion of host cells by extracellular parasites, replication of intracellular tachyzoites, and differentiation to a latent bradyzoite stage. We present the analysis of seven novel T. gondii insertional mutants that do not undergo normal differentiation to bradyzoites. Microarray quantification of the variation in genome-wide RNA levels for each parasite line and times after induction allowed us to describe states in the normal differentiation process, to analyze mutant lines in the context of these states, and to identify genes that may have roles in initiating the transition from tachyzoite to bradyzoite. Gene expression patterns in wild-type parasites undergoing differentiation suggest a novel extracellular state within the tachyzoite stage. All mutant lines exhibit aberrant regulation of bradyzoite gene expression and notably some of the mutant lines appear to exhibit high proportions of the intracellular tachyzoite state regardless of whether they are intracellular or extracellular. In addition to the genes identified by the insertional mutagenesis screen, mixture model analysis allowed us to identify a small number of genes, in mutants, for which expression patterns could not be accounted for using the three parasite states - genes that may play a mechanistic role in switching from the tachyzoite to bradyzoite stage.
PMID: 21209930 [PubMed - in process]
Thursday, January 06, 2011
Translation control is critical during acute and chronic stages of toxoplasmosis infection
Expert Rev Anti Infect Ther. 2011 Jan;9(1):1-3.
Translation control is critical during acute and chronic stages of toxoplasmosis infection
Joyce BR, Konrad C, Wek RC, Sullivan WJ Jr.
PMID: 21171869 [PubMed - in process]
Translation control is critical during acute and chronic stages of toxoplasmosis infection
Joyce BR, Konrad C, Wek RC, Sullivan WJ Jr.
PMID: 21171869 [PubMed - in process]
Intramembrane Cleavage of AMA1 Triggers Toxoplasma to Switch from an Invasive to a Replicative Mode
Science. 2010 Dec 23. [Epub ahead of print]
Intramembrane Cleavage of AMA1 Triggers Toxoplasma to Switch from an Invasive to a Replicative Mode
Santos JM, Ferguson DJ, Blackman MJ, Soldati-Favre D.
Department of Microbiology, Faculty of Medicine, University of Geneva, 1 rue-Michel Servet, 1211 Geneva 4, Switzerland.
Abstract
Apicomplexan parasites invade host cells and immediately initiate cell division. The extracellular parasite discharges transmembrane proteins onto its surface to mediate motility and invasion. These are shed by intramembrane cleavage, a process associated with invasion but otherwise poorly understood. Functional analysis of Toxoplasma rhomboid 4, a surface intramembrane protease, by conditional overexpression of a catalytically inactive form, produced a profound block in replication. This was completely rescued by expression of the cleaved cytoplasmic tail of Toxoplasma or Plasmodium apical membrane antigen 1 (AMA1). These results reveal an unexpected function for AMA1 in parasite replication, and suggest that invasion proteins help to promote parasite switch from an invasive to a replicative mode.
PMID: 21205639 [PubMed - as supplied by publisher]
Intramembrane Cleavage of AMA1 Triggers Toxoplasma to Switch from an Invasive to a Replicative Mode
Santos JM, Ferguson DJ, Blackman MJ, Soldati-Favre D.
Department of Microbiology, Faculty of Medicine, University of Geneva, 1 rue-Michel Servet, 1211 Geneva 4, Switzerland.
Abstract
Apicomplexan parasites invade host cells and immediately initiate cell division. The extracellular parasite discharges transmembrane proteins onto its surface to mediate motility and invasion. These are shed by intramembrane cleavage, a process associated with invasion but otherwise poorly understood. Functional analysis of Toxoplasma rhomboid 4, a surface intramembrane protease, by conditional overexpression of a catalytically inactive form, produced a profound block in replication. This was completely rescued by expression of the cleaved cytoplasmic tail of Toxoplasma or Plasmodium apical membrane antigen 1 (AMA1). These results reveal an unexpected function for AMA1 in parasite replication, and suggest that invasion proteins help to promote parasite switch from an invasive to a replicative mode.
PMID: 21205639 [PubMed - as supplied by publisher]
Full-parasites: database of full-length cDNAs of apicomplexa parasites, 2010 update
Nucleic Acids Res. 2011 Jan;39(Database issue):D625-31. Epub 2010 Nov 4.
Full-parasites: database of full-length cDNAs of apicomplexa parasites, 2010 update
Tuda J, Mongan AE, Tolba ME, Imada M, Yamagishi J, Xuan X, Wakaguri H, Sugano S, Sugimoto C, Suzuki Y.
Faculty of Medicine, Sam Ratulangi University, Kampus Unsrat, Bahu Manado 95115, Indonesia.
Abstract
Full-Parasites (http://fullmal.hgc.jp/) is a transcriptome database of apicomplexa parasites, which include Plasmodium and Toxoplasma species. The latest version of Full-Parasites contains a total of 105,786 EST sequences from 12 parasites, of which 5925 full-length cDNAs have been completely sequenced. Full-Parasites also contain more than 30 million transcription start sites (TSS) for Plasmodium falciparum (Pf) and Toxoplasma gondii (Tg), which were identified using our novel oligo-capping-based protocol. Various types of cDNA data resources were interconnected with our original database functionalities. Specifically, in this update, we have included two unique RNA-Seq data sets consisting of 730 million mapped RNA-Seq tags. One is a dataset of 16 time-lapse experiments of cultured bradyzoite differentiation for Tg. The other dataset includes 31 clinical samples of Pf. Parasite RNA was extracted together with host human RNA, and the extracted mixed RNA was used for RNA sequencing, with the expectation that gene expression information from the host and parasite would be simultaneously represented. By providing the largest unique full-length cDNA and dynamic transcriptome data, Full-Parasites is useful for understanding host-parasite interactions and will help to eventually elucidate how monophyletic organisms have evolved to become parasites by adopting complex life cycles.
PMID: 21051343 [PubMed - in process]
Full-parasites: database of full-length cDNAs of apicomplexa parasites, 2010 update
Tuda J, Mongan AE, Tolba ME, Imada M, Yamagishi J, Xuan X, Wakaguri H, Sugano S, Sugimoto C, Suzuki Y.
Faculty of Medicine, Sam Ratulangi University, Kampus Unsrat, Bahu Manado 95115, Indonesia.
Abstract
Full-Parasites (http://fullmal.hgc.jp/) is a transcriptome database of apicomplexa parasites, which include Plasmodium and Toxoplasma species. The latest version of Full-Parasites contains a total of 105,786 EST sequences from 12 parasites, of which 5925 full-length cDNAs have been completely sequenced. Full-Parasites also contain more than 30 million transcription start sites (TSS) for Plasmodium falciparum (Pf) and Toxoplasma gondii (Tg), which were identified using our novel oligo-capping-based protocol. Various types of cDNA data resources were interconnected with our original database functionalities. Specifically, in this update, we have included two unique RNA-Seq data sets consisting of 730 million mapped RNA-Seq tags. One is a dataset of 16 time-lapse experiments of cultured bradyzoite differentiation for Tg. The other dataset includes 31 clinical samples of Pf. Parasite RNA was extracted together with host human RNA, and the extracted mixed RNA was used for RNA sequencing, with the expectation that gene expression information from the host and parasite would be simultaneously represented. By providing the largest unique full-length cDNA and dynamic transcriptome data, Full-Parasites is useful for understanding host-parasite interactions and will help to eventually elucidate how monophyletic organisms have evolved to become parasites by adopting complex life cycles.
PMID: 21051343 [PubMed - in process]
Wednesday, January 05, 2011
Strain-specific activation of the NF-{kappa}B pathway by GRA15, a novel Toxoplasma gondii dense granule protein
J Exp Med. 2011 Jan 3. [Epub ahead of print]
Strain-specific activation of the NF-{kappa}B pathway by GRA15, a novel Toxoplasma gondii dense granule protein
Rosowski EE, Lu D, Julien L, Rodda L, Gaiser RA, Jensen KD, Saeij JP.
Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139.
Abstract
NF-κB is an integral component of the immune response to Toxoplasma gondii. Although evidence exists that T. gondii can directly modulate the NF-κB pathway, the parasite-derived effectors involved are unknown. We determined that type II strains of T. gondii activate more NF-κB than type I or type III strains, and using forward genetics we found that this difference is a result of the polymorphic protein GRA15, a novel dense granule protein which T. gondii secretes into the host cell upon invasion. A GRA15-deficient type II strain has a severe defect in both NF-κB nuclear translocation and NF-κB-mediated transcription. Furthermore, human cells expressing type II GRA15 also activate NF-κB, demonstrating that GRA15 alone is sufficient for NF-κB activation. Along with the rhoptry protein ROP16, GRA15 is responsible for a large part of the strain differences in the induction of IL-12 secretion by infected mouse macrophages. In vivo bioluminescent imaging showed that a GRA15-deficient type II strain grows faster compared with wild-type, most likely through its reduced induction of IFN-γ. These results show for the first time that a dense granule protein can modulate host signaling pathways, and dense granule proteins can therefore join rhoptry proteins in T. gondii's host cell-modifying arsenal.
PMID: 21199955 [PubMed - as supplied by publisher]
Strain-specific activation of the NF-{kappa}B pathway by GRA15, a novel Toxoplasma gondii dense granule protein
Rosowski EE, Lu D, Julien L, Rodda L, Gaiser RA, Jensen KD, Saeij JP.
Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139.
Abstract
NF-κB is an integral component of the immune response to Toxoplasma gondii. Although evidence exists that T. gondii can directly modulate the NF-κB pathway, the parasite-derived effectors involved are unknown. We determined that type II strains of T. gondii activate more NF-κB than type I or type III strains, and using forward genetics we found that this difference is a result of the polymorphic protein GRA15, a novel dense granule protein which T. gondii secretes into the host cell upon invasion. A GRA15-deficient type II strain has a severe defect in both NF-κB nuclear translocation and NF-κB-mediated transcription. Furthermore, human cells expressing type II GRA15 also activate NF-κB, demonstrating that GRA15 alone is sufficient for NF-κB activation. Along with the rhoptry protein ROP16, GRA15 is responsible for a large part of the strain differences in the induction of IL-12 secretion by infected mouse macrophages. In vivo bioluminescent imaging showed that a GRA15-deficient type II strain grows faster compared with wild-type, most likely through its reduced induction of IFN-γ. These results show for the first time that a dense granule protein can modulate host signaling pathways, and dense granule proteins can therefore join rhoptry proteins in T. gondii's host cell-modifying arsenal.
PMID: 21199955 [PubMed - as supplied by publisher]
Phosphorylation of Mouse Immunity-Related GTPase (IRG) Resistance Proteins Is an Evasion Strategy for Virulent Toxoplasma gondii
PLoS Biol. 2010 Dec 21;8(12):e1000576.
Phosphorylation of Mouse Immunity-Related GTPase (IRG) Resistance Proteins Is an Evasion Strategy for Virulent Toxoplasma gondii
Steinfeldt T, Könen-Waisman S, Tong L, Pawlowski N, Lamkemeyer T, Sibley LD, Hunn JP, Howard JC.
Institute for Genetics, University of Cologne, Cologne, Germany.
Abstract
Virulence of complex pathogens in mammals is generally determined by multiple components of the pathogen interacting with the functional complexity and multiple layering of the mammalian immune system. It is most unusual for the resistance of a mammalian host to be overcome by the defeat of a single defence mechanism. In this study we uncover and analyse just such a case at the molecular level, involving the widespread intracellular protozoan pathogen Toxoplasma gondii and one of its most important natural hosts, the house mouse (Mus musculus). Natural polymorphism in virulence of Eurasian T. gondii strains for mice has been correlated in genetic screens with the expression of polymorphic rhoptry kinases (ROP kinases) secreted into the host cell during infection. We show that the molecular targets of the virulent allelic form of ROP18 kinase are members of a family of cellular GTPases, the interferon-inducible IRG (immunity-related GTPase) proteins, known from earlier work to be essential resistance factors in mice against avirulent strains of T. gondii. Virulent T. gondii strain ROP18 kinase phosphorylates several mouse IRG proteins. We show that the parasite kinase phosphorylates host Irga6 at two threonines in the nucleotide-binding domain, biochemically inactivating the GTPase and inhibiting its accumulation and action at the T. gondii parasitophorous vacuole membrane. Our analysis identifies the conformationally active switch I region of the GTP-binding site as an Achilles' heel of the IRG protein pathogen-resistance mechanism. The polymorphism of ROP18 in natural T. gondii populations indicates the existence of a dynamic, rapidly evolving ecological relationship between parasite virulence factors and host resistance factors. This system should be unusually fruitful for analysis at both ecological and molecular levels since both T. gondii and the mouse are widespread and abundant in the wild and are well-established model species with excellent analytical tools available.
PMID: 21203588 [PubMed - in process]
Phosphorylation of Mouse Immunity-Related GTPase (IRG) Resistance Proteins Is an Evasion Strategy for Virulent Toxoplasma gondii
Steinfeldt T, Könen-Waisman S, Tong L, Pawlowski N, Lamkemeyer T, Sibley LD, Hunn JP, Howard JC.
Institute for Genetics, University of Cologne, Cologne, Germany.
Abstract
Virulence of complex pathogens in mammals is generally determined by multiple components of the pathogen interacting with the functional complexity and multiple layering of the mammalian immune system. It is most unusual for the resistance of a mammalian host to be overcome by the defeat of a single defence mechanism. In this study we uncover and analyse just such a case at the molecular level, involving the widespread intracellular protozoan pathogen Toxoplasma gondii and one of its most important natural hosts, the house mouse (Mus musculus). Natural polymorphism in virulence of Eurasian T. gondii strains for mice has been correlated in genetic screens with the expression of polymorphic rhoptry kinases (ROP kinases) secreted into the host cell during infection. We show that the molecular targets of the virulent allelic form of ROP18 kinase are members of a family of cellular GTPases, the interferon-inducible IRG (immunity-related GTPase) proteins, known from earlier work to be essential resistance factors in mice against avirulent strains of T. gondii. Virulent T. gondii strain ROP18 kinase phosphorylates several mouse IRG proteins. We show that the parasite kinase phosphorylates host Irga6 at two threonines in the nucleotide-binding domain, biochemically inactivating the GTPase and inhibiting its accumulation and action at the T. gondii parasitophorous vacuole membrane. Our analysis identifies the conformationally active switch I region of the GTP-binding site as an Achilles' heel of the IRG protein pathogen-resistance mechanism. The polymorphism of ROP18 in natural T. gondii populations indicates the existence of a dynamic, rapidly evolving ecological relationship between parasite virulence factors and host resistance factors. This system should be unusually fruitful for analysis at both ecological and molecular levels since both T. gondii and the mouse are widespread and abundant in the wild and are well-established model species with excellent analytical tools available.
PMID: 21203588 [PubMed - in process]
TgVTC2 is Involved in Polyphosphate Accumulation in Toxoplasma gondii
Mol Biochem Parasitol. 2010 Dec 29. [Epub ahead of print]
TgVTC2 is Involved in Polyphosphate Accumulation in Toxoplasma gondii
Rooney PJ, Ayong L, Tobin CM, Moreno SN, Knoll LJ.
Department of Medical Microbiology and Immunology, University of Wisconsin School of Medicine and Public Health, Microbial Sciences Building Room 3345, 1550 Linden Drive, Madison, WI 53706, United States.
Abstract
Polyphosphate is found in every cell, having roles in diverse processes, including differentiation and response to stress. In this study, we characterize a Toxoplasma gondii mutant containing an insertion within the carboxy-terminal end of a homolog of Saccharomyces cerevisiae Vtc2p, a component of the polyphosphate synthetic machinery. Locus TgVTC2 encodes a 140kDa protein containing conserved SPX, VTC and transmembrane domains. TgVTC2 localizes in punctate spots within the cytoplasm that do not co-localize with known markers. The TgVTC2 mutant showed dramatically reduced polyphosphate accumulation, a defect restored by introduction of TgVTC2 to the mutant. Insertion within TgVTC2 resulted in increased transcript levels for two loci, including a putative FIKK kinase. These transcript levels were restored to wild-type levels upon complementation with the TgVTC2 locus. The TgVTC2 locus was refractory to knockout, and may be essential. Analysis of this TgVTC2 mutant will facilitate dissection of the T. gondii polyphosphate synthesis pathway.
Copyright © 2010. Published by Elsevier B.V.
PMID: 21195114 [PubMed - as supplied by publisher]
TgVTC2 is Involved in Polyphosphate Accumulation in Toxoplasma gondii
Rooney PJ, Ayong L, Tobin CM, Moreno SN, Knoll LJ.
Department of Medical Microbiology and Immunology, University of Wisconsin School of Medicine and Public Health, Microbial Sciences Building Room 3345, 1550 Linden Drive, Madison, WI 53706, United States.
Abstract
Polyphosphate is found in every cell, having roles in diverse processes, including differentiation and response to stress. In this study, we characterize a Toxoplasma gondii mutant containing an insertion within the carboxy-terminal end of a homolog of Saccharomyces cerevisiae Vtc2p, a component of the polyphosphate synthetic machinery. Locus TgVTC2 encodes a 140kDa protein containing conserved SPX, VTC and transmembrane domains. TgVTC2 localizes in punctate spots within the cytoplasm that do not co-localize with known markers. The TgVTC2 mutant showed dramatically reduced polyphosphate accumulation, a defect restored by introduction of TgVTC2 to the mutant. Insertion within TgVTC2 resulted in increased transcript levels for two loci, including a putative FIKK kinase. These transcript levels were restored to wild-type levels upon complementation with the TgVTC2 locus. The TgVTC2 locus was refractory to knockout, and may be essential. Analysis of this TgVTC2 mutant will facilitate dissection of the T. gondii polyphosphate synthesis pathway.
Copyright © 2010. Published by Elsevier B.V.
PMID: 21195114 [PubMed - as supplied by publisher]
Foodborne illness acquired in the United States-major pathogens
Emerg Infect Dis. 2011 Jan;17(1):7-15.
Foodborne illness acquired in the United States-major pathogens
Scallan E, Hoekstra RM, Angulo FJ, Tauxe RV, Widdowson MA, Roy SL, Jones JL, Griffin PM.
Centers for Disease Control and Prevention, Atlanta, Georgia, USA.
Abstract
Estimates of foodborne illness can be used to direct food safety policy and interventions. We used data from active and passive surveillance and other sources to estimate that each year 31 major pathogens acquired in the United States caused 9.4 million episodes of foodborne illness (90% credible interval [CrI] 6.6-12.7 million), 55,961 hospitalizations (90% CrI 39,534-75,741), and 1,351 deaths (90% CrI 712-2,268). Most (58%) illnesses were caused by norovirus, followed by nontyphoidal Salmonella spp. (11%), Clostridium perfringens (10%), and Campylobacter spp. (9%). Leading causes of hospitalization were nontyphoidal Salmonella spp. (35%), norovirus (26%), Campylobacter spp. (15%), and Toxoplasma gondii (8%). Leading causes of death were nontyphoidal Salmonella spp. (28%), T. gondii (24%), Listeria monocytogenes (19%), and norovirus (11%). These estimates cannot be compared with prior (1999) estimates to assess trends because different methods were used. Additional data and more refined methods can improve future estimates.
PMID: 21192848 [PubMed - in process]
Foodborne illness acquired in the United States-major pathogens
Scallan E, Hoekstra RM, Angulo FJ, Tauxe RV, Widdowson MA, Roy SL, Jones JL, Griffin PM.
Centers for Disease Control and Prevention, Atlanta, Georgia, USA.
Abstract
Estimates of foodborne illness can be used to direct food safety policy and interventions. We used data from active and passive surveillance and other sources to estimate that each year 31 major pathogens acquired in the United States caused 9.4 million episodes of foodborne illness (90% credible interval [CrI] 6.6-12.7 million), 55,961 hospitalizations (90% CrI 39,534-75,741), and 1,351 deaths (90% CrI 712-2,268). Most (58%) illnesses were caused by norovirus, followed by nontyphoidal Salmonella spp. (11%), Clostridium perfringens (10%), and Campylobacter spp. (9%). Leading causes of hospitalization were nontyphoidal Salmonella spp. (35%), norovirus (26%), Campylobacter spp. (15%), and Toxoplasma gondii (8%). Leading causes of death were nontyphoidal Salmonella spp. (28%), T. gondii (24%), Listeria monocytogenes (19%), and norovirus (11%). These estimates cannot be compared with prior (1999) estimates to assess trends because different methods were used. Additional data and more refined methods can improve future estimates.
PMID: 21192848 [PubMed - in process]
Self-Mating in the Definitive Host Potentiates Clonal Outbreaks of the Apicomplexan Parasites Sarcocystis neurona and Toxoplasma gondii
PLoS Genet. 2010 Dec 23;6(12):e1001261.
Self-Mating in the Definitive Host Potentiates Clonal Outbreaks of the Apicomplexan Parasites Sarcocystis neurona and Toxoplasma gondii
Wendte JM, Miller MA, Lambourn DM, Magargal SL, Jessup DA, Grigg ME.
Molecular Parasitology Unit, Laboratory of Parasitic Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Abstract
Tissue-encysting coccidia, including Toxoplasma gondii and Sarcocystis neurona, are heterogamous parasites with sexual and asexual life stages in definitive and intermediate hosts, respectively. During its sexual life stage, T. gondii reproduces either by genetic out-crossing or via clonal amplification of a single strain through self-mating. Out-crossing has been experimentally verified as a potent mechanism capable of producing offspring possessing a range of adaptive and virulence potentials. In contrast, selfing and other life history traits, such as asexual expansion of tissue-cysts by oral transmission among intermediate hosts, have been proposed to explain the genetic basis for the clonal population structure of T. gondii. In this study, we investigated the contributing roles self-mating and sexual recombination play in nature to maintain clonal population structures and produce or expand parasite clones capable of causing disease epidemics for two tissue encysting parasites. We applied high-resolution genotyping against strains isolated from a T. gondii waterborne outbreak that caused symptomatic disease in 155 immune-competent people in Brazil and a S. neurona outbreak that resulted in a mass mortality event in Southern sea otters. In both cases, a single, genetically distinct clone was found infecting outbreak-exposed individuals. Furthermore, the T. gondii outbreak clone was one of several apparently recombinant progeny recovered from the local environment. Since oocysts or sporocysts were the infectious form implicated in each outbreak, the expansion of the epidemic clone can be explained by self-mating. The results also show that out-crossing preceded selfing to produce the virulent T. gondii clone. For the tissue encysting coccidia, self-mating exists as a key adaptation potentiating the epidemic expansion and transmission of newly emerged parasite clones that can profoundly shape parasite population genetic structures or cause devastating disease outbreaks.
PMID: 21203443 [PubMed - in process]
Self-Mating in the Definitive Host Potentiates Clonal Outbreaks of the Apicomplexan Parasites Sarcocystis neurona and Toxoplasma gondii
Wendte JM, Miller MA, Lambourn DM, Magargal SL, Jessup DA, Grigg ME.
Molecular Parasitology Unit, Laboratory of Parasitic Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Abstract
Tissue-encysting coccidia, including Toxoplasma gondii and Sarcocystis neurona, are heterogamous parasites with sexual and asexual life stages in definitive and intermediate hosts, respectively. During its sexual life stage, T. gondii reproduces either by genetic out-crossing or via clonal amplification of a single strain through self-mating. Out-crossing has been experimentally verified as a potent mechanism capable of producing offspring possessing a range of adaptive and virulence potentials. In contrast, selfing and other life history traits, such as asexual expansion of tissue-cysts by oral transmission among intermediate hosts, have been proposed to explain the genetic basis for the clonal population structure of T. gondii. In this study, we investigated the contributing roles self-mating and sexual recombination play in nature to maintain clonal population structures and produce or expand parasite clones capable of causing disease epidemics for two tissue encysting parasites. We applied high-resolution genotyping against strains isolated from a T. gondii waterborne outbreak that caused symptomatic disease in 155 immune-competent people in Brazil and a S. neurona outbreak that resulted in a mass mortality event in Southern sea otters. In both cases, a single, genetically distinct clone was found infecting outbreak-exposed individuals. Furthermore, the T. gondii outbreak clone was one of several apparently recombinant progeny recovered from the local environment. Since oocysts or sporocysts were the infectious form implicated in each outbreak, the expansion of the epidemic clone can be explained by self-mating. The results also show that out-crossing preceded selfing to produce the virulent T. gondii clone. For the tissue encysting coccidia, self-mating exists as a key adaptation potentiating the epidemic expansion and transmission of newly emerged parasite clones that can profoundly shape parasite population genetic structures or cause devastating disease outbreaks.
PMID: 21203443 [PubMed - in process]
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