No description available.

No description available.

The “seeds of disease” theory that emerged in Europe during the Renaissance period was not an entirely novel concept at the time. Humans were aware of the contagious properties of certain afflictions long before it was possible for them to observe the microorganisms responsible for disease transmission, and ancient authors had already speculated about the existence of imperceptible creatures as a cause of illness. This thesis will show that through ancient literary works of every type permeates the recognition of disease contagion not only between humans, but also between animals of the same species, animals of different species and between humans and animals. Chapter One will examine cases of intra-species infection, beginning with those that do not specify precisely the manner in which the illness in question is passed from one being to another. Instances in which particular factors are noted as contributing to the spread of disease will also be presented, followed by examples highlighting the recognition of intra-species infection in animals. Chapter Two will address the three varieties of inter-species infection of which ancient people were evidently aware: zoonosis, anthroponosis, and xenoosis. Chapter Three will explore the prevalent belief among the ancients that uninterred corpses incited pestilences. Chapter Four will discuss ancient views concerning the contamination of drinking water, as well as cases of deliberate infection with disease— ancient precursors to bioterrorism. Chapter Five will feature numerous theories of ancient authors regarding the presence of disease-causing microorganisms in the air. A variety of literary evidence will be examined throughout this paper and will prove that there was indeed a pervasive knowledge of disease contagion in the ancient world. / Thesis (Master, Classics) -- Queen's University, 2013-09-09 09:27:06.882

Boston University. University Professors Program Senior theses. / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / 2031-01-02

Les virus foamy simiens (VFS) sont la troisième famille des rétrovirus complexes exogènes infectant l'Homme. Ces virus, zoonotique, sont transmis par des fluides biologiques (principalement la salive), lors d'un contact direct entre un individu et un singe infecté. Ils établissent une infection chronique chez l'hôte infecté. À ce jour, aucune pathologie n'a été associée à au cas d'infections humaines par le VFS, et aucun cas de transmission secondaire n'a été rapporté dans la population. L'infection VFS représente un modèle naturel de la restriction de l'émergence d'un rétrovirus simien chez l'Homme. Lors de ma thèse, j'ai caractérisé la réponse humorale contre les VFS chez des personnes vivant au Cameroun ou au Gal infectées suite à des morsures lors d'épisodes de chasse. J'ai montré la présence d'anticorps neutralisants les VFS dans 48 sujets infectés, à des titres élevés. La population étudiée est infectée par des virus de deux génotypes qui diffèrent dans le domaine central de la protéine impliqué dans la liaison au récepteur cellulaire. J'ai montré des réponses neutralisantes spécifiques de chaque génotype des sujets étudiés et des réactivités croisées chez 40% d'entre-eux. Parmi ces derniers, la moitié est infectée par deux souches virales. En conclusion, mon travail de thèse est la première caractérisation des anticorps neutralisants chez des personnes infectées chroniquement par un VFS zoonotique : ces anticorps sont fréquemment détectés, à des titres élevés et sont dirigés contre des épitopes conservés entre les VFS de chimpanzé et de gorille. / Simian foamy virus (SFV) are the third family of exogenous complex retroviruses infecting humans. These viruses, of origins, are transmitted by body fluids (mainly saliva), through a direct contact between an individual and an infected m establish a chronic infection in the infected human host. To date, neither pathology, nor secondary transmission has be to be associated with SFV infection in humans. Therefore, SFV represents a natural model of restriction emerging simiar in humans. During my PhD, I characterized the humoral response against SFV in people living in Cameroon and Gabon, mainly infected bites during hunting episodes. I showed the presence of SFV neutralizing antibodies in the plasma of 48 infected individ titers. Our study population is infected with viruses of 2 different genotypes, which differ in the central region of the En region involved in binding to the cellular receptor.While in 60% of cases, neutralizing response was specific to a single genotype, 40% of cases showed cross-reactivity. Cr( was associated in 50% of cases with co-infection with viruses from both genotypes.In conclusion, my PhD is the first study to characterize neutralizing antibodies in individuals chronically infected with a zoonotic SFV : these antibodies are frequently detected at high titers and are directed against epitopes commonly found in chimpanzee and gorilla SFV.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1953. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 127-142).

CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior / Para melhor avaliar a transmissÃo interfamiliar da infecÃÃo por H. pylori durante a infÃncia, foi investigada a prevalÃncia de infecÃÃo por H. pylori em famÃlias de uma comunidade urbana pobre de Fortaleza no Cearà com alta prevalÃncia de H. pylori . A infecÃÃo por H. pylori foi investigada em 570 membros de 128 famÃlias dessa comunidade, atravÃs do teste respiratÃrio marcado com 13C-urÃia em crianÃas e atravÃs do teste ELISA em mÃes e outros parentes adultos. A prevalÃncia geral da infecÃÃo por H. pylori em todos os indivÃduos analisados foi 65.9% (376/570) a qual aumentou com a idade (p <0,001) variando de 28,9%, em crianÃas de 6 meses a 5 anos, para 82% em adultos com mais de 40 anos. A existÃncia de infecÃÃo materna e o nÃmero de irmÃos infectados foram fatores de risco independentes para a infecÃÃo por H. pylori na infÃncia (OR = 2,2, IC95% = 1,0-4,6 e OR = 4.3, IC95% = 2,3-8,1, respectivamente). O nÃmero de irmÃos, nÃmero de irmÃos mais novos, e o nÃmero de irmÃos mais novos infectados tambÃm foram associados à infecÃÃo na infÃncia atravÃs da anÃlise univariada. O nÃmero de irmÃos mais novos infectados permaneceu independentemente associado com a infecÃÃo (p = 0,000), mesmo apÃs o controle de todas as variÃveis acima citadas, alÃm do status H. pylori de irmÃos e mÃes, idade, nÃmero de pessoas por quarto, e nÃmero de crianÃas no mesmo domicÃlio / To further evaluate interfamilial transmission of H. pylori infection during childhood, we investigated the prevalence of H. pylori infection in family members from a poor H. pylori high prevalence urban community in the Northeast of Brazil. H pylori infection was investigated in 570 members of 128 households, by 13C-urea breath test in children and by ELISA in mothers and other adult relatives. The overall prevalence of H. pylori infection 65.9% (376/570) increased with age (p < 0.001) and ranged from 28.9%, in children aged 6 months to 5 years to 82% in adults over 40 years. An H. pylori positive mother and the number of infected siblings are independent risk factors for childhood H. pylori infection (OR = 2.2, 95% CI = 1.0-4.6 and OR = 4.3, 95% CI = 2.3-8.1, respectively). The number of siblings, number of younger siblings, and number of infected younger siblings were also associated with the infection in the univariate analysis. The number of infected younger siblings remained independently associated with the infection (p=0.000), even after controlling for all the above cited variables, in addition to the H. pylori status of siblings and mothers, age, number of people per room, and number of children in the household. The transmission of H. pylori occurs from infected mothers to their offspring and among siblings, notably from younger siblings to the older ones.

Objectives: The hypothesis that BRO-1 selectively replaced the BRO-2 isoform of the Moraxella catarrhalis BRO β-lactamase was tested by examining the temporal distribution, antibiotic resistance and epidemiological characteristics of isolates from a long-term collection at a single locale. Methods: A rapid, one-step PCR assay conducted on 354 isolates spanning 1984-1994 distinguished bro alleles in over 97% of the β-lactamase-producing isolates. Probes of dot blots were used to distinguish PCR failure from non-β-lactamase-mediated penicillin resistance. Results: BRO-2 isolates comprised 0-10% of the population per year with no evidence of a decline overtime. All β-lactamase producers exceeded the clinical threshold for penicillin resistance. Bimodality of penicillin MICs for β-lactamase producers was caused by variation within BRO-1 rather than differences between BRO-1 and BRO-2. Non-β-lactamase factors also confer resistance to penicillin and may contribute to the BRO-1 bimodality. The 13 BRO-2 isolates were associated with diverse genotypes within which there was evidence of epidemiologically linked clusters. The exclusive association of BRO-2 with four unrelated genotypes suggested maintenance of BRO-2 by recurrent mutation or horizontal exchange. Conclusions: The relative rarity of BRO-2 throughout the study, the absence of a declining temporal trend, and genetic diversity within BRO-2 all failed to support the hypothesis that BRO-2 was more common in the past and has been selectively replaced by BRO-1.

UA Open Access Publishing Fund / Background: Current understanding of tuberculosis (TB) genotype clustering in the US is based on individual risk factors. This study sought to identify whether area-based socioeconomic status (SES) was associated with genotypic clustering among culture-confirmed TB cases. Methods: A retrospective cohort analysis was performed on data collected on persons with incident TB in King County, Washington, 2004–2008. Multilevel models were used to identify the relationship between area-level SES at the block group level and clustering utilizing a socioeconomic position index (SEP). Results: Of 519 patients with a known genotyping result and block group, 212 (41%) of isolates clustered genotypically. Analyses suggested an association between lower area-based SES and increased recent TB transmission, particularly among US-born populations. Models in which community characteristics were measured at the block group level demonstrated that lower area-based SEP was positively associated with genotypic clustering after controlling for individual covariates. However, the trend in higher clustering odds with lower SEP index quartile diminished when additional block-group covariates. Conclusions: Results stress the need for TB control interventions that take area-based measures into account, with particular focus on poor neighborhoods. Interventions based on area-based characteristics, such as improving case finding strategies, utilizing location-based screening and addressing social inequalities, could reduce recent rates of transmission.

No description available.