RESUMO
Extended-spectrum-beta-lactamase (ESBL)- or AmpC beta-lactamase (ACBL)-producing Escherichia coli bacteria are the most common cause of community-acquired multidrug-resistant urinary tract infections (UTIs) in New Zealand. The carriage of antimicrobial-resistant bacteria has been found in both people and pets from the same household; thus, the home environment may be a place where antimicrobial-resistant bacteria are shared between humans and pets. In this study, we sought to determine whether members (pets and people) of the households of human index cases with a UTI caused by an ESBL- or ACBL-producing E. coli strain also carried an ESBL- or ACBL-producing Enterobacteriaceae strain and, if so, whether it was a clonal match to the index case clinical strain. Index cases with a community-acquired UTI were recruited based on antimicrobial susceptibility testing of urine isolates. Fecal samples were collected from 18 non-index case people and 36 pets across 27 households. Eleven of the 27 households screened had non-index case household members (8/18 people and 5/36 animals) positive for ESBL- and/or ACBL-producing E. coli strains. Whole-genome sequence analysis of 125 E. coli isolates (including the clinical urine isolates) from these 11 households showed that within seven households, the same strain of ESBL-/ACBL-producing E. coli was cultured from both the index case and another person (5/11 households) or pet dog (2/11 households). These results suggest that transmission within the household may contribute to the community spread of ESBL- or ACBL-producing E. coliIMPORTANCEEnterobacteriaceae that produce extended-spectrum beta-lactamases (ESBLs) and AmpC beta-lactamases (ACBLs) are important pathogens and can cause community-acquired illnesses, such as urinary tract infections (UTIs). Fecal carriage of these resistant bacteria by companion animals may pose a risk for transmission to humans. Our work evaluated the sharing of ESBL- and ACBL-producing E. coli isolates between humans and companion animals. We found that in some households, dogs carried the same strain of ESBL-producing E. coli as the household member with a UTI. This suggests that transmission events between humans and animals (or vice versa) are likely occurring within the home environment and, therefore, the community as a whole. This is significant from a health perspective, when considering measures to minimize community transmission, and highlights that in order to manage community spread, we need to consider interventions at the household level.
Assuntos
Proteínas de Bactérias/metabolismo , Doenças do Gato/microbiologia , Doenças do Cão/microbiologia , Infecções por Escherichia coli/microbiologia , Infecções por Escherichia coli/veterinária , Escherichia coli/isolamento & purificação , beta-Lactamases/metabolismo , Idoso , Animais , Gatos , Cães , Escherichia coli/enzimologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Nova ZelândiaRESUMO
OBJECTIVES: To assess whether having a pet in the home is a risk factor for community-acquired urinary tract infections associated with extended-spectrum ß-lactamase (ESBL)- or AmpC ß-lactamase (ACBL)- producing Enterobacterales. METHODS: An unmatched case-control study was conducted between August 2015 and September 2017. Cases (n = 141) were people with community-acquired urinary tract infection (UTI) caused by ESBL- or ACBL-producing Enterobacterales. Controls (n = 525) were recruited from the community. A telephone questionnaire on pet ownership and other factors was administered, and associations were assessed using logistic regression. RESULTS: Pet ownership was not associated with ESBL- or ACBL-producing Enterobacterales-related human UTIs. A positive association was observed for recent antimicrobial treatment, travel to Asia in the previous year, and a doctor's visit in the last 6 months. Among isolates with an ESBL-/ACBL-producing phenotype, 126/134 (94%) were Escherichia coli, with sequence type 131 being the most common (47/126). CONCLUSIONS: Companion animals in the home were not found to be associated with ESBL- or ACBL-producing Enterobacterales-related community-acquired UTIs in New Zealand. Risk factors included overseas travel, recent antibiotic use, and doctor visits.
Assuntos
Infecções Comunitárias Adquiridas , Infecções por Escherichia coli , Infecções Urinárias , Animais , Humanos , Antibacterianos/uso terapêutico , beta-Lactamases/genética , Estudos de Casos e Controles , Infecções Comunitárias Adquiridas/epidemiologia , Infecções Comunitárias Adquiridas/microbiologia , Escherichia coli , Infecções por Escherichia coli/epidemiologia , Nova Zelândia , Fatores de Risco , Infecções Urinárias/epidemiologia , Infecções Urinárias/microbiologiaRESUMO
During infection with human immunodeficiency virus (HIV), immune pressure from cytotoxic T-lymphocytes (CTLs) selects for viral mutants that confer escape from CTL recognition. These escape variants can be transmitted between individuals where, depending upon their cost to viral fitness and the CTL responses made by the recipient, they may revert. The rates of within-host evolution and their concordant impact upon the rate of spread of escape mutants at the population level are uncertain. Here we present a mathematical model of within-host evolution of escape mutants, transmission of these variants between hosts and subsequent reversion in new hosts. The model is an extension of the well-known SI model of disease transmission and includes three further parameters that describe host immunogenetic heterogeneity and rates of within host viral evolution. We use the model to explain why some escape mutants appear to have stable prevalence whilst others are spreading through the population. Further, we use it to compare diverse datasets on CTL escape, highlighting where different sources agree or disagree on within-host evolutionary rates. The several dozen CTL epitopes we survey from HIV-1 gag, RT and nef reveal a relatively sedate rate of evolution with average rates of escape measured in years and reversion in decades. For many epitopes in HIV, occasional rapid within-host evolution is not reflected in fast evolution at the population level.
Assuntos
Evolução Biológica , Transcriptase Reversa do HIV/genética , HIV-1/imunologia , Modelos Teóricos , Mutação/genética , Linfócitos T Citotóxicos/imunologia , Produtos do Gene gag do Vírus da Imunodeficiência Humana/genética , Produtos do Gene nef do Vírus da Imunodeficiência Humana/genética , Epitopos de Linfócito T , Infecções por HIV/genética , Infecções por HIV/imunologia , Infecções por HIV/patologia , HIV-1/genética , Humanos , FilogeniaRESUMO
We explore the feasibility of deriving generalised expressions for the probability mass function (PMF) of the final epidemic size of a Susceptible - Infected - Recovered (SIR) model on a finite network of an arbitrary number of nodes. Expressions for the probability that the infection progresses along a given pathway in a line of triangles (LoT) network are presented. Deriving expressions for the probability that the infection ends at any given node allows us to determine the corresponding final size of the epidemic, and hence produce PMFs of the final epidemic size. We illustrate how we can use the results from small networks derived in a previous study to describe how an infection spreads through a LoT network. The key here is to correctly decompose the larger network into an appropriate assemblage of small networks.
Assuntos
Doenças Transmissíveis/epidemiologia , Epidemias , Modelos Biológicos , Modelos Estatísticos , Epidemias/estatística & dados numéricos , HumanosRESUMO
AIM: To estimate the key transmission parameters associated with an outbreak of pandemic influenza in an institutional setting (New Zealand 1918). METHODS: Historical morbidity and mortality data were obtained from the report of the medical officer for a large military camp. A susceptible-exposed-infectious-recovered epidemiological model was solved numerically to find a range of best-fit estimates for key epidemic parameters and an incidence curve. Mortality data were subsequently modelled by performing a convolution of incidence distribution with a best-fit incidence-mortality lag distribution. RESULTS: Basic reproduction number (R0) values for three possible scenarios ranged between 1.3, and 3.1, and corresponding average latent period and infectious period estimates ranged between 0.7 and 1.3 days, and 0.2 and 0.3 days respectively. The mean and median best-estimate incidence-mortality lag periods were 6.9 and 6.6 days respectively. This delay is consistent with secondary bacterial pneumonia being a relatively important cause of death in this predominantly young male population. CONCLUSION: These R0 estimates are broadly consistent with others made for the 1918 influenza pandemic and are not particularly large relative to some other infectious diseases. This finding suggests that if a novel influenza strain of similar virulence emerged then it could potentially be controlled through the prompt use of major public health measures.
Assuntos
Surtos de Doenças , Influenza Humana/mortalidade , Influenza Humana/transmissão , Militares , Modelos Teóricos , Adulto , Causas de Morte , História do Século XX , Hospitais Militares/estatística & dados numéricos , Humanos , Influenza Humana/história , Masculino , Nova Zelândia/epidemiologia , Pneumonia Bacteriana/etiologia , Pneumonia Bacteriana/mortalidade , VirulênciaRESUMO
Many disease systems exhibit complexities not captured by current theoretical and empirical work. In particular, systems with multiple host species and multiple infectious agents (i.e., multi-host, multi-agent systems) require novel methods to extend the wealth of knowledge acquired studying primarily single-host, single-agent systems. We outline eight challenges in multi-host, multi-agent systems that could substantively increase our knowledge of the drivers and broader ecosystem effects of infectious disease dynamics.
Assuntos
Doenças Transmissíveis/epidemiologia , Doenças Transmissíveis/transmissão , Ecologia , Cadeia Alimentar , Interações Hospedeiro-Patógeno , Humanos , Estágios do Ciclo de Vida , Modelos Estatísticos , Dinâmica PopulacionalRESUMO
Despite some notable successes in the control of infectious diseases, transmissible pathogens still pose an enormous threat to human and animal health. The ecological and evolutionary dynamics of infections play out on a wide range of interconnected temporal, organizational, and spatial scales, which span hours to months, cells to ecosystems, and local to global spread. Moreover, some pathogens are directly transmitted between individuals of a single species, whereas others circulate among multiple hosts, need arthropod vectors, or can survive in environmental reservoirs. Many factors, including increasing antimicrobial resistance, increased human connectivity and changeable human behavior, elevate prevention and control from matters of national policy to international challenge. In the face of this complexity, mathematical models offer valuable tools for synthesizing information to understand epidemiological patterns, and for developing quantitative evidence for decision-making in global health.