scholarly journals Fighting microbial drug resistance: a primer on the role of evolutionary biology in public health

2015 ◽  
Vol 8 (3) ◽  
pp. 211-222 ◽  
Author(s):  
Gabriel G. Perron ◽  
R. Fredrik Inglis ◽  
Pleuni S. Pennings ◽  
Sarah Cobey
2014 ◽  
Vol 8 (01) ◽  
pp. 005-016 ◽  
Author(s):  
Suvash Chandra Ojha ◽  
Chayannan Jaide ◽  
Natini Jinawath ◽  
Porpon Rotjanapan ◽  
Pankaj Baral

The worldwide prevalence of geohelminths and their unique place in evolutionary biology have attracted research focus. These major soil-transmitted intestinal nematodes that cause human diseases are the nematode roundworm (Ascaris lumbricoides), the whipworm (Trichuris trichiura) and the two hookworms (Ancylostoma duodenale and Necator americanus), often collectively referred as geohelminths. Studies of geohelminthiasis in poorly nourished children in developing regions report that geohelminths contribute to stunted growth and cognitive impairment. Insights into immunology have shed light on the modulatory role of the parasite on the host immune system and have defined the role of T cells in controlling geohelminthic infection. Recent molecular biological techniques have created an opportunity to analyse the interaction between parasites and their hosts at the molecular level. This paper is a review of the recent literature that examined the prevalence of geohelminthiasis in developing countries, the association between geohelminths in relation to public health, parasitological/diagnostic features, and therapeutic and preventive aspects of these major soil-transmitted helminth (STH) pathogens in humans.


2018 ◽  
Author(s):  
C. Brandon Ogbunugafor ◽  
Rafael F. Guerrero ◽  
Margaret J. Eppstein

AbstractUnderstanding the forces that drive the dynamics of adaptive evolution is a goal of many subfields within evolutionary biology. The fitness landscape analogy has served as a useful abstraction for addressing these topics across many systems, and recent treatments have revealed how different environments can frame the particulars of adaptive evolution by changing the topography of fitness landscapes. In this study, we examine how the larger, ambient genotypic context in which the fitness landscape being modeled is embedded affects fitness landscape topography and subsequent evolution. Using simulations on empirical fitness landscapes, we discover that genotypic context, defined by genetic variability in regions outside of the locus under study (in this case, an essential bacterial enzyme target of antibiotics), influences the speed and direction of evolution in several surprising ways. These findings have implications for how we study the evolution of drug resistance in nature, and for presumptions about how biological evolution might be expected to occur in genetically-modified organisms. More generally, the findings speak to theory surrounding how “difference can beget difference” in adaptive evolution: that small genetic differences between organisms can greatly alter the specifics of how evolution occurs, which can rapidly drive even slightly diverged populations further apart.Author summaryTechnological advances enable scientists to engineer individual mutations at specific sites within an organism’s genome with increasing ease. These breakthroughs have provided scientists with tools to study how different engineered mutations affect the function of a given gene or protein, yielding useful insight into genotype-phenotype mapping and evolution. In this study, we use engineered strains of bacteria to show how the dynamics (speed and direction) of evolution of drug resistance in an enzyme depends on the species-type of that bacterial enzyme, and on the presence/absence of mutations in other genes in the bacterial genome. These findings have broad implications for public health, genetic engineering, and theories of speciation. In the context of public health and biomedicine, our results suggest that future efforts in managing antimicrobial resistance must consider genetic makeup of different pathogen populations before predicting how resistance will occur, rather than assuming that the same resistance pathways will appear in different pathogen populations. With regard to broader theory in evolutionary biology, our results show how even small genetic differences between organisms can alter how future evolution occurs, potentially causing closely-related populations to quickly diverge.


mSphere ◽  
2017 ◽  
Vol 2 (4) ◽  
Author(s):  
Tobias Weil ◽  
Rodrigo Santamaría ◽  
Wanseon Lee ◽  
Johan Rung ◽  
Noemi Tocci ◽  
...  

ABSTRACT Infectious diseases caused by drug-resistant fungi are an increasing threat to public health because of the high mortality rates and high costs associated with treatment. Thus, understanding of the molecular mechanisms of drug resistance is of crucial interest for the medical community. Here we investigated the role of regulated protein mistranslation, a characteristic mechanism used by C. albicans to diversify its proteome, in the evolution of fluconazole resistance. Such codon ambiguity is usually considered highly deleterious, yet recent studies found that mistranslation can boost adaptation in stressful environments. Our data reveal that CUG ambiguity diversifies the genome in multiple ways and that the full spectrum of drug resistance mechanisms in C. albicans goes beyond the traditional pathways that either regulate drug efflux or alter the interactions of drugs with their targets. The present work opens new avenues by which to understand the molecular and genetic basis of microbial drug resistance. Regulated erroneous protein translation (adaptive mistranslation) increases proteome diversity and produces advantageous phenotypic variability in the human pathogen Candida albicans. It also increases fitness in the presence of fluconazole, but the underlying molecular mechanism is not understood. To address this question, we evolved hypermistranslating and wild-type strains in the absence and presence of fluconazole and compared their fluconazole tolerance and resistance trajectories during evolution. The data show that mistranslation increases tolerance and accelerates the acquisition of resistance to fluconazole. Genome sequencing, array-based comparative genome analysis, and gene expression profiling revealed that during the course of evolution in fluconazole, the range of mutational and gene deregulation differences was distinctively different and broader in the hypermistranslating strain, including multiple chromosome duplications, partial chromosome deletions, and polyploidy. Especially, the increased accumulation of loss-of-heterozygosity events, aneuploidy, translational and cell surface modifications, and differences in drug efflux seem to mediate more rapid drug resistance acquisition under mistranslation. Our observations support a pivotal role for adaptive mistranslation in the evolution of drug resistance in C. albicans. IMPORTANCE Infectious diseases caused by drug-resistant fungi are an increasing threat to public health because of the high mortality rates and high costs associated with treatment. Thus, understanding of the molecular mechanisms of drug resistance is of crucial interest for the medical community. Here we investigated the role of regulated protein mistranslation, a characteristic mechanism used by C. albicans to diversify its proteome, in the evolution of fluconazole resistance. Such codon ambiguity is usually considered highly deleterious, yet recent studies found that mistranslation can boost adaptation in stressful environments. Our data reveal that CUG ambiguity diversifies the genome in multiple ways and that the full spectrum of drug resistance mechanisms in C. albicans goes beyond the traditional pathways that either regulate drug efflux or alter the interactions of drugs with their targets. The present work opens new avenues to understand the molecular and genetic basis of microbial drug resistance.


2015 ◽  
Vol 227 (06/07) ◽  
Author(s):  
J Fabian ◽  
J Ridinger ◽  
O Witt ◽  
I Oehme
Keyword(s):  

2020 ◽  
Vol 11 (SPL1) ◽  
pp. 967-971
Author(s):  
Poonam Thakre ◽  
Waqar M. Naqvi ◽  
Trupti Deshmukh ◽  
Nikhil Ingole ◽  
Sourabh Deshmukh

The emergence in China of 2019 of severe acute respiratory syndrome coronavirus2 (SARS-CoV-2) previously provisionally names 2019-nCoV disease (COVID19) caused major global outbreak and is a major public health problem. On 30 January 2020, the WHO declared COVID19 to be the sixth international public health emergency. This present pandemic has engrossed the globe with a high rate of mortality. As a front line practitioner, physiotherapists are expected to be getting in direct contact with patients infected with the virus. That’s why it is necessary for understanding the many aspects of their role in the identification, contains, reduces and treats the symptoms of this disease. The main presentation is the involvement of respiratory system with symptoms like fever, cough, sore throat, sneezing and characteristics of pneumonia leads to ARDS(Acute respiratory distress syndrome) also land up in multiorgan dysfunction syndrome. This text describes and suggests physiotherapy management of acute COVID-19 patients. It also includes recommendations and guidelines for physiotherapy planning and management. It also covers the guidelines regarding personal care and equipment used for treatment which can be used in the treatment of acute adult patients with suspected or confirmed COVID-19.


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