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In Exp. 1, Brachiaria ruziziensis (11.1 % CP) was inoculated or not with two sources of monensin, resulting in three treatments: 1) no monensin inoculation (CONT), 2) 20 mg of monensin sodium-A/kg of DM (Elanco Animal Health; MON-A), and 3) 20 mg of monensin sodium-B/kg of DM (Shandong Qilu King-Phar Pharmaceutical Co. Ltd.; MON-B). Three rumen-fistulated Jersey steers were offered a cool-season forage-based diet and were used as the rumen inoculum donors. Volatile fatty acids concentrations were evaluated at 0, 6, 12, 24, 30, and 48 h after treatment inoculation. Overall, acetate and butyrate concentrations were reduced in MON-A vs. CONT (P ≤ 0.02), whereas both monensin products reduced Ac:Pr ratio vs. CONT (P ≤ 0.01); however, MON-A also (P = 0.05) reduced the Ac:Pr ratio vs. MON-B. A treatment × hour interaction was detected for rumen propionate concentration (P = 0.01), primarily because MON-A resulted in greater propionate than CONT and MON-B at 24 and 48 h (P ≤ 0.03), but no differences were observed between CONT vs. MON-B (P ≥ 0.27). In Exp. 2, 240 Nellore bulls (initial BW = 363.2 ± 40.9 kg) were ranked and blocked according to initial BW, and within blocks animals were allotted into pens (n = 10 pens/treatment). Pens were randomly assigned into one of three treatments: 1) corn-based diet with no monensin (CONT), 2) CONT plus 28 mg of MON-A/kg of DM, and 3) CONT plus 28 mg of MON-B/kg of DM. The CONT diet was composed of sugarcane bagasse, ground corn, DDGS, urea, and a mineral-vitamin mix. The experimental period lasted 106 d and was divided into a 21-d adaptation period and an 85-d finishing phase. During the adaptation phase, both monensin sources increased (P ≤ 0.01) BW change, ADG, and F:G, as well as reduced DMI variation (P = 0.02). When the entire experimental period was evaluated, no treatment effects were detected for final BW, DMI, and ADG (P ≥ 0.26). Nonetheless, DMI variation was reduced as monensin was included (P = 0.01) and only MON-A improved the efficiency by reducing F:G vs. CONT (P = 0.05) and biological efficiency vs. MON-B (P = 0.05). Additionally, carcass ADG tended (P = 0.10) to be greater for MON-A vs. MON-B, whereas no other differences in the carcass characteristics were observed (P ≥ 0.53). In summary, the source of monensin inoculated in vitro and offered to Nellore bulls during the feedlot phase significantly affected the energetic efficiency and the performance of the animals.
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BACKGROUND: Multidrug-resistant tuberculosis poses a major threat to the success of tuberculosis control programs worldwide. Understanding how drug-resistant tuberculosis evolves can inform the development of new therapeutic and preventive strategies. METHODS: Here, we use novel genome-wide analysis techniques to identify polymorphisms that are associated with drug resistance, adaptive evolution and the structure of the phylogenetic tree. A total of 471 samples from different patients collected between 2009 and 2013 in the Lima suburbs of Callao and Lima South were sequenced on the Illumina MiSeq platform with 150bp paired-end reads. After alignment to the reference H37Rv genome, variants were called using standardized methodology. Genome-wide analysis was undertaken using custom written scripts implemented in R software. RESULTS: High quality homoplastic single nucleotide polymorphisms were observed in genes known to confer drug resistance as well as genes in the Mycobacterium tuberculosis ESX secreted protein pathway, pks12, and close to toxin/anti-toxin pairs. Correlation of homoplastic variant sites identified that many were significantly correlated, suggestive of epistasis. Variation in genes coding for ESX secreted proteins also significantly disrupted phylogenetic structure. Mutations in ESX genes in key antigenic epitope positions were also found to disrupt tree topology. CONCLUSION: Variation in these genes have a biologically plausible effect on immunogenicity and virulence. This makes functional characterization warranted to determine the effects of these polymorphisms on bacterial fitness and transmission.
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Farmacorresistencia Bacteriana Múltiple/genética , Mycobacterium tuberculosis/genética , Polimorfismo de Nucleótido Simple , Tuberculosis Resistente a Múltiples Medicamentos/microbiología , Adulto , Femenino , Genes Bacterianos , Humanos , Masculino , Mutación , Mycobacterium tuberculosis/efectos de los fármacos , Perú , Filogenia , Adulto JovenRESUMEN
An epidemic of post-surgical wound infections, caused by a non-tuberculous mycobacterium, has been on-going in Brazil. It has been unclear whether one or multiple lineages are responsible and whether their wide geographical distribution across Brazil is due to spread from a single point source or is the result of human-mediated transmission. 188 isolates, collected from nine Brazilian states, were whole genome sequenced and analysed using phylogenetic and comparative genomic approaches. The isolates from Brazil formed a single clade, which was estimated to have emerged in 2003. We observed temporal and geographic structure within the lineage that enabled us to infer the movement of sub-lineages across Brazil. The genome size of the Brazilian lineage was reduced relative to most strains in the three subspecies of Mycobacterium abscessus and contained a novel plasmid, pMAB02, in addition to the previously described pMAB01 plasmid. One lineage, which emerged just prior to the initial outbreak, is responsible for the epidemic of post-surgical wound infections in Brazil. Phylogenetic analysis indicates that multiple transmission events led to its spread. The presence of a novel plasmid and the reduced genome size suggest that the lineage has undergone adaptation to the surgical niche.
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Brotes de Enfermedades , Infecciones por Mycobacterium no Tuberculosas/epidemiología , Infecciones por Mycobacterium no Tuberculosas/microbiología , Mycobacterium abscessus/genética , Infección de la Herida Quirúrgica/epidemiología , Infección de la Herida Quirúrgica/microbiología , Adaptación Biológica/genética , Técnicas de Tipificación Bacteriana , Brasil/epidemiología , Infección Hospitalaria , Transmisión de Enfermedad Infecciosa , Eliminación de Gen , Genes Bacterianos , Genómica , Humanos , Mycobacterium abscessus/clasificación , Mycobacterium abscessus/aislamiento & purificación , Fenotipo , Filogenia , Plásmidos/genética , Secuenciación Completa del GenomaRESUMEN
Modern strains of Mycobacterium tuberculosis from the Americas are closely related to those from Europe, supporting the assumption that human tuberculosis was introduced post-contact. This notion, however, is incompatible with archaeological evidence of pre-contact tuberculosis in the New World. Comparative genomics of modern isolates suggests that M. tuberculosis attained its worldwide distribution following human dispersals out of Africa during the Pleistocene epoch, although this has yet to be confirmed with ancient calibration points. Here we present three 1,000-year-old mycobacterial genomes from Peruvian human skeletons, revealing that a member of the M. tuberculosis complex caused human disease before contact. The ancient strains are distinct from known human-adapted forms and are most closely related to those adapted to seals and sea lions. Two independent dating approaches suggest a most recent common ancestor for the M. tuberculosis complex less than 6,000 years ago, which supports a Holocene dispersal of the disease. Our results implicate sea mammals as having played a role in transmitting the disease to humans across the ocean.
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Caniformia/microbiología , Genoma Bacteriano/genética , Mycobacterium tuberculosis/genética , Tuberculosis/historia , Tuberculosis/microbiología , Zoonosis/historia , Zoonosis/microbiología , Animales , Huesos/microbiología , Europa (Continente)/etnología , Genómica , Historia Antigua , Migración Humana/historia , Humanos , Perú , Filogenia , Tuberculosis/transmisión , Zoonosis/transmisiónRESUMEN
Vibrio cholerae is a globally important pathogen that is endemic in many areas of the world and causes 3-5 million reported cases of cholera every year. Historically, there have been seven acknowledged cholera pandemics; recent outbreaks in Zimbabwe and Haiti are included in the seventh and ongoing pandemic. Only isolates in serogroup O1 (consisting of two biotypes known as 'classical' and 'El Tor') and the derivative O139 can cause epidemic cholera. It is believed that the first six cholera pandemics were caused by the classical biotype, but El Tor has subsequently spread globally and replaced the classical biotype in the current pandemic. Detailed molecular epidemiological mapping of cholera has been compromised by a reliance on sub-genomic regions such as mobile elements to infer relationships, making El Tor isolates associated with the seventh pandemic seem superficially diverse. To understand the underlying phylogeny of the lineage responsible for the current pandemic, we identified high-resolution markers (single nucleotide polymorphisms; SNPs) in 154 whole-genome sequences of globally and temporally representative V. cholerae isolates. Using this phylogeny, we show here that the seventh pandemic has spread from the Bay of Bengal in at least three independent but overlapping waves with a common ancestor in the 1950s, and identify several transcontinental transmission events. Additionally, we show how the acquisition of the SXT family of antibiotic resistance elements has shaped pandemic spread, and show that this family was first acquired at least ten years before its discovery in V. cholerae.
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Cólera/epidemiología , Cólera/transmisión , Pandemias/estadística & datos numéricos , Vibrio cholerae/genética , Vibrio cholerae/aislamiento & purificación , Cólera/microbiología , Genoma Bacteriano/genética , Haití/epidemiología , Humanos , Funciones de Verosimilitud , Epidemiología Molecular , Filogenia , Polimorfismo de Nucleótido Simple/genética , Vibrio cholerae/clasificación , Zimbabwe/epidemiologíaRESUMEN
Current methods for differentiating isolates of predominant lineages of pathogenic bacteria often do not provide sufficient resolution to define precise relationships. Here, we describe a high-throughput genomics approach that provides a high-resolution view of the epidemiology and microevolution of a dominant strain of methicillin-resistant Staphylococcus aureus (MRSA). This approach reveals the global geographic structure within the lineage, its intercontinental transmission through four decades, and the potential to trace person-to-person transmission within a hospital environment. The ability to interrogate and resolve bacterial populations is applicable to a range of infectious diseases, as well as microbial ecology.