Background While single nucleotide polymorphisms (SNPs) in Mycoplasma genitalium parC contribute to fluoroquinolone treatment failure, data are limited for the homologous gene, gyrA. This study investigated the prevalence of gyrA SNPs, and their contribution to fluoroquinolone failure. Methods Samples from 411 patients (male and female) undergoing treatment for M. genitalium infection (Melbourne Sexual Health Centre, March 2019–February 2020) were analyzed by Sanger sequencing (gyrA and parC). For patients treated with moxifloxacin (n=194), the association between SNPs and microbiologic treatment outcome was analyzed. Results The most common parC SNP was G248T/S83I (21.1% of samples), followed by D87N (2.3%). The most common gyrA SNP was G285A/M95I (7.1%). Dual parC/gyrA SNPs were found in 8.6% of cases. One third of infections harboring parC G248T/S83I SNP had a concurrent SNP in gyrA conferring M95I. SNPs in gyrA co-occurred with parC S83I variations. Treatment failure was higher in patients with parC S83I/gyrA dual SNPs, when compared to infections with single S83I SNP alone from analysis of (i) 194 cases in this study (81.2% vs 45.8%, p=0.047), and (ii) pooled analysis of a larger population of 535 cases (80.6% vs 43.2%; p=0.0027), indicating a strong additive effect. Conclusions Compared to parC S83I SNP alone, M. genitalium infections with dual mutations affecting parC/gyrA had twice the likelihood of failing moxifloxacin. While AMR varies by region globally, these data indicate that gyrA should be considered as a target for future resistance assays in Australasia. We propose a strategy for the next generation of resistance-guided therapy incorporating parC and gyrA testing.
Although encephalomyocarditis virus (EMCV) infection has been commonly documented among domestic animals, less is known about EMCV transmission among humans. Recently, we described the isolation of EMCV from two febrile patients in Peru. To further investigate EMCV transmission in Peru, we screened febrile patients reporting to health clinics in Peru for serological evidence of recent EMCV infection. We also conducted a serological survey for EMCV-neutralizing antibodies in the city of Iquitos, located in the Amazon basin department of Loreto, Peru. Additionally, we screened serum from rodents collected from 10 departments in Peru for evidence of EMCV exposure. EMCV infection was found to be only rarely associated with acute febrile disease in Peru, accounting for <1% of febrile episodes analyzed. Despite the low acute disease burden associated with the virus, human exposure was quite common, as prevalence of EMCV-neutralizing antibodies ranged between 6.0% in the coastal city of Tumbes and >17% in cities in the tropical rainforest of northeastern Peru (Iquitos and Yurimaguas). On the basis of the serological survey conducted in Iquitos, risk factors for past infection include increased age, socioeconomic indicators such as residence construction materials and neighborhood, and swine ownership. Evidence from the rodent survey indicates that EMCV exposure is common among Murinae subfamily rodents in Peru (9.4% EMCV IgG positive), but less common among Sigmodontinae rodents (1.0% positive). Further studies are necessary to more precisely delineate the mode of EMCV transmission to humans, other potential disease manifestations, and the economic impact of EMCV transmission among swine in Peru.
Since deer were introduced into Australia in the mid-1800s, their wild populations have increased in size and distribution, posing a potential risk to the livestock industry, through their role in pathogen transmission cycles. In comparison to livestock, there are limited data on viral infections in all wildlife, including deer. The aim of this study was to assess blood samples from wild Australian deer for serological evidence of exposure to relevant viral livestock diseases. Blood samples collected across eastern Australia were tested by ELISA to detect antigens and antibodies against Pestivirus and antibodies against bovine herpesvirus 1. A subset of samples was also assessed by RT-PCR for Pestivirus, Simbu serogroup, epizootic hemorrhagic disease virus and bovine ephemeral fever virus. Our findings demonstrated a very low seroprevalence (3%) for ruminant Pestivirus, and none of the other viruses tested were detected. These results suggest that wild deer may currently be an incidental spill-over host (rather than a reservoir host) for Pestivirus. However, deer could be a future source of viral infections for domestic animals in Australia. Further investigations are needed to monitor pathogen activity and quantify possible future infectious disease impacts of wild deer on the Australian livestock industry.
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