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Severe Strongyloides stercoralis, such as hyperinfection syndrome, carries a high mortality risk. Even with appropriate treatment, patients may experience infectious complications and failure of therapy. Currently, there are no Food and Drug administration--approved parenteral therapies available for treatment in patients who develop gastrointestinal complications from hyperinfection, including small bowel obstruction. A veterinary form of ivermectin is available as a subcutaneous injection, although current literature in humans is limited. We report on the successful treatment of two surviving immunocompromised patients with S. stercoralis hyperinfection syndrome after prompt recognition and initiation of veterinary subcutaneous ivermectin therapy. [ABSTRACT FROM AUTHOR]

Clostridium difficile is an important cause of nosocomial acquired antibiotic-associated diarrhea causing an estimated 453,000 cases with 29,000 deaths yearly in the U.S. Both antibiotic resistance and toxin expression of C. difficile correlate with the severity of C. difficile infection (CDI). In this report, a total of 139 C. difficile isolates from patients diagnosed with CDI in Tampa General Hospital (Florida) in 2016 were studied for antibiotic resistance profiles of 12 types of antibiotics and toxin production. Antibiotic resistance determined by broth microdilution method showed that strains resistant to multi-antibiotics are common. Six strains (4.32%) showed resistance to six types of antibiotics. Twenty strains (14.39%) showed resistance to five types of antibiotics. Seventeen strains (12.24%) showed resistance to four types of antibiotics. Thirty-nine strains (28.06%) showed resistance to three types of antibiotic. Thirty-four strains (24.46%) showed resistance to two types of antibiotics. While, all isolates were susceptible to metronidazole, and rifaximin, we found that one isolate (0.72%) displayed resistance to vancomycin (MIC ≥ 8μg/ml), and another one was resistant to fidaxomicin (MIC >1μg/ml). The percentage of isolates resistant to cefoxitin, ceftriaxone, chloramphenicol, ampicillin, clindamycin, erythromycin, gatifloxacin, and moxifloxacin was 75.54, 10.79, 5.76, 67.63, 82.70, 45.32, 28.06, and 28.78%, respectively. Toxin profiling by PCR showed the isolates include 101 (72.66%) A+B+CDT-strains, 23 (16.55%) A+B+CDT+ strains, 3 (2.16%) A-B+CDT+ strains, 1 (0.72%) A-B+CDT-strains, and 11 (7.91%) A-B-CDT-strains. Toxin production determined by ELISA using supernatants of bacterial culture harvested at 12, 24, 48, and 72 h of post inoculation (hpi) showed that the toxins were mainly produced between 48 and 72 hpi, and toxin B (TcdB) was produced faster than toxin A (TcdA) during the experimental time (72 hpi). In addition, the binary-positive strains were likely to yield more toxins compared to the binary-negative strains. This work contributes to the current understanding of the antibiotic resistance and virulence of C. difficile clinical strains. [ABSTRACT FROM AUTHOR]

Background: Approaches to treatment-experienced HIV-infected patients with persistent low-level viremia are limited by current commercial resistance genotyping assays when the viral load (VL) is <500 copies/mL. The best intervention to achieve virologic suppression in this population is unclear. Methods: This is a case control retrospective chart review study of 149 HIV-infected patients with a VL of 50 to 1000 copies/mL. Patients were in either regimen unchanged group or intervention group (intensification of regimen or switch without guidance from resistance testing). End point was VL < 100 copies/mL. Results: At 6 months post change, 30.8% of patients with intervention versus 36.6% with no intervention achieved a complete virologic suppression. There were no statistically significant differences between these 2 groups (P = .254). The majority of patients without regimen change eventually progressed to complete virologic failure. Conclusion: Patients with persistent low levels of viremia are likely to progress to have virologic failure. This supports the adoption of a more proactive approach to treatment and more sensitive technique to identify drug resistance. [ABSTRACT FROM PUBLISHER]

Clostridioides difficile, the primary cause of nosocomial antibiotic-associated diarrhea, has a complex relationship with antibiotics. While the use of broad-spectrum antibiotics disrupts the gut microbiota and increases the risk of C. difficile infection (CDI), antibiotics are also the primary treatment for CDI. However, only a few antibiotics, including vancomycin, fidaxomicin, and rifaximin, are effective against CDI, and resistance to these antibiotics has emerged recently. In this study, we report the identification of two RT027 C. difficile clinical isolates (TGH35 and TGH64) obtained from symptomatic CDI-diagnosed patients in Tampa, Florida in 2016. These two strains showed an elevated minimum inhibitory concentration (MIC) of vancomycin (MIC = 4 μg/mL, compared to the EUCAST breakpoint of 2 μg/mL) and contained a vanR Cd 343A>G mutation resulting in a Thr115Ala substitution in the VanR Cd response regulator. This mutation was absent in the vancomycin-sensitive control epidemic strain RT027/R20291. TGH64 was also resistant to rifaximin (MIC ≥ 128 μg/mL) and carried the previously reported Arg505Lys and Ile548Met mutations in RpoB. Furthermore, we report on the antimicrobial resistance (AMR) and genomic characterization of additional C. difficile isolates, including RT106/TGH120, RT017/TGH33, and RT017/TGH51, obtained from the same patient sample cohort representing the highly prevalent and regionally distributed C. difficile ribotypes worldwide. Considering that the VanR Cd Thr115Ala mutation was also independently reported in seven C. difficile clinical isolates from Texas and Israel in 2019, we recommend epidemiological surveillance to better understand the impact of this mutation on vancomycin resistance. IMPORTANCE The perpetually evolving antimicrobial resistance (AMR) of C. difficile is an important contributor to its epidemiology and is a grave concern to global public health. This exacerbates the challenge of treating the infections caused by this multidrug-resistant causative organism of potentially life-threatening diarrhea. Further, the novel resistance-determining factors can be transferred between different strains and species of bacteria and cause the spread of AMR in clinical, environmental, and community settings. In this study, we have identified a mutation ( vanR Cd 343A>G) that causes a Thr115Ala substitution and is linked to an increased MIC of vancomycin in clinical isolates of C. difficile obtained from Florida in 2016. Understanding the mechanisms of AMR, especially those of newly evolving strains, is essential to effectively guide antibiotic stewardship policies to combat antibiotic resistance as well as to discover novel therapeutic targets., Competing Interests: The authors declare no conflict of interest.

Background: Approaches to treatment-experienced HIV-infected patients with persistent low-level viremia are limited by current commercial resistance genotyping assays when the viral load (VL) is <500 copies/mL. The best intervention to achieve virologic suppression in this population is unclear., Methods: This is a case control retrospective chart review study of 149 HIV-infected patients with a VL of 50 to 1000 copies/mL. Patients were in either regimen unchanged group or intervention group (intensification of regimen or switch without guidance from resistance testing). End point was VL < 100 copies/mL., Results: At 6 months post change, 30.8% of patients with intervention versus 36.6% with no intervention achieved a complete virologic suppression. There were no statistically significant differences between these 2 groups (P = .254). The majority of patients without regimen change eventually progressed to complete virologic failure., Conclusion: Patients with persistent low levels of viremia are likely to progress to have virologic failure. This supports the adoption of a more proactive approach to treatment and more sensitive technique to identify drug resistance.