Rhodococcus erythropolis septic arthritis.

A woman in her 50s presented with a 4-day history of left knee pain, erythema, swelling as well as malaise and rigours 1 month after undergoing a left knee meniscectomy. She was diagnosed with left native knee septic arthritis and underwent arthroscopic irrigation and debridement of the knee; cultures from synovial tissue grew Rhodococcus erythropolis. Rhodococcus spp are soil-dwelling and livestock-dwelling bacteria which occasionally cause disease in immunocompromised hosts. Infection in immunocompetent hosts is rare, and septic arthritis secondary to Rhodococcus erythropolis has not been reported previously.

Outbreak of Adenovirus in a Neonatal Intensive Care Unit: Critical Importance of Equipment Cleaning During Inpatient Ophthalmologic Examinations.

PURPOSE: Outbreaks of adenovirus in neonatal intensive care units (NICUs) can lead to widespread transmission and serious adverse outcomes. We describe the investigation, response, and successful containment of an adenovirus outbreak in a NICU associated with contaminated handheld ophthalmologic equipment used during retinopathy of prematurity (ROP) screening. DESIGN: Epidemiologic outbreak investigation. PARTICIPANTS: A total of 23 hospitalized neonates, as well as NICU staff and parents of affected infants. MAIN OUTCOME MEASURES: Routine surveillance identified an adenovirus outbreak in a level IV NICU in August 2016. Epidemiologic investigation followed, including chart review, staff interviews, and observations. Cases were defined as hospital-acquired adenovirus identified from any clinical specimen (NICU patient or employee) or compatible illness in a family member. Real-time polymerase chain reaction (PCR) and partial- and whole-genome sequencing assays were used for testing of clinical and environmental specimens. RESULTS: We identified 23 primary neonatal cases and 9 secondary cases (6 employees and 3 parents). All neonatal case-patients had respiratory symptoms. Of these, 5 developed pneumonia and 12 required increased respiratory support. Less than half (48%) had ocular symptoms. All neonatal case-patients (100%) had undergone a recent ophthalmologic examination, and 54% of neonates undergoing examinations developed adenovirus infection. All affected employees and parents had direct contact with infected neonates. Observations revealed inconsistent disinfection of bedside ophthalmologic equipment and limited glove use. Sampling of 2 handheld lenses and 2 indirect ophthalmoscopes revealed adenovirus serotype 3 DNA on each device. Sequence analysis of 16 neonatal cases, 2 employees, and 2 lenses showed that cases and equipment shared 100% identity across the entire adenovirus genome. Infection control interventions included strict hand hygiene, including glove use; isolation precautions; enhanced cleaning of lenses and ophthalmoscopes between all examinations; and staff furlough. We identified no cases of secondary transmission among neonates. CONCLUSIONS: Adenovirus outbreaks can result from use of contaminated ophthalmologic equipment. Even equipment that does not directly contact patients can facilitate indirect transmission. Patient-to-patient transmission can be prevented with strict infection control measures and equipment cleaning. Ophthalmologists performing inpatient examinations should take measures to avoid adenoviral spread from contaminated handheld equipment.

Mycoplasma hominis Empyema in an 18-Year-old Stem Cell and Lung Transplant Recipient: Case Report and Review of the Literature.

Mycoplasma hominis has been identified as a rare cause of respiratory infections in immunocompromised adults. Here, we describe a case of Mycoplasma hominis empyema in an 18-year-old immunocompromised patient with a review of the literature highlighting diagnostic challenges associated with this infection.

Comparative analysis of measures of viral reservoirs in HIV-1 eradication studies.

HIV-1 reservoirs preclude virus eradication in patients receiving highly active antiretroviral therapy (HAART). The best characterized reservoir is a small, difficult-to-quantify pool of resting memory CD4(+) T cells carrying latent but replication-competent viral genomes. Because strategies targeting this latent reservoir are now being tested in clinical trials, well-validated high-throughput assays that quantify this reservoir are urgently needed. Here we compare eleven different approaches for quantitating persistent HIV-1 in 30 patients on HAART, using the original viral outgrowth assay for resting CD4(+) T cells carrying inducible, replication-competent viral genomes as a standard for comparison. PCR-based assays for cells containing HIV-1 DNA gave infected cell frequencies at least 2 logs higher than the viral outgrowth assay, even in subjects who started HAART during acute/early infection. This difference may reflect defective viral genomes. The ratio of infected cell frequencies determined by viral outgrowth and PCR-based assays varied dramatically between patients. Although strong correlations with the viral outgrowth assay could not be formally excluded for most assays, correlations achieved statistical significance only for integrated HIV-1 DNA in peripheral blood mononuclear cells and HIV-1 RNA/DNA ratio in rectal CD4(+) T cells. Residual viremia was below the limit of detection in many subjects and did not correlate with the viral outgrowth assays. The dramatic differences in infected cell frequencies and the lack of a precise correlation between culture and PCR-based assays raise the possibility that the successful clearance of latently infected cells may be masked by a larger and variable pool of cells with defective proviruses. These defective proviruses are detected by PCR but may not be affected by reactivation strategies and may not require eradication to accomplish an effective cure. A molecular understanding of the discrepancy between infected cell frequencies measured by viral outgrowth versus PCR assays is an urgent priority in HIV-1 cure research.

Quantitation of integrated proviral DNA in viral reservoirs.

PURPOSE OF REVIEW: Integrated HIV DNA can give rise to infectious virus, and therefore may be a surrogate of reservoir size. How this form reflects the amount of replication competent virus in vivo remains to be established. This review highlights the technical hurdles involved in measuring integrated HIV DNA, progress toward overcoming these hurdles by repetitive sampling and recent important in-vivo findings monitoring this HIV DNA intermediate. RECENT FINDINGS: The dynamics of integration levels after antiretroviral therapy may provide clues to how reservoirs accumulate over time and why early intervention may be beneficial. Recent studies including a multilab collaboration showed that integrated HIV DNA correlate with several viral DNA intermediates including replication competent virus as measured by a quantitative coculture assay. Because this assay performs robustly over a large dynamic range and is reproducible, it may be useful for detecting small changes in reservoir size in trials that target reservoirs as suggested by a recent trial with interferon-α. SUMMARY: Integrated HIV DNA provides an important surrogate for reservoir size and may be useful in trials that target HIV reservoirs. By performing large replicates (repetitive sampling), it is possible to provide more robust estimates and to detect small changes that other assays may overlook. This in turn is critical for evaluating eradication therapies that may have modest but important effects.

HIV reservoirs and latency models.

The main impediment to a cure for HIV is the existence of long-lasting treatment resistant viral reservoirs. In this review, we discuss what is currently known about reservoirs, including their formation and maintenance, while focusing on latently infected CD4+ T cells. In addition, we compare several different in vivo and in vitro models of latency. We comment on how each model may reflect the properties of reservoirs in vivo, especially with regard to cell phenotype, since recent studies demonstrate that multiple CD4+ T cell subsets contribute to HIV reservoirs and that with HAART and disease progression the relative contribution of different subsets may change. Finally, we focus on the direct infection of resting CD4+ T cells as a source of reservoir formation and as a model of latency, since recent results help explain the misconception that resting CD4+ T cells appeared to be resistant to HIV in vitro.