IMPORTANCE Antibiotic resistance in ocular infections can affect treatment outcomes. Surveillance data on evolving antibacterial susceptibility patterns inform the treatment of such infections. OBJECTIVE To assess overall antibiotic resistance profiles and trends among bacterial isolates from ocular sources collected during 10 years. DESIGN, SETTING, AND PARTICIPANTS This cross-sectional study of longitudinal data from the ongoing, nationwide, prospective, laboratory-based surveillance study, the Antibiotic Resistance Monitoring in Ocular Microorganisms (ARMOR) study, included clinically relevant isolates of Staphylococcus aureus, coagulase-negative staphylococci (CoNS), Streptococcus pneumoniae, Pseudomonas aeruginosa, and Haemophilus influenzae cultured from patients with ocular infections at US centers from January 1, 2009, to December 31, 2018.MAIN OUTCOMES AND MEASURES Minimum inhibitory concentrations were determined for various combinations of antibiotics and species. Odds ratios (ORs) were determined for concurrent antibiotic resistance; analysis of variance and χ 2 tests were used to evaluate resistance rates by patient age and geographic region; Cochran-Armitage tests identified changing antibiotic susceptibility trends over time.RESULTS A total of 6091 isolates (2189 S aureus, 1765 CoNS, 590 S pneumoniae, 767 P aeruginosa, and 780 H influenzae) from 6091 patients were submitted by 88 sites. Overall, 765 S aureus (34.9%) and 871 CoNS (49.3%) isolates were methicillin resistant and more likely to be concurrently resistant to macrolides
A ntibiotic resistance among ocular pathogens is a public health concern. The multicenter, prospective Antibiotic Resistance Monitoring in Ocular micRoorganisms (ARMOR) study is an ongoing surveillance study designed to report on antibiotic resistance rates and trends among Staphylococcus aureus, coagulase-negative staphylococci (CoNS; includes Staphylococcus epidermidis), Streptococcus pneumoniae, Pseudomonas aeruginosa, and Haemophilus influenzae isolates from ocular infections. Results for more than 4,000 isolates collected from 2009 -2015, representing 7 years of ARMOR, were recently presented. More than a third of S. aureus and almost half of all CoNS isolates were found to be resistant to methicillin. Staphylococcal isolates also showed high levels of multidrug resistance (resistance to ≥3 antibacterial drug classes) with 76.4% and 73.7% of methicillin-resistant S. aureus (MRSA) and methicillin-resistant CoNS (MRCoNS) isolates, respectively, demonstrating multidrug resistance. Resistance among S. pneumoniae was notable for azithromycin (36.8%) and for penicillin (34.0%), whereas P. aeruginosa and H. influenzae were generally susceptible to the antibiotic classes tested. Longitudinal analyses demonstrated a small decrease in methicillin resistance among S. aureus over the 7-year study period, which may be a result of improved antibiotic stewardship. Continued surveillance of antibiotic resistance among ocular pathogens is warranted.
Streptococcus pneumoniae, an inhabitant of the upper respiratory mucosa, causes respiratory and invasive infections as well as conjunctivitis. Strains that lack the capsule, a main virulence factor and the target of current vaccines, are often isolated from conjunctivitis cases. Here we perform a comparative genomic analysis of 271 strains of conjunctivitis-causing S. pneumoniae from 72 postal codes in the US. We find that the vast majority of conjunctivitis strains are members of a distinct cluster of closely related unencapsulated strains. These strains possess divergent forms of pneumococcal virulence factors (such as CbpA and neuraminidases) that are not shared with other unencapsulated nasopharyngeal S. pneumoniae. They also possess putative adhesins that have not been described in encapsulated pneumococci. These findings suggest that the unencapsulated strains capable of causing conjunctivitis utilize a pathogenesis strategy substantially different from that described for S. pneumoniae at other infection sites.
IMPORTANCE The Antibiotic Resistance Monitoring in Ocular Microorganisms (ARMOR) study is the only ongoing nationwide antibiotic resistance surveillance program specific to ocular pathogens. OBJECTIVE To report resistance rates and trends among common ocular isolates collected during the first 5 years of the ARMOR study. DESIGN, SETTING, AND PARTICIPANTS This antibiotic resistance surveillance study was performed at an independent central laboratory. Clinical centers across the United States were invited to submit ocular isolates of Staphylococcus aureus, coagulase-negative staphylococci (CoNS), Streptococcus pneumoniae, Haemophilus influenzae, and
Apoptosis is a highly regulated programmed cell death process which is activated during normal development and by various stimuli, such as viral infection, which disturb cellular metabolism and physiology. That herpes simplex virus type 1 (HSV-1) induces apoptosis but then prevents its killing of infected cells is well-established. However, little is known about the viral factor/event which triggers the apoptotic process. We previously reported that infections with either (i) a temperature-sensitive virus at its nonpermissive temperature which does not inject viral DNA into nuclei or (ii) various UV-inactivated wild-type viruses do not result in the induction of apoptosis (C. M. Sanfilippo, F. N. W. Chirimuuta, and J. A. Blaho, J. Virol. 78: [224][225][226][227][228][229][230][231][232][233][234][235][236][237][238][239] 2004). This indicates that virus receptor binding/attachment to cells, membrane fusion, virion disassembly/ tegument dispersal, virion RNAs, and capsid translocation to nuclei are not responsible for induction and implicates viral immediate-early (IE) gene expression in the process. Here, we systematically evaluated the contribution of each IE gene to the stimulation of apoptosis. Using a series of viruses individually deleted for ␣27, ␣4, and ␣22, we determined that these genes are not required for apoptosis induction but rather that their products play roles in its prevention, likely through regulatory effects. Sole expression of ␣0 acted as an "apoptoxin" that was necessary and sufficient to trigger the cell death cascade. Importantly, results using a recombinant virus which contains a stop codon in ␣0 showed that it was not the ICP0 protein which acted as the apoptotic inducer. Based on these findings, we propose that ␣0 gene expression acts as an initial inducer of apoptosis during HSV-1 infection. This represents the first description of apoptosis induction in infected cells triggered as a result of expression of a single viral gene. Expression of apoptotic viral genes is a unique mechanism through which human pathogens may modulate interactions with their host cells.Abnormalities in apoptotic control mechanisms contribute to the development of an assortment of human diseases, including cancer and autoimmunity. Due to the cell's innate ability to self-destruct, apoptosis is also an important mechanism of host response to viral infection. Human herpes simplex virus type 1 (HSV-1) is a large DNA virus (25) whose infection is characterized by the establishment of latency in neuronal cells (60) and the recurrence of lytic infection in epithelial cells (reviewed in reference 52). While productive HSV-1 replication induces major biochemical changes in infected cells, collectively referred to as cytopathic effect, it is now recognized that the virus also triggers apoptosis in transformed or tumor cells, not primary cells (3), but the subsequent synthesis of infected cell proteins during an apoptotic-prevention window (3 to 6 hours postinfection [hpi]) delays the cell death process from killing t...
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