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1.
BMC Infect Dis ; 24(1): 717, 2024 Jul 22.
Article in English | MEDLINE | ID: mdl-39039476

ABSTRACT

BACKGROUND: The use of telemedicine has grown significantly since the COVID-19 pandemic and has the potential to improve access to specialized care for otherwise underserved populations. Incarcerated people living with HIV (PLWH) could potentially benefit from expanded access to HIV care through telemedicine. METHODS: All PLWH who were incarcerated within the Tennessee Department of Corrections and received care through the HIV telemedicine clinic at Regional One Hospital between 5/1/2019 through 2/28/2022 were identified from the electronic health records (EHR). Demographics, laboratory data, vaccine history, and treatment outcomes were abstracted from the EHR. Retention in care and viral suppression were defined using Centers for Disease Control and Prevention definitions. RESULTS: Of the 283 incarcerated PLWH receiving care from this telemedicine clinic, 78% remained retained in care and 94% achieved or maintaining viral suppression at 12 months. Many preventative care measures remained unperformed or undocumented, including vaccinations and testing for concurrent sexually transmitted infections. There were 56 patients (20%) found to have chronic hepatitis C in this population, with 71% either cured or still on treatment in this study period. CONCLUSIONS: Retention in care and viral suppression rates were excellent among incarcerated PLWH receiving telemedicine care for their HIV. HIV related primary health care screenings and vaccinations, however, were less consistently documented and represent areas for improvement.


Subject(s)
COVID-19 , HIV Infections , Prisoners , Telemedicine , Humans , HIV Infections/therapy , Male , Female , Adult , Middle Aged , COVID-19/therapy , COVID-19/epidemiology , Cohort Studies , Delivery of Health Care , SARS-CoV-2 , Tennessee
2.
J Clin Microbiol ; 48(9): 3438-9, 2010 Sep.
Article in English | MEDLINE | ID: mdl-20631098

ABSTRACT

Yersinia enterocolitica rarely causes extraintestinal disease. A 54-year-old construction worker with chronic hepatitis C developed an axillary abscess following an injury to his finger. An aspirate from the axillary mass grew Y. enterocolitica. Direct inoculation is proposed as the mode of transmission of this classically enteric pathogen.


Subject(s)
Abscess/microbiology , Axilla/pathology , Finger Injuries/complications , Yersinia Infections/diagnosis , Yersinia enterocolitica/isolation & purification , Abscess/pathology , Axilla/microbiology , Hepatitis C, Chronic/complications , Humans , Male , Middle Aged , Yersinia Infections/microbiology , Yersinia Infections/pathology
3.
Infect Immun ; 74(12): 6847-54, 2006 Dec.
Article in English | MEDLINE | ID: mdl-16954397

ABSTRACT

The human beta-defensin 3 (hBD-3) is an inducible epithelial peptide antibiotic that has potent antistaphylococcal activity. Infection of skin epithelial cells with viable Staphylococcus aureus, a common skin pathogen, induces increased gene expression of hBD-3 and other antimicrobial peptides. The aim of this study was to identify signaling pathways and nuclear responses that contribute to the gene expression of hBD-3 in primary human keratinocytes upon contact with S. aureus. Increased hBD-3 peptide was observed by immunofluorescence microscopy in keratinocytes exposed to S. aureus and to lipoteichoic acid (LTA). Both are ligands for the cell surface Toll-like receptor 2 (TLR2), and thus the contribution of TLR2 signaling in hBD-3 expression was examined. Functional inhibition of TLR2 prior to S. aureus stimulation significantly decreased hBD-3 mRNA levels by 37%, attesting to the involvement of this surface receptor in the initial recognition and downstream signaling for hBD-3 expression. Treatment of keratinocytes with a p38 mitogen-activated protein kinase (MAPK) inhibitor prior to either S. aureus or LTA stimulation was associated with reduced hBD-3 mRNA transcripts and peptide. We also propose a role for the MAPK-regulated transcriptional activating protein 1 in S. aureus-induced hBD-3 gene expression. Combined, these studies indicate a role for TLR2 signaling and MAPK activation in the upregulation of hBD-3 and demonstrate the innate immune capacity of skin keratinocytes under conditions of S. aureus challenge to enhance the local expression of this antistaphylococcal peptide antibiotic.


Subject(s)
Keratinocytes/microbiology , Staphylococcus aureus/physiology , Toll-Like Receptor 2/physiology , beta-Defensins/genetics , Cells, Cultured , Gene Expression , Humans , Keratinocytes/chemistry , Keratinocytes/metabolism , Lipopolysaccharides/pharmacology , RNA, Messenger/analysis , RNA, Messenger/metabolism , Signal Transduction , Skin/cytology , Skin/metabolism , Skin/microbiology , Teichoic Acids/pharmacology , Toll-Like Receptor 2/agonists , Toll-Like Receptor 2/antagonists & inhibitors , Transcription Factor AP-1/metabolism , Transcription, Genetic , beta-Defensins/analysis , beta-Defensins/metabolism , p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors , p38 Mitogen-Activated Protein Kinases/metabolism
4.
Infect Immun ; 73(8): 5241-4, 2005 Aug.
Article in English | MEDLINE | ID: mdl-16041048

ABSTRACT

Keratinocytes upregulate expression of endogenous antimicrobial peptides in response to inflammatory stimuli. We show that both viable and heat-inactivated Staphylococcus aureus and lipoteichoic acid differentially alter expression of these peptides upon contact with human keratinocytes. The findings indicate a diversity of staphylococcal factors involved in upregulation of antimicrobial peptide expression in cutaneous epithelia.


Subject(s)
Antimicrobial Cationic Peptides/genetics , Keratinocytes/microbiology , Staphylococcal Infections/metabolism , Staphylococcus aureus , Antimicrobial Cationic Peptides/biosynthesis , Epidermis/immunology , Epidermis/metabolism , Epidermis/microbiology , Humans , Keratinocytes/immunology , Keratinocytes/metabolism , Lipopolysaccharides/metabolism , Teichoic Acids/metabolism
5.
Curr Opin Infect Dis ; 16(3): 225-9, 2003 Jun.
Article in English | MEDLINE | ID: mdl-12821812

ABSTRACT

PURPOSE OF REVIEW: Staphylococcus aureus produces two closely-related fibronectin-binding proteins (FnBPs) that facilitate attachment by this versatile pathogen. Recent studies of staphylococcal FnBP have increased our understanding of the molecular mechanisms that are critical in bacterial-host cell interactions and in infection. RECENT FINDINGS: This review will summarize current knowledge of the role of the FnBPs of Staphylococcus aureus in the pathogenesis of infection. The FnBPs, which facilitate attachment of this pathogen to host cells and to fibronectin-coated biomaterials, are important mediators of infection in experimental endocarditis. In addition, recent vaccine studies utilizing FnBP derivatives have shown partial protection in animals. FnBPs also act as invasins permitting uptake of the staphylococcus by cultured non-professional phagocytes using host fibronectin to bridge with integrins on the cell surface. However, the precise role of FnBP in tissue invasion and the relevance of intracellular invasion in disease remain to be elucidated. SUMMARY: FnBP is one of many adhesins expressed by S. aureus that influence host tissue adherence by binding to host fibronectin. FnBP-based vaccine strategies and novel anti-adherence tools based upon FnBP derivatives are in the early stages of investigation but may show promise in preventing staphylococcal infections.


Subject(s)
Adhesins, Bacterial , Bacterial Proteins/physiology , Carrier Proteins/physiology , Staphylococcal Infections/microbiology , Staphylococcus aureus/pathogenicity , Bacterial Proteins/chemistry , Bacterial Proteins/metabolism , Bacterial Vaccines/immunology , Carrier Proteins/chemistry , Carrier Proteins/metabolism , Models, Biological , Staphylococcal Infections/immunology , Staphylococcus aureus/immunology , Virulence Factors/physiology
6.
J Infect Dis ; 185(7): 937-43, 2002 Apr 01.
Article in English | MEDLINE | ID: mdl-11920318

ABSTRACT

Adherence of Staphylococcus aureus to host tissues is a critical step for colonization and initiation of infection. The fibronectin-binding proteins (FnBPs) of S. aureus have been implicated in adherence and internalization in nonprofessional phagocytes. A recombinant fragment of the fibronectin-binding domains (rFnBF) that potently inhibits S. aureus entry into host cells was generated. To test the hypothesis that rFnBF may attenuate the establishment of infection, the ability of intermuscularly administered rFnBF to prevent abscess formation was determined in a guinea pig model of wound infection. rFnBF exhibited dose-dependent inhibition of abscess formation and, at a 100-microg dose, raised the median infective dose approximately 170-fold, compared with the control. In addition, rFnBF potentiated the benefit of prophylaxis with cefazolin. Thus, exogenous administration of the fibronectin-binding domain of FnBP reduces the risk of staphylococcal abscess formation and should be investigated further as a novel agent for prevention of wound infection.


Subject(s)
Adhesins, Bacterial , Antibiotic Prophylaxis , Bacterial Proteins/therapeutic use , Carrier Proteins/therapeutic use , Staphylococcal Infections/prevention & control , Staphylococcus aureus , Staphylococcus aureus/pathogenicity , Wound Infection/prevention & control , Animals , Bacterial Proteins/genetics , Carrier Proteins/genetics , Cefazolin/therapeutic use , Cells, Cultured , Cephalosporins/therapeutic use , Disease Models, Animal , Drug Synergism , Endothelium, Vascular/cytology , Endothelium, Vascular/microbiology , Female , Guinea Pigs , Humans , Male , Recombinant Proteins/genetics , Recombinant Proteins/therapeutic use , Staphylococcus aureus/drug effects , Staphylococcus aureus/physiology , Umbilical Veins
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