Ultra late onset group B streptococcal sepsis with acute renal failure in a child with urethral obstruction: a case report

<p>Abstract</p> <p>Introduction</p> <p>Group B streptococci are a well-known cause of early and late onset sepsis. In neonates and older children gram-negative bacteria are mostly found in urinary tract infections and urosepsis. In adults predisposing factors for group B streptococci urinary tract infection may include diabetes mellitus and chronic renal failure.</p> <p>Case presentation</p> <p>We present a rare case of a five-month-old Caucasian boy with ultra late onset urosepsis and acute renal failure caused by group B streptococci serotype V. Excretion urography showed a subvesical obstruction that consequently was surgically corrected after antibiotic treatment of the acute infection.</p> <p>Conclusions</p> <p>Group B streptococci serotype V, urogenitary tract malformations, previous hospitalization and medical interventions may be important risk factors for the development of ultra late onset Group B streptococci sepsis in non-neonates.</p

An exploratory study to examine intentions to adopt an evidence-based HIV linkage-to-care intervention among state health department AIDS directors in the United States

<p>Abstract</p> <p>Background</p> <p>Widespread dissemination and implementation of evidence-based human immunodeficiency virus (HIV) linkage-to-care (LTC) interventions is essential for improving HIV-positive patients' health outcomes and reducing transmission to uninfected others. To date, however, little work has focused on identifying factors associated with intentions to adopt LTC interventions among policy makers, including city, state, and territory health department AIDS directors who play a critical role in deciding whether an intervention is endorsed, distributed, and/or funded throughout their region.</p> <p>Methods</p> <p>Between December 2010 and February 2011, we administered an online questionnaire with state, territory, and city health department AIDS directors throughout the United States to identify factors associated with intentions to adopt an LTC intervention. Guided by pertinent theoretical frameworks, including the Diffusion of Innovations and the "push-pull" capacity model, we assessed participants' attitudes towards the intervention, perceived organizational and contextual demand and support for the intervention, likelihood of adoption given endorsement from stakeholder groups (<it>e.g</it>., academic researchers, federal agencies, activist organizations), and likelihood of enabling future dissemination efforts by recommending the intervention to other health departments and community-based organizations.</p> <p>Results</p> <p>Forty-four participants (67% of the eligible sample) completed the online questionnaire. Approximately one-third (34.9%) reported that they intended to adopt the LTC intervention for use in their city, state, or territory in the future. Consistent with prior, related work, these participants were classified as LTC intervention "adopters" and were compared to "nonadopters" for data analysis. Overall, adopters reported more positive attitudes and greater perceived demand and support for the intervention than did nonadopters. Further, participants varied with their intention to adopt the LTC intervention in the future depending on endorsement from different key stakeholder groups. Most participants indicated that they would support the dissemination of the intervention by recommending it to other health departments and community-based organizations.</p> <p>Conclusions</p> <p>Findings from this exploratory study provide initial insight into factors associated with public health policy makers' intentions to adopt an LTC intervention. Implications for future research in this area, as well as potential policy-related strategies for enhancing the adoption of LTC interventions, are discussed.</p

Processes and dynamics of linkage to care from mobile/outreach and facility‑based HIV testing models in hard‑to‑reach settings in rural Tanzania. Qualitative findings of a mixed methods study

BACKGROUND: Like other countries, Tanzania instituted mobile and outreach testing approaches to address low HIV testing rates at health facilities and enhance linkage to care. Available evidence from hard-to-reach rural settings of Mbeya region, Tanzania suggests that clients testing HIV+ at facility-based sites are more likely to link to care, and to link sooner, than those testing at mobile sites. This paper (1) describes the populations accessing HIV testing at mobile/outreach and facility-based testing sites, and (2) compares processes and dynamics from testing to linkage to care between these two testing models from the same study context. METHODS: An explanatory sequential mixed-method study (a) reviewed records of all clients (n = 11,773) testing at 8 mobile and 8 facility-based testing sites over 6 months; (b), reviewed guidelines; (c) observed HIV testing sites (n = 10) and Care and Treatment Centers (CTCs) (n = 8); (d) applied questionnaires at 0, 3 and 6 months to a cohort of 1012 HIV newly-diagnosed clients from the 16 sites; and (e) conducted focus group discussions (n = 8) and in-depth qualitative interviews with cohort members (n = 10) and health care providers (n = 20). RESULTS: More clients tested at mobile/outreach than facility-based sites (56% vs 44% of 11,733, p < 0.001). Mobile site clients were more likely to be younger and male (p < 0.001). More clients testing at facility sites were HIV positive (21.5% vs. 7.9% of 11,733, p < 0.001). All sites in both testing models adhered to national HIV testing and care guidelines. Staff at mobile sites showed more proactive efforts to support linkage to care, and clients report favouring the confidentiality of mobile sites to avoid stigma. Clients who tested at mobile/outreach sites faced longer delays and waiting times at treatment sites (CTCs). CONCLUSIONS: Rural mobile/outreach HIV testing sites reach more people than facility based sites but they reach a different clientèle which is less likely to be HIV +ve and appears to be less “linkage-ready”. Despite more proactive care and confidentiality at mobile sites, linkage to care is worse than for clients who tested at facility-based sites. Our findings highlight a combination of (a) patient-level factors, including stigma; and (b) well-established procedures and routines for each step between testing and initiation of treatment in facility-based sites. Long waiting times at treatment sites are a further barrier that must be addressed

Pathogenesis of Streptococcus urinary tract infection depends on bacterial strain and β-hemolysin/cytolysin that mediates cytotoxicity, cytokine synthesis, inflammation and virulence

Streptococcus agalactiae can cause urinary tract infection (UTI) including cystitis and asymptomatic bacteriuria (ABU). The early host-pathogen interactions that occur during S. agalactiae UTI and subsequent mechanisms of disease pathogenesis are poorly defined. Here, we define the early interactions between human bladder urothelial cells, monocyte-derived macrophages, and mouse bladder using uropathogenic S. agalactiae (UPSA) 807 and ABU-causing S. agalactiae (ABSA) 834 strains. UPSA 807 adhered, invaded and killed bladder urothelial cells more efficiently compared to ABSA 834 via mechanisms including low-level caspase-3 activation, and cytolysis, according to lactate dehydrogenase release measures and cell viability. Severe UPSA 807-induced cytotoxicity was mediated entirely by the bacterial β-hemolysin/cytolysin (β-H/C) because an β-H/C-deficient UPSA 807 isogenic mutant, UPSA 807ΔcylE, was not cytotoxic in vitro; the mutant was also significantly attenuated for colonization in the bladder in vivo. Analysis of infection-induced cytokines, including IL-8, IL-1β, IL-6 and TNF-α in vitro and in vivo revealed that cytokine and chemokine responses were dependent on expression of β-H/C that also elicited severe bladder neutrophilia. Thus, virulence of UPSA 807 encompasses adhesion to, invasion of and killing of bladder cells, pro-inflammatory cytokine/ chemokine responses that elicit neutrophil infiltration, and β-H/C-mediated subversion of innate immune-mediated bacterial clearance from the bladder.Full Tex

Increased Age, but Not Parity Predisposes to Higher Bacteriuria Burdens Due to Streptococcus Urinary Tract Infection and Influences Bladder Cytokine Responses, Which Develop Independent of Tissue Bacterial Loads

Streptococcus agalactiae causes urinary tract infection (UTI) in pregnant adults, non-pregnant adults, immune-compromised individuals and the elderly. The pathogenesis of S. agalactiae UTI in distinct patient populations is poorly understood. In this study, we used murine models of UTI incorporating young mice, aged and dam mice to show that uropathogenic S. agalactiae causes bacteriuria at significantly higher levels in aged mice compared to young mice and this occurs coincident with equivalent levels of bladder tissue colonisation at 24 h post-infection (p.i.). In addition, aged mice exhibited significantly higher bacteriuria burdens at 48 h compared to young mice, confirming a divergent pattern of bacterial colonization in the urinary tract of aged and young mice. Multiparous mice, in contrast, exhibited significantly lower urinary titres of S. agalactiae compared to age-matched nulliparous mice suggesting that parity enhances the ability of the host to control S. agalactiae bacteriuria. Additionally, we show that both age and parity alter the expression levels of several key regulatory and pro-inflammatory cytokines, which are known to be important the immune response to UTI, including Interleukin (IL)-1β, IL-12(p40), and Monocyte Chemoattractant Protein-1 (MCP-1). Finally, we demonstrate that other cytokines, including IL-17 are induced significantly in the S. agalactiae-infected bladder regardless of age and parity status. Collectively, these findings show that the host environment plays an important role in influencing the severity of S. agalactiae UTI; infection dynamics, particularly in the context of bacteriuria, depend on age and parity, which also affect the nature of innate immune responses to infection