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Bacterial infection often results in the formation of tissue abscesses, which represent the primary site of interaction between invading bacteria and the innate immune system. We identify the host protein calprotectin as a neutrophil-dependent factor expressed inside Staphylococcus aureus abscesses. Neutrophil-derived calprotectin inhibited S. aureus growth through chelation of nutrient Mn²⁺ and Zn²⁺: an activity that results in reprogramming of the bacterial transcriptome. The abscesses of mice lacking calprotectin were enriched in metal, and staphylococcal proliferation was enhanced in these metal-rich abscesses. These results demonstrate that calprotectin is a critical factor in the innate immune response to infection and define metal chelation as a strategy for inhibiting microbial growth inside abscessed tissue.

Background As disseminated extrapulmonary tuberculosis infection can involve multiple systems and result in atypical clinical manifestations that mimic other diseases, the diagnosis may be difficult, especially in elderly patients. Delaying treatment can adversely affect the prognosis. And to achieve better prognosis, early detection and diagnosis are necessary, as well as early initiation of comprehensive treatment. Case presentation We present the case of a 78-year-old man with disseminated tuberculosis who developed the uncommon complication of urinary retention due to a psoas abscess, meningoencephalitis, and the rare secondary hemophagocytic lymphohistiocytosis syndrome. The patient achieved a favorable outcome following targeted therapy with antitubercular medications. Conclusions This case highlights that disseminated extrapulmonary tuberculosis infection can present with a variety of manifestations, and may exhibit many rare and complex clinical presentations. Prompt and accurate diagnosis and treatment play a crucial role in improving prognosis for the patients with persistent fever.

Type 2 diabetes mellitus patients are immunocompromised, particularly under poorly controlled conditions, and thereby they could develop rare inflammatory diseases, such as spontaneous discitis, pyogenic psoas abscess, spinal epidural abscess and bacterial meningitis. Herein we report a pyogenic psoas abscess on the dorsal side, and bacterial meningitis and spinal epidural abscess on the ventral side, both of which were induced by spontaneous discitis in a patient with poorly controlled type 2 diabetes mellitus. This case was very rare and interesting, because we successfully treated various infections with antibiotics over a long period of time, complicated by hyperglycemic crises, although the patient suffered severe bone destruction and required rehabilitation for a long time. Type 2 diabetes mellitus patients are immunocompromised, particularly under poorly controlled conditions, and thereby they could develop rare inflammatory diseases, such as spontaneous discitis, pyogenic psoas abscess, spinal epidural abscess and bacterial meningitis. Herein we report a pyogenic psoas abscess on the dorsal side, and bacterial meningitis and spinal epidural abscess on the ventral side, both of which were induced by spontaneous discitis in a patient with poorly controlled type 2 diabetes mellitus. This case was very rare and interesting, because we successfully treated various infections with antibiotics over a long period of time, complicated by hyperglycemic crises, although the patient suffered severe bone destruction and required rehabilitation for a long time.

This study aimed to describe the clinical presentation, microbiological profile and management of complications of bone wax usage for surgical procedures at the skull base. The case records of a series of five patients who developed post-operative surgical site complications because of bone wax usage during skull base surgery were reviewed. In all five patients, persistent site-specific clinical features were noted along with intra-operative presence of excessive bone wax. Three unique cases of presentation, one with a fungal brain abscess because of Aspergillus flavus infection, another with fungal osteomyelitis because of Trichosporon beigelii infection and a third with intradural migration of bone wax into the cerebellopontine angle cistern are highlighted. The presentation of surgical site infection at the skull base because of excessive use of bone wax can be manifold. The need for testing appropriate cultures including fungal culture is highlighted.

Fusobacterium nucleatum is a commensal pathogen typically found in the oral cavity, digestive tract, and urogenital system which has been associated with Lemierre’s syndrome, periodontal diseases, sinusitis, endocarditis, and intra-abdominal and brain abscesses. Our case is of a 62-year-old male who presented with headaches, nausea, and vision loss. Brain imaging identified a right occipito-parietal brain abscess. Following surgery and abscess drainage, Fusobacterium nucleatum was isolated from intraoperative cultures, and the infectious disease service was consulted for antibiotic recommendations. Additional history uncovered that he had also been experiencing night sweats, generalized weakness and 40-pound weight loss for 2 months, and had a prior history of colon polyps and diverticulitis. Furthermore, the patient disclosed having substandard oral hygiene practices, particularly in relation to the care of his dental appliances. Despite negative blood cultures, suspicion for hematogenous seeding was high. Imaging ruled out periodontal disease, but identified a colovesical fistula and liver abscesses, indicating potential translocation of bacteria via portal circulation to his liver. Echocardiogram workup revealed a 1-cm mobile vegetation on the aortic valve. His course was complicated by breakthrough seizures, renal failure, and drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome, and he ultimately completed 16 weeks of antibiotics. This case illustrates an uncommon presentation of brain abscess in an immunocompetent adult, with a prior episode of diverticulitis as the probable primary infection source, leading to development of a colovesical fistula and bacterial dissemination to the liver, heart, and brain. It highlights the importance of a comprehensive diagnostic approach, including consideration of atypical pathogens in immunocompetent adults.

Staphylococcus aureus is a human commensal that can also cause systemic infections. This transition requires evasion of the immune response and the ability to exploit different niches within the host. However, the disease mechanisms and the dominant immune mediators against infection are poorly understood. Previously it has been shown that the infecting S. aureus population goes through a population bottleneck, from which very few bacteria escape to establish the abscesses that are characteristic of many infections. Here we examine the host factors underlying the population bottleneck and subsequent clonal expansion in S. aureus infection models, to identify underpinning principles of infection. The bottleneck is a common feature between models and is independent of S. aureus strain. Interestingly, the high doses of S. aureus required for the widely used \"survival\" model results in a reduced population bottleneck, suggesting that host defences have been simply overloaded. This brings into question the applicability of the survival model. Depletion of immune mediators revealed key breakpoints and the dynamics of systemic infection. Loss of macrophages, including the liver Kupffer cells, led to increased sensitivity to infection as expected but also loss of the population bottleneck and the spread to other organs still occurred. Conversely, neutrophil depletion led to greater susceptibility to disease but with a concomitant maintenance of the bottleneck and lack of systemic spread. We also used a novel microscopy approach to examine abscess architecture and distribution within organs. From these observations we developed a conceptual model for S. aureus disease from initial infection to mature abscess. This work highlights the need to understand the complexities of the infectious process to be able to assign functions for host and bacterial components, and why S. aureus disease requires a seemingly high infectious dose and how interventions such as a vaccine may be more rationally developed.

A 36-year-old man with a history of substance abuse was admitted for two days of fever, cough, and confusion. Aside from dental caries, which had worsened due to methamphetamine use, he had no medical history. A CT-guided core biopsy of the lung mass demonstrated inflammatory debris histologically, with culture yielding Streptococcus intermedius.

Intra-abdominal candidiasis (IAC) is poorly understood compared to candidemia. We described the clinical characteristics, microbiology, treatment and outcomes of IAC, and identified risk factors for mortality. We performed a retrospective study of adults diagnosed with IAC at our center in 2012-2013. Risk factors for mortality were evaluated using multivariable logistic regression. We identified 163 patients with IAC, compared to 161 with candidemia. Types of IAC were intra-abdominal abscesses (55%), secondary peritonitis (33%), primary peritonitis (5%), infected pancreatic necrosis (5%), and cholecystitis/cholangitis (3%). Eighty-three percent and 66% of secondary peritonitis and abscesses, respectively, stemmed from gastrointestinal (GI) tract sources. C. albicans (56%) and C. glabrata (24%) were the most common species. Bacterial co-infections and candidemia occurred in 67% and 6% of patients, respectively. Seventy-two percent of patients underwent an early source control intervention (within 5 days) and 72% received early antifungal treatment. 100-day mortality was 28%, and highest with primary (88%) or secondary (40%) peritonitis. Younger age, abscesses and early source control were independent predictors of survival. Younger age, abscesses and early antifungal treatment were independently associated with survival for IAC stemming from GI tract sources. Infectious diseases (ID) consultations were obtained in only 48% of patients. Consulted patients were significantly more likely to receive antifungal treatment. IAC is a common disease associated with heterogeneous manifestations, which result in poor outcomes. All patients should undergo source control interventions and receive antifungal treatment promptly. It is important for the ID community to become more engaged in treating IAC.

Klebsiella pneumoniae is a well known human nosocomial pathogen. Most community-acquired K pneumoniae infections cause pneumonia or urinary tract infections. During the past two decades, however, a distinct invasive syndrome that causes liver abscesses has been increasingly reported in Asia, and this syndrome is emerging as a global disease. In this Review, we summarise the clinical presentation and management as well the microbiological aspects of this invasive disease. Diabetes mellitus and two specific capsular types in the bacterium predispose a patient to the development of liver abscesses and the following metastatic complications: bacteraemia, meningitis, endophthalmitis, and necrotising fasciitis. For patients with this invasive syndrome, appropriate antimicrobial treatment combined with percutaneous drainage of liver abscesses increases their chances of survival. Rapid detection of the hypervirulent strain that causes this syndrome allows earlier diagnosis and treatment, thus minimising the occurrence of sequelae and improving clinical outcomes.

Bacterial invasion of host tissues triggers polymorphonuclear leukocytes to release DNA [neutrophil extracellular traps (NETs)], thereby immobilizing microbes for subsequent clearance by innate defenses including macrophage phagocytosis. We report here that Staphylococcus aureus escapes these defenses by converting NETs to deoxyadenosine, which triggers the caspase-3–mediated death of immune cells. Conversion of NETs to deoxyadenosine requires two enzymes, nuclease and adenosine synthase, that are secreted by S. aureus and are necessary for the exclusion of macrophages from staphylococcal abscesses. Thus, the pathogenesis of S. aureus infections has evolved to anticipate host defenses and to repurpose them for the destruction of the immune system.