Microbiology of Actinomyces Species Isolated From Patients With Invasive Disease and Contaminated Samples in a Comprehensive Cancer Center.

Background: Actinomyces are mucous membrane commensals that infrequently cause invasive disease. Our goal was to define Actinomyces species prevalence, the predominant disease site and risk factors for actinomycosis. Methods: We retrospectively reviewed patients with growth of Actinomyces species from cultures in a single-cancer center from July 2007 to June 2020. Proven invasive actinomycosis was defined as the presence of compatible clinical syndrome and radiographic findings with histopathological confirmation or culture from a normally sterile site. Probable invasive actinomycosis was defined based on the same criteria but without histologic confirmation. Contaminants were defined as culture growth in the absence of clinical or radiological findings consistent with disease. Speciation of Actinomyces was performed by the bioMerieux VITEK 2 anaerobic and coryneform identification card. Results: Of 235 patients, 179 (76.2%) had malignancy. Among 90 (38.3%) patients with invasive actinomycosis, A odontolyticus was isolated in 32 (35.6%), followed by A meyeri in 20 (22.2%), and A naeslundii in 17 (18.9%). Among 145 (61.7%) colonized patients, A odontolyticus was isolated in 67 (46.2%), followed by A naeslundii in 27 (18.6%). Abdominopelvic infection was the most common site for invasive actinomycosis documented in 54 patients (60.0%) followed by orocervicofacial in 14 (15.6%) and thoracic in 10 (11.1%). Conclusions: A odontolyticus, A meyeri, and A naeslundi were the most frequently isolated species causing invasive actinomycosis, and A odontolyticus and A nauslendii among colonizers. Abdominopelvic represented the most frequent site for invasive disease. Further studies are needed to investigate the epidemiology of Actinomyces species in this population.

Unlocking the Biological Enigma: Influence of Host Length and Infection Site on Parasite Abundance in Ompok bimaculatus.

PURPOSE: The influence of two key factors, host length and infection site, on the host-parasite interaction in Ompok bimaculatus (Butter catfish) from Mukutmanipur Dam Lake, were investigated. METHODS: Present study involved 192 specimens of Ompok bimaculatus with varying body lengths, subjected to diverse statistical analyses. One-way analysis of variance (ANOVA) was performed for the parasite numbers for three groups (cestode, nematode and trematode). Subsequently, we conducted one-way permutational multivariate analysis of variance (PERMANOVA) followed by pairwise test to assess parasite numbers across three body sites (intestine, mesentery, and bodycavity), employing the Bray-Curtis index. Additionally, Principal Coordinate Analysis (PCoA) for the same dataset was performed using the same index. Linear regression analysis was performed for the fish length-cestode number, fish length-nematode number, fish length-trematode number and fish length-total parasite number. RESULTS: One-way ANOVA revealed no significant differences in parasite numbers among the three endo-helminth groups (cestode, nematode, and trematode). The results of PERMANOVA revealed significant differences in parasite numbers across the three body sites of the host fishes (groups) (F = 9.41, p = 0.0001). Pairwise tests further demonstrated significant differences between the intestine-mesentery, intestine-body-cavity, and mesentery-body-cavity. Additionally, Principal Coordinate Analysis (PCoA) unveiled a significant relationship between infection site and parasite number. However, linear regression analysis examining the relationship between fish length and parasite abundance indicated no significant associations. CONCLUSIONS: Through a detailed exploration of the statistical analyses, we provide insights into the host-parasite interaction, elucidating both established knowledge and novel findings in fish parasitology.

An Infected Dog Bite With Neisseria canis: A Case Report and Review of the Literature.

Neisseria is a common bacteria that colonizes in humans. Of the 11 species, only two, N. meningitidis and N. gonorrhea, are pathogenic. Although sparse, there are case reports of other Neisseria species causing infections in humans. Neisseria canis, which is a part of normal flora in the mouths of dogs and cats, has been shown to have potential to be pathogenic in humans. The standard treatment for dog and cat bites is oral amoxicillin/clavulanic acid (Augmentin) or IV ampicillin/sulbactam (Unasyn). However, in cases where the patient has multiple antibiotic allergies, careful antibiotic selection must be made to ensure resolution of infection.

Primary Hydatid Cyst of the Gluteal Muscle: A Case Report.

Hydatid disease, also known as cystic echinococcus, is a parasitic infection initiated by Echinococcus granulosus. It primarily affects the lungs and liver, but it can also occur in other organs. Hydatid cysts in the gluteal muscle are an exceedingly rare phenomenon, even in areas with high prevalence. We report the case of a 29-year-old farmer who presented with a painful mass in the gluteal region. The diagnostic findings unveiled the existence of a hydatid cyst within the gluteal muscle managed with complete pericystectomy and chemotherapy with antiparasitic drugs. In regions where hydatid cysts are prevalent, it is essential to include them in the list of potential diagnoses for any cystic mass. Diagnosing such cases can be difficult, and surgery remains the most effective treatment.

Etiologies of Extreme Leukocytosis.

OBJECTIVE: The objective of this study was to determine the etiologies and co-morbidities associated with extreme leukocytosis, which is characterized by a white blood cell (WBC) count ≥ 35 × 109 leukocytes/L.  Method: Retrospective chart review was conducted for all patients, aged 18 years and older, admitted to the internal medicine department between 2015 and 2021 with an elevated WBC count ≥ 35 × 109 leukocytes/L within the first 24 hours of admission.  Results: Eighty patients were identified to have WBC count ≥ 35 × 109 leukocytes/L. The overall mortality was 16% and increased to 30% in those presenting with shock. Mortality increased from 2.8% in patients with WBC count in the range of 35-39.9 × 109 leukocytes/L to 33% in those with WBC count in the range of 40-50 × 109 leukocytes/L. There was no correlation with underlying co-morbidities or age. Pneumonia was the most common infection (38%), followed by UTI or pyelonephritis (28%) and abscesses (10%). There was no predominant organism responsible for these infections. The most common etiology for WBC count between 35-39.9 × 109 leukocytes/L and 40-50 × 109 leukocytes/L was infections, while malignancies (especially chronic lymphocytic leukemia) were more common with WBC count > 50 × 109 leukocytes/L.  Conclusion: For WBC counts in the range of 35-50 × 109 leukocytes/L, infections were the main reason for admission to the internal medicine department. Mortality increased from 2.8% to 33% as WBC counts increased from 35-39.9 × 109 leukocytes/L to 40-50 × 109 leukocytes/L. Overall, mortality for all WBC counts ≥ 35 × 109 leukocytes/L was 16%. The most common infections were pneumonia, followed by UTI or pyelonephritis and abscesses. The underlying risk factors did not correlate with WBC counts or mortality.

Delayed Activation of T Cells at the Site of Infection Facilitates the Establishment of Trypanosoma cruzi in Both Naive and Immune Hosts.

Although parasite entry through breaks in the skin or mucosa is one of the main routes of natural transmission of Trypanosoma cruzi, little is known about the host cell types initially invaded nor the ability of those host cells to initiate immune responses at the site of infection. To gain insights into these early events, we studied the fate of fluorescently tagged T. cruzi delivered subcutaneously in mouse footpads or ears. We demonstrate that the majority of parasites introduced into the skin initially proliferate there until 8 to 10 days postinfection, when the parasite load decreases. This decline in parasite numbers is dependent on the presence of an intact T cell compartment and on the ability of hosts to produce gamma interferon (IFN-γ). Many of the parasite-containing cells at the initial infection site display a macrophage/monocyte phenotype but with low expression of activation markers, suggesting that these cells provide an early niche for T. cruzi proliferation, rather than being active in parasite control. It is only after the first round of T. cruzi replication and release from host cells that signs of immune activation and control of parasites become apparent. The delay in the activation and failure to rapidly control parasite replication are observed even when T. cruzi-primed T cells are present, such as in chronically infected mice. This failure of a primed immune system to recognize and react prior to extensive parasite expansion at the infection site likely poses a significant challenge for the development of vaccines aiming to prevent T. cruzi infection. IMPORTANCE Trypanosoma cruzi, the parasite causing Chagas disease, usually infects through the mucosa or breaks in the skin, but little is known about the parasite's fate at the site of entry or the early events involving immune control there. Here, we track the local proliferation and subsequent dissemination of fluorescently tagged T. cruzi and the initial immune response at the point of entry. We show that T. cruzi preferentially infects innate immune cells in the skin and that the stimulation of an adaptive T cell response does not occur until after the release of parasites from this first round of infected host cells. This first immunologically "silent" proliferation occurs even in the presence of a strong immune T cell memory generated by previous infection. This capacity of T. cruzi to establish infections while avoiding initial immune recognition has important implications for the potential to develop vaccines to prevent T. cruzi infection.

Source-specific host response and outcomes in critically ill patients with sepsis: a prospective cohort study.

PURPOSE: There is limited knowledge on how the source of infection impacts the host response to sepsis. We aimed to compare the host response in sepsis patients with a single, known source at admission (< 24 h) to the intensive care unit. METHODS: From the molecular diagnosis and risk stratification of sepsis (MARS) prospective cohort, we measured 16 plasma host response biomarkers reflective of key host response pathways in 621 sepsis patients. In a subgroup (n = 335), blood leukocyte transcriptomes were compared between the sources. Differences in clinical patient profiles and survival were compared in the whole sepsis cohort (n = 2019). RESULTS: The plasma biomarker cohort was categorized into sepsis originating from the respiratory tract (n = 334, 53.8%), abdomen (n = 159, 25.6%), urinary tract (n = 44, 7.1%), cardiovascular (n = 41, 6.6%), central nervous system (CNS) (n = 18, 2.9%), or skin (n = 25, 4%). This analysis revealed stronger inflammatory and cytokine responses, loss of vascular integrity and coagulation activation in abdominal sepsis relative to respiratory. Endothelial cell activation was prominent in urinary, cardiovascular and skin infections, while CNS infection was associated with the least host response aberrations. The leukocyte transcriptional response showed the largest overlap between abdominal and pulmonary infections (76% in common); notable differences between the sources were detected regarding hemostasis, cytokine signaling, innate and adaptive immune, and metabolic transcriptional pathways. After adjustment for confounders, the source of infection remained an independent contributor to 30-day mortality (unadjusted p = 0.001, adjusted p = 0.028). CONCLUSION: Sepsis heterogeneity is partly explained by source-specific host response dysregulations and should be considered when selecting patients for trials testing immune modulatory drugs.

Effective Use of F-18-Fluorodeoxyglucose Positron Emission Tomography/Computed Tomography to Rule Out Prosthetic Aortic Valve as the Source of Infection.

Several nuclear imaging techniques can be used to diagnose infectious and inflammatory processes. F-18-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) is a useful diagnostic technique to detect inflammation and infection quickly and accurately. We report the case of a patient with end-stage renal disease (ESRD) and recurrent bacterial infections where FDG PET/CT was used to identify the source of infection as sternal osteomyelitis and rule out suspected infection of the aortic valve prosthesis.

F-18-Fluorodeoxyglucose Positron Emission Tomography/CT Effectively Identifying Source of Infection in a Patient With Multiple Dialysis Arteriovenous Fistula Access Points.

Radiologic imaging techniques, such as F-18-fluorodeoxyglucose positron emission tomography/computerized tomography (FDG PET/CT), provide diagnostic value in a variety of diseases. In cases of suspected infection, FDG PET/CT can find areas of fluorodeoxyglucose metabolism, correlating with local acute inflammation. The following case involves a man with end-stage renal disease (ESRD), who presented with symptoms of infection and positive blood cultures with high suspicion of arteriovenous fistula as the source of infection. The patient also had two central lines that could be a site of infection. Concerns for patient's persistent positive blood cultures necessitated FDG PET/CT to confirm site of infection. Confirming active infection and the source of infection guides therapeutic measures and eliminates concern for other disease etiologies common in patients with ESRD.

Phenotypic heterogeneity by site of infection in surgical sepsis: a prospective longitudinal study.

BACKGROUND: The role of site of infection in sepsis has been poorly characterized. Additionally, sepsis epidemiology has evolved. Early mortality has decreased, but many survivors now progress into chronic critical illness (CCI). This study sought to determine if there were significant differences in the host response and current epidemiology of surgical sepsis categorized by site of infection. STUDY DESIGN: This is a longitudinal study of surgical sepsis patients characterized by baseline predisposition, insult characteristics, serial biomarkers, hospital outcomes, and long-term outcomes. Patients were categorized into five anatomic sites of infection. RESULTS: The 316 study patients were predominantly Caucasian; half were male, with a mean age of 62 years, high comorbidity burden, and low 30-day mortality (10%). The primary sites were abdominal (44%), pulmonary (19%), skin/soft tissue (S/ST, 17%), genitourinary (GU, 12%), and vascular (7%). Most abdominal infections were present on admission and required source control. Comparatively, they had more prolonged proinflammation, immunosuppression, and persistent organ dysfunction. Their long-term outcome was poor with 37% CCI (defined as > 14 in ICU with organ dysfunction), 49% poor discharge dispositions, and 30% 1-year mortality. Most pulmonary infections were hospital-acquired pneumonia. They had similar protracted proinflammation and organ dysfunction, but immunosuppression normalized. Long-term outcomes are similarly poor (54% CCI, 47% poor disposition, 32% 1-year mortality). S/ST and GU infections occurred in younger patients with fewer comorbidities, less perturbed immune responses, and faster resolution of organ dysfunction. Comparatively, S/ST had better long-term outcomes (23% CCI, 39% poor disposition, 13% 1-year mortality) and GU had the best (10% CCI, 20% poor disposition, 10% 1-year mortality). Vascular sepsis patients were older males, with more comorbidities. Proinflammation was blunted with baseline immunosuppression and organ dysfunction that persisted. They had the worst long-term outcomes (38% CCI, 67% poor disposition, 57% 1-year mortality). CONCLUSION: There are notable differences in baseline predisposition, host responses, and clinical outcomes by site of infection in surgical sepsis. While previous studies have focused on differences in hospital mortality, this study provides unique insights into the host response and long-term outcomes associated with different sites of infection.

Anisakis spp. in fishery products from Japanese waters: Updated insights on host prevalence and human infection risk factors.

The nematodes of the genus Anisakis are among the most relevant parasitic hazards in fishery products since they are responsible for human infection and allergy cases. In a food safety and epidemiological perspective, several marine hosts from different locations around Japan were examined to characterize the parasitism of Anisakis larvae. Chum salmon (Oncorhynchus keta) and Alaska pollock (Gadus chalcogrammus) showed the highest overall prevalence (100%), followed by blue mackerel (Scomber australasicus) (97.5%), Pacific cod (Gadus macrocephalus) (80%), chub mackerel (Scomber japonicus) (60.1%), Japanese flying squid (Todarodes pacificus) (17%) and Japanese pilchard (Sardinops sagax melanostictus) (2%). In Pacific krill (Euphausia pacifica), apart from one Hysterothylacium aduncum larva, no Anisakis specimens were detected. Anisakis simplex sensu stricto was molecularly identified (PCR-RFLP) for the first time in Japanese flying squid and Japanese pilchard distributed in the Northwestern Pacific ocean. That was the most frequent parasitic species detected followed by A. pegreffii, mostly in the western areas of Japan, hybrid genotypes between the two sibling species as well as A. typica and A. berlandi. Surprisingly, A. simplex s.s. was the most abundant species in one batch of chub mackerel from the East China Sea and A. pegreffii was the main species found in one batch from the Pacific coast of Aomori, which seems to indicate that the ranges of these two sibling species might be more variable than previously thought.

Monocytic HLA-DR expression kinetics in septic shock patients with different pathogens, sites of infection and adverse outcomes.

BACKGROUND: Decreased monocytic (m)HLA-DR expression is the most studied biomarker of sepsis-induced immunosuppression. To date, little is known about the relationship between sepsis characteristics, such as the site of infection, causative pathogen, or severity of disease, and mHLA-DR expression kinetics. METHODS: We evaluated mHLA-DR expression kinetics in 241 septic shock patients with different primary sites of infection and pathogens. Furthermore, we used unsupervised clustering analysis to identify mHLA-DR trajectories and evaluated their association with outcome parameters. RESULTS: No differences in mHLA-DR expression kinetics were found between groups of patients with different sites of infection (abdominal vs. respiratory, p = 0.13; abdominal vs. urinary tract, p = 0.53) and between pathogen categories (Gram-positive vs. Gram-negative, p = 0.54; Gram-positive vs. negative cultures, p = 0.84). The mHLA-DR expression kinetics differed between survivors and non-survivors (p < 0.001), with an increase over time in survivors only. Furthermore, we identified three mHLA-DR trajectories ('early improvers', 'delayed or non-improvers' and 'decliners'). The probability for adverse outcome (secondary infection or death) was higher in the delayed or non-improvers and decliners vs. the early improvers (delayed or non-improvers log-rank p = 0.03, adjusted hazard ratio 2.0 [95% CI 1.0-4.0], p = 0.057 and decliners log-rank p = 0.01, adjusted hazard ratio 2.8 [95% CI 1.1-7.1], p = 0.03). CONCLUSION: Sites of primary infection or causative pathogens are not associated with mHLA-DR expression kinetics in septic shock patients. However, patients showing delayed or no improvement in or a declining mHLA-DR expression have a higher risk for adverse outcome compared with patients exhibiting a swift increase in mHLA-DR expression. Our study signifies that changes in mHLA-DR expression over time, and not absolute values or static measurements, are of clinical importance in septic shock patients.

Beyond tissue concentrations: antifungal penetration at the site of infection.

Despite advances in antifungal therapy, invasive fungal infections remain a significant cause of morbidity and mortality worldwide. One important factor contributing to the relative ineffectiveness of existing antifungal drugs is insufficient drug exposure at the site of infection. Despite the importance of this aspect of antifungal therapy, we generally lack a full appreciation of how antifungal drugs distribute, penetrate, and interact with their target organisms in different tissue subcompartments. A better understanding of drug distribution will be critical to guide appropriate use of currently available antifungal drugs, as well as to aid development of new agents. Herein we briefly review current perspectives of antifungal drug exposure at the site of infection and describe a new technique, matrix-assisted laser desorption ionization (MALDI) mass spectrometry imaging, which has the potential to greatly expand our understanding of drug penetration.

Site of infection and mortality in patients with severe sepsis or septic shock. A cohort study of patients admitted to a Danish general intensive care unit.

BACKGROUND: The search for the site of infection has high priority in patients with severe sepsis and septic shock. However, it is questionable whether mortality is associated with the specific site of infection in patients admitted to an intensive care unit (ICU). Therefore, the 30-day and 90-day mortalities in ICU patients admitted with suspected or confirmed community-acquired infection were studied. METHODS: A retrospective cohort study was conducted, including all adult patients admitted to a multi-specialty tertiary ICU with severe sepsis or septic shock from November 2008 to October 2010. The site of infection was classified according to criteria set for healthcare associated infections and infections in the acute care setting by Centers for Disease Control and Prevention (CDC). Kaplan-Meier curves and Poisson regression analysis were used to evaluate the association between site of infection and 30- and 90-day all-cause mortality, adjusting for age, sex and comorbidities. RESULTS: Three hundred and eighty-eight patients were included. One or more comorbidities were present in 76% of patients. Across all sites of infection, there were more patients with septic shock than patients with severe sepsis. The most frequent site of infection was pneumonia, followed by gastrointestinal infection. Urinary tract infection was found to be an independent predictor of mortality among septic ICU patients when adjusting for sex, age and comorbidities. CONCLUSIONS: The results suggest that identification of correct site of infection is important in the management of severe sepsis and septic shock.