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Brucellosis is a common, worldwide zoonosis. Clinical presentation is protean and often goes unrecognized. Hepatic brucelloma is a rare local complication of chronic brucellosis. We report a case in which magnetic resonance imaging and positron emission tomography imaging prompted suspicion of a hepatic malignancy. Diagnosis was ultimately made by serology and polymerase chain reaction of resected liver tissue.

Breakthrough candidemia (BTC) on fluconazole was associated with non-susceptible Candida spp. and increased mortality. This nationwide FUNGINOS study analyzed clinical and mycological BTC characteristics.A 3-year prospective study was conducted in 567 consecutive candidemias. Species identification and antifungal susceptibility testing (CLSI) were performed in the FUNGINOS reference laboratory. Data were analyzed according to STROBE criteria.43/576 (8%) BTC occurred: 37/43 (86%) on fluconazole (28 prophylaxis, median 200 mg/day). 21% BTC vs. 23% non-BTC presented severe sepsis/septic shock. Overall mortality was 34% vs. 32%. BTC was associated with gastrointestinal mucositis (multivariate OR 5.25, 95%CI 2.23-12.40, p 0.001) and graft-versus-host-disease (6.25, 1.00-38.87, p = 0.05), immunosuppression (2.42, 1.03-5.68, p = 0.043), and parenteral nutrition (2.87, 1.44-5.71, p = 0.003). Non-albicans Candida were isolated in 58% BTC vs. 35% non-BTC (p = 0.005). 63% of 16 BTC occurring after 10-day fluconazole were non-susceptible (Candida glabrata, Candida krusei, Candida norvegensis) vs. 19% of 21 BTC (C. glabrata) following shorter exposure (7.10, 1.60-31.30, p = 0.007). Median fluconazole MIC was 4 mg/l vs. 0.25 mg/l (p 0.001). Ten-day fluconazole exposure predicted non-susceptible BTC with 73% accuracy.Outcomes of BTC and non-BTC were similar. Fluconazole non-susceptible BTC occurred in three out of four cases after prolonged low-dose prophylaxis. This implies reassessment of prophylaxis duration and rapid de-escalation of empirical therapy in BTC after short fluconazole exposure.

Donor PTX3 polymorphisms were shown to influence the risk of invasive aspergillosis among hematopoietic stem cell transplant recipients. Here, we show that PTX3 polymorphisms are independent risk factors for invasive mold infections among 1101 solid organ transplant recipients, thereby strengthening their role in mold infection pathogenesis and patients' risk stratification.

BACKGROUND: Natural killer cell function is regulated by inhibitory and activating killer cell immunoglobulin-like receptors (KIR). Previous studies have documented associations of KIR genotype with the risk of cytomegalovirus (CMV) replication after solid organ transplantation. METHODS: In this study of 649 solid organ transplant recipients, followed prospectively for infectious disease events within the Swiss Transplant Cohort Study, we were interested to see if KIR genotype associated with virus infections other than CMV. RESULT: We found that KIR B haplotypes (which have previously been linked to protection from CMV replication) were associated with protection from varicella zoster virus infection (hazard ratio, 0.43; 95% confidence interval, 0.21-0.91; P = 0.03). No significant associations were detected regarding the risk of herpes simplex, Epstein-Barr virus or BK polyomavirus infections. CONCLUSIONS: In conclusion, these data provide evidence that the relative protection of KIR haplotype B from viral replication after solid organ transplantation may extend beyond CMV to other herpes viruses, such as varicella zoster virus and possibly Epstein-Barr virus.

Background Homo sapiens mature micro-ribonucleic acid (miRNA)-200b-3p and 200c-3p are predicted to bind to 3' untranslated region of mRNA encoding human cytomegalovirus (HCMV) immediate early protein 2 (IE2). We hypothesized that expression of these miRNAs pretransplant could predict HCMV replication after solid organ transplantation (SOT). Methods A total of 272 SOT recipients were HCMV-seropositive pretransplant and were managed using preemptive therapy. Pretransplant peripheral blood mononuclear cells were stimulated with HCMV followed by collection of RNA 1 day poststimulation. The miRNAs were quantified using real-time reverse transcription-polymerase chain reaction. Human foreskin fibroblasts were transfected with 200b-3p and 200c-3p and infected with HCMV 1 hour post-transfection. Protein was collected at 3 days postinfection (dpi) and 7 dpi underwent immunoblotting for IE2. Results Medians of 200b-3p and 200c-3p were significantly lower in recipients with HCMV replication (n = 144) (361.6 vs 552.6, P = .035; 3586.8 vs 12986.8 copies/μL, P = .03, respectively). Multivariate regression revealed that 200b-3p ≥100 copies/μL (odds ratio [OR]: 0.53; P = .02), was associated with less HCMV replication. Transfection with 200b-3p resulted in 2.7- and 2.5-fold decreased IE2 at 3 dpi and 7 dpi, respectively, compared to mock cells. Conclusions MicroRNAs may play a biologically relevant role in controlling HCMV replication post-transplant.

Supplemental digital content is available in the text., Background Occurring frequently after solid organ and hematopoietic stem cell transplantation, cytomegalovirus (CMV) replication remains a relevant cause of mortality and morbidity in affected patients. Despite these adverse effects, an increased alloreactivity of natural killer (NK) cells after CMV infection has been assumed, but the underlying physiopathological mechanisms have remained elusive. Methods We used serial analyses of NK cells before and after CMV infection in kidney transplant recipients as an in vivo model for CMV primary infection to explore the imprint of CMV infection using every patient as their own control: We analyzed NK cell phenotype and function in 47 CMV seronegative recipients of CMV seropositive kidney grafts, who developed CMV primary infection posttransplant. Seronegative recipients of seronegative kidney grafts served as controls. Results We observed a significant increase of NKG2C expressing NK cells after CMV infection (mean increase, 17.5%; 95% confidence interval [95% CI], 10.2-24.9, P < 0.001), whereas cluster of differentiation (CD)57 expressing cells decreased (mean decrease, 14.1%; 95% CI, 8.0-20.2; P < 0.001). Analysis of killer immunoglobulin-like receptor (KIR) expression showed an increase of cells expressing KIR2DL1 as their only inhibitory KIR in patients carrying the cognate ligand HLA-C2 (mean increase, 10.0%; 95% CI, 1.7-18.3; P = 0.018). In C2-negative individuals, KIR2DL1 expression decreased (mean decrease, 3.9%; 95% CI, 1.6-6.2; P = 0.001). As for activating KIR, there was no conclusive change pattern. Most importantly, we observed a significantly higher NK cell degranulation and IFNγ production in response to different target cells (target K562, CD107a: mean increase, 9.9%; 95% CI, 4.8-15.0; P < 0.001; IFNγ: mean increase, 6.6%; 95% CI, 1.6-11.1; P < 0.001; target MRC-5, CD107a: mean increase, 6.9%; 95% CI, 0.7-13.1; P = 0.03; IFNγ: mean increase, 4.8%; 95% CI, 1.7-7.8; P = 0.002). Conclusions We report evidence for an increased function of NK cells induced by CMV infection. This increased in vitro functionality was seen in NKG2C-positive and NKG2C-negative subsets, arguing for an NKG2C independent mechanism of action.

Contains fulltext : 153038.pdf (Publisher’s version ) (Closed access) BACKGROUND: Single-nucleotide polymorphisms (SNPs) in immune genes have been associated with susceptibility to invasive mold infection (IMI) among hematopoietic stem cell but not solid-organ transplant (SOT) recipients. METHODS: Twenty-four SNPs from systematically selected genes were genotyped among 1101 SOT recipients (715 kidney transplant recipients, 190 liver transplant recipients, 102 lung transplant recipients, 79 heart transplant recipients, and 15 recipients of other transplants) from the Swiss Transplant Cohort Study. Association between SNPs and the end point were assessed by log-rank test and Cox regression models. Cytokine production upon Aspergillus stimulation was measured by enzyme-linked immunosorbent assay in peripheral blood mononuclear cells (PBMCs) from healthy volunteers and correlated with relevant genotypes. RESULTS: Mold colonization (n = 45) and proven/probable IMI (n = 26) were associated with polymorphisms in the genes encoding interleukin 1beta (IL1B; rs16944; recessive mode, P = .001 for colonization and P = .00005 for IMI, by the log-rank test), interleukin 1 receptor antagonist (IL1RN; rs419598; P = .01 and P = .02, respectively), and beta-defensin 1 (DEFB1; rs1800972; P = .001 and P = .0002, respectively). The associations with IL1B and DEFB1 remained significant in a multivariate regression model (P = .002 for IL1B rs16944; P = .01 for DEFB1 rs1800972). The presence of 2 copies of the rare allele of rs16944 or rs419598 was associated with reduced Aspergillus-induced interleukin 1beta and tumor necrosis factor alpha secretion by PBMCs. CONCLUSIONS: Functional polymorphisms in IL1B and DEFB1 influence susceptibility to mold infection in SOT recipients. This observation may contribute to individual risk stratification.

BACKGROUND: The burden of enterococcal infections has increased over the last decades with vancomycin-resistant enterococci (VRE) being a major health problem. Solid organ transplantation is considered as a risk factor. However, little is known about the relevance of enterococci in solid organ transplantation recipients in areas with a low VRE prevalence. METHODS: We examined the epidemiology of enterococcal events in patients followed in the Swiss Transplant Cohort Study between May 2008 and September 2011 and analyzed risk factors for infection, aminopenicillin resistance, treatment, and outcome. RESULTS: Of the 1234 patients, 255 (20.7%) suffered from 392 enterococcal events (185 [47.2%] infections, 205 [52.3%] colonizations, and 2 events with missing clinical information). Only 2 isolates were VRE. The highest infection rates were found early after liver transplantation (0.24/person-year) consisting in 58.6% of Enterococcus faecium. The highest colonization rates were documented in lung transplant recipients (0.33/person-year), with 46.5% E. faecium. Age, prophylaxis with a betalactam antibiotic, and liver transplantation were significantly associated with infection. Previous antibiotic treatment, intensive care unit stay, and lung transplantation were associated with aminopenicillin resistance. Only 4/205 (2%) colonization events led to an infection. Adequate treatment did not affect microbiological clearance rates. Overall mortality was 8%; no deaths were attributable to enterococcal events. CONCLUSIONS: Enterococcal colonizations and infections are frequent in transplant recipients. Progression from colonization to infection is rare. Therefore, antibiotic treatment should be used restrictively in colonization. No increased mortality because of enterococcal infection was noted

Objectives: To assess the safety of discontinuation of primary prophylaxis in HIV-infected patients on antiretroviral combination therapy at high risk of developing Pneumocystis carinii pneumonia. Design: Prospective multicentre study. Patients and methods: The incidence of P. carinii pneumonia after discontinuation of primary prophylaxis was studied in 396 HIV-infected patients on antiretroviral combination therapy who experienced an increase in their CD4 cell count to at least 200 × 10 6 / and 14% of total lymphocytes; the study population included 191 patients with a history of CD4 cell counts below 100 × 10 6 /l (245 person-years) and 144 patients with plasma HIV RNA above 200 copies/ml (215 person-years). Results: There was one case of Pneumocystis pneumonia, an incidence of 0.18 per 100 person-years [95% confidence interval (CI), 0.005-1.0 per 100 person-years]. No case was diagnosed in groups with low nadir CD4 cell counts (95% Cl, 0-1.2 per 100 person-years) or detectable plasma HIV RNA (95% Cl, 0-1.4 per 100 person-years). Conclusions: Discontinuation of primary prophylaxis against Pneumocystis pneumonia is safe in patients who have responded with a sustained increase in their CD4 cell count to antiretroviral combination therapy, irrespective of the CD4 cell count nadir and the viral load at the time of stopping prophylaxis.

Summary Background Hepatitis C virus (HCV) infection is highly prevalent among HIV-1-infected individuals, but its contribution to the morbidity and mortality of coinfected patients who receive potent antiretroviral therapy is controversial. We used data from the ongoing Swiss HIV Cohort Study to analyse clinical progression of HIV-1, and the virological and immunological response to potent antiretroviral therapy in HIV-1-infected patients with or without concurrent HCV infection. Methods We analysed prospective data on survival, clinical disease progression, suppression of HIV-1 replication, CD4-cell recovery, and frequency of changes in antiretroviral therapy according to HCV status in 3111 patients starting potent antiretroviral therapy. Results 1157 patients (37·2%) were coinfected with HCV, 1015 of whom (87·7%) had a history of intravenous drug use. In multivariate Cox's regression, the probability of progression to a new AIDS-defining clinical event or to death was independently associated with HCV sero-positivity (hazard ratio 1·7 [95% Cl 1·26–2·30]), and with active intravenous drug use (1·38 [1·02–1·88]). Virological response to antiretroviral therapy and the probability of treatment change were not associated with HCV serostatus. In contrast, HCV seropositivity was associated with a smaller CD4-cell recovery (hazard ratio for a CD4-cell count increase of at least 50 cells/μL=0·79 [0·72–0·87]). Interpretation HCV and active intravenous drug use could be important factors in the morbidity and mortality among HIV-1-infected patients, possibly through impaired CD4-cell recovery in HCV seropositive patients receiving potent antiretroviral therapy. These findings are relevant for decisions about optimum timing for HCV treatment in the setting of HIV infection.

Objective: The amount of HIV in semen likely influences infectiousness. Antiretroviral therapy decreases HIV-RNA in semen, but data on HIV concentrations in semen in a large cohort of men with suppressed HIV-RNA in blood is unavailable. Methods: Male patients with a treatment-induced reduction of HIV-RNA load in plasma below 400 copies/ml were asked to donate a semen and blood sample. Blood and seminal plasma were tested for the presence of HIV-RNA by the NucliSens method (detection limit 400 copies/ml). Seminal cell samples from 67 patients were further analysed for the presence of HIV-DNA using a nested DNA-polymerase chain reaction. Results of RNA and DNA testing in semen were compared with 55 HIV-positive antiretroviral therapy-naive men. Results: A total of 114 patients participated in the study. Seminal plasma HIV-RNA was detectable in only two patients [1.8%, 95% confidence ratio (CI), 0-4.2%] compared with a detection frequency of 67% in untreated controls [Odds ratio (OR), 0.01; 95% CI, 0-0.03]. Detection of cell-associated HIV-DNA in semen was significantly less frequent (16 versus 38%) in patients receiving suppressive therapy compared with untreated controls (OR, 0.32; 95% Cl, 0.12-0.80). Conclusion: In patients with treatment-induced suppression of blood viral load the likelihood of having detectable HIV in semen is very low (< 4%). In addition, seminal shedding of cell-free and cell-associated HIV is significantly lower than in an untreated population of HlV-infected asymptomatic men. On a population basis, this effect of therapy may help to reduce sexual transmission of HIV. However, individual patients may still be infected as evidenced by continued shedding of cells harbouring the HIV provirus.

We present a 63-year-old man treated with alemtuzumab for chronic lymphocytic leukemia who developed multiple angiomatous papules and fever. Real-time polymerase chain reaction (RT-PCR) from a skin lesion and blood sample revealedBartonella quintanaas causative agent confirming the diagnosis of bacillary angiomatosis with bacteremia. Treatment with doxycycline, initially in combination with gentamicin, led to complete resolution of the lesions. This case shows the importance of considering bacillary angiomatosis as a rare differential diagnosis of angiomatous lesions in the immunocompromised patient, particularly in chronic lymphocytic leukemia and following lymphocyte depleting treatments as alemtuzumab.

We assessed the impact of antiviral prophylaxis and preemptive therapy on the incidence and outcomes of cytomegalovirus (CMV) disease in a nationwide prospective cohort of solid organ transplant recipients. Risk factors associated with CMV disease and graft failure-free survival were analyzed using Cox regression models. One thousand two hundred thirty-nine patients transplanted from May 2008 until March 2011 were included; 466 (38%) patients received CMV prophylaxis and 522 (42%) patients were managed preemptively. Overall incidence of CMV disease was 6.05% and was linked to CMV serostatus (D+/R− vs. R+, hazard ratio [HR] 5.36 [95% CI 3.14–9.14], p

PURPOSE OF REVIEW: The debate on the merits of observational studies as compared with randomized trials is ongoing. We will briefly touch on this subject, and demonstrate the role of cohort studies for the description of infectious disease patterns after transplantation. The potential benefits of cohort studies for the clinical management of patients outside of the expected gain in epidemiological knowledge are reviewed. The newly established Swiss Transplantation Cohort Study and in particular the part focusing on infectious diseases will serve as an illustration. RECENT FINDINGS: A neglected area of research is the indirect value of large, multicenter cohort studies. These benefits can range from a deepened collaboration to the development of common definitions and guidelines. Unfortunately, very few data exist on the role of such indirect effects on improving quality of patient management. SUMMARY: This review postulates an important role for cohort studies, which should not be viewed as inferior but complementary to established research tools, in particular randomized trials. Randomized trials remain the least bias-prone method to establish knowledge regarding the significance of diagnostic or therapeutic measures. Cohort studies have the power to reflect a real-world situation and to pinpoint areas of knowledge as well as of uncertainty. Prerequisite is a prospective design requiring a set of inclusive data coupled with the meticulous insistence on data retrieval and quality.

Background Burkholderia pseudomallei, the etiologic agent of melioidosis, is endemic to tropic regions, mainly in Southeast Asia and northern Australia. Melioidosis occurs only sporadically in travellers returning from disease-endemic areas. Severe clinical disease is seen mostly in patients with alteration of immune status. In particular, pericardial effusion occurs in 1-3% of patients with melioidosis, confined to endemic regions. To our best knowledge, this is the first reported case of melioidosis in a traveller complicated by a hemodynamically significant pericardial effusion without predisposing disease. Case presentation A 44-year-old Caucasian man developed pneumonia, with bilateral pleural effusions and complicated by a hemodynamically significant pericardial effusion, soon after his return from Thailand to Switzerland. Cultures from different specimens including blood cultures turned out negative. Diagnosis was only accomplished by isolation of Burkholderia pseudomallei from the pericardial aspirate, thus finally enabling the adequate antibiotic treatment. Conclusions Melioidosis is a great mimicker and physicians in non-endemic countries should be aware of its varied manifestations. In particular, melioidosis should be considered in differential diagnosis of pericardial effusion in travellers , even without risk factors predisposing to severe disease.

To the Editors: We describe the presentation of an Echinococcus multilocularis (EM) infection (alveolar echinococcosis (AE)) with progressive massive orthopnoea and progressive dyspnoea on exertion due to infiltration of the diaphragm and phrenic nerves. Diagnosis was proved using a combination of computed tomography (CT), lung function in the supine and sitting position, sniff test during radioscopy and AE serology. Because of diffuse infiltration of the retroperitoneal and mediastinal space a surgical intervention was inapplicable. Thus, medical treatment was initiated using albendazole. Noninvasive ventilation (NIV) resolved orthopnoea and the patient was discharged. AE occurs in the northern hemisphere but in Switzerland it is classified as a rare disease. To our knowledge this is the first described case of this rare infection with a consecutive bilateral paresis of the diaphragm. But despite its unique entity, this case report demonstrates that clinical findings and routine diagnostic methods may lead to the correct diagnosis. Progressive phrenic paresis is a rare cause of orthopnoea and dyspnoea on exertion [1]. Relevant paresis is often overseen and diagnosed late in the course of the disease. The main reasons for bilateral phrenic paresis are traumatic, inflammatory, neuropathic, idiopathic or tumour related [1]. We present a case of a non-malignant compression caused by AE leading to bilateral phrenic paresis. A 60-yr-old farmer’s wife presented to a district hospital with progressive dyspnoea on exertion for 2 yrs. A cardiologic consultation at that time including echocardiography and exercise testing was unremarkable. Within the last year, the patient complained about weight …

Summary During the 2009/10 influenza A/H1N1v pandemic in Switzerland, we followed the disease course of of all 15 patients with A/H1N1v-associated pneumonia whom we identified at our tertiary care hospital. Eight of the patients had previously known risk factors for A/H1N1v disease compliction, according to WHO criteria. All patients showed signs and/or symptoms of complicated influenza. 14 patients had to be hospitalised with a median hospital stay of 8‐9 days; 6 were admitted to intensive care, of whom 3 required intubation. According to WHO recommendations, oseltamivir should be started as early as possible, both in patients with risk factors for severe disease and in any patient presenting with symptoms of progressive disease. If treated early according to these guidelines, half of our patients might not have developed pneumonia at all. In the remaining patients without preexisting risk factors, the clinical course of pneumonia might have been milder. It is questionable whether the delayed oseltamivir treatment still influenced the clinical outcome, but no patient died; the two patients who were discharged with new home oxygen therapy apparatus had presented massive preexisting morbidities.

Relapsing or persisting skin and soft tissue infections after injury with biological materials should prompt consideration of atypical mycobacteria, even in non-immunocompromized hosts. We report 3 cases where diagnosis was delayed for 3-10 months. Insidiously, Mycobacterium marinum infection can occur without any contact to fish tank or swimming pool.

We prospectively assessed the 1-month prevalence of abnormal body fat distribution in HIV-infected individuals. Of 1,359 patients treated with antiretroviral drugs, 578 (43%) had signs of abnormal fat distribution. Peripheral fat loss was observed in 382 patients (28%), whereas 412 (30%) had signs of fat accumulation. The presence of lipodystrophy (peripheral fat loss with or without fat accumulation) was found to be independently associated with increasing age (less than 35 years of age as a reference group: 35 to 41 years of age, OR = 1.5 [95% CI, 1.1-2.3]; and older than 41 years of age, OR = 2.4 [95% CI, 1.7-3.5]), current use of stavudine (OR = 2.4 [95% CI, 1.8-3.3]), current use of abacavir (OR = 2.1 [95% CI, 1.3-3.4]), and elevated lactate level (OR = 1.6 [95% CI, 1.1-2.4]). The prevalence of lipodystrophy was higher among patients who had received stavudine for a longer period (no stavudine in the current combination as a reference group: 24 months, OR = 3.2 [95% CI, 2.4-4.3]). This study confirms the association between the use of stavudine and lipodystrophy.

Previous studies have associated activating Killer cell Immunoglobulin like Receptor (KIR) genes with protection from cytomegalovirus (CMV) replication after organ transplantation. Whether KIR associated protection is operating in the context of primary infection re activation or both remains unknown. Here we correlated KIR genotype and CMV serostatus at the time of transplantation with rates of CMV viremia in 517 heart (n=57) kidney (n=223) liver (n=165) or lung (n=72) allograft recipients reported to the Swiss Transplant Cohort Study. Across the entire cohort we found B haplotypes which in contrast to A haplotypes may contain multiple activating KIR genes to be protective in the most immunosuppressed patients (receiving anti thymocyte globulin induction and intensive maintenance immunosuppression) (hazard ratio after adjustment for covariates 0.46 95 confidence interval 0.29 0.75 P=0.002). Notably a significant protection was detected only in recipients who were CMV seropositive at the time of transplantation (HR 0.45 95 CI 0.26 0.77 P=0.004) but not in CMV seronegative recipients (HR 0.59 95 CI 0.22 1.53 P=0.28). These data indicate a prominent role for KIR and presumably natural killer (NK) cells in the control of CMV replication in CMV seropositive organ transplant recipients treated with intense immunosuppression.Genes and Immunity advance online publication 10 July 2014; doi:10.1038/gene.2014.39.

CT findings (figures 1 and 2) were consistent with infection of a liver metastasis as a result of gas-producing bacteria. Culture specimens grew C. septicum. The patient died 28 h after onset of symptoms despite intensive medical treatment. Clostridium species are anaerobic, gram-positive, spore-forming bacteria. Clostridial infections are believed to be more prevalent among patients with malignant diseases than among the general population [1-5]. C. septicum, however, may have a specific relationship with colorectal adenocarcinoma. In several case series, C. septicum appeared to be highly associated with rightsided colon cancer, which is often occult at the time that infection occurs [1-4]. Further predisposing conditions include hematological malignancies, cyclic neutropenia following chemotherapy, and diabetes [1, 7]. Metastatic myonecrosis, a myonecrosis in the absence of local trauma, is an uncommon presentation of C. septicum infection [6, 7]. C. septicum myonecrosis is characterized by fulminant destruction of muscles and septicemia, with 100% mortality rates for patients not receiving early treatment with antibiotics and aggressive surgical debridement [ 1-3, 7]. Even with prompt and aggressive surgical debridement and appropriate antibiotic treatment, metastatic infection with C. septicum is associated with a high mortality rate (70%-80%) [1-3, 7]. Extremity myonecrosis has been described secondary to intraabdominal abscesses extending directly along fascial planes, but hematogenous lesions were also described as "spontaneous gas gangrene" [8]. Myonecrosis must be differentiated from cellulitis on the basis of the depth of the infection and whether the infection is necrotizing. It has been proposed that tumors of the colon act as a source for systemic contamination from C. septicum bacteria. The gas-containing hepatic lesions in our patient represented infected metastases. It can be speculated that the number of cases of C. septicum myonecrosis might increase in the future as a result of changing practices in the treatment of colon cancer with advanced synchronous metastases, including the increasing use of primary chemotherapy before surgery.

A commercially available test for the serologic diagnosis of tuberculosis was evaluated for its applicability in human immunodeficiency virus (HIV)-positive patients. Antibodies to lipoarabinomannan were detectable in sera from only 9 of 85 HIV-positive patients with a confirmed diagnosis of tuberculosis. Given the low degree of sensitivity of the assay with sera from HIV-infected patients, the study does not support the use of this serologic assay for the diagnosis of tuberculosis in HIV-infected patients.

In the original publication the members of the FUNGINOS network were provided in such a way that they could not be indexed as collaborators on PubMed.