The Mucosally-Adherent Rectal Microbiota Contains Features Unique to Alcohol-Related Cirrhosis.

Most studies examining correlations between the gut microbiota and disease states focus on fecal samples due to ease of collection, yet there are distinct differences when compared to samples collected from the colonic mucosa. Although fecal microbiota has been reported to be altered in cirrhosis, correlation with mucosal microbiota characterized via rectal swab has not been previously described in this patient population. We conducted a cross-sectional analysis using 39 stool and 39 rectal swabs from adult patients with cirrhosis of different etiologies and performed shotgun metagenomic sequencing. Bacterial growth studies were performed with Escherichia coli. Two asaccharolytic bacterial taxa, Finegoldia magna and Porphyromonas asaccharolytica, were increased in rectal swabs relative to stool (FDR < 0.01). Genomic analysis of the microbiome revealed 58 genes and 16 pathways that differed between stool and rectal swabs (FDR < 0.05), where rectal swabs were enriched for pathways associated with protein synthesis and cellular proliferation but decreased in carbohydrate metabolism. Although no features in the fecal microbiome differentiated cirrhosis etiologies, the mucosal microbiome revealed decreased abundances of E. coli and Enterobacteriaceae in alcohol-related cirrhosis relative to non-alcohol related cirrhosis (FDR < 0.05). In vitro bacterial culture studies showed that physiological concentrations of ethanol and its oxidative metabolites inhibited E. coli growth in a pH- and concentration-dependent manner. Characterization of the mucosally associated gut microbiome via rectal swab revealed findings consistent with amino acid/nitrogen abundance versus carbohydrate limitation in the mucosal microenvironment as well as unique features of alcohol-related cirrhosis possibly consistent with the influence of host-derived metabolites on the composition of mucosally adherent microbiota.

Role of Bacterial Infection in the Development of Acute Liver Failure in Patients with Decompensated Alcoholic Liver Cirrhosis.

We examined 74 patients with acute decompensation of alcoholic liver cirrhosis: 34 (45.9%) with bacterial infection (group 1) and 40 (54.1%) without bacterial infection (group 2). The degree and index of acute-on-chronic liver failure (ACLF) were determined using an on-line CLIF-C ACLF Calculator and the levels of cytokeratin-18 fragments, TNFα, IL-1ß, IL-4, IL-6, and IL-8. In group 1, AST, cytokeratin-18, TNFα, IL-1ß, IL-6, degree and score of ACLF were significantly higher than in group 2. ACLF developed in 18 (52.9%) patients in group 1 and in 11 (27.5%) (p<0.05) patients in group 2. Within 1 month, 10 (29.4%) patients of group 1 and 2 (5%) patients of group 2 died (p<0.05). Patients with bacterial infection showed a more severe course of alcoholic liver cirrhosis and ACLF than those without bacterial infection.

Beneficial effects of LRP6-CRISPR on prevention of alcohol-related liver injury surpassed fecal microbiota transplant in a rat model.

Alcohol intake can modify gut microbiota composition, increase gut permeability, and promote liver fibrogenesis. LRP6 is a signal transmembrane protein and a co-receptor for the canonical Wnt signaling pathway. This study compared the curative effect of LRP6-CRISPR on alcohol-related liver injury with that of traditional fecal microbiota transplant (FMT) and investigated the alteration of the gut microbiome following the treatment. A rat model of alcohol-related liver injury was established and injected with lentiviral vectors expressing LRP6-CRISPR or administered with fecal filtrate from healthy rats, with healthy rat served as the control. Liver tissues of rats were examined by HE staining, Sirius staining, and Oil red O staining, respectively. The expression of LRP6 and fibrosis biomarkers were tested by PCR. The fecal sample of rats was collected and examined by 16S rRNA sequencing. Our data indicated that LRP6-CRISPR was more efficient in the prevention of alcohol-related liver injury than FMT. Microbiome analysis showed that alcohol-related liver injury related to gut microbiota dysbiosis, while treatment with LRP6-CRISPR or FMT increased gut microflora diversity and improved gut symbiosis. Further, bacteria specific to the disease stages were identified. Genera Romboutsia, Escherichia-Shigella, Pseudomonas, Turicibacter, and Helicobacter were prevalent in the intestine of rats with alcohol-related liver injury, while the domination of Lactobacillus was found in rats treated with LRP6-CRISPR or FMT. Besides, Lactobacillus and genera belonging to family Lachnospiraceae, Bacteroidales S24-7 group, and Ruminococcaceae were enriched in healthy rats. LRP6-CRISPR and FMT have beneficial effects on the prevention of alcohol-related liver injury, and correspondently, both treatments altered the disrupted gut microflora to a healthy one.

Genomic Features, Comparative Genomic Analysis, and Antimicrobial Susceptibility Patterns of Chryseobacterium arthrosphaerae Strain ED882-96 Isolated in Taiwan.

Bacteria belonging to the genus Chryseobacterium are ubiquitously distributed in natural environments, plants, and animals. Except C. indologenes and C. gleum, other Chryseobacterium species rarely cause human diseases. This study reported the whole-genome features, comparative genomic analysis, and antimicrobial susceptibility patterns of C. arthrosphaerae ED882-96 isolated in Taiwan. Strain ED882-96 was collected from the blood of a patient who had alcoholic liver cirrhosis and was an intravenous drug abuser. This isolate was initially identified as C. indologenes by using matrix-assisted laser desorption ionization-time of flight mass spectrometry. The analysis of 16S ribosomal RNA gene sequence revealed that ED882-96 shared 100% sequence identity with C. arthrosphaerae type strain CC-VM-7T. The results of whole-genome sequencing of ED882-96 showed two chromosome contigs and one plasmid. The total lengths of the draft genomes of chromosome and plasmid were 4,249,864 bp and 435,667 bp, respectively. The findings of both in silico DNA-DNA hybridization and average nucleotide identity analyses clearly demonstrated that strain ED882-96 was a species of C. arthrosphaerae. A total of 83 potential virulence factor homologs were predicted in the whole-genome sequencing of strain ED882-96. This isolate was resistant to all tested antibiotics, including ß-lactams, ß-lactam/ß-lactamase inhibitor combinations, aminoglycosides, fluoroquinolones, tetracycline, glycylcycline, and trimethoprim-sulfamethoxazole. Only one antibiotic resistance gene was recognized in the plasmid. By contrast, many antibiotic resistance genes were identified in the chromosome. The findings of this study suggest that strain ED882-96 is a highly virulent and multidrug-resistant pathogen. Knowledge regarding genomic characteristics and antimicrobial susceptibility patterns provides valuable insights into this uncommon species.

Bile acid homeostasis and intestinal dysbiosis in alcoholic hepatitis.

BACKGROUND: Intestinal microbiota plays an important role in bile acid homeostasis. AIM: To study the structure of the intestinal microbiota and its function in bile acid homeostasis in alcoholic patients based on the severity of alcoholic liver disease. METHODS: In this prospective study, we included four groups of active alcoholic patients (N = 108): two noncirrhotic, with (noCir_AH, n = 13) or without alcoholic hepatitis (noCir_noAH, n = 61), and two cirrhotic, with (Cir_sAH, n = 17) or without severe alcoholic hepatitis (Cir_noAH, n = 17). Plasma and faecal bile acid profiles and intestinal microbiota composition were assessed. RESULTS: Plasma levels of total bile acids (84.6 vs 6.8 µmol/L, P < 0.001) and total ursodeoxycholic acid (1.3 vs 0.3 µmol/L, P = 0.03) were higher in cirrhosis with severe alcoholic hepatitis (Cir_sAH) than Cir_noAH, whereas total faecal (2.4 vs 11.3, P = 0.01) and secondary bile acids (0.7 vs 10.7, P < 0.01) levels were lower. Cir_sAH patients had a different microbiota than Cir_noAH patients: at the phyla level, the abundance of Actinobacteria (9 vs 1%, P = 0.01) was higher and that of Bacteroidetes was lower (25 vs 40%, P = 0.04). Moreover, the microbiota of Cir_sAH patients showed changes in the abundance of genes involved in 15 metabolic pathways, including upregulation of glutathione metabolism, and downregulation of biotin metabolism. CONCLUSIONS: Patients with Cir_sAH show specific changes of the bile acid pool with a shift towards more hydrophobic and toxic species that may be responsible for the specific microbiota changes. Conversely, the microbiota may also alter the bile acid pool by transforming primary to secondary bile acids, leading to a vicious cycle.

Antifibrotic and molecular aspects of rifaximin in alcoholic liver disease: study protocol for a randomized controlled trial.

BACKGROUND: Alcoholic liver disease is the leading cause of cirrhosis worldwide. Due to an increase in alcohol overuse, alcoholic liver disease has become an increased burden on health care systems. Abstinence from alcohol remains the cornerstone of alcoholic liver disease treatment; however, this approach is hampered by frequent relapse and lack of specific therapy for treating advanced cases of liver disease. In the present study, we hypothesized that gut microbiota drive the development of liver fibrosis and that modulation of gut microbiota with the gut-selective, nonabsorbable antibiotic rifaximin attenuates alcoholic liver fibrosis. METHODS/DESIGN: Our double-blind, placebo-controlled trial will include 136 participants with biopsy-verified alcoholic fibrosis (Ishak liver fibrosis score of 1-4). Participants are randomized 1:1 to receive placebo or 550 mg of rifaximin twice daily for 18 months. A liver biopsy will be performed at the end of the treatment period to evaluate the effect of drug treatment on liver fibrosis. Stool, urine, and saliva specimens will be collected before treatment begins, at 1 month, and at the end of the treatment period. Fecal samples are used for microbiome deep sequencing. Changes in microbiome composition are compared before and after the trial medication period and linked to changes in liver fibrosis. DISCUSSION: This is the first clinical trial to evaluate the effect of gut microbiota on liver fibrosis in humans. If gut microbiota are an important promoter of alcoholic liver disease, current results may open new therapeutic avenues and revolutionize the current understanding of chronic liver diseases. TRIAL REGISTRATION: EudraCT, 2014-001856-51 . Registered on 16 August 2014.

A tip from the nose: rhinocerebral mucormycosis in a patient with alcoholic liver cirrhosis and cocaine abuse, an uncommon association.

We present the case of a 28-year-old man with a long-standing history of cocaine abuse and Child-Pugh class C alcoholic liver cirrhosis who developed severe lower respiratory tract infection complicated with septic shock and multiple organ dysfunction. He was managed in the intensive care unit. On the eighth day after admission, he developed a nose discolouration, which was initially thought to be associated with high-dose vasopressors. Despite the reduction of vasopressors, the lesion progressed rapidly. It was later diagnosed as rhinocerebral mucormycosis. Amphotericin B was administered, but unfortunately the patient succumbed to the complications postinfection. The association between alcoholic liver cirrhosis and rhinocerebral mucormycosis should be known and prompt recognition warrants immediate treatment.

Bidirectional Communication between Liver and Gut during Alcoholic Liver Disease.

Alcoholic liver disease is a major medical burden. Alcohol abuse is the cause for end-stage liver disease in approximately 50% of all patients with cirrhosis. Chronic alcohol consumption is associated with changes in the composition of the intestinal microbiota and gut barrier dysfunction. The portal vein is the major communication route between the intestine and the liver. Increased intestinal permeability allows microbial components, bacteria, and metabolites to translocate to the liver. The liver communicates with the intestine via mediators in the systemic circulation and the biliary system. In this review, the authors describe the changes that occur in the intestinal microbiota with chronic alcohol consumption. They further review the bilateral communication between the liver and the gut, and discuss how this interaction affects the progression of alcoholic liver disease.

Changes in gut bacterial populations and their translocation into liver and ascites in alcoholic liver cirrhotics.

BACKGROUND: The liver is the first line of defence against continuously occurring influx of microbial-derived products and bacteria from the gut. Intestinal bacteria have been implicated in the pathogenesis of alcoholic liver cirrhosis. Escape of intestinal bacteria into the ascites is involved in the pathogenesis of spontaneous bacterial peritonitis, which is a common complication of liver cirrhosis. The association between faecal bacterial populations and alcoholic liver cirrhosis has not been resolved. METHODS: Relative ratios of major commensal bacterial communities (Bacteroides spp., Bifidobacterium spp., Clostridium leptum group, Enterobactericaea and Lactobacillus spp.) were determined in faecal samples from post mortem examinations performed on 42 males, including cirrhotic alcoholics (n = 13), non-cirrhotic alcoholics (n = 15), non-alcoholic controls (n = 14) and in 7 healthy male volunteers using real-time quantitative PCR (RT-qPCR). Translocation of bacteria into liver in the autopsy cases and into the ascites of 12 volunteers with liver cirrhosis was also studied with RT-qPCR. CD14 immunostaining was performed for the autopsy liver samples. RESULTS: Relative ratios of faecal bacteria in autopsy controls were comparable to those of healthy volunteers. Cirrhotics had in median 27 times more bacterial DNA of Enterobactericaea in faeces compared to the healthy volunteers (p = 0.011). Enterobactericaea were also the most common bacteria translocated into cirrhotic liver, although there were no statistically significant differences between the study groups. Of the ascites samples from the volunteers with liver cirrhosis, 50% contained bacterial DNA from Enterobactericaea, Clostridium leptum group or Lactobacillus spp.. The total bacterial DNA in autopsy liver was associated with the percentage of CD14 expression (p = 0.045). CD14 expression percentage in cirrhotics was significantly higher than in the autopsy controls (p = 0.004). CONCLUSIONS: Our results suggest that translocation of intestinal bacteria into liver may be involved as a one factor in the pathogenesis of alcoholic liver cirrhosis.

Altered profile of human gut microbiome is associated with cirrhosis and its complications.

BACKGROUND & AIMS: The gut microbiome is altered in cirrhosis; however its evolution with disease progression is only partly understood. We aimed to study changes in the microbiome over cirrhosis severity, its stability over time and its longitudinal alterations with decompensation. METHODS: Controls and age-matched cirrhotics (compensated/decompensated/hospitalized) were included. Their stool microbiota was quantified using multi-tagged pyrosequencing. The ratio of autochthonous to non-autochthonous taxa was calculated as the cirrhosis dysbiosis ratio (CDR); a low number indicating dysbiosis. Firstly, the microbiome was compared between controls and cirrhotic sub-groups. Secondly, for stability assessment, stool collected twice within 6months in compensated outpatients was analyzed. Thirdly, changes after decompensation were assessed using (a) longitudinal comparison in patients before/after hepatic encephalopathy development (HE), (b) longitudinal cohort of hospitalized infected cirrhotics MELD-matched to uninfected cirrhotics followed for 30days. RESULTS: 244 subjects [219 cirrhotics (121 compensated outpatients, 54 decompensated outpatients, 44 inpatients) and 25 age-matched controls] were included. CDR was highest in controls (2.05) followed by compensated (0.89), decompensated (0.66), and inpatients (0.32, p<0.0001) and negatively correlated with endotoxin. Microbiota and CDR remained unchanged in stable outpatient cirrhotics (0.91 vs. 0.86, p=0.45). In patients studied before/after HE development, dysbiosis occurred post-HE (CDR: 1.2 to 0.42, p=0.03). In the longitudinal matched-cohort, microbiota were significantly different between infected/uninfected cirrhotics at baseline and a low CDR was associated with death and organ failures within 30days. CONCLUSIONS: Progressive changes in the gut microbiome accompany cirrhosis and become more severe in the setting of decompensation. The cirrhosis dysbiosis ratio may be a useful quantitative index to describe microbiome alterations accompanying cirrhosis progression.

[A NEW APPROACH TO TREATMENT LIVER CIRRHOSIS IN CONNECTION WITH INTESTINAL DYSBIOSIS].

In order to increase the effectiveness of treatment of the liver cirrhosis were examined 65 patients, we studied the effect on the features flow of intestine microbiocenosis and were are included to the combined treatment the synbiotic medications "Bifilakt extra". Inclusion to the combined treatment of the examined patients with liver cirrhosis synbiotic medications "Bifilakt extra" probably led to better reduction of subjective and objective signs of cirrhosis and intensity of functional biochemical syndromes, symptoms of hepatic encephalopathy.

Identification of bacterial DNA in neutrocytic and non-neutrocytic cirrhotic ascites by means of a multiplex polymerase chain reaction.

BACKGROUND: Even though bacterial cultures of ascitic fluid are negative in up to 65% of the cases of spontaneous bacterial peritonitis (SBP); bacterial DNA (bactDNA) has been frequently detected in episodes of SBP as well as in culture-negative non-neutrocytic ascites. AIMS: To evaluate multiplex polymerase chain reaction (PCR) for pathogen identification in SBP and to determine the prevalence of ascitic bactDNA and its prognostic relevance in hospitalized patients with liver cirrhosis. METHODS: Ascitic fluid from 68 consecutive patients who underwent diagnostic paracentesis was analysed for polymorphonuclear leucocyte (PMN) count, bacterial culture and bactDNA. BactDNA was identified by gel analysis after multiplex PCR of selectively enriched prokaryotic nucleic acids. Correlations of bactDNA status with PMN count, bacterial culture result and 3-month mortality were determined for neutrocytic and for non-neutrocytic ascites. RESULTS: 11/68 patients presented with an elevated ascitic PMN count. BactDNA was detected in 5/5 culture-positive neutrocytic samples, in 1/6 culture-negative neutrocytic samples and in 8/56 culture-negative non-neutrocytic samples. Three-month mortality did not differ with respect to ascitic bactDNA status (7/14 vs. 14/47, P=0.162). 3-month mortality was increased in the presence of ascitic bactDNA for patients older than 65 years (4/5 vs. 4/14, P=0.046) and for patients with a model for end-stage liver disease score >15 (7/10 vs. 9/30, P=0.025). CONCLUSIONS: Identification of ascitic bactDNA is an appropriate alternative to bacterial ascite culture for pathogen identification in patients at risk for SBP. Its prognostic relevance as a proposed marker of bacterial translocation for certain risk groups has to be further evaluated.

[Infections in hospitalized patients with cirrhosis]. / Infecciones en pacientes hospitalizados por cirrosis.

We evaluated the prevalence and the clinical relevance of bacterial and nonbacterial infections in predominantly alcoholic cirrhotic patients, admitted to an intermediate complexity hospital, and we also compared the clinical characteristics, laboratory and evolution of these patients with and without bacterial infection in a prospective study of cohort. A total of 211 consecutive admissions in 132 cirrhotic patients, between April 2004 and July 2007, were included. The mean age was 51.8 (+/-8) years, being 84.8% male. The alcoholic etiology of cirrhosis was present in 95.4%. One hundred and twenty nine episodes of bacterial infections were diagnosed in 99/211 (46.9%) admissions, community-acquired in 79 (61.2%) and hospital-acquired in 50 (38.8%): spontaneous bacterial peritonitis (23.3%); urinary tract infection (21.7%); pneumonia (17.8%); infection of the skin and soft parts (17.1%), sepsis by spontaneous bacteremia (7.7%); other bacterial infections (12.4%). Gram-positive organisms were responsible for 52.2% of total bacterial infections documented cases. There were eight serious cases of tuberculosis, fungal and parasitic infections; the prevalence of tuberculosis was 6% with an annual mortality of 62.5%; 28.1% (9/32) of the coproparasitological examination had Strongyloides stercolaris. The in-hospital mortality was significantly higher in patients with bacterial infection than in non-infected patients (32.4% vs. 13.2%; p=0.02). The independent factors associated with mortality were bacterial infections, the score of Child-Pügh and creatininemia > 1.5 mg/dl. By the multivariate analysis, leukocytosis and hepatic encephalopathy degree III/IV were independent factors associated to bacterial infection. This study confirms that bacterial and nonbacterial infections are a frequent and severe complication in hospitalized cirrhotic patients, with an increase of in-hospital mortality.

Infecciones en pacientes hospitalizados por cirrosis / Infections in hospitalized patients with cirrhosis

Evaluamos la prevalecencia y relevancia clínica de las infecciones bacterianas y no bacterianas en pacientes cirróticos predominantemente alcohólicos internados en un hospital de mediana complejidad, y comparamos las características clínicas, de laboratorio y la evolución de pacientes con y sin infección bacteriana en un estudio prospectivo de cohorte. Se incluyeron 211 internaciones consecutivas de 132 pacientes con diagnóstico de cirrosis, de abril 2004 a julio 2007. El promedio de edad (±DS) fue 51.8 (±8) años, 112 fueron hombres (84.8%); etiología alcohólica 95.4%. Se diagnosticaron 129 episodios de infecciones bacterianas en 99/211 (46.9%) internaciones, adquiridos en la comunidad 79 (61.2%) y 50 (38.8%) intrahospitalarios: peritonitis bacteriana espontánea (23.3%); infección urinaria (21.7%); neumonías (17.8%); infecciones de piel y partes blandas (17.1%); sepsis por bacteriemia espontánea (7.7%); otras infecciones bacterianas (12.4%). El 52.2% fueron por gérmenes gram-positivos. Hubo ocho casos de tuberculosis e infecciones graves por hongos y parásitos. La prevalecencia de tuberculosis fue del 6% con una mortalidad anual de 62.5%. El 28.1% (9/32) de los exámenes coproparasitológicos tuvieron Strongyloides stercolaris. La mortalidad hospitalaria fue mayor en los pacientes con infección bacteriana (32.4% vs. 13.2%; p=0.02). Fueron identificados como predictores independientes de mortalidad: las infecciones bacterianas, el score de Child-Pügh y creatininemia > 1.5 mg/dl. En el análisis multivariado fueron factores independientes asociados a infección bacteriana la leucocitosis y la encefalopatía hepática grado III/IV. Este estudio confirma que las infecciones bacterianas y no bacterianas son una complicación frecuente y grave en pacientes cirróticos internados, con un aumento de la mortalidad hospitalaria.

We evaluated the prevalence and the clinical relevance of bacterial and nonbacterial infections in predominantly alcoholic cirrhotic patients, admitted to an intermediate complexity hospital, and we also compared the clinical characteristics, laboratory and evolution of these patients with and without bacterial infection in a prospective study of cohort. A total of 211 consecutive admissions in 132 cirrhotic patients, between April 2004 and July 2007, were included. The mean age was 51.8 (±8) years, being 84.8% male. The alcoholic etiology of cirrhosis was present in 95.4%. One hundred and twenty nine episodes of bacterial infections were diagnosed in 99/211 (46.9%) admissions, community- acquired in 79 (61.2%) and hospital-acquired in 50 (38.8%): spontaneous bacterial peritonitis (23.3%); urinary tract infection (21.7%); pneumonia (17.8%); infection of the skin and soft parts (17.1%), sepsis by spontaneous bacteremia (7.7%); other bacterial infections (12.4%). Gram-positive organisms were responsible for 52.2% of total bacterial infections documented cases. There were eight serious cases of tuberculosis, fungal and parasitic infections; the prevalence of tuberculosis was 6% with an annual mortality of 62.5%; 28.1% (9/32) of the coproparasitological examination had Strongyloides stercolaris. The in-hospital mortality was significantly higher in patients with bacterial infection than in non-infected patients (32.4% vs. 13.2%; p=0.02). The independent factors associated with mortality were bacterial infections, the score of Child-Pügh and creatininemia > 1.5 mg/dl. By the multivariate analysis, leukocytosis and hepatic encephalopathy degree III/IV were independent factors associated to bacterial infection. This study confirms that bacterial and nonbacterial infections are a frequent and severe complication in hospitalized cirrhotic patients, with an increase of in-hospital mortality.

Influence of pretransplantation bacterial and fungal culture positivity on outcome after living donor liver transplantation.

BACKGROUND: Bacterial and fungal infections are serious complications in patients with cirrhosis and are among the main causes of morbidity and mortality. The effects of pretransplantation infection on the outcome after orthotopic liver transplantation (OLT), however, have not been fully described. OBJECTIVE: To assess the influence of pretransplantation infection on OLT by analyzing the clinical profiles of liver recipients with preexisting bacterial or fungal infection. PATIENTS AND METHODS: We retrospectively reviewed the medical records of 223 adult patients who underwent living donor OLT between October 1, 2005, and September 30, 2006. In all patients, routine blood culture, was performed, and in patients with suspected bacterial or fungal infection; sputum, urine, and ascitic fluid cultures were performed. RESULTS: Of 223 patients, 37 (16.6%) had a positive culture in one or more samples. Culture-positive and culture-negative groups differed significantly in end-stage liver disease score but showed no differences in Child-Turcotte-Pugh score, existence of spontaneous bacterial peritonitis, hemodialysis, or duration of stay in the intensive care unit or hospital. Six of 37 patients with positive cultures (16.2%) and 4 (2.2%) of 186 patients with negative cultures (2.2%) died during the first 90 days after OLT (P = .007). The causes of death among culture-positive patients were brain edema (n = 2), brain hemorrhage (n = 1), hepatic dysfunction (n = 1), and sepsis (n = 2), whereas all 4 culture-negative patients died of infectious complications. CONCLUSION: Prompt OLT accompanied by adequate antibiotic or antifungal therapy may be acceptable in patients with preexisting bacterial or fungal infection unless there are overt manifestations of active infection.

[Saccharomyces cerevisiae fungemia associated with multifocal pneumonia in a patient with alcohol-related hepatic cirrhosis]. / Fungemia da Saccharomyces cerevisiae con polmonite a focolai multipli in paziente con cirrosi epatica alcool correlata.

Saccharomyces cerevisiae is usually considered non-pathogenic and has rarely been reported as a cause of fungemia in immunocompromised patients, especially those admitted to an intensive care unit or those affected by acquired immune deficiency syndrome or under immunosuppressive treatment. In all described cases the use of probiotic yeast has been given as the main risk factor. We report a case of S. cerevisiae sepsis complicated by pneumonia in a patient affected by alcohol-related cirrhosis with no evidence of probiotic drug intake. In this case recovery was obtained after a treatment course with liposomal amphotericin B. S. cerevisiae should be taken into consideration when sepsis lacks to isolate any aetiological agent.