Surgical wound infection by Aspergillus fumigatus in liver transplant recipients.

Cutaneous aspergillosis is generally associated with immunosuppression, burns, and major trauma. Most cases are acquired by direct inoculation, although cutaneous involvement does occasionally occur with disseminated disease. Surgical wound infections caused by Aspergillus species are very unusual and to our knowledge have not been described in the setting of organ transplantation. We describe two liver transplant recipients who developed wound aspergillosis during a nosocomial outbreak of Aspergillus infection. Infection developed in the second and fourth postoperative week respectively, and in both cases wound appearance mimicked necrotizing fasciitis. Both patients died despite local debridement and antifungal therapy with amphotericin B. Aspergillus must be added to the list of potential pathogens of surgical wounds, especially in the setting of organ transplantation.     

The magnitude and encephalogenic potential of autoimmune response to MOG is enhanced in MOG deficient mice

Myelin oligodendrocyte glycoprotein (MOG) is a minor component of central nervous system myelin presumably implicated in the pathogenesis of Multiple Sclerosis (MS). Immunization with MOG leads to the development of Experimental Autoimmune Encephalomyelitis (EAE), the experimental model of MS. It has been suggested that its encephalitogenic potential may be due to the lack of MOG self-immune tolerance. To clarify this, we have generated a MOG deficient mouse (MOG(-/-)) strain. Surprisingly, MOG(35-55)specific proliferation and Th1-type cytokine production were markedly enhanced in MOG(-/-)mice compared to wild type control. Furthermore, adoptive transfer of MOG(35-55)specific T cells, isolated from MOG deficient mice, into wild-type recipients resulted in the development of a more severe disease, indicating a high capacity of MOG(-/-)T cells to initiate effector responses. Interestingly, T cell reactivity to overlapping MOG peptides in MOG(-/-)mice did not reveal new potential immunodominant epitopes in H-2(b)mice. Taken together, our data suggests that MOG self-tolerance modulates the encephalitogenic potential of autoreactive MOG T cells in the periphery.     

Cranial epidural empyema with osteomyelitis caused by actinomyces, CT, and MRI appearance

Actinomycosis is an uncommon cause of intracranial infection. Epidural empyema represents about 6% of CNS actinomycotic lesions. A case of an epidural empyema with parietal bone osteomyelitis caused by Actinomyces israelii is presented. Relevant neuroimaging features were bone erosions and a multiloculated collection with annular contrast enhancing on CT. Postoperative MRI revealed extensive involvement of the neighbor dura, falx, and subdural space. MRI was crucial to follow-up the response to antibiotic treatment.     

Hepatic and systemic haemodynamic changes after MARS in patients with acute on chronic liver failure

Abstract Hyperdynamic circulation and portal hypertension characterize acute on chronic liver failure (AoCLF), partially because of circulating mediators. Molecular Absorbents Recirculating System (MARS) may remove some of these substances. The objective of this study was to evaluate the effect of MARS on portal pressure, systemic haemodynamic and endogenous vasoactive systems. MARS treatment was performed in four patients with AoCLF (mean age 36.2 ± 3.1 years; Child–Pugh C 11 ± 1.8 points; three AAH and one NASH). Systemic and splanchnic haemodynamic measurements were performed before and after each session. Plasmatic renin activity (PRA) and NE were measured at baseline, at the end of the sessions and 10 days after MARS. All patients had severe portal hypertension (HVPG = 23 ± 7 mmHg) and pronounced hyperdynamic circulation (MAP 77.8 ± 11.7 mmHg; CO 11.2 ± 1.6 L/min; SVRI 478.5 ± 105 dyne s/cm⁵). HVPG decreased at the end of the first session in all patients (23 ± 7 mmHg vs 17.3 ± 9.9 mmHg; P = 0.05; mean decrease 32 ± 24%) because of a decrease in WHVP (40.7 ± 5.6 mmHg vs 34 ± 9.6 mmHg; P = 0.025; mean decrease 18 ± 19%). MARS significantly attenuated hyperdynamic circulation as shown by a decrease in CO (11.2 ± 1.6 L/min vs 9.4 ± 2.1 L/min; mean decrease 12.3%), with an increase in MAP (77.8 ± 11.7 mmHg vs 84.2 ± 8 mmHg; mean increase 9.2%) and in SVRI (478.5 ± 105 dyne s/cm⁵ vs 622 ± 198 dyne s/cm⁵; mean increase 41%). PRA and NE decreased significantly (14.2 ± 17.2 ng/mL/h vs 3.7 ± 3.4 ng/mL/h; 1319 ± 1002 pg/mL vs 617 ± 260 pg/mL, respectively). The NE decrease was correlated to HVPG decrease (r = 1, P = 0.01). MARS decreases portal hypertension and ameliorates hyperdynamic circulation in patients with AoCLF, probably mediated by clearance of vasoactive substances. Further studies are necessary to confirm these results.     

Polymeric enteral diets as primary treatment of active Crohn's disease: a prospective steroid controlled trial.

Thirty two patients with active Crohn's disease were included in a controlled randomised trial to determine the efficacy and safety of polymeric enteral nutrition compared with steroids, to achieve and maintain clinical remission. The polymeric diet was administered through a fine bore nasogastric tube by continuous, pump assisted infusion (2800 (SEM 120) kcal/day). The steroid group received 1 mg/kg/day of prednisone. Both treatments were effective in inducing clinical remission: 15 of the 17 patients given steroids and 12 of the 15 patients assigned to the polymeric diet went into clinical remission (defined by a Van Hees index < 120) within four weeks of treatment. The percentage reduction of the Van Hees index was 34.8 (4.9)% for steroids and 32.3 (5)% for enteral nutrition (mean difference 2.5%; 95% CI--11.8% to +16.8%). Mean time elapsed to achieve remission was similar in both groups (2.0 (1) v 2.4 (1.2) weeks). Tolerance of the enteral diet was excellent. Four patients in the steroid group had mild complications attributable to this treatment. Ten patients (66.6%) in the steroid group and five (41.6%) in the enteral nutrition group relapsed within a year of discharge, but no differences were found in the cumulative probability of relapse during the follow up period. These results suggest that polymeric enteral nutrition is as safe and effective as steroids in inducing short term remission in active Crohn's disease.     

Hepatocellular carcinoma risk after viral response in hepatitis C virus-advanced fibrosis: Who to screen and for how long?

Hepatitis C virus (HCV) chronic infection is associated with fibrosis progression, end-stage liver complications and HCC. Not surprisingly, HCV infection is a leading cause of liver-related morbidity and mortality worldwide. After sustained virological response (SVR), the risk of developing hepatocellular carcinoma is not completely eliminated in patients with established cirrhosis or with advanced fibrosis. Therefore, lifelong surveillance is currently recommended. This strategy is likely not universally cost-effective and harmless, considering that not all patients with advanced fibrosis have the same risk of developing HCC. Factors related to the severity of liver disease and its potential to improve after SVR, the molecular and epigenetic changes that occur during infection and other associated comorbidities might account for different risk levels and are likely essential for identifying patients who would benefit from screening programs after SVR. Efforts to develop predictive models and risk calculators, biomarkers and genetic panels and even deep learning models to estimate the individual risk of HCC have been made in the direct-acting antiviral agents era, when thousands of patients with advanced fibrosis and cirrhosis have reached SVR. These tools could help to identify patients with very low HCC risk in whom surveillance might not be justified. In this review, factors affecting the probability of HCC development after SVR, the benefits and risks of surveillance, suggested strategies to estimate individualized HCC risk and the current evidence to recommend lifelong surveillance are discussed.     

Pneumococcal peritonitis in adult patients: report of 64 cases with special reference to emergence of antibiotic resistance

BACKGROUND: Few data are available regarding pneumococcal peritonitis. We studied the clinical characteristics of intra-abdominal infections caused by Streptococcus pneumoniae and its prognosis in relation to antibiotic resistance. METHODS: We reviewed all cases of culture-proved pneumococcal peritonitis. Patients with liver cirrhosis and primary pneumococcal peritonitis were compared with patients with Escherichia coli peritonitis. RESULTS: Between January 1, 1979, and December 31, 1998, we identified 45 cases of primary pneumococcal peritonitis in patients with cirrhosis and 19 cases of secondary (or tertiary) pneumococcal peritonitis. Patients with cirrhosis and primary pneumococcal peritonitis vs those with primary E coli peritonitis had more frequent community-acquired infection, 73% vs 47%; pneumonia, 36% vs 2%; and bacteremia, 76% vs 33%; and higher attributable mortality (early mortality), 27% vs 9% (P<.05 for all). Secondary (or tertiary) pneumococcal peritonitis was associated with upper or lower gastrointestinal tract diseases; in most cases, the infection appeared after surgery. A hematogenous spread of S pneumoniae from a respiratory tract infection might be the most important origin of peritonitis; also, S pneumoniae might directly reach the gastrointestinal tract favored by endoscopic procedures or hypochlorhydria. There was an increased prevalence of penicillin and cephalosporin resistance up to 30.7% and 17.0%, respectively, although it was not associated with increased mortality rates. CONCLUSIONS: Primary pneumococcal peritonitis in patients with cirrhosis more often spread hematogenously from the respiratory tract and was associated with early mortality. In secondary (and tertiary) pneumococcal peritonitis, a transient gastrointestinal tract colonization and inoculation during surgery might be the most important mechanisms. Current levels of resistance were not associated with increased mortality rates.     

Characteristics and antibiotic therapy of adult meningitis due to penicillin-resistant pneumococci

Of 66 episodes of pneumococcal meningitis seen in Bellvitge Hospital, Barcelona, Spain (January 1981 to June 1987), 15 (23 percent) were due to penicillin-resistant pneumococci [minimal inhibitory concentrations (MICs) of 0.1 to 4 micrograms/ml]. Fifty percent of these strains were also resistant to chloramphenicol. Most were sporadic community-acquired cases. Clinical characteristics were similar in both penicillin-resistant and penicillin-sensitive cases. Those cases with MICs of greater than 1 microgram/ml did not show a response to penicillin therapy. Of nine patients treated with cefotaxime (200 to 350 mg/kg per day) with penicillin G MICs of 0.1 to 4 micrograms/ml and cefotaxime MICs of less than or equal to 0.03 to 1 microgram/ml, seven recovered, one experienced a relapse after 14 days of therapy and the infection was cured with intravenous vancomycin, and one patient died with sterile cerebrospinal fluid. Thus, adults with meningitis due to penicillin-resistant pneumococci may be adequately treated with high doses (around 300 mg/kg per day) of intravenous cefotaxime if MICs of penicillin G are less than or equal to 4 micrograms/ml. Cases with higher resistance may require another antibiotic such as vancomycin.