[Effects of SARS-CoV-2 Infection on Symptoms and Therapy of Inflammatory Bowel Disease]. / Auswirkungen einer SARS-CoV-2-Infektion auf Symptomatik und Therapie chronisch-entzündlicher Darmerkrankungen.

INTRODUCTION: The influence of a SARS-CoV-2 infection on inflammatory bowel disease (IBD) has not yet been well characterized and it is unclear whether this requires an adaptation of the immunosuppressive therapy. METHODS: A national register was established for the retrospective documentation of clinical parameters and changes in immunosuppressive therapy in SARS-CoV-2 infected IBD patients. RESULTS: In total, only 3 of 185 IBD patients (1.6 %) were tested for SARS-CoV-2 infection because of abdominal symptoms. In the course of COVID-19 disease, 43.5 % developed diarrhea, abdominal pain or hematochezia (risk of hospitalization with vs. without abdominal symptoms: 20.0 % vs. 10.6 %, p < 0.01). With active IBD at the time of SARS-CoV-2 detection, there was an increased risk of hospitalization (remission 11.2 %, active IBD 23.3 % p < 0.05). IBD-specific therapy remained unchanged in 115 patients (71.4 %); the most common change was an interruption of systemic therapy (16.2 %). DISCUSSION: New abdominal symptoms often appeared in SARS-CoV-2 infected IBD patients. However, these only rarely led to SARS-CoV-2 testing. A high IBD activity at the time of SARS-CoV-2 detection was associated with an increased risk of hospitalization.

Microevolution of the chromosomal region of acute disease antigen A (adaA) in the query (Q) fever agent Coxiella burnetii.

The acute disease antigen A (adaA) gene is believed to be associated with Coxiella burnetii strains causing acute Q fever. The detailed analysis of the adaA genomic region of 23 human- and 86 animal-derived C. burnetii isolates presented in this study reveals a much more polymorphic appearance and distribution of the adaA gene, resulting in a classification of C. burnetii strains of better differentiation than previously anticipated. Three different genomic variants of the adaA gene were identified which could be detected in isolates from acute and chronic patients, rendering the association of adaA positive strains with acute Q fever disease disputable. In addition, all adaA positive strains in humans and animals showed the occurrence of the QpH1 plasmid. All adaA positive isolates of acute human patients except one showed a distinct SNP variation at position 431, also predominant in sheep strains, which correlates well with the observation that sheep are a major source of human infection. Furthermore, the phylogenetic analysis of the adaA gene revealed three deletion events and supported the hypothesis that strain Dugway 5J108-111 might be the ancestor of all known C. burnetii strains. Based on our findings, we could confirm the QpDV group and we were able to define a new genotypic cluster. The adaA gene polymorphisms shown here improve molecular typing of Q fever, and give new insights into microevolutionary adaption processes in C. burnetii.

Paenibacillus larvae Bacteremia in injection drug users.

Paenibacillus larvae causes American foulbrood in honey bees. We describe P. larvae bacteremia in 5 injection drug users who had self-injected honey-prepared methadone proven to contain P. larvae spores. That such preparations may be contaminated with spores of this organism is not well known among pharmacists, physicians, and addicts.

Nosocomial acquisition of dengue.

Recent transmission of dengue viruses has increased in tropical and subtropical areas and in industrialized countries because of international travel. We describe a case of nosocomial transmission of dengue virus in Germany by a needlestick injury. Diagnosis was made by TaqMan reverse transcription-polymerase chain reaction when serologic studies were negative.

Small intestinal bacterial overgrowth in human cirrhosis is associated with systemic endotoxemia.

OBJECTIVES: Systemic endotoxemia has been implicated in various pathophysiological sequelae of chronic liver disease. One of its potential causes is increased intestinal absorption of endotoxin. We therefore examined the association of small intestinal bacterial overgrowth with systemic endotoxemia in patients with cirrhosis. METHODS: Fifty-three consecutive patients with cirrhosis (Child-Pugh group A, 23; group B, 18; group C, 12) were included. Jejunal secretions were cultivated quantitatively and systemic endotoxemia determined by the chromogenic Limulus amoebocyte assay. Patients were followed up for 1 yr. RESULTS: Small intestinal bacterial overgrowth, defined as > or = 10(5) total colony forming units per milliliter of jejunal secretions, was present in 59% of patients and strongly associated with acid suppressive therapy. The mean plasma endotoxin level was 0.86 +/- 0.48 endotoxin units/ml (range = 0.03-1.44) and was significantly associated with small intestinal bacterial overgrowth (0.99 vs 0.60 endotoxin units/ml, p = 0.03). During the 1-yr follow-up, seven patients were lost to follow up or underwent liver transplantation and 12 patients died. Multivariate Cox regression showed Child-Pugh group to be the only predictor for survival. CONCLUSIONS: Small intestinal bacterial overgrowth in cirrhotic patients is common and associated with systemic endotoxemia. The clinical relevance of this association remains to be defined.

Daily norfloxacin is more effective than weekly rufloxacin in prevention of spontaneous bacterial peritonitis recurrence.

Our aim was to compare weekly rufloxacin with daily norfloxacin in the secondary prophylaxis of spontaneous bacterial peritonitis and to examine changes in antibiotic susceptibility in fecal Escherichia coli. The method used was an open randomized clinical trial including 79 patients who received either norfloxacin 400 mg/day or rufloxacin 400 mg/week and followed up for one year. E. coli counts, quinolone susceptibility, and drug concentrations in feces were investigated in 12 patients. Cumulative one-year probability of peritonitis recurrence was 26% for patients on norfloxacin and 36% for those on rufloxacin (P = 0.16). Norfloxacin was more effective in the prevention of peritonitis recurrence due to Enterobacteriaceae (0% vs 22%, P = .01). At the end of follow-up, all 12 patients had E. coli resistant to quinolones in their feces. In conclusion, weekly rufloxacin is not an alternative to daily norfloxacin in the prevention of peritonitis recurrence. The development of quinolone-resistant E. coli in feces may be an important problem in patients on long-term quinolone prophylaxis.

Failure of Lactobacillus spp. to prevent bacterial translocation in a rat model of experimental cirrhosis.

BACKGROUND/AIMS: Prophylaxis of spontaneous bacterial peritonitis in cirrhotic patients with norfloxacin is associated with emergence of quinolone-resistant Enterobacteriaceae. We investigated whether an alternative strategy with Lactobacillus prevents bacterial translocation and ascitic fluid infection in cirrhotic rats. METHODS: CCl(4)-induced cirrhotic rats with ascites (n=34) were allocated to treatment with oral Lactobacillus strain GG at 1-2 x 10(9) cfu/day for 8-10 days (group LGG) or milk (group MILK). In addition, 20 cirrhotic rats were given a single dose of 15 mg norfloxacin orally and then allocated to Lactobacillus (group NOR-LGG) or milk (group NOR-MILK). Ten healthy rats served as control. After sacrifice the cecal flora were analyzed and the prevalence of bacterial translocation and ascitic fluid infection assessed. RESULTS: Cecal colonization with Lactobacillus was achieved in 90% of treated rats. The prevalence of bacterial translocation to mesenteric lymph nodes was 10% in control rats and 93, 84, 70 and 100% in groups MILK, LGG, NOR-MILK and NOR-LGG, respectively (P>0.1 for comparison of treatment groups), the prevalence of ascitic fluid infection was 60, 32, 40 and 40% (P>0.1). Bacterial translocation of Lactobacillus was observed in 24% of rats treated. CONCLUSION: Lactobacilli fail to prevent bacterial translocation and ascitic fluid infection in experimental cirrhosis in spite of successful intestinal colonization.