Spontaneous bacterial peritonitis (SBP) is a common complication of cirrhosis. Based on our current understanding of SBP, the most common etiologies for SBP in cirrhosis are Enterobacter and Streptococcal species. Th e Aeromonas species are ubiquitous in fresh or sea water. Aeromonas caviae is never identified as etiology in cases of SBP. A patient, who had a history of liver cirrhosis related to chronic hepatitis B virus infection for 1 year, presented with diarrhea. He had diarrhea 1 week later returned from coastal city. He was hospitalized and treated with norfloxacin after 7 days of severe symptoms, including fever, abdominal distention, and diarrhea. Analysis of the ascitic specimen revealed a white-cell count of 4.42 × 109 cells/L with 88% neutrophils. Analysis of stool specimen showed a white-cell count of 60 cells per high-power field. Th e patient started the injection of cefriaxone at a dose of 4 g/d. However, the situation was not improved. Th ree days later, stool and ascitic fluid culture showed positive for Aeromonas caviae. Antibiotic susceptibility testing revealed that imipenem, meropenem, amikacin, and cefoperazone-sulbactam were highly sensitive to the Aeromonas caviae. However, the bacilli resisted to ceftriaxone, ceftazidime, ampicillin-sulbactam, levofloxacin, and sulfamethoxazole. Ceftriaxone was then switched to imipenem. The patient was fully recovered 14 days later. Aeromonas caviae is a rare pathogen of SBP in cirrhosis. It resists to third-generation of cephalosporin and fluroquinolone, which are of frequently used dependent on clinical experience. It needs a special attention.
Aeromonas caviae ; Anti-Infective Agents ; Ascitic Fluid ; Gram-Negative Bacterial Infections ; pathology ; Humans ; Leukocyte Count ; Liver Cirrhosis ; Male ; Microbial Sensitivity Tests ; Peritonitis ; microbiology ; pathology

ObjectiveTo investigate the incidence rate of primary liver cancer （PLC） and the progression of liver fibrosis in chronic hepatitis B （CHB） patients with low-level viremia （LLV） （HBV DNA<2 000 IU/mL but ≥20 IU/mL） after treatment adjustment， and to provide more robust evidence for clinical practice. MethodsA retrospective analysis was performed for the clinical data of LLV patients who initially received nucleos（t）ide analogue （NAs） for at least 48 weeks at the Fifth Medical Center of PLA General Hospital from August 2007 to April 2017 and subsequently underwent NAs adjustment due to LLV， and according to the virologic response after 48 weeks of treatment adjustment， the patients were divided into LLV group and complete virological response （CVR） group （HBV DNA<20 IU/mL）. The patients were followed up once every 3‍ ‍—‍ ‍6 months till the primary endpoint event of PLC or October 2024. The incidence rate of PLC and the progression of liver fibrosis were observed， and the progression of liver fibrosis was defined as an increase of ≥1 grade in fibrosis-4 （FIB-4） index. The independent-samples t test was used for comparison of normally distributed continuous data between two groups， and the Mann-Whitney U test was used for comparison of continuous data with skewed distribution between two groups； the chi-square test was used for comparison of categorical data between groups. The Kaplan-Meier method was used to calculate the cumulative incidence rate of PLC， and the Log-rank test was used for comparison between groups； the Cox regression analysis was used to investigate the risk factors for PLC， and the Logistic regression analysis was used to investigate the influencing factors for the progression of liver fibrosis. ResultsA total of 307 patients were enrolled， with a mean age of 50.0 years， and the male patients accounted for 80.5%. After 48 weeks of treatment with the adjusted NAs regimen， 254 patients （82.7%） achieved CVR， and 53 patients （17.3%） still had LLV. For the LLV group， the incidence rate of PLC was 30.2% and the rate of liver fibrosis progression was 22.6%， while for the CVR group， the incidence rate of PLC was only 13.4%， and the rate of liver fibrosis progression was 7.5%. The multivariate regression analyses showed that LLV was an independent risk factor for the onset of PLC （hazard ratio=2.623， 95% confidence interval ［CI］： 1.315‍ ‍—‍ ‍5.234， P=0.006） and the progression of liver fibrosis （odds ratio=3.213， 95%CI： 1.385‍ ‍—‍ ‍7.455， P=0.007）. ConclusionActive adjustment of treatment is needed immediately after the diagnosis of LLV to improve CVR， and if LLV persists after treatment adjustment， it is necessary to enhance the monitoring of liver fibrosis progression and PLC， so as to facilitate early diagnosis and treatment.