ABSTRACT
In summary the carbon tetrachloride/phenobarbital of cirrhosis in rats mimics human cirrhosis very closely, with development of ascites and SBP. This model shows us that bacterial overgrowth occurs as cirrhosis progresses and that bacterial translocation from the gut to extra-intestinal sites is part of the early pathogenesis of SBP. SID with norfloxacin dramatically reduced translocation and SBP at the expense of grampositive overgrowth and infection with gram-positives and colonization with strange gram negatives. SID with TMP-SMZ actually delayed development of ascites and prolonged survival.
Subject(s)
Animals , Rats , Ascites/microbiology , Liver Cirrhosis, Experimental/complications , Peritonitis/microbiology , Bacterial Translocation/physiology , Ascites/prevention & control , Liver Cirrhosis, Experimental/chemically induced , Liver Cirrhosis, Experimental/microbiology , Trimethoprim, Sulfamethoxazole Drug Combination/therapeutic use , Bacterial Physiological Phenomena , Carbon Tetrachloride Poisoning , Norfloxacin/therapeutic use , Peritonitis/prevention & control , Antibiotic Prophylaxis , Bacterial TranslocationSubject(s)
Humans , Liver Cirrhosis/microbiology , Bacterial Infections/complications , Peritonitis/microbiology , Peritonitis/drug therapy , Anti-Bacterial Agents/therapeutic use , Cefotaxime/therapeutic use , Ceftriaxone/therapeutic use , Liver Cirrhosis/complications , Escherichia coli/pathogenicity , Ascitic Fluid/microbiology , Norfloxacin/therapeutic use , Peritonitis/diagnosis , PrognosisABSTRACT
Patients with cirrhosis are regularly infected with a plethora of bacteria, fungi and mycobacteria. A high index of suspicion of infection and a low threshold for culturing, ascitic fluid, blood, urine, pleural fluid, spinal fluid, joint fluid, etc will lead to a rapid diagnosis of infection and perhaps prolong survival of these very fragile patients.