Anıl Delik

By Sadık Dincer, Fatima Masume Uslu and Anil Delik

Biofilms can be found on several living and nonliving surfaces, which are formed by a group of microorganisms, complex assembly of proteins, polysaccharides, and DNAs in an extracellular polymeric matrix. By forming a biofilm, bacteria protect themselves from host defense, disinfectants, and antibiotics. Bacteria inside biofilm are much more resistant to antimicrobial agents than planktonic forms since bacteria that are unresisting to antimicrobial agents in any way can turn resistant after forming a biofilm. Low penetration of antibiotics into the biofilm, slow reproduction, and the existence of adaptive stress response constitute the multiphased defense of the bacterium. This antibiotic resistance, which is provided by biofilm, makes the treatments, which use effective antibiotic doses on the bacterium in planktonic shape, difficult. Biofilm formation potential of bacteria appears as an important virulence factor in ensuring the colonization on the living tissues or medical devices and makes the treatment difficult. The aim of this chapter is to overview the current knowledge of antimicrobial resistance mechanisms in biofilms.

Part of the book: Bacterial Biofilms

By Anıl Delik and Yakup Ülger

Chronic liver disease and decompensated cirrhosis are the major causes of morbidity and mortality in the world. According to current data, deaths due to liver cirrhosis constitute 2.4% of the total deaths worldwide. Cirrhosis is characterized by hepatocellular damage that leads to fibrosis and regenerative nodules in the liver. The most common causes of cirrhosis include alcohol consumption, hepatitis C, hepatitis B, and non-alcoholic fatty liver disease. Dysbiosis and intestinal bacterial overgrowth play a role in the development of complications of cirrhosis through translocation. In liver cirrhosis, ascites, gastrointestinal variceal bleeding, spontaneous bacterial peritonitis infection, hepatic encephalopathy, hepatorenal syndrome, hepatocelluler carcinoma are the most common complications. In addition, there are refractory ascites, hyponatremia, acute on-chronic liver failure, relative adrenal insufficiency, cirrhotic cardiomyopathy, hepatopulmonary syndrome and portopulmonary hypertension. In the primary prophylaxis of variceal bleeding, non-selective beta blockers or endoscopic variceal ligation are recommended for medium and large variceal veins. In current medical treatment, vasoactive agents, antibiotics, blood transfusion, endoscopic band ligation are the standard approach in the treatment of acute variceal bleeding. Sodium-restricted diet, diuretics and large-volume paracentesis are recommended in the management of ascites. In the treatment of hepatic encephalopathy, lactulose, branched chain amino acids, rifaximin and L-ornithine L-aspartate can be used. New therapeutic approaches such as ornithine phenyl acetate spherical carbon and fecal microbiota transplantation have shown beneficial effects on hepatic encephalopathy symptoms. In addition to their antioxidative, anti-proliferative and anti-inflammatory properties, statins have been shown to reduce the risk of decompensation and death by reducing portal pressure in compensated cirrhosis. In the treatment of liver failure, some artificial liver devices such as molecular adsorbent recirculating system, the single albumin dialysis system, fractionated plasma separation and adsorption are used until transplantation or regeneration. The purpose of this chapter is to review the most up-to-date information on liver cirrhosis and to explain the complications assessment, current management and potential treatment strategies in decompensated cirrhosis.

Part of the book: Advances in Hepatology