HOST FACTORS CAUSING INCREASED SUSCEPTIBILITY TO INFECTION IN PATIENTS WITH LAENNEC'S CIRRHOSIS

Infection is one of the common precipitating factors of hepatic coma in patients with cirrhosis. It is also the immediate cause of death of about of the patients with Laennec's cirrhosis.' This paper will deal with the effects of cirrhosis on host-defense mechanisms that increase the risk of infection, but it will not cover the influences of acute alcoholic intoxication on these mechanisms. The types of infections found in cirrhotics are many, but pyogenic bacterial infections as a group tend to predominate. Organisms arising from the gastrointestinal tract, such as gram-negative bacilli and anaerobes, are most common, but pneumococcal, staphylococcal, and streptococcal infections frequently occur. 1-4 Pneumonia, peritonitis, bacteremia, and pyelonephritis are the most common sites of these infections. The facets of the host-defense mechanisms that appear to be most important in preventing pyogenic infections are (1) the reticuloendothelial system (fixed macrophages), (2) antibodies, (3) complement, and (4) neutrophilic granulocytes. The major steps in the prevention of pyogenic infections are the phagocytosis of bacteria by granulocytes and fixed macrophages and the subsequent intracellular killing of these organisms. The serum factors primarily serve to facilitate these activities. Current knowledge about the functional capacity of these systems in cirrhotics will be reviewed individually. The reticuloendothelial system is important for clearing organisms from the blood that enter from the gastrointestinal tract, lungs, skin, and other sites. Since the liver is the major organ of the reticuloendothelial system, it would not be surprising if function were abnormal in cirrhotic patients. In a study of cirrhotic rats, Rutenberg et al.,5 demonstrated that intravenously injected bacteria were normally cleared from the blood; however, there was a delay in bacterial killing in these animals. As cirrhosis progresses, additional difficulty probably results from shunting of blood around the cirrhotic liver and thereby bypassing this very important reticuloendothelial organ. Antibodies function as opsonins to facilitate phagocytosis of bacteria by granulocytes and to initiate the inflammatory process that ultimately limits and controls the infection. The antibody-forming ability of the cirrhotic does not appear to be deficient and may even be greater than normal. Cirrhotic patients commonly have a polyclonal hypergammaglobulinemia.6 Triger et al.' found increased levels of antibodies to E. coli in patients with liver disease; however, the antibody levels t o Hemophilus influenzae were within the normal range. They concluded that patients with liver disease are unable to degrade the antigen from bacterial products that arise in the gastrointestinal tract and consequently make antibodies to this increased level of bacterial antigen. Since Hemophilus influenzae is not a normal inhabitant of the gastrointestinal tract, it would not be ex-