Vascular seeding, most often through the portal system via the gastrointestinal tract
Direct invasion, from an adjacent source (e.g., bacterial cholecystitis)
Bacteria that may establish an infection in the liver via the blood include Staphylococcus aureus in toxic shock syndrome, Salmonella typhi in typhoid fever, and Treponema pallidum in secondary or tertiary syphilis. Ascending infections are most common in the setting of partial or complete biliary tract obstruction and are typically caused by gut flora, which may colonize the static bile in the ducts. Whatever the source of the bacteria, with pyogenic organisms intrahepatic abscesses may develop, producing fever, right upper-quadrant pain, and tender hepatomegaly. Although antibiotic therapy may sterilize small abscesses, surgical drainage is often necessary for larger lesions. More commonly, extrahepatic bacterial infections, particularly sepsis, induce mild hepatic inflammation and varying degrees of hepatocellular cholestasis indirectly, without establishing an infectious nidus in the liver.
Other non-viral infectious agents cause liver disease with important or unusual pathogenic features that merit specific comment. These include the following: • Schistosomiasis, most commonly found in Asia, Africa, and South America, is one of the most common causes of noncirrhotic portal hypertension worldwide. Adult worms in the gut produce numerous eggs, some of which find their way into the portal circulation, where they lodge and induce a granulomatous reaction associated with marked fibrosis.
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Entamoeba histolytica, an important cause of dysentery (Chapter 15), sometimes ascends to the liver through portal circulation and produces secondary foci of infection that can progress to large necrotic areas called amebic liver abscesses. Amebic abscesses are more common in the right lobe of the liver. The abscess cavity contains necrotic liver cells, but unlike pyogenic abscesses, neutrophils are absent.
Liver fluke infection, most common in Southeast Asia, is associated with a high rate of cholangiocarcinoma. Responsible organisms include Fasciola hepatica, Opisthorcis species, and Clonorchis sinensis.
Echinococcal infections may cause the formation of intrahepatic hydatid cysts that produce symptoms due to pressure on surrounding structures or following rupture.
Autoimmune hepatitis is a chronic, progressive hepatitis with all the features of autoimmune diseases in general: genetic predisposition, association with other autoimmune diseases, the presence of autoantibodies, and therapeutic response to immunosuppression.
Risk for autoimmune hepatitis is associated with certain HLA alleles, such as the DRB1* allele in Caucasians, but as in other autoimmune disorders the mechanistic basis for this relationship is unclear. Triggers for the immune reaction may include viral infections or drug or toxin exposures.
The annual incidence is highest among white northern Europeans at 1.9 in 100,000, but all ethnic groups are susceptible. There is a female predominance (78%). Autoimmune hepatitis is classified into two types, based on the patterns of circulating antibodies.
Type 1, more common in middle-age and older individuals, is characterized by the presence of antinuclear (ANA), anti–smooth muscle actin (SMA), antimitochondrial (AMA), and anti–soluble liver antigen/ liver-pancreas antigen (anti-SLA/LP) antibodies.
Type 2, usually seen in children and teenagers, is chararcterized by the presence of anti–liver kidney microsome-1 antibodies and anti–liver cytosol-1 antibodies.