INTRODUCTION

Hepatitis is defined as any inflammatory cell infiltrate within the hepatic parenchyma, and the term cholangiohepatitis describes extension of that inflammation to include the intrahepatic bile ducts.¹ A diagnosis of these conditions is based on histopathologic examination of hepatic biopsy specimens. The histopathologic appearance will give clues as to the duration of the inflammation. Acute hepatitis is characterized by a combination of inflammation, hepatocellular apoptosis, necrosis, and possibly regeneration, but there is a lack of fibrosis. Chronic hepatitis (CH), on the other hand, is identified by the presence of fibrosis, proliferation of ductular structures, and regenerative nodules in addition to the inflammatory infiltrate.² The type of inflammatory cellular infiltrate may give the clinician some clues regarding the etiology. Occasionally, etiologic agents will be identified within biopsy specimens. However, the etiology remains unknown for many cases of hepatitis and cholangiohepatitis in dogs and cats. This chapter will discuss the clinical presentation of animals with hepatitis and cholangiohepatitis and outline the most commonly recognized clinical syndromes with respect to diagnosis and treatment of the specific disease. Effective treatment of patients with hepatitis or cholangiohepatitis includes specific therapy of any identified inciting cause and aggressive symptomatic and supportive therapy. A discussion of symptomatic treatment and supportive therapy for the sequelae of hepatitis and cholangiohepatitis can be found in Chapter 127, Hepatic Failure.

HISTORICAL FINDINGS

In general, the historical findings associated with hepatitis are nonspecific, as with most types of liver disease. Exposure to certain etiologic agents or toxins may be ascertained from the owner and history and thus raise the suspicion for hepatic involvement. It is important to remember that because of the large reserve capacity of the liver, a short duration of clinical signs does not necessarily indicate acute disease. Animals with CH may not show outward clinical signs until a significant portion of their hepatic function is affected. Presenting owner complaints for animals with hepatitis may include vomiting, diarrhea, anorexia, lethargy, polyuria, polydipsia, abdominal distention, dysuria, neurologic abnormalities associated with hepatic encephalopathy or vascular accidents, and icterus.

PHYSICAL EXAMINATION FINDINGS

Similar to historical findings, the physical examination findings in animals with hepatitis are often nonspecific. Icterus, when present in the absence of hemolytic anemia, suggests disease of the hepatic parenchyma or extrahepatic biliary system. Animals with acute hepatitis are more likely to have fever and abdominal pain, and those with CH are more likely to have ascites. Hepatomegaly may be present in some patients, especially those with acute hepatitis. Many animals with hepatitis will not have any of these physical abnormalities present on the initial examination, and serum biochemical changes in those cases are likely to direct the clinician toward the liver as the site of disease.

MECHANISMS OF HEPATOCELLULAR INJURY

The pathogenesis whereby hepatitis and cholangiohepatitis lead to hepatocellular necrosis and apoptosis is incompletely understood. Experimental studies have suggested many mechanisms of hepatocellular injury, but their specific evaluation in dogs and cats with hepatitis is lacking. Mechanisms of hepatocellular injury that are not specific to hepatitis include tissue hypoxia, lipid peroxidation, intracellular cofactor depletion, intracellular toxin production, cholestatic injury, endotoxic insults, and hepatocyte plasma membrane injury.³

Hepatocytes are especially susceptible to anoxia because the liver receives a mixture of venous and arterial blood. Hypoxic damage quickly leads to plasma membrane and cytosolic organelle injury secondary to adenosine triphosphate (ATP) depletion. Free radicals may cause oxidative cellular injury that can result in lipid peroxidation and subsequent plasma membrane damage.

Cellular toxins may bind to nucleic acids and inhibit protein synthesis. Cholestasis causes retention of bile acids that directly damage cellular organelles. Endotoxins work via various mechanisms, most of which involve stimulation of inflammatory cells to produce inflammatory mediators (cytokines such as prostaglandins and leukotrienes) that perpetuate hepatitis. Experimental work in mouse models suggests an important role for tumor necrosis factor-alpha (TNF-α) in the initiation and perpetuation of hepatitis. TNF-α, production of which is induced by the interaction of the costimulatory molecules CD154 on T cells and CD40 on hepatocytes and Kupffer cells, stimulates hepatocyte apoptosis through the Fas-Fas ligand pathway.⁴ A better understanding of the complex mechanisms of hepatocellular injury in animals with hepatitis may encourage the development of novel therapeutic modalities for affected patients.

CAUSES OF HEPATITIS AND CHOLANGIOHEPATITIS IN DOGS AND CATS

Box 126-1 lists the reported causes of hepatitis and cholangiohepatitis in dogs and cats. A complete discussion of all disease entities is beyond the scope of this chapter. A discussion of the most common clinical syndromes follows.

Box 126-1 Causes of Hepatitis and Cholangiohepatitis in Dogs and Cats

Idiopathic

Canine chronic hepatitis

Feline cholangitis-cholangiohepatitis complex

Nonspecific reactive hepatitis

Lobular dissecting hepatitis

Viral

Infectious canine hepatitis (adenovirus type I)

Acidophil cell hepatitis

Herpesvirus (neonates)

Feline infectious peritonitis

Bacterial

Feline cholangitis-cholangiohepatitis complex

Leptospirosis

Bartonellosis

Tyzzers disease (Clostridium piliformis)

Salmonellosis

Listeriosis

Tularemia

Brucellosis

Yersiniosis

Helicobacter spp

Mycobacteria

Septicemia

Rickettsial

Ehrlichiosis

Rocky Mountain spotted fever

Protozoal

Toxoplasmosis

Neosporosis

Leishmaniasis

Cytauxzoonosis

Hepatozoonosis

Schistosomiasis

Coccidiosis

Parasitic

Visceral larval migrans

Dirofilariasis (caudal vena caval syndrome)

Liver fluke migration

Fungal

Histoplasmosis

Blastomycosis

Coccidioidomycosis

Aspergillosis (disseminated)

Phycomycosis

Algal

Protothecosis

Select Drugs and Toxins

Amiodarone

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