Diagnosis of Hepatic Disease by Presenting Sign
Abdominal Pain
Pressure on the liver capsule from parenchymal swelling, such as occurs in acute diffuse hepatitis or trauma to the capsule itself, can cause liver-associated pain.
If severe, the animal may adopt a guarded, tucked-up stance with an arched back and be reluctant to move. This, of course, can also occur as a result of non-hepatic causes of abdominal pain, so pain must be localized to the liver by palpation over the right anterior ventrolateral aspect of the abdomen and the last few ribs. The most commonly reported causes of hepatic pain in goats are the acute forms of liver fluke disease and acute toxic hepatitis.Anemia
Liver-associated causes of anemia are limited to the parasitic diseases, chronic copper toxicosis, and some experimentally induced plant poisonings. In acute liver fluke disease, the cause of anemia is severe hemorrhage into the peritoneal cavity associated with large numbers of larvae penetrating the liver capsule. In chronic fascioliasis, the anemia is caused by mechanical trauma and feeding activity of adult Fasciola spp. within the biliary tree, resulting in continuous blood loss. Anemia is accompanied by hypoproteinemia in these chronic cases.
Anorexia
Loss of appetite is a consistent finding in diffuse liver disease, but is non-specific.
Ascites and/or Edema
Hypoproteinemia is a common outcome of chronic liver disease and the most common clinical manifestation of liver-related hypoproteinemia is intermandibular edema, often seen in chronic liver fluke disease. However, non- hepatic causes of hypoproteinemia, most notably gastrointestinal helminthiasis, also produce the same sign.
Generalized ascites as a result of caprine liver disease is uncommon. One exception is a disease known as “waterpens” or “water belly,” seen in goats and sheep in South Africa grazing the plant Galenia africana (kraalbos).
At necropsy, there is severe ascites and evidence of liver and cardiac disease. It is unclear if ascites is caused by a primary cardiac or primary hepatic abnormality (van der Lugt et al. 1988). Experimental challenge studies with toxic plant extracts indicate that the hepatic lesions precede the cardiac lesions in the development of the condition (van der Lugt et al. 1992).In Texas, consumption of the range plant Sartwellia flaveriae by Angora goats leads to marked ascites, abdominal distension, and weight loss associated with hepatic cirrhosis (Mathews 1940b). Although a rare occurrence, bile duct carcinoma has also been reported as a cause of ascites in a goat in India (Chauhan and Singh 1969).
Bleeding Tendency
Coagulopathies are uncommon in goats and are rarely associated with liver problems. Only three reported instances of prolonged clotting time in goats have been associated with hepatic disease (Bassir and Bababunmi 1972; Saad et al. 1972; Jones and Shah 1982).
Diarrhea and Constipation
Diarrhea can occur in chronic fascioliasis. Diarrhea occurs in hepatotoxic plant poisonings, but concurrent enteritis also may be responsible for the diarrhea. Constipation is characteristic of Lantana poisoning in goats and other ruminants.
Alternating diarrhea and constipation have been associated with liver disease in large animals due to decreases in bile salt excretion and reflex intestinal activity associated with liver distension. This pattern is not well documented in goats with hepatitis.
Jaundice (Icterus)
Hyperbilirubinemia caused by obstructive biliary conditions is rare in goats. Jaundice is most likely to result from hemolytic anemia and primarily involves increases in indirect unconjugated bilirubin. Table 7.6 lists the causes of anemia in goats and identifies which may be associated with jaundice. Chronic copper poisoning produces both liver damage and hemolytic anemia with resultant jaundice, but the condition is rare in goats, which are much more tolerant of copper than sheep.
The plant Acanthospermum hispidum, native to Central and South America but now distributed widely around the world, also produces both hepatic necrosis and hemolytic anemia in goats (Ali and Adam 1978).No cases have been reported of complete, extrahepatic biliary obstruction in goats. Nonhemolytic jaundice may occur in Rift Valley fever (RVF) and Wesselsbron disease in Africa, and has been reported sporadically in goats in association with other diverse causes, including aflatoxicosis (Wanasinghe 1974), suspect halothane toxicity (O'Brien et al. 1986), sawfly larvae poisoning (Thamsborg et al. 1987), hepatic fibrosarcoma (Higgins et al. 1985), and consumption of the plants sacahuiste (Nolina texana) in Texas (Mathews 1940a) and signal grass (Brachiaria decumbens) in Malaysia and Nigeria (Mazni et al. 1985; Opasina 1985). In general, the occurrence of jaundice in caprine liver disease carries an unfavorable prognosis.
Neurologic Signs
Altered states of mentation and other neurologic signs are often seen in goats with diffuse liver disease and are associated with disruptions in normal liver metabolism. The pathogenesis of this hepatoencephalopathy is not completely understood, but is presumed to be multifactorial. There is general consensus that ammonia plays a key role, especially since therapeutic interventions that decrease blood and cerebrospinal fluid ammonia levels usually mitigate the neurologic signs associated with hepatic encephalopathy (Katayama 2004).
Clinical presentations associated with hepatoencepha- lopathy range from signs of hypoexcitability, including depression, head pressing, generalized weakness, ataxia, and coma, to signs of hyperexcitability, such as hyperesthesia, muscle tremors, and convulsions. In a series of 11 cases of hepatoencephalopathy in young goats associated with congenital portosystemic shunts, the most common clinical signs were ataxia, blindness, tremors, head bobbing, head pressing, seizures, circling, weakness, and ill-thrift (Kinde et al.
2014). Young goats experimentally infected with the gastrointestinal parasite Strongyloides papillosus developed hepatosis and showed signs consistent with hepatoencephalopathy, such as ataxia, a wide-based stance, stupor, nystagmus, and head pressing. As lesions were also found in the brain, all the signs could not be attributed to hepatoencephalopathy. However, liver involvement was significant in these experimental infections, as rupture of the liver with sudden death occurred in 6% of the challenged goats (Pienaar et al. 1999).While all the causes of diffuse liver disease in goats have the potential to produce neurologic signs, the most common causes are pregnancy toxemia and toxic hepatitis. The known causes of toxic hepatitis in goats are discussed later in this chapter.
Non-hepatic causes of neurologic signs are numerous in goats and must be differentiated from hepatoencephalopa- thy. Primary neurologic diseases are discussed in Chapter 5.
Photodermatitis
Hepatic or secondary photosensitization occurs in goats. Signs of photosensitization are varied and include uneasiness and pruritus with much scratching and rubbing activity, severe dermatitis with erythema, extensive subcutaneous edema, and eventual ulceration and sloughing of skin. Ophthalmia with excessive lacrimation, photophobia, and corneal cloudiness may also occur. The dermatitis and edema are particularly evident on the head and ears. In some outbreaks, jaundice is seen in conjunction with signs of photodermatitis. Secondary blindness, pyoderma, loss of body condition, and occasional deaths are possible sequelae. Light-colored animals are more severely affected.
Photosensitization associated with hepatotoxicity has been reported in goats consuming a variety of plants around the world, including sacahuiste weed (N. texana) (Mathews 1940a), green oats (Avena sativa) and wheat (Schmidt 1931), lechuguilla (Agave Iecheguilla) (Mathews 1937), and kleingrass (Panicum coloratum) (Bailey 1986) in the United States; signal grass (B.
decumbens) in Malaysia and Nigeria (Mazni et al. 1985; Opasina 1985); caltrop (Tribulus terrestris) in South Africa (Kellerman et al. 1980); and caltrop, boobiala tree (Myoporum tetrandrum), and Ellangowan poison bush (Myoporum deserti) in Australia (Allen et al. 1978; Glastonbury and Boal 1985; Jacob and Peet 1987). Additional details are given in the discussion of toxic hepatitis at the end of this chapter. Primary, non-hepatic photodermatitis also occurs in goats and must be differentiated from the hepatic form. It is discussed in Chapter 2.Weight Loss
Chronic liver fluke disease is important in the differential diagnosis for wasting in goats. Weight loss may be the only sign associated with liver abscesses. It is one of many signs associated with a wide range of hepatotoxic plants that cause prolonged hepatic insufficiency.
Yawning
Occasional yawning in goats is normal. Repeated yawning may suggest liver disease in goats as in other species, although the causal relationship is not clear. Goats with pregnancy toxemia or other causes of hepatic lipidosis are most likely to exhibit repeated yawning.