Epidemiology

The morbidity of BH varies between 0.25% and 12%, but the lethality can reach 80% to 100%. The geographic distribution of the disease is dependent both on the soil characteristics and on the presence of liver flukes. In most cases, BH occurs sporadically, but it may be endemic in areas where fascioliasis abounds. Therefore, the main determining factor for the incidence of the disease is the number of liver fluke metacercariae present on pastures where animals graze.

BH may occur at any time during the year, but most cases occur in summer and early fall. Dry weather conditions may induce animals to concentrate on portions of the pastures infested with liver flukes, including areas surrounding small ponds, drains, dams, swamps, and other bodies of water, thus being exposed to an increased intake of metacercariae. For these reasons, the disease is far more frequently seen on pasture-grazing cattle rather than in intensively reared animals. BH occurs mostly in animals older than 1 year, although cases can occasionally be seen in younger animals. Affected animals are usually in good nutritional condition and BH is most frequently seen in animals recently introduced to an infected area. No apparent sex or breed predisposition has been determined. Clinically healthy animals may eliminate spores through feces and urine, thus contaminating pastures. The movement of flood or drainage water may also spread the microorganism, and decomposing carcasses of dead animals due to BH represent a potential additional source of infection.

Pathogenesis

The spores of C. haemolyticum are found in soil, where they are very resistant to environmental conditions and can survive for several years, especially in poorly drained pastures with alkaline water pH, usually 8.0 or higher. Spores are ingested by animals and absorbed from the intestine into the bloodstream, reaching the liver via portal circulation. It is thought that in the liver, the spores are phagocytized by Kupffer cells, in the cytoplasm of which they can survive for long periods of time. Spores of C. haemolyticum have also been found in the intestine, kidney, and bone marrow of healthy cattle.

In the great majority of cases, BH occurs after initiating hepatic damage largely attributable to liver flukes, mainly Fasciola hepatica, although other trematodes including Fascioloides magna and Dicrocoelium dendriticum may also be involved. When immature forms of liver flukes penetrate into the liver, the necrosis and hemorrhage associated with migration create the anaerobic conditions allowing for spore germination and bacterial multiplication, with consequent production of toxins. Large quantities of beta toxin result in hemolysis. In addition, activation of the arachidonic acid cascade, production of thromboxane and leukotrienes, platelet aggregation, and increase in capillary permeability are thought to be consequences of the action of beta toxin. Both hepatocyte necrosis and thrombus formation due to endothelial disruption contribute to the development of a large focus of coagulative necrosis. This focus is probably a consequence of both ischemia related to thrombosis and of the direct action of beta toxin on the hepatocytes. Hemolysis results in hemoglobinuria and jaundice, two of the main clinical features of the disease, and in severe hypoxia that leads to hemoglobinuric nephrosis.

Sporadically, BH occurs in animals free from liver flukes. In those cases, the initial germination of the spores of C. haemolyticum has been suggested to be associated with a variety of insults, including Fusobacterium necrophorum and Cysticercus tenuicollis infection, liver biopsies, telangiectasia, metabolic disturbances, and reduced hepatic blood circulation associated with pressure of the pregnant uterus against the liver. However, the role of these predisposing factors in the development of BH has not been definitively determined.

Clinical signs

Most clinical signs of BH in cattle are a consequence of the severe hemolytic anemia characteristic of this condition, which may be acute or sub-acute. In range farming conditions, animals may be found dead without clinical signs having been observed. The clinical course in the acute form of the disease lasts between 10 and 12 hours, whereas the clinical course in sub-acute cases may last 3 to 4 days. The latter is less common. Both forms of BH are clinically characterized by hemoglobinuria, jaundice, and high initial fever (40–41 °C) which drops rapidly just before death. Animals become lethargic and there is an abrupt decrease in rumination, milk production, and defecation, increased heart rate, severe dyspnea, and blood in the feces. Hematological changes are characterized by a marked reduction in hematocrit, red blood cell count, and hemoglobin concentration, accompanied by initial leukocytosis. The latter reverts quickly into leukopenia as a consequence of the severe toxemia. Death results from severe hemolysis-associated anoxia and toxemia.

Clinical signs in other species are essentially similar to those seen in cattle.

Gross changes

Carcasses of animals dying of BH present with dehydration, varying degrees of jaundice, and the perineal region and tail soiled with dark, liquid feces. The subcutaneous tissue is diffusely edematous and presents widespread multifocal petechiae and ecchymoses, which also extend to the fascia and muscles. In the great majority of cases of BH, a large and usually single area of necrosis delimited by a hyperemic rim, frequently visible on the diaphragmatic surface of the liver (Figure 22.1), is considered a pathognomonic finding. Less frequently, additional smaller foci of necrosis may also be present around the main lesion or widespread in the liver parenchyma. The foci of necrosis are usually pale and roughly conical with their base on the surface of the liver (Figure 22.2

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