8 Francisco A. Uzal Clostridium perfringens type A is frequently associated with enteric disease of poultry, ruminants, horses, pigs, dogs, and other species. However, while the role of this microorganism in avian necrotic enteritis is beyond doubt, with a few exceptions mentioned in this section, there is very little evidence supporting a role for C. perfringens type A in the pathogenesis of enteric disease of mammals. Type A strains producing NetF, a newly discovered toxin, seem to be strongly associated with canine hemorrhagic gastroenteritis (Chapter 9). A small percentage of C. perfringens type A strains producing enterotoxin (CPE) are responsible for highly prevalent food poisoning and antibiotic-associated diarrhea in humans. CPE-positive strains may also be associated with enteric disease in other mammalian species. Yellow lamb disease is a rare disease of sheep for which only a few references exist. The condition has been reported in the US and Europe, and anecdotal evidence indicates that a few cases may have been diagnosed in South America. Because C. perfringens type A is the most ubiquitous of all C. perfringens strains, and since it is found in the intestines of most clinically healthy mammals, diagnosis of yellow lamb disease is challenging; the mere isolation of this microorganism is of no diagnostic significance. Because of this, the occurrence of this disease may be underestimated. Yellow lamb disease has traditionally been associated with strains of C. perfringens type A that produce high levels of alpha toxin (CPA). Recently, however, an outbreak of what was thought to be yellow lamb disease was reported in lambs infected by a strain of C. perfringens type D that produced an unusually high amount of CPA. This toxin is a hemolytic lecithinase (phospholipase), which is consistent with the severe hemolysis and jaundice in yellow lamb disease. Because of the similarity in clinical signs and lesions, both type A and type D-associated yellow lamb disease are discussed in this section. Information on the epidemiology of yellow lamb disease is very scant. Factors predisposing to C. perfringens type D enterotoxemia (that is, sudden changes in diet to foods rich in carbohydrates) are also thought to predispose yellow lamb disease. Definitive evidence that this is the case is, however, lacking. The most common clinical manifestations of yellow lamb disease are depression, anemia, icterus, and hemoglobinuria. Sudden death has occasionally been described. The cases of yellow lamb disease associated with C. perfringens type D were characterized by similar clinical signs plus abdominal pain, trembling, and tachycardia. Lethality in both forms of the disease has been reported to be close to 100%. Necropsy findings in yellow lamb disease are not specific and may be compatible with several other diseases. The most frequently described gross findings include generalized icterus (Figure 8.1), red urine in the bladder, enlarged, pale, and friable spleen, enlarged liver with an acinar pattern, and dark, swollen kidneys. Cases of type D-associated yellow lamb disease presented, in addition, serosanguineous fluid free in body cavities and severe pulmonary edema; these changes are presumably produced by epsilon toxin, the main action of which is to increase vascular permeability. Figure 8.1 Sheep with yellow lamb disease showing severe, diffuse icterus. Microscopic changes include centrilobular necrosis of the liver (Figure 8.2), pigmentary (hemoglobinuric) nephrosis (Figures 8.3 and 8.4), splenic congestion, and pulmonary congestion and edema. The liver lesions are characterized by centrilobular to mid-zonal hepatocellular degeneration and necrosis, and bile stasis in bile canaliculi. The kidney lesions include multiple hemoglobin casts in the tubular lumen and the presence of numerous multifocal, eosinophilic, and granular to globular intracytoplasmic hyaline droplets that stain positively for hemoglobin, in the proximal and distal convoluted tubules (Figures 8.3 and 8.4). The lungs show diffuse proteinaceous alveolar and interstitial edema and fibrin in the alveoli. Most histological lesions are thought to be associated with acute intravascular hemolysis and anemia produced by CPA. These changes are not, by any means, specific to this condition, and a diagnosis of yellow lamb disease cannot be established on histological changes alone. Figure 8.2 Liver of a lamb with yellow lamb disease showing centrilobular necrosis. HE, 100x. Figure 8.3 Kidney of a lamb with yellow lamb disease showing tubular degeneration and multiple protein (hemoglobin) droplets in the cytoplasm of tubular epithelial cells. HE, 400x. Courtesy of F. Giannitti.
Diseases produced by Clostridium perfringens type A in mammalian species
Introduction
Yellow lamb disease
Introduction
Etiology
Epidemiology and clinical signs
Gross changes
Microscopic changes
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