INFECTED HEPATITIS. NODULAR NECROBIOSIS OF THE LIVER.
In ox, sheep, pig, dog, horse. Necrotic areas projecting on surface of liver. Causes: bacteria, toxins, from bowels, womb, navel. Lesions: In cattle dirty gray nodules in brownish red liver, nodules firm, granular, necrotic, elements do not stain, later leucocytes and fibro-plastic growth in periphery. In lambs the nodules are white, common to the lungs and pleura, pathogenic to rabbit. In pigs nutmeg liver, cells without nuclei, fatty, granular, pathogenic to rabbits, guinea pigs, rats and young pigs. In dog, nutmeg liver, with violet areas, and white spots, 1–2 lines, having granular, fatty cells without nuclei. Symptoms: fever, constant lying, tarry fæces, icterus, tender right hypochondrium, and those of the primary disease. Treatment: antisepsis of primary seat, and bowels, elimination by kidneys, general antisepsis, stimulants, etc. Case usually hopeless. Prevention.
This has been observed particularly in cattle, but also in sheep, pig, dog and horse. It is characterized by the formation of circumscribed areas of gangrene, becoming hard, dry, yellowish and usually slightly projecting beyond the adjacent surface. Its infected character is shown by the presence in the lesion and adjacent parts of the hepatic tissue of an abundance of bacteria, which, from the varied description, appear to differ in different cases. The cause may however be safely stated as one of the bacteria of gangrene. It is alleged with some show of reason, that the lesion may be determined by the action of toxins and ptomaines produced by bacteria in the alimentary canal and carried to the liver with the portal blood (Cadeac). The bacteria themselves commonly come from the same source, (Stubbe), but also from the uterus (Berndt), the mammæ (LeBlanc), and above all from the suppurating or septic umbilicus. McFadyean in five cases found a long slender bacillus, Hamilton in a single case in the horse found cocci, Rivolta in an infectious hepatitis in sheep found bacterium subtilis agnorum, and Semmer found the same condition in young pigs from micrococci introduced through the diseased umbilicus.
Lesions. In cattle the liver has a general brownish red, or greenish white color, and shows projecting, hard nodules of a dirty gray color more or less tinged with yellowish brown. The margins of these hard nodules are very sharply defined, and on section show a homogeneous granular surface, devoid of areas of softening or of connective tissue, and formed of the hepatic parenchyma in a state of necrobiosis. The granules and nuclear elements do not stain like those of healthy liver. As the disease advances the periphery of the nodule may be invaded by leucocytes and become the seat of a fibro-plastic hypertrophy (McFadyean) with the ultimate formation of cicatricial tissue (Stubbe).
In lambs Rivolta found the necrosed nodules standing out as white patches under the capsule of the liver, but similar lesions were met with in the lungs and pleuræ, an observation which has been confirmed by Hanbold. The affection was conveyed by inoculation to the rabbit.
In pigs Semmer found nutmeg liver, deep red or grayish yellow, hypertrophied, the hepatic cells swollen and divested of nuclei but containing fatty and pigmentary granules. It was inoculable on rabbits, guinea pigs, white rats and on young pigs.
In the dog, Courmont and Doyon found congested liver (portal congestion) with projecting patches of a deep violet color and sharply defined borders, and one to two lines in diameter, also salient white spots with distinct outlines. In the white spots the hepatic cells had lost their nuclei and were charged with fatty granules.
Symptoms. These are indications of hepatic disease. In parturient cows, Berndt noted fever (102° to 104°), anorexia, stiffness, cough, labored breathing, intense thirst, constant decubitus, and constipation followed by lowering temperature, tarry fæces and icterus. The region of the liver was very sensitive to pressure or percussion. In the other animals the symptoms appear to be largely over-shadowed by those of the primary disease, but the same general indications of jaundice, hepatic tenderness and digestive disorder are superadded.
Treatment when it can be intelligently adopted, consists largely in evacuation and antisepsis of the seat of primary infection, and of the prima viœ, and in maintaining elimination by the kidneys. In this way, as in congestion and hepatitis, the concentration of the poison is as far as possible counteracted, and an opportunity may sometimes be furnished for the recuperation of the liver cells. As a rule, however, the case is hopeless, and thus preventive measures, by cleanliness, disinfection and antisepsis of the ascertained sources of the infection are indicated.