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.