Hepatic Abscesses in Feedlot Cattle
Liver abscesses negatively affect feedlot cattle performance
both in the feedyard and on the rail, causing financial loss
to cattle feeders and packers through decreased feed intake,average
daily gain, feed efficiency, dressing percentage and liver
Causative agents of this condition include Fusobacteriumnecrophorum,
a gram negative obligate anaerobe which is the most commonly
isolated bacterium (up to 100%), and Arcanobacter
(Actinomyces) pyogenes, a gram positive facultative anaerobe
which is the second most commonly isolated (35%) pathogen.
Other bacteria which may be cultured include Staphylococcus
spp., Streptococcus spp., and Bacteroidesspp.
The two subspecies of F. necrophorum are subsp.
necrophorum (biotype A) and subsp. funduliforme
(biotype B). Of these, the subspecies necrophorum
is the most pathogenic. The two virulence factors of major
importance are leukotoxin and endotoxiclipopolysaccharide
which help to prevent phagocytosis of F. necrophorum.
F. necrophorum and A. pyogenes are part of
the normal bacterial flora of the rumen. Damage to the wall
of the rumen secondary to rumen acidosis leads to bacterial
colonization. Subsequently, the bacteria enter the bloodstream
via the portal circulation, which seeds bacteria throughout
the liver. The bacteria readily proliferate forming abscesses.
Liver abscesses begin as areas of coagulative necrosis that
develop into encapsulated abscesses over time. Eventually,
these areas may heal by forming a fibrous scar.
Cattle with liver abscesses usually do not show clinical
signs; however, some cattle may be febrile, anorexic, depressed
and experience weight loss. Cattle with ruptured liver abscesses
may be severely depressed, anorexic, and febrile due to peritonitis.
Sudden death may occur due to anaphylactic shock if an abscess
ruptures and releases a large amount of purulent material
into the bloodstream. In these cases, the lungs will appear
markedly congested and edematous at necropsy. In some instances,
abscesses may involve the posterior vena cava, causing phlebitis
and, eventually, thrombosis. Clinical signs of caudal vena
caval thrombosis include chronic diarrhea, emaciation, mild
ascites, and distended subcutaneous abdominal veins. Clinical
signs of pulmonary thromboemboli include epistaxis and/or
hemoptysis, coughing, dyspnea, tachypnea, anemia, and melena.
Diagnostic techniques available to diagnose liver abscesses
include laboratory changes and ultrasonography. Common laboratory
changes include increased gamma glutamyltransferase (GGT),
sorbitoldehydrogenase (SDH), globulin, bilirubin, fibrinogen,
and leukocyte counts, as well as hypoalbuminemia and significantly
decreased sulfobromophthalein clearance. Ultrasonography
is a useful diagnostic tool, although it may be unable to
detect abscesses in some areas of the liver. Ultrasonography
detects areas where the hepatic parenchyma has coagulative
necrosis and therefore has a necrotic fluid center. These
changes may be visible as soon as three days after experimental
Histologically, liver abscesses have a necrotic center containing
leukocytes, hepatocytes and cellular debris. The area surrounding
the necrotic center contains macrophages and multinucleated
giant cells. The next layer contains plasma cells, degenerating
hepatocytes, immature fibroblasts, neutrophils, macrophages,
and immature collagen strands. The capsule consists of fibrous
connective tissue. At necropsy, the liver may contain a single
abscess or numerous abscesses that range in size from pinpoint
to over 15 cm in diameter. Peritonitis may be present if
an abscess has ruptured into the abdominal cavity. The liver
may be adhered to the diaphragm with fibrous connective tissue.
In a study conducted by Lechtenberget. al,Fusobacteriumnecrophorum
was found to be generally susceptible to penicillins, tetracyclines
(chlortetracycline and oxytetracycline), licosamides (clindamycin
and lincomycin), and macrolides (tylosin and erythromycin),
and was resistant to aminoglycosides (kanamycin, neomycin,
gentamicin, and streptomycin), ionophores (except narasin),
and peptides (avoparcin, polymyxin, and thiopeptin). However,
long term antiobiotic therapy using approved antimicrobials
is of questionable benefit.
Fortunately, feeding diets supplemented with antimicrobials
can reduce the incidence of naturally occurring liver abscess.
Oxytetracycline, chlortetracycline, baci-tracin, methylenedisalicyclate,
virgin-amycin, and tylosin are antimicrobial feed additives
labeled for the prevention of liver abscesses in feedlot cattle.
Another preventative measure may include gradually increasing
the amount of concentrate in the ration to reduce acidosis.
Research by Saginala et al demonstrated that a leukotoxoid
vaccine reduced the incidence of liver abscesses; however,
this vaccine and other similar vaccines are not available
-by Jennifer Fairchild, Class of 2000
-edited by Randy White, DVM,PhD