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Winter 2000 Newsletter

Hepatic Abscesses in Feedlot Cattle
Why Necropsy Abortions?
Canine Ehrlichiosis
Equine Polysaccharide Storage Myopathy
Poultry Quality Monitoring
SCID in Arabian Foals
Turkey Corona Virus by ELISA
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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 condemnation.

  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 infection.

 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 commercially.

-by Jennifer Fairchild, Class of 2000

-edited by Randy White, DVM,PhD


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