INFECTION
AND IMMUNITY
Vol. 74, No. 4, 2006; Pages: 2015–2021
Leukotoxin
Confers Beta-Hemolytic Activity to Actinobacillus actinomycetemcomitans
Nataliya V. Balashova, Juan A. Crosby,
Lourdes Al Ghofaily, and Scott C. Kachlany*
Department of Oral Biology, Medical Science Building C-636,
University of Medicine and
Dentistry of NJ, 185 S. Orange Avenue, Newark, NJ 07103.
Abstract
Actinobacillus actinomycetemcomitans
is the etiologic agent of localized aggressive periodontitis,
a rapidly progressing oral disease that occurs in adolescents.
A. actinomycetemcomitans can also cause systemic
disease, including infective endocarditis. In early work on
A. actinomycetemcomitans workers concluded that this bacterium
is not beta-hemolytic. More recent reports have suggested
that A. actinomycetemcomitans does have the potential
to be beta-hemolytic. While growing A. actinomycetemcomitans
on several types of growth media, we noticed a beta-hemolytic
reaction on media from one manufacturer. Beta-hemolysis occurred
on Columbia agar from Accumedia with either sheep or horse
blood, but not on similar media from other manufacturers.
A surprising result was that mutants of A. actinomycetemcomitans
defective for production of leukotoxin, a toxin that is reportedly
highly specific for only human and primate white blood cells,
are not beta-hemolytic. Purified leukotoxin was able to lyse
sheep and human erythrocytes in vitro. This work showed that
in contrast to the accepted view, A. actinomycetemcomitans
leukotoxin can indeed destroy erythrocytes and that the production
of this toxin results in beta-hemolytic colonies on solid
medium. In light of these results, the diagnostic criteria
for clinical identification of A. actinomycetemcomitans
and potentially related bacteria should be reevaluated. Furthermore,
in studies on A. actinomycetemcomitans leukotoxin workers
should now consider this toxin’s ability to destroy
red blood cells.
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