Parasitogical Examination of Wasting Disease in Black
Abalone, Haliotis cracherodii
Shields, Jeffrey D. and Perkins, Frank O.
March 31, 1997
Marine Fisheries Service, Southwest Region, 501 West Ocean
Boulevard, Suite 4200, Long Beach, CA 90802-4213.
PHONE: (562) 980-4000
in southern California are afflicted with chronic intestinal
infections of a rickettsia-like organism that causes a
debilitating and fatal withering syndrome. The hematology
of withered animals indicated that cellular degradation
and apoptosis occurred in tandem with the decline and
catabolism of abalone tissues. Two types of hemocytes
were found in the hemolymph. Type I and Type II Hyalinocytes
were distinguished by subtle differences in their cytoplasmic
vesicles. Densities of both types hemocytes declined in
abundance, and small, presumptive stem cells increased
in abundance with the progression of the disease. No circulating
granulocytes were present in hemolymph; but serous cells
were present as fixed granulocytes in hemal spaces. Cellular
inclusions, dying cells, and vacuolate cells increased
in abundance with the disease. An evaluation of cellular
immunity resulted in disparate findings associated with
serum levels and types of buffer used. In the presence
of micronutrients, and divalent metal ions, however, hemocytes
from infected abalone showed increased degrees of phagocytosis
(percent phagocytosis, and number of yeast particles per
hemocyte) compared to hemocytes from uninfected animals.
Experimental transmission of the disease was effected
in healthy, unexposed abalone held together with asymptomatic,
exposed abalone. Clinical signs of infection appeared
after 180 days of cohabitation. The chronic nature of
the disease progressed relatively unnoticed until 6 to
8 months infected abalone began to show signs of withering.
The withered condition represented an end stage of the
disease and probably resulted from starvation caused by
rickettisial disruption of the digestive processes.