cultures); in one experiment (unpublished data) 
viable bacteria were reduced so quickly that they 
dropped below the counting range in 30 min. 
Presumably, the older (72-hr) bacteria are in a more 
dormant state, which is less susceptible to an- 
tibacterial metabolites. 
One clue regarding the mechanism of cadmium ac- 
tion is given by this work. It appears that within 
phagocytic cells cadmium may prevent the delivery of 
lysosomal substances to the phagocytic vacuole or in- 
hibit the action of these substances on bacteria. On 
the other hand, cadmium does not appear to inhibit 
events leading to protein formation. This is indicated 
because lymphocytic cells exposed to cadmium in 
vivo actively proliferate and produce antibody protein 
to the same extent as cells not exposed to cadmium. 
This work also suggests one way in which cadmium 
could reduce fish populations. Since bacteria are more 
slowly killed within phagocytes of cadmium-exposed 
fish, it follows that certain marginally pathogenic 
bacteria may multiply within phagocytes and even- 
tually overwhelm the fish with infection. Studies of 
the effects of chemical agents in other animals suggest 
a common mechanism for phagocytic dysfunction. 
Laurenzi et al. (1963) found reduced clearance of 
aerosolized bacteria from lungs of mice exposed to 
ethanol, cortisone, or cigarette smoke. Green and 
Carolin (1967) found that cigarette smoke inhibited 
the capacity of rabbit pulmonary macrophages to in- 
activate bacteria. Kass and Finland (1953) reviewed a 
large body of literature showing that treatment of 
animals with cortisone and other adrenocortical hor- 
mones increases severity of bacterial, viral, fungal, 
protozoan, and helminth infections. Sidransky, 
Verney, and Beede (1965) showed that mice treated 
with cortisone or cytotoxic cancer therapy drugs 
became highly susceptible to pneumonia from 
aerosols of Aspergillus flavus spores. Merkow et al. 
(1968) then demonstrated that lysosomes in 
phagocytes of cortisone-treated mice failed to fuse 
with vacuoles containing the spores. Consequently, 
the substances in these lysosomes were not delivered 
to the vacuole. Jones and Hirsch (1972) have also 
demonstrated absence of lysosomal fusion with 
phagocytic vacuoles containing living toxoplasma 
parasites. These studies indicate a possible universal 
mechanism for shutting off microbicidal activities 
within phagocytes. If so, it is likely that a number of 
environmental pollutants may be found to cause 
similar phagocytic dysfunction in fish. 
LITERATURE CITED 
BENACERRAF, B., G. BIOZZI, B. N. HALPERN, and C. STIFFEL. 
1957. Physiology of phagocytosis of particles by the R.E.S. 
In B. N. Halpern, B. Benacerraf, and J. F. Delafresnaye 
(editors), Physiopathology of the reticulo-endothelial system, 
p. 52-77. Blackwell Sci. Publ., Oxford. 
CALABRESE, A., R. S. COLLIER, and J. E. MILLER. 
1974. Physiological response of the cunner, Tautogolabrus 
adspersus, to cadmium. I. Introduction and experimental 
design. In Physiological response of the cunner, Tauto- 
golabrus adspersus, to cadmium, p. 1-3. NOAA Tech. 
Rep. NMFS SSRF 681. 
CHILLER, J.M., H.O. HODGINS, V.C. CHAMBERS, and 
R. S. WEISER. 
1969. Antibody response in rainbow trout (Salmo gairdneri). 
J. Immunol. 102:1193-1201. 
FRIBERG, L., M. PISCATOR, and G. NORDBERG. 
1971. Cadmium in the environment. CRC Press, Cleveland, 
166 p. 
GARDNER, G. R., and P. P. YEVICH. 
1970. Histological and hematological responses of an estuarine 
teleost to cadmium. J. Fish. Res. Board Can. 27:2185- 
2196. 
GREEN, G. M., and D. CAROLIN. 
1967. The depressant effect of cigarette smoke on the in vitro 
antibacterial activity of alveolar macrophages. N. Engl. J. 
Med. 276:421-427. 
GREIG, R. A., A. E. ADAMS, and B. A. NELSON. 
1974. Physiological response of the cunner, Tautogolabrus 
adspersus, to cadmium. I. Uptake of cadmium by organs 
and tissues. In Physiological response of the cunner, 
Tautogolabrus adspersus, to cadmium, p. 5-9. NOAA Tech. 
Rep. NMFS SSRF 681. 
HOLMES, B., A. R. PAGE, and R. A. GOOD. 
1967. Studies of the metabolic activity of leukocytes from 
patients with genetic abnormality of phagocytic function. 
J. Clin. Invest. 46:1422-1482. 
JACKIM, E., J. M. HAMLIN, and S. SONIS. 
1970. Effects of metal poisoning on five liver enzymes in the 
killifish (Fundulus heteroclitus). J. Fish. Res. Board 
Can. 27:383-390. 
JONES, T.C., and J. G. HIRSCH. 
1972. The interaction between Toxoplasma gondii and mam- 
malian cells. II. The absence of lysosomal fusion with 
phagocytic vacuoles containing living parasites. J. Exp. 
Med. 136:1173-1194. 
KASS, E. H., and M. FINLAND. 
1953. Adrenocortical hormones in infection and immunity. 
Annu. Rev. Microbiol. 7:361-388. 
LAURENZI, G. A., J. J. GUARNERI, R. B. ENDRIGA, and 
J. P. CAREY. 
1963. Clearance of bacteria by the lower respiratory tract. 
Science (Wash., D.C.) 142:1572-1573. 
McCLOSKEY, R. V. 
1972. Uptake and killing of Mima polymorpha and Herellea 
vaginicola by the reticuloendothelial system of neonatally 
thymectomized nonwasted mice. Infect. Immun. 6:21- 
26. 
MERKOW, L., M. PARDO, S. M. EPSTEIN, E. VERNEY, and 
H. SIDRANSKY. 
1968. Lysosomal stability during phagocytosis of Aspergillus 
flavus spores by alveolar macrophages of cortisone- 
treated mice. Science (Wash., D.C.) 160:79-81. 
MOUNT, D.I., and C. E. STEPHAN. 
1967. A method for detecting cadmium poisoning in fish. 
J. Wildl. Manage. 31:168-172. 
PIPPY, J. H. C., and G. M. HARE. 
1969. Relationship of river pollution to bacterial infection 
in salmon (Salmo salar) and suckers (Catostomus 
commersoni). Trans. Am. Fish. Soc. 98:685-690. 
