Several genera of microsporidia have been identified morphologically in human tissue but none has yet been propagated in vitro. These primitive, obligate intracellular parasitic protozoa are poorly understood pathogens of a wide variety of vertebrates and invertebrates. In humans they are especially important as opportunistic pathogens in AIDS patients. A microsporidian was recovered from a human patient and propagated in vitro. The organism has diplokarya, divides by binary fission, and often is found free in the host cell cytoplasm. The name Nosema corneum is suggested.

Tracheal explants were used to evaluate the relative ciliostatic and cytotoxic potential of heavy metal salts (cadmium chloride, chromium chloride, nickel chloride, and copper sulfate). Explants from hamster, rat, and guinea pig were all sensitive to the metals, though guinea pig explants showed the greatest difference between the untreated and metal treated tissues. Dosage levels were 50, 100, and 500 microM, for 24 to 148 h. Cadmium caused the greatest degree of ciliostasis and cell necrosis. Copper was less toxic, and nickel and chromium caused marginal damage when tested at 100 microM or lower. In each instance, damage became detectable at approximately 24 to 48 h and was nearly stabilized by 72 h. A significant loss of ciliary motion was always accompanied by a decrease in metabolic activity (dehydrogenase activity and ATP content). Transmission and scanning electron microscopy revealed a severely necrotic epithelium after exposure to cadmium, with only subtle morphological alterations after exposure to other metals. With all of the treatments there was no overt structural damage to cilia and little alteration in membranes of cells remaining in the epithelium. Some coagulation or vacuolization was noted in cadmium and copper treated explants but most cellular organelles did not display obvious damage. The most significant changes in the tracheal epithelium exposed to heavy metal salts in vitro were a loss of ciliary motion and a decrease in total ATP content.

Cadmium salts were examined for their biological effects on ciliated respiratory epithelium in hamster tracheal explants. Cadmium chloride and cadmium acetate both caused significant decreases in ciliary motion when tested at 100 micrograms M and above. Reductions in relative ciliary activity were dose-dependent and were first demonstrable at 8-32 hr. The decreased ciliary motion was accompanied by decreases in two key metabolic compound (ATP and dehydrogenase) which are normally associated with cell viability. Histopathological examination of cadmium-treated tissues showed an epithelium thinner than normal, with extensive vacuolization and few, if any, intact ciliated cells. The various biological effects exerted by cadmium are presented, along with potential mechanisms of pathogenesis for the observed ciliostasis and cytonecrosis. Decreases in adenosine triphosphate appear to play a critical role in the development of cadmium-related effects on cellular function and metabolism.ImagesFIGURE 3.

Cadmium salts were examined for their biological effects on ciliated respiratory epithelium in hamster tracheal explants. Cadmium chloride and cadmium acetate both caused significant decreases in ciliary motion when tested at 100 ,uM and above. Reductions in relative ciliary activity were dose-dependent and were first demonstrable at 8-32 hr. The decreased ciliary motion was accompanied by decreases in two key metabolic compounds (ATP and dehydrogenase) which are normally associated with cell viability. Histopathological examination of cadmium-treated tissues showed an epithelium thinner than normal, with extensive vacuolization and few, if any, intact ciliated cells. The various biological effects exerted by cadmium are presented, along with potential mechanisms of pathogenesis for the observed ciliostasis and cytonecrosis. Decreases in adenosine triphosphate appear to play a critical role in the development of cadmium-related effects on cellular function and metabolism.