Ownby C L, Odell G V
Exp Mol Pathol. 1983 Jun;38(3):283-96. doi: 10.1016/0014-4800(83)90069-2.
The pathogenesis of myonecrosis induced by venoms of the Arkansas tarantula (Dugesiella hentzi, Girard) and the Honduran tarantula (Aphonopelma spp.) was studied using light and electron microscopy, scanning electron microscopy and x-ray microprobe analysis, and histochemistry. White mice were injected intraperitoneally with a sublethal dose of tarantula venom. Gross examination 24 hr after injection revealed white areas of apparent calcification in the diaphragm muscle. Light microscopic examination at 15 min revealed hypercontracted muscle cells, and necrotic masses containing areas of condensed myofibrils and clumps of mitochondria. By 12 hr numerous phagocytic cells were present around degenerated muscle cells. Electron microscopic examination revealed a myonecrosis of rapid onset with plasma membrane rupture and contraction bands 15 min after injection. At 3 hr only small patches of plasma membrane remained and mitochondrial changes such as swelling, dense intracristal spaces, partitioning, and flocculent densities were prominent. By 12 and 24 hr very dark spicular densities were present in mitochondria and numerous phagocytic cells were located within the intact basal lamina of necrotic cells. X-ray analysis and histochemistry of 24 hr samples showed that necrotic cells contained very high levels of calcium and phosphate. These two tarantula venoms caused a rapid onset myonecrosis in which the primary injury was rupture of the plasma membrane followed by inability of mitochondria and sarcoplasmic reticulum to maintain normal levels of calcium in the cytoplasm leading to cell death.
