Wannamaker L W
Rev Infect Dis. 1983 Sep-Oct;5 Suppl 4:S723-32. doi: 10.1093/clinids/5.supplement_4.s723.
Few of the cellular components of group A streptococci appear to be directly toxic for animals or humans. Some preparations of M protein produce an immunotoxic effect on human platelets and neutrophils. Cell wall fragments produce a chronic multinodular inflammatory lesion of dermal connective tissue. The peptidoglycan component of cell walls has many of the biologic features of endotoxins. The exotoxins of group A streptococci include the erythrogenic toxins (pyrogenic exotoxins) and the cytolytic toxins (streptolysins S and O). The high prevalence of erythrogenic, toxin-producing strains is difficult to reconcile with the epidemiologic behavior of scarlet fever; the variations may be due to quantitative differences in toxin production or to a shift from the early scarlet fever-associated strains that produce A toxin to the currently prevalent strains that produce B and C toxins. Experiments with animals suggest that a positive Dick test and the rash of scarlet fever result not from a direct toxic effect but rather from enhancement by pyrogenic exotoxin(s) of acquired hypersensitivity to diverse streptococcal products. The mechanism of toxigenic phage conversion is not clear. The pyrogenic exotoxins are associated with the enhancement of endotoxin shock and a wide variety of other biologic properties. Streptolysin S is a nonantigenic polypeptide associated with various stabilizing carrier molecules. It lyses a wide range of mammalian cells, influences T lymphocyte functions, and is probably responsible for the leukotoxic property of group A streptococci. Rheumatic fever has been associated with a streptococcal outbreak due to a nonhemolytic (streptolysin S-negative) strain. Streptolysin O is an oxygen-labile (thiol-activated) cytolysin. It is inhibited by nonesterified cholesterol and binds to cholesterol in the membranes of mammalian cells and organelles, an interaction producing ring-like and C-shaped structures demonstrable by electron microscopy. Streptolysin O affects a number of leukocyte functions. It produces profound electrocardiographic changes in experimental animals and toxic effects on pulsating heart cells in tissue culture. The observation that rheumatic fever is not associated with infection of the skin due to group A streptococci has suggested that nonesterified cholesterol in the epidermis may inhibit a toxic effect of streptolysin O, an effect necessary for the development of rheumatic fever.
A组链球菌的细胞成分中似乎很少有对动物或人类具有直接毒性的。某些M蛋白制剂对人类血小板和中性粒细胞产生免疫毒性作用。细胞壁片段会引起皮肤结缔组织的慢性多结节性炎性病变。细胞壁的肽聚糖成分具有许多内毒素的生物学特性。A组链球菌的外毒素包括致热毒素（热原性外毒素）和溶细胞毒素（链球菌溶血素S和O）。产致热毒素菌株的高流行率难以与猩红热的流行病学行为相协调；这些差异可能是由于毒素产生的数量差异，或者是由于从早期产生A毒素的与猩红热相关的菌株转变为目前流行的产生B和C毒素的菌株。动物实验表明，狄克氏试验阳性和猩红热皮疹并非源于直接毒性作用，而是由热原性外毒素增强了对多种链球菌产物的获得性超敏反应所致。产毒噬菌体转化的机制尚不清楚。热原性外毒素与内毒素休克的增强以及多种其他生物学特性有关。链球菌溶血素S是一种与各种稳定载体分子相关的非抗原性多肽。它能溶解多种哺乳动物细胞，影响T淋巴细胞功能，可能是A组链球菌白细胞毒性的原因。风湿热与非溶血性（链球菌溶血素S阴性）菌株引起的链球菌暴发有关。链球菌溶血素O是一种对氧不稳定（硫醇激活）的溶细胞素。它被非酯化胆固醇抑制，并与哺乳动物细胞和细胞器膜中的胆固醇结合，这种相互作用产生电子显微镜下可见的环状和C形结构。链球菌溶血素O影响多种白细胞功能。它在实验动物中产生深刻的心电图变化，并对组织培养中的搏动心脏细胞产生毒性作用。A组链球菌引起的皮肤感染与风湿热无关，这一观察结果表明，表皮中的非酯化胆固醇可能抑制链球菌溶血素O的毒性作用，而这种作用是风湿热发展所必需的。
