Sabir Sarah, Perera Thomas B.
Kansas University School of Medicine
Hofstra Northwell
Scarlet fever is a syndrome characterized by a blanching, erythematous, maculopapular rash often described as “sandpaper-like,” a “strawberry tongue,” and exudative pharyngitis (see Scarlet Fever). The causative organism, (group A Streptococcus, or “GAS”), is a gram-positive bacterium adapted to humans. This organism grows in pairs and chains and causes a range of infections, including superficial, deep, and invasive conditions such as cellulitis, pharyngitis, erysipelas, and necrotizing fasciitis. GAS produces streptococcal pyrogenic exotoxins (SPEs), which act as superantigens released during infection. These exotoxins are the primary cause of the erythematous rash associated with scarlet fever. GAS bacterial pharyngitis and scarlet fever most commonly affect school-age and adolescent children due to higher transmissibility in school settings. However, these infections can also occur in other age groups, particularly in crowded environments such as households and nursing homes. Scarlet fever caused by GAS infections can occur at any age. Although it is most commonly associated with GAS pharyngitis, it may also develop with other GAS infections, whether invasive or noninvasive, such as erysipelas or necrotizing fasciitis. Historically, GAS serotypes have displayed cyclic epidemiological patterns. Notably, GAS is among the few bacteria that produce superantigen exotoxins, which are exceptionally potent T-cell activators. GAS superantigens, also referred to as erythrogenic or scarlet fever toxins, are responsible for the characteristic erythematous, sandpaper-like rash and strawberry tongue seen in scarlet fever. Superantigen genes, such as , and enhance the fitness and virulence of GAS, contributing to the development of invasive disease. Scarlet fever epidemics and invasive GAS infections were common in the 19th century. While the prevalence of scarlet fever declined in the 20th century, a resurgence of GAS infections occurred in the 1980s. Over the past decade, more virulent epidemic strains of GAS have emerged, leading to increased GAS infections and scarlet fever. Suppurative and nonsuppurative complications can arise from GAS infections, including rheumatic heart disease and poststreptococcal glomerulonephritis. Prompt treatment of acute infections is essential to prevent these complications.
猩红热是一种综合征,其特征为出现可消退的、红斑性的斑丘疹,常被描述为“砂纸样”,伴有“草莓舌”和渗出性咽炎(见猩红热)。致病微生物A组链球菌(GAS)是一种适应人类的革兰氏阳性细菌。这种细菌成对或成链生长,可导致一系列感染,包括浅表、深部和侵袭性疾病,如蜂窝织炎、咽炎、丹毒和坏死性筋膜炎。GAS产生链球菌致热外毒素(SPEs),这些毒素在感染期间作为超抗原释放。这些外毒素是与猩红热相关的红斑皮疹的主要原因。GAS细菌性咽炎和猩红热最常影响学龄儿童和青少年,因为在学校环境中传播性更高。然而,这些感染也可发生在其他年龄组,特别是在家庭和养老院等拥挤环境中。由GAS感染引起的猩红热可发生在任何年龄。虽然它最常与GAS咽炎相关,但也可能与其他GAS感染有关,无论是侵袭性还是非侵袭性的,如丹毒或坏死性筋膜炎。从历史上看,GAS血清型呈现周期性流行模式。值得注意的是,GAS是少数产生超抗原外毒素的细菌之一,这些外毒素是T细胞的超强激活剂。GAS超抗原,也称为致红斑毒素或猩红热毒素,是猩红热中特征性红斑、砂纸样皮疹和草莓舌的原因。超抗原基因,如、和,可增强GAS的适应性和毒力,促进侵袭性疾病的发展。猩红热流行和侵袭性GAS感染在19世纪很常见。虽然20世纪猩红热的发病率有所下降,但20世纪80年代GAS感染有所复发。在过去十年中,出现了毒性更强的GAS流行菌株,导致GAS感染和猩红热都有所增加。GAS感染可引起化脓性和非化脓性并发症,包括风湿性心脏病(RHD)和链球菌感染后肾小球肾炎(PSGN)。及时治疗急性感染对于预防这些并发症至关重要。