129 Streptococcal Diseases
Streptococci are responsible for many common and not so common human and animal diseases. Streptococcal pharyngitis, scarlet fever, impetigo, erysipelas, neonatal meningitis and sepsis, puerperal sepsis, and bacterial endocarditis all follow infection with streptococci.
In addition, some streptococci provoke two peculiar postinfectious conditions: acute rheumatic fever and acute glomerulonephritis. Rebecca Lancefield (1933) divided streptococci into distinct serologic groups, labeled A, B, C, D..., each with a number of separate subgroups. In addition to these groups, microbiologists further classify streptococci on whether and how they hemolyze red blood cells {alpha: incomplete or green hemolysis; beta: complete or clear hemolysis). According to this tradition, the streptococcus responsible for pharyngitis is known as a “group A beta-hemolytic streptococcus.” Another member of the genus Streptococcus is the Streptococcus pneumoniae, the bacteria responsible for pneumonia.The streptococcus has a number of biological peculiarities that alter its ability to infect humans. The genetic insertion of a bacteriophage produces a toxin responsible for the rash of scarlet fever. A group of proteins, known as the M protein, renders the streptococcus impervious to the normal bodily defense of phagocytosis. Hemolysins and enzymes, when present, help the streptococcus to invade the host. One can speculate that this potential biological variability is responsible for the abrupt changes that streptococcal illnesses have made in the past (Gallis 1984).
Streptococcal illness can be extremely common. Few have escaped streptococcal pharyngitis or superficial impetigo of the skin. Alternately, some forms of streptococcal illness are rare. An example is streptococcal endocarditis. Most streptococcal diseases are spread through respiratory droplets.
Others can be spread by bacterial contamination of food or milk, by soiled hands or instruments touching open wounds, or when normal resident bacteria invade the bloodstream (for example, when endocarditis follows dental work).Group A streptococci produce several common illnesses. Streptococcal pharyngitis presents a clinical picture of fever, headache, sore throat, and abdominal discomfort. Before therapy with penicillin, the disease was often self-limited, but in certain cases the streptococci could disseminate to other anatomic sites, producing otitis media, mastoiditis, tonsillar abscesses, or osteomyelitis. Puerperal sepsis, or childbed fever, occurs when streptococci, introduced at delivery, invade the internal lining of the uterus. Group A streptococci can cause impetigo (a superficial skin infection), cellulitis, and erysipelas (a life-threatening, rapidly progressing soft tissue infection).
Group A streptococci are responsible for two striking postinfectious conditions: The first is acute rheumatic fever, which follows streptococcal pharyngitis after 2 to 3 weeks. Rheumatic fever can include one or more of the following: carditis (pericarditis, myocarditis, and/or endocarditis); migratory, nondeforming arthritis; chorea; subcutaneous, fibrous nodules; and erythema marginatum. The second postinfectious condition is acute glomerulonephritis, a usually temporary form of renal failure.
Group B streptococci form part of the normal flora of the vagina and usually do not produce illness in adult women. These bacteria, however, can infect babies during delivery, producing meningitis and sepsis.
Group C streptococci are usually pathogenic only for animals.
Group D streptococci, normal residents of the human body, can produce endocarditis in people with deformed heart valves. Some streptococci cannot be so readily grouped, such as Streptococcus viridans. These can also cause endocarditis, and they play a role in the formation of dental caries.
History and Geography
Women have suffered from puerperal fever, presumably due to streptococci, since ancient times. Many case studies in the books OiEpidemics within the Hippocratic corpus indicate that women suffered from postpartum fever, debility, and death. Nevertheless, childbed fever was probably never common. Oliver Wendell Holmes, in his masterfully argued “Contagiousness of Puerperal Fever” (1842-3), claimed that childbed fever was rare. When it occurred, it clustered around the practice of an individual physician. Holmes pointed to the need for cleanliness to prevent further victims.
Similarly, in the other classical study of puerperal sepsis first published in 1861, Ignaz Semmelweis (1983) demonstrated that physicians who followed their dead patients to the autopsy room and then returned to the lying-in room to deliver more babies had more of their patients die of puerperal fever than did midwives who did not perform autopsies. These observations of Holmes and Semmelweis (each unaware of the work of the other) point to the tremendous gulf in personal cleanliness that existed between the pre- and post-germ-theory practitioners.
Holmes, for example, tells of distinguished obstetricians who carried pelvic organs removed at autopsy in their street coat pockets. Both accounts also underscore the irony in the fact that the most scientifically oriented physicians, the ones who performed autopsies, were responsible for spreading the illness! Those accounts, however, treat with silence the plight of infants bom of infected mothers. We know from twentieth-century experience that many infants emerged unscathed. But in the past, some may have developed a fatal infection, and even the lucky surviving infants would have faced an uncertain future if their mothers were unable to nurse them.
Erysipelas’s role in history was an inevitable accompaniment of wounds, whether accidental or surgical (Simpson 1872). Any deep cut through uncleansed skin risked injecting streptococci into susceptible tissue.
Erysipelas also accompanied other streptococcal-related illnesses, such as childbed fever. Scarlet fever (streptococcal pharyngitis produced by peculiar strains of streptococci that release a toxin yielding a rash) crosses medical history in a number of places. In the early years of bacteriology, Friedrich Loffler (1884) had to sort out scarlet fever cocci from diphtheria bacilli (both produced sore throats). Scarlet fever often occurred in epidemics passed both in the usual droplet fashion and in contaminated food - especially milk — supplies.Streptococcal pharyngitis, with or without rash, provoked a prominent postinfectious state: acute rheumatic fever. For a period of about a century, rheumatic fever injured more hearts than any other disease. It struck children and young adults, usually less than 25 years of age, in temperate climates. Although mentioned by prominent seventeenth-century writers, such as Thomas Sydenham, rheumatic fever appears not to have become a major problem until the late eighteenth and early nineteenth centuries, when carditis emerged as the major component of rheumatic fever. This seems to have been the result of a biological change in the way the streptococcus provoked the body to respond (rheumatic fever is not an infection in the usual sense, but rather an immunologic response to the streptococcus), coupled with the introduction of the stethoscope that made diagnosis easier (Cheadle 1889).
All streptococcal diseases, except newborn sepsis and meningitis, have become less virulent since the end of the nineteenth century, a phenomenon that has yet to be explained. Their incidence was clearly on the decline before the arrival of specific measures to treat these illnesses. The puzzle to be sorted out is the possibility that the streptococcus, with its biological variability, could have become less inherently invasive in natural fashion. But it did so at the precise time in history (at least in Europe and the United States) when nutrition, housing, and standards of living substantially improved.
Today, however, the streptococcus is usually sensitive to sulfonamides and to penicillins; thus most infections are curable with appropriate antibiotics.
Peter C. English
Bibliography
Cheadle, Walter Butler. 1889. Various manifestations of the rheumatic state. London.
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Holmes, Oliver Wendell. 1842-3. On the contagiousness of puerperal fever. New England Quarterly Journal of Medicine 1: 503—30.
Lancefield, Rebecca C. 1933. A serological differentiation of human and other groups Ofhemolytic streptococci. Journal OfExperimental Medicine 57: 571.
Loffler, Friedrich. 1884. Untersuchungen iiber die Bedeu- tung der Micro-Organismen fur die Entstehung der Diphtherie beim Menschen, bei der Taube und beim Kalbe. Mittheilungen aus dem Kaiserlichen Gesund- heitsamte 2: 421.
Semmelweis, Ignaz. 1983. The etiology, concept, and prophylaxis of childbed fever, trans. K. Codell Carter. Madison, Wis.
Simpson, James Y. 1872. Anesthesia, hospitalism, hermaphroditism, and a proposal to stamp out smallpox and other contagious diseases. New York.