Infectious Diseases in Obstetrics and Gynecology 1:252-255 (1994) (C) 1994 Wiley-Liss, Inc. Group A Streptococcal Puerperal Sepsis: Historical Review and 1990s Resurgence Lawrence Nathan and Kenneth J. Leveno Department of Obstetrics and Gynecology, University of Texas Southwestern Medical School, Dallas, TX ABSTRACT There appears to be a resurgence of puerperal sepsis due to a historically important pathogen, group A I-hemolytic streptococcus. (C) 1994 Wiley-Liss, Inc. Kv WORDS Group A streptococcus, puerperal fever, sepsis dramatic decline in the prevalence of serious infection caused by group A streptococci has been observed throughout most of the 20th cen- tury, and Streptococcus pyogenes is currently an un- common cause of maternal morbidity and mortal- ity. However, recent reports 1- have suggested a resurgence of virulent group A streptococci causing sepsis, severe soft-tissue invasion, toxic shock-like syndrome, disseminated intravascular coagulation, and death. In view of the apparent reemergence of classic childbed sepsis due to this organism, we have written this review to emphasize the return of a historically important pathogen in the annals of puerperal infection. In 1772, John Leake4 first recognized that puerperal fever was contagious. Later that century, Alexander Gordon 5 of Aberdeen suggested that puerperal fever was a communicable disease. In 1843, Oliver Wendell Holmes 6 described the con- tagiousness of puerperal fever as "a momentous fact which is no longer to be considered as a subject for trivial discussion He became convinced that childbed fever was contagious when he witnessed the death of a physician who, prior to his death, performed an autopsy on a woman with puerperal fever and attended several other parturients with similar infection. A controversy ensued and contin- ued for many years between Holmes and American obstetricians Hugh Lennox Hodge and Charles Meigs, who vehemently opposed the theory that doctors could spread this deadly disease to their patients. In the mid-19th century, Ignaz Semmelweis 7 noticed that puerperal fever was significantly more common in of the 2 maternity divisions of the Vienna Lying-In Hospital; patients attended by medical students were more frequently afflicted with childbed fever than were patients cared for by midwives. Semmelweis 7 was therefore convinced that childbed fever could be spread from person to person and insisted that students wash their hands in chlorine solution before examining women in labor. Remarkably, maternal mortality decreased from 5 % to 1.3 % after implementation of this mea- sure. Eighteen years later, Pasteur demonstrated that the disease described by Holmes 6 and Semmel- weis 7 was caused by the same hemolytic streptococ- cus that was responsible for erysipelas, scarlet fe- ver, and surgical wound infections. 8 Although obstetrical texts from the beginning of the 20th century contain descriptions of what is now considered puerperal sepsis due to group A Address correspondence/reprint requests to Dr. Lawrence Nathan, Department of Gynecology and Obstetrics, Emory University School of Medicine, 69 Butler Street, S.E., Atlanta, GA 30303. Review Aicle Received February 8, 1994 Accepted April 13, 1994
Transcript
Infectious Diseases in Obstetrics and Gynecology 1:252-255 (1994)(C) 1994 Wiley-Liss, Inc.
Group A Streptococcal Puerperal Sepsis:Historical Review and 1990s Resurgence
Lawrence Nathan and Kenneth J. LevenoDepartment of Obstetrics and Gynecology, University of Texas Southwestern Medical School,
Dallas, TX
ABSTRACT
There appears to be a resurgence ofpuerperal sepsis due to a historically important pathogen, groupA I-hemolytic streptococcus. (C) 1994 Wiley-Liss, Inc.
Kv WORDS
Group A streptococcus, puerperal fever, sepsis
dramatic decline in the prevalence of seriousinfection caused by group A streptococci has
been observed throughout most of the 20th cen-
tury, and Streptococcus pyogenes is currently an un-common cause of maternal morbidity and mortal-ity. However, recent reports1- have suggested a
resurgence ofvirulent group A streptococci causingsepsis, severe soft-tissue invasion, toxic shock-likesyndrome, disseminated intravascular coagulation,and death. In view of the apparent reemergence ofclassic childbed sepsis due to this organism, wehave written this review to emphasize the return ofa historically important pathogen in the annals ofpuerperal infection.
In 1772, John Leake4 first recognized thatpuerperal fever was contagious. Later that century,Alexander Gordon5 of Aberdeen suggested thatpuerperal fever was a communicable disease. In1843, Oliver Wendell Holmes6 described the con-
tagiousness of puerperal fever as "a momentous factwhich is no longer to be considered as a subject fortrivial discussion He became convinced thatchildbed fever was contagious when he witnessedthe death of a physician who, prior to his death,performed an autopsy on a woman with puerperalfever and attended several other parturients with
similar infection. A controversy ensued and contin-ued for many years between Holmes and Americanobstetricians Hugh Lennox Hodge and CharlesMeigs, who vehemently opposed the theory thatdoctors could spread this deadly disease to theirpatients.
In the mid-19th century, Ignaz Semmelweis7
noticed that puerperal fever was significantly morecommon in of the 2 maternity divisions of theVienna Lying-In Hospital; patients attended bymedical students were more frequently afflictedwith childbed fever than were patients cared for bymidwives. Semmelweis7 was therefore convincedthat childbed fever could be spread from person to
person and insisted that students wash their handsin chlorine solution before examining women inlabor. Remarkably, maternal mortality decreasedfrom 5% to 1.3% after implementation of this mea-sure. Eighteen years later, Pasteur demonstratedthat the disease described by Holmes6 and Semmel-weis7 was caused by the same hemolytic streptococ-cus that was responsible for erysipelas, scarlet fe-ver, and surgical wound infections. 8
Although obstetrical texts from the beginning ofthe 20th century contain descriptions of what isnow considered puerperal sepsis due to group A
Address correspondence/reprint requests to Dr. Lawrence Nathan, Department of Gynecology and Obstetrics, EmoryUniversity School of Medicine, 69 Butler Street, S.E., Atlanta, GA 30303.
Review AicleReceived February 8, 1994Accepted April 13, 1994
GROUP A STREPTOCOCCUS NATHAN AND LEVENO
streptococci, similar descriptions are not availablein modern texts. 9-11 For example, J. WhitridgeWilliams, 12 in the 1st edition of Williams Obstetricsin 1903, described S. pyogenes as the most frequentcause of epidemic and fatal puerperal infection. Hedistinguished these infections from those caused byanaerobic bacteria by emphasizing that the latterwere characterized by "putrefaction" (suppuration).Williams 12 observed that "the local changes of vir-ulent (aerobic) streptococcal infections are compar-atively slight, the process rapidly spreading throughthe lymphatics or veins past the uterus and givingrise to a peritonitis or a general systemic infection."He13 continued, "In a certain number of cases theinfection is so virulent that the organisms do not
have a chance to become localized to any one organ,and both they and their toxins are found in abun-dance in the circulating blood, with very slightimplication (involvement) of the uterus."
In the 1930s, Fry advanced our understandingof puerperal infection with his careful studies of themorbid anatomy in fatal infections. 14 He showedthat each of the more common organisms tended to
produce its own pathologic lesions. Fry’s work gaverise to a better clinical understanding of these com-mon infections, particularly of aerobic and anaero-bic puerperal infections. The characteristic find-ings in aerobic streptococcal infections includedextreme invasiveness such that the organisms rap-idly spread through the uterine wall with hardlyany inflammatory reaction to halt them, quicklyreaching the peritoneal cavity and pelvic tissues.Such aerobic streptococcal infections were also char-acterized by early onset and relatively severe sys-temic illness, yet unobtrusive localized clinical find-ings. Specifically, high pyrexia and rapid pulse ratewere typically most prominent, while other clinicalfindings, with the exception of paralytic ileus, werelacking. Fry also observed innumerable loci of bac-teria within the uterine wall that he concluded es-caped into the bloodstream so that a sustained septi-cemia resulted. In contrast, anaerobic streptococcalpuerperal infections were characterized by promi-nent clinical findings that included putrid lochia,suppurative wounds, and pelvic abscesses. Puer-peral women with anaerobic infections were typi-cally not overwhelmed at the outset, as is seen withaerobic infections. Anaerobic infections typicallyprogressed to abscess formation, which often in-cluded sites as distant as the lung. Pelvic throm-
bophlebitis along with thromboembolism was theproposed mechanism for lung involvement.
Also in the 193 0s, Rebecca C. Lancefieldl 5 re-
ported that streptococci could be differentiated intoseveral groups. Lancefield’s is group A [3-hemolyticstreptococcus is now recognized as the organismresponsible for a variety of human diseases includ-ing puerperal sepsis and thought to be the organismresponsible for the epidemics of puerperal infec-tions in the past.
In the early 20th century, epidemics of group Astreptococcal puerperal infection occurred withvariable frequency and intensity. The death rate inBritain from puerperal infection was 1-2/1,000between 1925 and 1935,16 while an epidemic inNew York’s Sloan Hospital described by Watson 17
had a fatality rate of 3 6%. Over the subsequent 2-3decades, aerobic streptococcal puerperal infectionsbecame a rarity that even antedated the availabilityof sulfa and penicillin. This decline was presumedto be related to development of knowledge on thecontagiousness of aerobic streptococci resulting inthe use of aseptic techniques during parturition.Moreover, part of the improvement in maternalinfections was attributed to the better managementof labor and elimination of those procedures thatcontributed to prolonged labor. 18
In the preantibiotic era, obstetricians were con-cerned about gram-positive aerobes such as groupA [-hemolytic streptococci (S. pyogenes) and anaer-
obes (Peptostreptococcus) such as S. putridus. 19 Allthese organisms shared a remarkable susceptibilityto penicillin, and the introduction of penicillin intoclinical practice in the mid-1940s greatly reducedclinical concerns about infections due to these patho-gens.2 Indeed, contemporary views on the patho-genesis ofpuerperal infections changed significantlyin the postantibiotic period with group A [3-he-molytic streptococci being infrequently recoveredfrom women with postpartum metritis, and mostsuch infections occurred only after cesarean sec-tion. 21 At our institution, most puerperal infectionsfollow cesarean section, are typically polymicrobial(2.5 bacterial species/infection), and are associatedwith suppuration. 22 The most frequent bacteria iso-lated in these infections are Peptostreptococcus, Bac-teroides, and Enterobacteriaceae. Indeed, group A[-hemolytic streptococci were isolated from only2% of women developing puerperal infection fol-lowing cesarean section, and heretofore we have not
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GROUP A STREPTOCOCCUS NATHAN AND LEVENO
witnessed septic shock due to this organism. Dur-ing the 1960s, ’70s, and early ’80s, puerperal in-fections due to group A streptococci became spo-radic with only minor geographic epidemics thatwere limited and controlled23-26 such that group Astreptococcus was considered an infrequent cause ofserious puerperal infections. For example, in 1981,Blanco and colleagues27 reported that group Astreptococcus was isolated from 3.3% of patientswith puerperal endometritis.
Beginning in the mid-1980s, some investigatorssuggested that aerobic streptococci were reemerg-ing as a cause of life-threatening soft-tissue infec-tions. Stevens and co-workers reported an out-break of 20 group A [3-hemolytic streptococcalinfections in the Rocky Mountain region. Theseinfections were remarkable because of the severityof the soft-tissue destruction and associated life-threatening systemic toxicity. The mortality ratewas 30% despite the median age of the patientsbeing 36 years with no underlying evidence ofimmune incompetence. They postulated that thehistorical disappearance of serious streptococcal in-fections was partially correlated with the disappear-ance of type A exotoxin produced by S. pyogenes.The exotoxin, also called scarlet fever toxin, is be-lieved to cause life-threatening systemic effects dueto group A [3-hemolytic streptococci. Other inves-tigators2’28-31 have also observed a resurgence ofS. pyogenes infections with complications, includingrheumatic fever, sepsis, and toxic shock-like syn-drome. Cleary and co-workers2 investigated theassociation of the return of scarlet fever toxin, sys-temic toxicity, and the possibility that a new highlyvirulent clone of S. pyogenes had emerged. Usingrestriction enzyme methodology and gene probes,they studied isolates from patients with sepsis andcompared these with S. pyogenes isolates not associ-ated with sepsis. They observed that streptococcalstrains from patients with sepsis are a unique clonecapable of producing exotoxin A, which is pro-posed to explain the apparent return of life-threat-ening group A [3-hemolytic streptococci.
Importantly, group A streptococci have increas-ingly been associated with life-threatening infec-tions on obstetric services on both sides of the At-lantic. In Europe, virulent group A [3-hemolyticstreptococci causing sepsis, soft-tissue infection,toxic shock syndrome, disseminated intravascularcoagulation, and maternal death have been re-
ported,-6 while in the United States, toxic shockdue to this organism has been described in SanAntonio, TX, 37 and Chapel Hill, NC.8 Recently,Silver and associates described 2 patients with life-threatening puerperal infection due to group A[3-hemolytic streptococcus. Both women presentedwith bacteremia and shock, failed aggressive medi-cal intervention, and required hysterectomy. Fi-nally, we9 reported 2 pregnancies complicated bygroup A [3-hemolytic streptococcal sepsis after al-most 2 decades without such infections at our hospi-tal, during which time almost 200,000 women havebeen delivered.
It therefore appears that puerperal sepsis causedby group A [3-hemolytic streptococcus, recentlyconsidered to be of historic interest only, has re-sumed importance and should be returned to ob-stetric concepts of contemporary causes of severepuerperal infection. The recent increase in both thefrequency and virulence of group A streptococcalinfections serves notice that this pathogen is with us
today.
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