Chapter 148_ Streptococcal Infections.pdf

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University of the Philippines ­ Manila Access Provided by: Harrison's Principles of Internal Medicine, 21e Chapter 148: Streptococcal Infections Michael R. Wessels INTRODUCTION Many varieties of streptococci are found as part of the normal flora colonizing the human respiratory, gastrointestinal, and genitourinary tracts. Several species are important causes of human disease. Group A Streptococcus (GAS, Streptococcus pyogenes) is responsible for streptococcal pharyngitis, one of the most common bacterial infections of school­age children, and for the postinfectious syndromes of acute rheumatic fever (ARF) and poststreptococcal glomerulonephritis (PSGN). Group B Streptococcus (GBS, Streptococcus agalactiae) is the leading cause of bacterial sepsis and meningitis in newborns and a major cause of endometritis and fever in parturient women. Viridans streptococci are the most common cause of bacterial endocarditis. Enterococci, which are morphologically similar to streptococci, are now considered a separate genus on the basis of DNA homology studies. Thus, the species previously designated as Streptococcus faecalis and Streptococcus faecium have been renamed Enterococcus faecalis and Enterococcus faecium, respectively. The enterococci are discussed in Chap. 149. Streptococci are gram­positive, spherical to ovoid bacteria that characteristically form chains when grown in liquid media. Most streptococci that cause human infections are facultative anaerobes, although some are strict anaerobes. Streptococci are relatively fastidious organisms, requiring enriched media for growth in the laboratory. Clinicians and clinical microbiologists identify streptococci by several classification systems, including hemolytic pattern, Lancefield group, species name, and common or trivial name. Many streptococci associated with human infection produce a zone of complete (β) hemolysis around the bacterial colony when cultured on blood agar. The β­hemolytic streptococci that form large (≥0.5­mm) colonies on blood agar can be classified by the Lancefield system, a serologic grouping based on the reaction of specific antisera with bacterial cell­wall carbohydrate antigens. With rare exceptions, organisms belonging to Lancefield groups A, B, C, and G are all β­hemolytic, and each is associated with characteristic patterns of human infection. Other streptococci produce a zone of partial (α) hemolysis, often imparting a greenish appearance to the agar. These α­ hemolytic streptococci are further identified by biochemical testing and include Streptococcus pneumoniae (Chap. 146), an important cause of pneumonia, meningitis, and other infections, and the several species referred to collectively as the viridans streptococci, which are part of the normal oral flora and are important agents of subacute bacterial endocarditis. Finally, some streptococci are nonhemolytic, a pattern sometimes called γ hemolysis. Among the organisms classified serologically as group D streptococci, the enterococci are assigned to a distinct genus (Chap. 149). The classification of the major streptococcal groups causing human infections is outlined in Table 148­1. TABLE 148­1 Classification of Streptococci LANCEFIELD HEMOLYTIC REPRESENTATIVE SPECIES TYPICAL INFECTIONS GROUP PATTERN A S. pyogenes β Pharyngitis, impetigo, cellulitis, scarlet fever B S. agalactiae β Neonatal sepsis and meningitis, puerperal infection, urinary tract infection, diabetic ulcer infection, endocarditis C, G S. dysgalactiae subsp. equisimilis β Cellulitis, bacteremia, endocarditis D Enterococcia: E. faecalis, E. faecium Usually Urinary tract infection, nosocomial bacteremia, endocarditis nonhemolytic Nonenterococci: S. gallolyticus (formerly S. Usually Bacteremia, endocarditis Downloaded 2024­8­4 6:40 A Your IP is 49.147.196.41 bovis) Infections, Michael R. Wessels Chapter 148: Streptococcal nonhemolytic Page 1 / 16 ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Variable or Viridans streptococci: S. sanguis, S. mitis α Endocarditis, dental abscess, brain abscess nongroupable pneumonia, meningitis, and other infections, and the several species referred to collectively as the viridans streptococci, which are part of the normal University of the Philippines ­ Manila oral flora and are important agents of subacute bacterial endocarditis. Finally, some streptococci are nonhemolytic, a pattern sometimes called γ Access Provided by: hemolysis. Among the organisms classified serologically as group D streptococci, the enterococci are assigned to a distinct genus (Chap. 149). The classification of the major streptococcal groups causing human infections is outlined in Table 148­1. TABLE 148­1 Classification of Streptococci LANCEFIELD HEMOLYTIC REPRESENTATIVE SPECIES TYPICAL INFECTIONS GROUP PATTERN A S. pyogenes β Pharyngitis, impetigo, cellulitis, scarlet fever B S. agalactiae β Neonatal sepsis and meningitis, puerperal infection, urinary tract infection, diabetic ulcer infection, endocarditis C, G S. dysgalactiae subsp. equisimilis β Cellulitis, bacteremia, endocarditis D Enterococcia: E. faecalis, E. faecium Usually Urinary tract infection, nosocomial bacteremia, endocarditis nonhemolytic Nonenterococci: S. gallolyticus (formerly S. Usually Bacteremia, endocarditis bovis) nonhemolytic Variable or Viridans streptococci: S. sanguis, S. mitis α Endocarditis, dental abscess, brain abscess nongroupable Intermedius or milleri group: S. intermedius, Variable Brain abscess, visceral abscess S. anginosus, S. constellatus Anaerobic streptococcib: Peptostreptococcus Usually Sinusitis, pneumonia, empyema, brain abscess, liver abscess magnus nonhemolytic aSee Chap. 149. b See Chap. 177. GROUP A STREPTOCOCCI Lancefield group A consists of a single species, S. pyogenes. As its species name implies, this organism is associated with a variety of suppurative infections. In addition, GAS can trigger the postinfectious syndromes of ARF (which is uniquely associated with S. pyogenes infection; Chap. 359) and PSGN (Chap. 314). Worldwide, GAS infections and their postinfectious sequelae (primarily ARF and rheumatic heart disease) account for an estimated 500,000 deaths per year. Although data are incomplete, the incidence of all forms of GAS infection and that of rheumatic heart disease are thought to be tenfold higher in resource­limited countries than in developed countries (Fig. 148­1). FIGURE 148­1 Prevalence of rheumatic heart disease in children 5–14 years old. The circles within Australia and New Zealand represent indigenous populations (and also Pacific Islanders in New Zealand). (Reproduced with permission from JR Carapetis et al: The global burden of group A streptococcal diseases. Lancet Infect Dis 5:685, 2005.) Downloaded 2024­8­4 6:40 A Your IP is 49.147.196.41 Chapter 148: Streptococcal Infections, Michael R. Wessels Page 2 / 16 ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility FIGURE 148­1 University of the Philippines ­ Manila Prevalence of rheumatic heart disease in children 5–14 years old. The circles within Australia and New Zealand represent indigenous Access Provided by: populations (and also Pacific Islanders in New Zealand). (Reproduced with permission from JR Carapetis et al: The global burden of group A streptococcal diseases. Lancet Infect Dis 5:685, 2005.) PATHOGENESIS GAS elaborates a number of cell­surface components and extracellular products important in both the pathogenesis of infection and the human immune response. The cell wall contains a carbohydrate antigen that may be released by acid treatment. The reaction of such acid extracts with group A–specific antiserum is the basis for definitive identification of a streptococcal strain as S. pyogenes. Rarely, the group A antigen may be present on isolates of S. dysgalactiae ssp. equisimilis, which usually express the group C or G antigen (see “Streptococci of Groups C and G,” below). The major surface protein of GAS is M protein, which is the basis for the serotyping of strains with specific antisera. The M protein molecules are fibrillar structures anchored in the cell wall of the organism that extend as hairlike projections away from the cell surface. The amino acid sequence of the distal or amino­terminal portion of the M protein molecule is variable, accounting for the antigenic variation of the different M types, while more proximal regions of the protein are relatively conserved. Traditional M­typing by serologic methods has been largely supplanted by a newer technique for assignment of M type to GAS isolates by use of the polymerase chain reaction to amplify the variable region of the emm gene, which encodes M protein. DNA sequence analysis of the amplified gene segment can be compared with an extensive database (developed at the Centers for Disease Control and Prevention [CDC]) for assignment of emm type. Use of emm typing has increased the number of identified emm types to more than 200. This method eliminates the need for typing sera, which are available in only a few reference laboratories. The presence of M protein on a GAS isolate correlates with its capacity to resist phagocytic killing in fresh human blood. This phenomenon appears to be due, at least in part, to the binding of plasma fibrinogen to M protein molecules on the streptococcal surface, which interferes with complement activation and deposition of opsonic complement fragments on the bacterial cell. This resistance to phagocytosis may be overcome by M protein–specific antibodies; thus, individuals with antibodies to a given M type acquired as a result of prior infection are protected against subsequent infection with organisms of the same M type but not against that with different M types. GAS also elaborates, to varying degrees, a polysaccharide capsule composed of hyaluronic acid. While most clinical isolates of GAS produce a hyaluronic acid capsule, strains of M type 4 or 22 lack a capsule, as do some isolates of M type 89. The fact that acapsular strains have been associated with pharyngitis and invasive infection implies that the capsule is not essential for virulence. The production of large amounts of capsule by certain strains imparts a characteristic mucoid appearance to the colonies. The capsular polysaccharide plays an important role in protecting GAS from ingestion and killing by phagocytes. In contrast to M protein, the hyaluronic acid capsule is a weak immunogen, and antibodies to hyaluronate have not been shown to be important in protective immunity. The presumed explanation is the apparent structural identity between streptococcal hyaluronic acid and the hyaluronic acid of mammalian connective tissues. The capsular polysaccharide may also play a role in GAS colonization of the pharynx by binding to CD44, a hyaluronic acid–binding protein expressed on human pharyngeal epithelial cells. GAS produces a large number of extracellular products that may be important in local and systemic toxicity and in the spread of infection through tissues. These products include streptolysins S and O, toxins that damage cell membranes and account for the hemolysis produced by the organisms; streptokinase; DNAses; SpyCEP, a serine protease that cleaves and inactivates the chemoattractant cytokine interleukin 8, thereby inhibiting neutrophil recruitment to the site of infection; and several pyrogenic exotoxins. Previously known as erythrogenic toxins, the pyrogenic exotoxins cause the rash of scarlet fever. Since the mid­1980s, pyrogenic exotoxin–producing strains of GAS have been linked to unusually severe invasive infections, including necrotizing fasciitis and the streptococcal toxic shock syndrome (TSS). Several extracellular products stimulate specific antibody responses useful for serodiagnosis of recent streptococcal infection. Tests for antibodies to streptolysin O and DNase B are used most commonly for detection of preceding Downloaded streptococcal2024­8­4 6:40 infection in A Your cases IP is 49.147.196.41 of suspected ARF or PSGN. Chapter 148: Streptococcal Infections, Michael R. Wessels Page 3 / 16 ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility CLINICAL MANIFESTATIONS Pharyngitis tissues. These products include streptolysins S and O, toxins that damage cell membranes and account for the hemolysis produced by the organisms; University streptokinase; DNAses; SpyCEP, a serine protease that cleaves and inactivates the chemoattractant cytokine interleukin of theinhibiting 8, thereby Philippines ­ Manila neutrophil recruitment to the site of infection; and several pyrogenic exotoxins. Previously known as erythrogenic toxins, the Access pyrogenic Providedexotoxins by: cause the rash of scarlet fever. Since the mid­1980s, pyrogenic exotoxin–producing strains of GAS have been linked to unusually severe invasive infections, including necrotizing fasciitis and the streptococcal toxic shock syndrome (TSS). Several extracellular products stimulate specific antibody responses useful for serodiagnosis of recent streptococcal infection. Tests for antibodies to streptolysin O and DNase B are used most commonly for detection of preceding streptococcal infection in cases of suspected ARF or PSGN. CLINICAL MANIFESTATIONS Pharyngitis Although seen in patients of all ages, GAS pharyngitis is one of the most common bacterial infections of childhood, accounting for 20–40% of all cases of exudative pharyngitis in children; it is rare among those under the age of 3. Younger children may manifest streptococcal infection with a syndrome of fever, malaise, and lymphadenopathy without exudative pharyngitis. Infection is acquired through contact with another individual carrying the organism. Respiratory droplets are the usual mechanism of spread, although other routes, including food­borne outbreaks, have been well described. The incubation period is 1–4 days. Symptoms include sore throat, fever and chills, malaise, and sometimes abdominal complaints and vomiting, particularly in children. Both symptoms and signs are quite variable, ranging from mild throat discomfort with minimal physical findings to high fever and severe sore throat associated with intense erythema and swelling of the pharyngeal mucosa and the presence of purulent exudate over the posterior pharyngeal wall and tonsillar pillars. Enlarged, tender anterior cervical lymph nodes commonly accompany exudative pharyngitis. The differential diagnosis of streptococcal pharyngitis includes the many other bacterial and viral etiologies (Table 148­2). Streptococcal infection is an unlikely cause when symptoms and signs suggestive of viral infection are prominent (conjunctivitis, coryza, cough, hoarseness, or discrete ulcerative lesions of the buccal or pharyngeal mucosa). Because of the range of clinical presentations of streptococcal pharyngitis and the large number of other agents that can produce the same clinical picture, diagnosis of streptococcal pharyngitis on clinical grounds alone is not reliable. The throat culture remains the diagnostic gold standard. Culture of a throat specimen that is properly collected (i.e., by vigorous rubbing of a sterile swab over both tonsillar pillars) and properly processed is the most sensitive and specific means of definitive diagnosis. A rapid diagnostic test for latex agglutination or enzyme immunoassay of swab specimens is a useful adjunct to throat culture. While precise figures on sensitivity and specificity vary, rapid diagnostic tests generally are >95% specific. Thus, a positive result can be relied upon for definitive diagnosis and eliminates the need for throat culture. In settings in which the incidence of rheumatic fever is low, a confirmatory throat culture is not recommended for routine evaluation of most adults with a negative rapid test. However, because rapid diagnostic tests are less sensitive than throat culture (relative sensitivity in comparative studies, 70–90%), a negative result should be confirmed by throat culture for individuals at higher risk such as those with a history of rheumatic fever or immunocompromise or a family member with such a history; patients living in congregate settings of young adults such as dormitories or military facilities where the incidence of GAS pharyngitis may be elevated; individuals with household exposure to someone with proven GAS infection; and those living in an area in which rheumatic fever is endemic. TABLE 148­2 Infectious Etiologies of Acute Pharyngitis ORGANISM ASSOCIATED CLINICAL SYNDROME(S) Viruses Rhinovirus Common cold Coronavirus Common cold, COVID­19 Adenovirus Pharyngoconjunctival fever Influenza virus Influenza Parainfluenza virus Cold, croup Coxsackievirus Herpangina, hand­foot­and­mouth disease Herpes simplex virus Gingivostomatitis (primary infection) Downloaded 2024­8­4 6:40 A Your IP is 49.147.196.41 Epstein­Barr virus Infectious mononucleosis Chapter 148: Streptococcal Infections, Michael R. Wessels Page 4 / 16 ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Cytomegalovirus Mononucleosis­like syndrome  Parainfluenza virus Cold, croup University of the Philippines ­ Manila Access Provided by: Coxsackievirus Herpangina, hand­foot­and­mouth disease Herpes simplex virus Gingivostomatitis (primary infection) Epstein­Barr virus Infectious mononucleosis Cytomegalovirus Mononucleosis­like syndrome HIV Acute (primary) infection syndrome Bacteria Group A streptococci Pharyngitis, scarlet fever Group C or G streptococci Pharyngitis Mixed anaerobes Vincent’s angina Arcanobacterium haemolyticum Pharyngitis, scarlatiniform rash Neisseria gonorrhoeae Pharyngitis Treponema pallidum Secondary syphilis Francisella tularensis Pharyngeal tularemia Corynebacterium diphtheriae Diphtheria Yersinia enterocolitica Pharyngitis, enterocolitis Yersinia pestis Plague Chlamydiae Chlamydia pneumoniae Bronchitis, pneumonia Chlamydia psittaci Psittacosis Mycoplasmas Mycoplasma pneumoniae Bronchitis, pneumonia TREATMENT OF GAS PHARYNGITIS In the usual course of uncomplicated streptococcal pharyngitis, symptoms resolve after 3–5 days. The course is shortened little by treatment, which is given primarily to prevent suppurative complications and ARF. Prevention of ARF depends on eradication of the organism from the pharynx, not simply on resolution of symptoms, and requires 10 days of penicillin treatment (Table 148­3). A first­generation cephalosporin, such as cephalexin or cefadroxil, may be substituted for penicillin in cases of penicillin allergy if the nature of the allergy is not an immediate hypersensitivity reaction (anaphylaxis or urticaria) or another potentially life­threatening manifestation (e.g., severe rash and fever). TABLE 148­3 Treatment of Group A Streptococcal Infections INFECTION a Downloaded 2024­8­4 6:40 A Your IP isTREATMENT 49.147.196.41 Chapter 148: Streptococcal Infections, Michael R. Wessels Page 5 / 16 ©2024Pharyngitis McGraw Hill. All Rights Reserved.Benzathine Terms of Use Privacy penicillin G (1.2 mUPolicy Notice V (250 IM) or penicillin Accessibility mg PO tid or 500 mg PO bid) × 10 days (Children 24 h before delivery), prolonged labor, fever, or chorioamnionitis. Because the usual source of the organisms infecting a neonate is the mother’s birth canal, efforts have been made to prevent GBS infections by the identification of high­risk carrier mothers and their treatment with various forms of antibiotic prophylaxis or immunoprophylaxis. Prophylactic administration of ampicillin or penicillin to such patients during delivery reduces the risk of infection in the newborn. This approach has been hampered by logistical difficulties in identifying colonized women before delivery; the results of vaginal cultures early in pregnancy are poor predictors of carrier status at delivery. The CDC recommends screening for anogenital colonization at 35–37 weeks of pregnancy by a swab culture of the lower vagina and anorectum; intrapartum chemoprophylaxis is recommended for culture­positive women and for women who, regardless of culture status, have previously given birth to an infant with GBS infection or have a history of GBS bacteriuria during pregnancy. Women whose culture status is unknown and who develop premature labor (18 h), or intrapartum fever or who have a positive intrapartum nucleic acid amplification test for GBS also should receive intrapartum chemoprophylaxis. The recommended regimen for chemoprophylaxis is a loading dose of 5 million units of penicillin G followed by 2.5 million units every 4 h until delivery. Cefazolin is an alternative for women with a history of penicillin allergy who are thought not to be at high risk for anaphylaxis. For women with a history of immediate hypersensitivity, clindamycin may be substituted, but only if the colonizing isolate has been demonstrated to be susceptible. If susceptibility testing results are not available or indicate resistance, vancomycin should be used in this situation. Treatment of all pregnant women who are colonized or have risk factors for neonatal infection will result in exposure of up to one­third of pregnant women and newborns to antibiotics, with the attendant risks of allergic reactions and selection for resistant organisms. Although still in the developmental stages, a GBS vaccine may ultimately offer a better solution to prevention. Because transplacental passage of maternal antibodies produces protective antibody levels in newborns, efforts are underway to develop a vaccine against GBS that can be given to childbearing­age women before or during pregnancy. Results of phase 1 clinical trials of GBS capsular polysaccharide–protein conjugate vaccines suggest that a multivalent conjugate vaccine would be safe and highly immunogenic. INFECTION IN ADULTS Downloaded The majority of2024­8­4 6:40 A inYour GBS infections IP is 49.147.196.41 otherwise healthy adults are related to pregnancy and parturition. Peripartum fever, the most common Chapter 148: Streptococcal Infections, Michael R. Wessels Page 14 / 16 manifestation, is sometimes accompanied by symptoms and signs of endometritis or chorioamnionitis (abdominal distention and uterine or adnexal ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility tenderness). Blood and vaginal swab cultures are often positive. Bacteremia is usually transitory but occasionally results in meningitis or endocarditis. Infections in adults that are not associated with the peripartum period generally involve individuals who are elderly or have an underlying chronic produces protective antibody levels in newborns, efforts are underway to develop a vaccine against GBS that can be given to childbearing­age women University before or during pregnancy. Results of phase 1 clinical trials of GBS capsular polysaccharide–protein conjugate vaccines of the suggest Philippines that ­ Manila a multivalent conjugate vaccine would be safe and highly immunogenic. Access Provided by: INFECTION IN ADULTS The majority of GBS infections in otherwise healthy adults are related to pregnancy and parturition. Peripartum fever, the most common manifestation, is sometimes accompanied by symptoms and signs of endometritis or chorioamnionitis (abdominal distention and uterine or adnexal tenderness). Blood and vaginal swab cultures are often positive. Bacteremia is usually transitory but occasionally results in meningitis or endocarditis. Infections in adults that are not associated with the peripartum period generally involve individuals who are elderly or have an underlying chronic illness, such as diabetes mellitus or a malignancy. Among the infections that develop with some frequency in adults are cellulitis and soft tissue infection (including infected diabetic skin ulcers), urinary tract infection, pneumonia, endocarditis, and septic arthritis. Other reported infections include meningitis, osteomyelitis, and intraabdominal or pelvic abscesses. Relapse or recurrence of invasive infection weeks to months after a first episode is documented in ~4% of cases. TREATMENT OF GROUP B STREPTOCOCCAL INFECTION IN ADULTS GBS is less sensitive to penicillin than GAS, requiring somewhat higher doses. Adults with serious localized infections (pneumonia, pyelonephritis, abscess) should receive doses of ~12 million units of penicillin G daily; patients with endocarditis or meningitis should receive 18–24 million units per day in divided doses. Vancomycin is an acceptable alternative for penicillin­allergic patients. NONENTEROCOCCAL GROUP D STREPTOCOCCI The main nonenterococcal group D streptococci that cause human infections were previously considered a single species, Streptococcus bovis. The organisms encompassed by S. bovis have been reclassified into two species, each of which has two subspecies: Streptococcus gallolyticus subspecies gallolyticus, S. gallolyticus subspecies pasteurianus, Streptococcus infantarius subspecies infantarius, and S. infantarius subspecies coli. Endocarditis caused by these organisms is often associated with neoplasms of the gastrointestinal tract—most frequently, a colon carcinoma or polyp—but is also reported in association with other bowel lesions. When occult gastrointestinal lesions are carefully sought, abnormalities are found in >60% of patients with endocarditis due to S. gallolyticus or S. infantarius. In contrast to the enterococci, nonenterococcal group D streptococci like these organisms are reliably killed by penicillin as a single agent, and penicillin is the agent of choice for the infections they cause. VIRIDANS AND OTHER STREPTOCOCCI VIRIDANS STREPTOCOCCI Consisting of multiple species of α­hemolytic streptococci, the viridans streptococci are a heterogeneous group of organisms that are important agents of bacterial endocarditis (Chap. 128). Several species of viridans streptococci, including Streptococcus salivarius, Streptococcus mitis, Streptococcus sanguis, and Streptococcus mutans, are part of the normal flora of the mouth, where they live in close association with the teeth and gingiva. Some species contribute to the development of dental caries. Previously known as Streptococcus morbillorum, Gemella morbillorum has been placed in a separate genus, along with Gemella haemolysans, on the basis of genetic­relatedness studies. These species resemble viridans streptococci with respect to habitat in the human host and associated infections. The transient viridans streptococcal bacteremia induced by eating, toothbrushing, flossing, and other sources of minor trauma, together with adherence to biologic surfaces, is thought to account for the predilection of these organisms to cause endocarditis (see Fig. 128­1). Viridans streptococci are also isolated, often as part of a mixed flora, from sites of sinusitis, brain abscess, and liver abscess. Viridans streptococcal bacteremia occurs relatively frequently in neutropenic patients, particularly after bone marrow transplantation or high­dose chemotherapy for cancer. Some of these patients develop a sepsis syndrome with high fever and shock. Risk factors for viridans streptococcal bacteremia include chemotherapy with high­dose cytosine arabinoside, prior treatment with trimethoprim­sulfamethoxazole or a fluoroquinolone, treatment with antacids or histamine antagonists, mucositis, and profound neutropenia. The S. milleri group (also referred to as the S. intermedius or S. anginosus group) includes three species that cause human disease: S. intermedius, S. anginosus, and Streptococcus constellatus. These organisms are often considered viridans streptococci, although they differ somewhat from other viridans streptococci in both their hemolytic pattern (they may be α­, β­, or nonhemolytic) and the disease syndromes they cause. This group commonly produces suppurative infections, particularly abscesses of brain and abdominal viscera, and infections related to the oral cavity or respiratory tract, such as peri​tonsillar abscess, lung abscess, and empyema. Downloaded 2024­8­4 6:40 A Your IP is 49.147.196.41 TREATMENT OF INFECTION Chapter 148: Streptococcal WITH Infections, VIRIDANS Michael STREPTOCOCCI R. Wessels Page 15 / 16 ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Isolates from neutropenic patients with bacteremia are often resistant to penicillin; thus these patients should be treated presumptively with vancomycin until the results of susceptibility testing become available. Viridans streptococci isolated in other clinical settings usually are sensitive to The S. milleri group (also referred to as the S. intermedius or S. anginosus group) includes three species that cause human disease: S. intermedius, S. anginosus, and Streptococcus constellatus. These organisms are often considered viridans streptococci, althoughUniversity they differofsomewhat the Philippines ­ Manila from other Access Provided by: viridans streptococci in both their hemolytic pattern (they may be α­, β­, or nonhemolytic) and the disease syndromes they cause. This group commonly produces suppurative infections, particularly abscesses of brain and abdominal viscera, and infections related to the oral cavity or respiratory tract, such as peri​tonsillar abscess, lung abscess, and empyema. TREATMENT OF INFECTION WITH VIRIDANS STREPTOCOCCI Isolates from neutropenic patients with bacteremia are often resistant to penicillin; thus these patients should be treated presumptively with vancomycin until the results of susceptibility testing become available. Viridans streptococci isolated in other clinical settings usually are sensitive to penicillin. Susceptibility testing should be performed to guide treatment of serious infections. ABIOTROPHIA AND GRANULICATELLA SPECIES (NUTRITIONALLY VARIANT STREPTOCOCCI) Occasional isolates cultured from the blood of patients with endocarditis fail to grow when subcultured on solid media. These nutritionally variant streptococci require supplemental thiol compounds or active forms of vitamin B6 (pyridoxal or pyridoxamine) for growth in the laboratory. The nutritionally variant streptococci are generally grouped with the viridans streptococci because they cause similar types of infections. However, they have been reclassified on the basis of 16S ribosomal RNA sequence comparisons into two separate genera: Abiotrophia, with a single species (Abiotrophia defectiva), and Granulicatella, with three species associated with human infection (Granulicatella adiacens, Granulicatella para­adiacens, and Granulicatella elegans). TREATMENT OF INFECTION WITH NUTRITIONALLY VARIANT STREPTOCOCCI Treatment failure and relapse appear to be more common in cases of endocarditis due to nutritionally variant streptococci than in those due to the usual viridans streptococci. Thus, the addition of gentamicin (1 mg/kg every 8 h for patients with normal renal function) to the penicillin regimen is recommended for endocarditis due to the nutritionally variant organisms. OTHER STREPTOCOCCI Streptococcus suis is an important pathogen in swine and has been reported to cause meningitis in humans, usually in individuals with occupational exposure to pigs. S. suis has been reported to be the most common cause of bacterial meningitis in Vietnam, and it has been responsible for outbreaks in China. Strains of S. suis associated with human infections have generally reacted with Lancefield group R typing serum and sometimes with group D typing serum as well. Isolates may be α­ or β­hemolytic and are sensitive to penicillin. Streptococcus iniae, a pathogen of fish, has been associated with infections in humans who have handled live or freshly killed fish. Cellulitis of the hand is the most common form of human infection, although bacteremia and endocarditis have been reported. Anaerobic streptococci, or peptostreptococci, are part of the normal flora of the oral cavity, bowel, and vagina. Infections caused by the anaerobic streptococci are discussed in Chap. 177. FURTHER READING Bruckner L, Gigliotti F: Viridans group streptococcal infections among children with cancer and the importance of emerging antibiotic resistance. Semin Pediatr Infect Dis 17:153, 2006. [PubMed: 16934710] Parks T et al: Polyspecific intravenous immunoglobulin in clindamycin­treated patients with streptococcal toxic shock syndrome: A systematic review and meta­analysis. Clin Infect Dis 67:1434, 2018. [PubMed: 29788397] Raabe V, Shane A: Group B Streptococcus (Streptococcus agalactiae ), in Gram­Positive Pathogens, 3rd ed, Fischetti V et al (eds). Washington, DC, ASM Press, 2019, pp 228–238. Shulman ST et al: Clinical practice guideline for the diagnosis and management of group A streptococcal pharyngitis: 2012 update by the Infectious Diseases Society of America. Clin Infect Dis 55:1279, 2012. [PubMed: 23091044] Stevens DL, Bryant AE: Necrotizing soft tissue infections. N Engl J Med 377:2253, 2017. [PubMed: 29211672] Downloaded 2024­8­4 6:40 A Your IP is 49.147.196.41 Chapter 148: Streptococcal Infections, Michael R. Wessels Page 16 / 16 ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility