Harrison's Internal Medicine

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Diagnosis The diagnosis of diphtheria is based on clinical signs and symptoms plus laboratory confirmation. Respiratory diphtheria should be considered in patients with sore throat, pharyngeal exudates, and fever. Other symptoms may include hoarseness, stridor, or palatal paralysis. The presence of a pseudomembrane should prompt consideration of diphtheria. Once a clinical diagnosis of diphtheria is made, diphtheria antitoxin should be administered as soon as possible. Laboratory diagnosis is based either on cultivation of C. diphtheriae or toxigenic C.

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Management Patients in whom diphtheria is suspected should be hospitalized in respiratory isolation rooms, with close monitoring of cardiac and respiratory function. A cardiac workup is recommended to assess the possibility of myocarditis. In patients with extensive pseudomembranes, consultation with an anesthesiologist or an ear, nose, and throat specialist is recommended because of the possibility that tracheostomy or intubation will be required. In some settings, pseudomembranes can be removed surgically.

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Clinical Manifestations Respiratory Diphtheria The clinical diagnosis of diphtheria is based on the constellation of sore throat; adherent tonsillar, pharyngeal, or nasal pseudomembranous lesions; and low-grade fever. In addition, diagnosis requires the isolation of C. diphtheriae or the histopathologic isolation of compatible gram-positive organisms.

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Harrison's Internal Medicine Chapter 131. Diphtheria and Other Infections Caused by Corynebacteria and Related Species Diphtheria Diphtheria is a nasopharyngeal and skin infection caused by Corynebacterium diphtheriae. Toxigenic strains of C. diphtheriae produce a protein toxin that causes systemic toxicity, myocarditis, and polyneuropathy. The toxin is associated with the formation of pseudomembranes in the pharynx during respiratory diphtheria. While toxigenic strains most frequently cause pharyngeal diphtheria, nontoxigenic strains commonly cause cutaneous disease.

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Infection with Viridans Streptococci: Treatment 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. Abiotrophia Species (Nutritionally Variant Streptococci) Occasional isolates cultured from the blood of patients with endocarditis fail to grow when subcultured on solid media.

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Pathogenesis and Immunology Diphtheria toxin, produced by toxigenic strains of C. diphtheriae, is the primary virulence factor in clinical disease. The toxin is synthesized in precursor form; is released as a 535-amino-acid, single-chain protein; and has an LD50 of ~100 ng/kg of body weight. The toxin is produced in the pseudomembranous lesion and is taken up into the bloodstream, through which it is distributed to all organ systems.

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Enterococci may be resistant to penicillins via two distinct mechanisms. The first is β-lactamase production (mediating resistance to penicillin and ampicillin), which has been reported for E. faecalis isolates from several locations in the United States and other countries. Because the amount of β-lactamase produced may be insufficient for detection by routine antibiotic susceptibility testing, isolates from serious infections should be screened specifically for βlactamase production with a chromogenic cephalosporin or another method.

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Group B Streptococcal Infection in Adults: Treatment 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 penicillin-allergic patients.

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Streptococcal Toxic Shock Syndrome: Treatment In light of the possible role of pyrogenic exotoxins or other streptococcal toxins in streptococcal TSS, treatment with clindamycin has been advocated by some authorities (Table 130-3), who argue that, through its direct action on protein synthesis, clindamycin is more effective in rapidly terminating toxin production than penicillin—a cell-wall agent. Support for this view comes from studies of an experimental model of streptococcal myositis, in which mice given clindamycin had a higher rate of survival than those given penicillin.

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Infection in Neonates Two general types of GBS infection in infants are defined by the age of the patient at presentation. Early-onset infections occur within the first week of life, with a median age of 20 h at onset. Approximately half of these infants have signs of GBS disease at birth. The infection is acquired during or shortly before birth from the colonized maternal genital tract. Surveillance studies have shown that 5– 40% of women are vaginal or rectal carriers of GBS.

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Erysipelas is a streptococcal infection of the superficial dermis and consists of well-demarcated, erythematous, edematous, warm plaques Classic cases of erysipelas, with typical features, are almost always due to β-hemolytic streptococci, usually GAS and occasionally group C or G. Often, however, the appearance of streptococcal cellulitis is not sufficiently distinctive to permit a specific diagnosis on clinical grounds.

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Deep Soft-Tissue Infections: Treatment Once necrotizing fasciitis is suspected, early surgical exploration is both diagnostically and therapeutically indicated. Surgery reveals necrosis and inflammatory fluid tracking along the fascial planes above and between muscle groups, without involvement of the muscles themselves. The process usually extends beyond the area of clinical involvement, and extensive debridement is required. Drainage and debridement are central to the management of necrotizing fasciitis; antibiotic treatment is a useful adjunct (Table 130-3), but surgery is lifesaving.

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Asymptomatic Pharyngeal Colonization with Gas: Treatment When a carrier is transmitting infection to others, attempts to eradicate carriage are warranted. Data are limited on the best regimen to clear GAS after penicillin alone has failed. The combination of penicillin V (500 mg four times daily for 10 days) and rifampin (600 mg twice daily for the last 4 days) has been used to eliminate pharyngeal carriage. A 10-day course of oral vancomycin (250 mg four times daily) and rifampin (600 mg twice daily) has eradicated rectal colonization.

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Impetigo contagiosa is a superficial streptococcal or Staphylococcus aureus infection consisting of honey-colored crusts and erythematous weeping erosions. Occasionally, bullous lesions may be seen. (Courtesy of Mary Spraker, MD.) The classic presentation of impetigo usually poses little diagnostic difficulty. Cultures of impetiginous lesions often yield S. aureus as well as GAS. In almost all cases, streptococci are isolated initially and staphylococci appear later, presumably as secondary colonizing flora. In the past, penicillin was nearly always effective against these infections.

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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.

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Gas Pharyngitis: Treatment 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 130-3). Erythromycin may be substituted for penicillin in cases of penicillin allergy.

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Group A Streptococci Lancefield's 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. 315) and PSGN (Chap. 277). Worldwide, GAS infections and their postinfectious sequelae (primarily ARF and rheumatic heart disease) account for an estimated 500,000 deaths per year.

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Harrison's Internal Medicine Chapter 130. Streptococcal and Enterococcal Infections Streptococcal and Enterococcal Infections: 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, S.

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Antimicrobial Therapy for Selected Settings For uncomplicated skin and soft tissue infections, the use of oral antistaphylococcal agents is usually successful. For other infections, parenteral therapy is indicated. S. aureus endocarditis is usually an acute, life-threatening infection. Thus prompt collection of blood for cultures must be followed immediately by empirical antimicrobial therapy. For S. aureus native-valve endocarditis, a combination of antimicrobial agents is often used.

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