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92 INFECTIONS CAUSED BY HAEMOPHILUS, BORDETELLA, MORAXELLA, AND HACEK GROUP ORGANISMS

92 INFECTIONS CAUSED BY HAEMOPHILUS, BORDETELLA, MORAXELLA, AND HACEK GROUP ORGANISMS
Harrison’s Manual of Medicine

92

INFECTIONS CAUSED BY HAEMOPHILUS, BORDETELLA, MORAXELLA, AND HACEK GROUP ORGANISMS

Haemophilus Influenzae
Bordetella Pertussis
Moraxella Catarrhalis
Hacek Group Organisms
Bibliography

HAEMOPHILUS INFLUENZAE
ETIOLOGY   H. influenzae is a small pleomorphic coccobacillary gram- negative pathogen that often stains only faintly with phenosafranin and therefore can easily be overlooked. The six capsular polysaccharide–based serotypes are designated a through f. H. influenzae type b (Hib) and unencapsulated strains, termed nontypable H. influenzae (NTHi), are the most frequently isolated pathogens.
PATHOGENESIS   H. influenzae is part of the normal oropharyngeal flora and causes systemic disease by invasion and hematogenous spread to distant sites such as the meninges, bones, and joints. The type b capsular polysaccharide is an antiphagocytic barrier. NTHi strains cause disease by local invasion of mucosal surfaces. The incidence of invasive disease caused by nontypable strains is low but increasing.
EPIDEMIOLOGY   H. influenzae is spread by airborne droplets or by direct contact with secretions or fomites. NTHi strains colonize up to 75% of healthy adults. Since 1991, vaccines of type b capsular polysaccharide conjugated to carrier proteins have greatly reduced rates of Hib meningitis among children. The rate of nasopharyngeal colonization by Hib strains has similarly decreased.
CLINICAL MANIFESTATIONS   H. influenzae is the second most common cause of community-acquired pneumonia, especially in elderly adults, pts with chronic lung disease or prolonged tobacco use, and pts with HIV infection. More than 80% of isolates from cases of pneumonia are NTHi. Obstetric infections caused by NTHi are severe and are an important source of neonatal bacteremia. NTHi causes sinusitis in adults and children. In addition, it is a less common cause of empyema, adult epiglottitis, pericarditis, cellulitis, septic arthritis, osteomyelitis, endocarditis, cholecystitis, intraabdominal infection, UTI, mastoiditis, aortic graft infection, and bacteremia without a detectable focus.
Hib is a pathogen affecting mainly children, causing meningitis, epiglottitis, cellulitis, and pneumonia.
DIAGNOSIS   The most reliable method for diagnosing H. influenzae infection is culture. Agglutination assays, immunoelectrophoresis, and ELISA are useful for antigen detection in clinical specimens.

TREATMENT
Initial therapy for meningitis due to Hib in adults should consist of 1–2 weeks of ceftriaxone (2 g q12h IV) or cefotaxime (2 g q4–6h IV); pediatric doses are 75–100 (mg/kg)/d of ceftriaxone, given in 2 doses 12 h apart, and 200 (mg/kg)/d of cefotaxime, given in 4 doses 6 h apart. An alternative regimen is ampicillin (200–300 mg/kg qd in 4 divided doses) plus chloramphenicol (75–100 mg/kg qd in 4 divided doses). Early administration of glucocorticoids (dexamethasone, 0.6 mg/kg IV qd for 2 d) protects against hearing loss in children with Hib meningitis. Invasive infections other than meningitis are treated with the same regimens. Approximately 25% of NTHi strains produce b-lactamase and are resistant to ampicillin. Infections caused by ampicillin- resistant strains can be treated with trimethoprim-sulfamethoxazole (TMP- SMZ), amoxicillin/clavulanic acid, various extended-spectrum cephalosporins, clarithromycin, and azithromycin. Fluoroquinolones are highly active against H. influenzae but are not currently recommended for treatment of children or pregnant women. Unvaccinated school and household contacts of children infected with Hib should receive prophylaxis with rifampin (20 mg/ kg qd, up to 600 mg, for 4 d). All children should be immunized with an Hib conjugate vaccine.

BORDETELLA PERTUSSIS
ETIOLOGY   Humans are the sole host for the gram-negative coccobacillus B. pertussis, which grows slowly on selective media.
PATHOGENESIS   B. pertussis attaches to the ciliated epithelial cells of the nasopharynx, adhering via filamentous hemagglutinin and pertactin. The organism elaborates pertussis toxin, which exerts a number of biologic effects and probably plays a role in producing the pertussis clinical syndrome.
EPIDEMIOLOGY   Pertussis (whooping cough) is probably underdiagnosed. Rates of communicability to nonimmune household contacts of pertussis pts are 80–100%. There is an increasing incidence of pertussis among adolescents and adults. A number of studies suggest that pertussis may be the etiology in 12–30% of adults with cough that does not improve within 2 weeks. Severe morbidity and mortality are virtually restricted to infants.
CLINICAL MANIFESTATIONS   Pertussis infection incubates for 7–10 d. The three stages of illness are catarrhal (1–2 weeks), paroxysmal (2–4 weeks), and convalescent (1–3 months). Coughing is distinctive: 5–10 coughs per spasm, which may be terminated by an audible whoop. Features predictive of pertussis are vomiting with cough, nighttime cough, and exposure to persons with a prolonged coughing illness.
DIAGNOSIS   In the absence of classic symptoms, distinguishing pertussis from other causes of respiratory tract infection is difficult. Lymphocytosis is common only in young children. For the isolation of B. pertussis, a nasopharyngeal swab or aspirate is immediately inoculated onto selective media. Polymerase chain reaction of nasopharyngeal specimens may increase the yield and is helpful in pts treated with antibiotics. At present, no serologic test is commercially available, and no specific serologic criteria are defined.

TREATMENT
Treatment does not alter the clinical course unless given early in the catarrhal phase; thus the purpose of therapy is to eradicate B. pertussis from the nasopharynx. Erythromycin (preferably estolate), at 50 (mg/kg)/d (maximum, 2 g/d) in 3 divided doses, is the recommended regimen; 1 g/d is effective and may be better tolerated. A 7-d course of therapy is as effective as a 2-week course. It is recommended that household and other close contacts be treated with the same regimen, regardless of age and immunization status. The average estimated efficacy for whole-cell vaccine is 85%. New acellular vaccines cause fewer adverse reactions.

MORAXELLA CATARRHALIS
ETIOLOGY/EPIDEMIOLOGY   Moraxella (Branhamella) is a gram- negative diplococcus that colonizes the upper airways of 50% of healthy school children and 7% of adults. The incidence of infections peaks in late winter/early spring.
CLINICAL MANIFESTATIONS   M. catarrhalis causes otitis media, tracheobronchitis, pneumonia, and rare cases of empyema, bacteremia, septic arthritis, meningitis, and endocarditis. The majority of respiratory infections occur in patients >50 years of age who have chronic pulmonary disease.
DIAGNOSIS   Gram’s staining of sputum reveals gram-negative diplococci. M. catarrhalis is easily grown on blood or chocolate agar.

TREATMENT
b-Lactamase production is detected in 85% of M. catarrhalis isolates. Amoxicillin/clavulanate, a second- or third-generation cephalosporin, erythromycin, quinolones, tetracycline, chloramphenicol, and TMP-SMZ are all effective against M. catarrhalis infection. A 5-day course cures respiratory infection.

HACEK GROUP ORGANISMS
ETIOLOGY   Haemophilus aphrophilus, H. paraphrophilus, H. parainfluenzae, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae are fastidious, CO2-requiring pathogens.
PATHOGENESIS   The HACEK organisms colonize the oral cavity and can cause severe systemic infections, most often endocarditis. In fact, up to 3% of endocarditis cases are caused by HACEK organisms, most commonly the Haemophilus species, A. actinomycetemcomitans, and C. hominis.
CLINICAL MANIFESTATIONS   Endocarditis due to HACEK organisms can be insidious or complicated, with major emboli in 28–60% of cases.
DIAGNOSIS   Blood cultures may require up to 30 days to become positive, although most are positive in the first week.

TREATMENT
Treatment with ceftriaxone (2 g/d IV) is a reasonable initial approach for HACEK endocarditis. Most cases of C. hominis endocarditis are treated with penicillin (16–18 million U/d IV in 6 divided doses) with or without an aminoglycoside (5–6 mg/kg qd IV in 3 divided doses). Treatment should be administered for 6 weeks. Unlike prosthetic valve endocarditis caused by other gram-negative rods, that due to HACEK organisms is often cured with antibiotics alone.

Bibliography

For a more detailed discussion, see Musher DM: Moraxella catarrhalis and Other Moraxella Species, Chap. 148, p. 938; Murphy TF: Haemophilus Infections, Chap. 149, p. 939; Kasper DL, Barlam TF: Infections due to the HACEK Group and Miscellaneous Gram-Negative Bacteria, Chap. 150, p. 942; and Halperin SA: Pertussis and Other Bordetella Infections, Chap. 152, p. 949, in HPIM-15.

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