Version May 2024
INTRODUCTION — Haemophilus influenzae are pleomorphic gram-negative rods that commonly colonize and infect the human respiratory tract. The H. influenzae species is divided into typeable (encapsulated) and nontypeable (unencapsulated) strains.
Among typeable strains, H. influenzae serotype b (Hib) is the most virulent. In areas of the world where Hib vaccination is not widespread, Hib is a leading of cause of meningitis and epiglottitis in children and pneumonia in adults. By contrast, in areas where vaccination is routine, the prevalence of Hib has declined, while the prevalence of nontypeable H. influenzae has increased. Nontypeable strains tend to be less virulent than Hib and most commonly cause otitis media and infections of the respiratory tract such as acute rhinosinusitis, acute bronchitis, acute exacerbations of chronic obstructive pulmonary disease, and pneumonia.
The bacteriology, epidemiology, and treatment of H. influenzae are reviewed here. Postexposure chemoprophylaxis and H. influenzae type b vaccination are discussed separately. (See "Prevention of Haemophilus influenzae type b infection".)
MICROBIOLOGY
Taxonomy — There are six typeable (encapsulated) strains of H. influenzae and multiple nontypeable (nonencapsulated) biotypes [1,2]. Typeable strains are classified serologically (a through f) based on distinct polysaccharide antigens on their capsular surfaces. Type b is the most prominent strain, historically accounting for the majority of cases of invasive disease.
Nontypeable strains are classified into biotypes based upon the presence or absence of indole, urease, and ornithine decarboxylase. Nontypeable strains are genetically heterogenous and differ in their pathogenic potential [1,2].
Pathogen — H. influenzae are small, pleomorphic gram-negative rods that are oxidase positive, facultatively anaerobic, and nonmotile. In clinical specimens obtained from patients who have received beta-lactam antibiotics, H. influenzae can appear as filamentous rods.
In vitro growth requires a CO2-enriched atmosphere, hemin (factor X), and nicotinamide adenine dinucleotide (NAD; factor V); therefore, isolation from clinical specimens on solid medium requires the use of chocolate agar or other X and V factor supplemented media. H. influenzae appear as transparent or slightly opaque colonies on solid media.
Transmission — H. influenzae is primarily spread from person to person via airborne droplets or by direct contact with respiratory secretions from infected or colonized individuals [2]. Humans are the only known reservoir for H. influenzae. The nasopharynx is the most common site of long-term colonization. Rarely, H. influenzae can colonize the lower genital tract; direct contact with genital secretions or aspiration of amniotic fluid can lead to infection in neonates [3,4]. The incubation period is unknown [5].
Before widespread immunization, the secondary attack rate with encapsulated type B strains among children who were household contacts of an index case was 0.3 percent, which is 500-fold higher than the age-adjusted risk in the general population [6]. This risk of secondary infection increased inversely with age; children <4 years of age were at greatest risk, and clinical disease was most likely in the first 30 days after exposure to the index case [7-13].
PATHOGENESIS
●Colonization – Colonization of the respiratory mucosa is the first step in pathogenesis for most infections caused by typeable and nontypeable H. influenzae. The outer membrane of H. influenzae contains several adhesins that mediate attachment to the respiratory tract epithelium including pili, fimbriae, high molecular weight factors (HMW1 and HMW2), and Hia (homologous to the pertussis hemagglutinin) [14-18]. Bacterial cell wall lipoproteins (including lipooligosaccharide [LOS]) impair ciliary function, hindering clearance of H. influenzae from the respiratory tract, and also induce local inflammation.
Colonization is a dynamic process, with new strains routinely transiting through the respiratory mucosa [19-21]. In some instances, acquisition of a new strain alone can be sufficient to cause symptomatic respiratory tract infection (eg, a cold in a child or a chronic obstructive pulmonary disease exacerbation in an adult). Other infections, such as acute otitis media or rhinosinusitis, result from direct extension along the respiratory mucosa to a new site. Direct extension is likely facilitated by a high density of colonizing bacteria coupled with their ability to form biofilms.
●Mucosal infection – Infection at mucosal surfaces is further facilitated by bacterial production of immunoglobulin (Ig)A proteases, which cleave IgA at its hinge region thereby inhibiting agglutination, bacterial binding, and opsonization [22-24]. Nontypeable strains also evade the immune system by surviving intracellularly in respiratory epithelial cells and macrophages, providing a site for persistent colonization.
●Invasive infection – Tissue invasion is also a critical pathogenic feature. Invasive disease refers to infection that extends beyond the respiratory tract. Invasive clinical syndromes caused by H. influenzae include meningitis, bacteremia, epiglottitis, septic arthritis, cellulitis, purulent pericarditis, endocarditis, and osteomyelitis [25].
Most invasive infections are caused by H. influenzae type b (Hib). The type b capsule contains polyribitol ribose phosphate, a potent virulence factor, which enables invasion of local tissue, the bloodstream, and, in some instances, the central nervous system [21,26]. The other capsular serotypes have a different glycosylation pattern and less frequently cause invasive disease compared with Hib. Nontypeable strains are less invasive but can access the vascular system by transmural migration through epithelial tight junctions or by an independent intercellular mechanism [27].
IMMUNITY — Innate and acquired humoral immunity play important roles in host defense. Structural defenses such as mucociliary function are first-line defenses. The mucociliary apparatus promotes clearance and prevents spread to the lower respiratory tract. When impaired (eg, cystic fibrosis, chronic obstructive pulmonary disease, other structural lung diseases), rates of lower respiratory tract colonization and infection rise.
H. influenzae lipooligosaccharide activates the alternative complement pathway, stimulating C3b opsonization and subsequent bacterial phagocytosis. The importance of early complement in immune control is evinced by the observation that individuals with early complement deficiency are at increased risk for H. influenzae infections [28].
Mechanisms for adaptive immune control of typeable and nontypeable H. influenzae differ. The antibody response to nontypeable strains is typically strong and bactericidal [29]. Bactericidal activity is mediated by the membrane-attack complex of the classical (antibody-mediated) complement pathway. In animal models, immunization with one nontypeable strain appears to provide protection against invasive infection with other nontypeable strains. This finding may explain why nontypeable strains are primarily mucosal pathogens that rarely spread beyond the respiratory tract. By contrast, typeable strains have a dense polysaccharide capsule, which renders greater resistance to complement-mediated killing and phagocytosis, thus enabling systemic infection.
Protection against invasive H. influenzae type b (Hib) infections is mediated by antibodies to the type b capsular polysaccharide polyribitol ribose phosphate (PRP). Newborns are protected against Hib by maternal antibodies, but they are susceptible to infection with nontypeable (unencapsulated) strains [30]. Breastfeeding affords some protection against H. influenzae [31]. As maternal antibody levels wane, children become susceptible to invasive Hib infection from around age 3 months to 3 years. Conjugate vaccines targeting PRP are highly effective at reducing systemic infections in young children and subsequently infections in the population via herd immunity.
Prior to routine use of conjugate vaccines, children older than three years of age progressively gained protection against invasive disease with repeated exposure and subsequent nasopharyngeal colonization. The decline in individual serum anti-Hib antibody levels observed since introduction of Hib vaccination suggests that ongoing antigen exposure in the setting of Hib colonization may play a role Hib immunity [30,32].
EPIDEMIOLOGY
Colonization
Nasopharyngeal colonization — H. influenzae, particularly nontypeable H. influenzae (NTHi), is a common commensal of the nasopharynx [33-35]. Approximately 20 percent of infants are colonized in the first year of life, and more than one half of children are colonized by age 5 years [35]. Children may simultaneously be colonized by multiple distinct strains and colonizing strains may change over time [6,36-38]. Colonization can persist for months, during which intercurrent upper respiratory infection may promote invasive disease and transmission to close contacts [6,39-41]. Colonization persists throughout adulthood [42].
The use of conjugate H. influenzae serotype b (Hib) vaccines in infancy has been associated with reduced prevalence of nasopharyngeal Hib carriage (from approximately 2 to 7 percent in the prevaccine era to <1 percent in the postvaccine era in the United States [43,44]). Reduction in carriage appears to be influenced by the number and type of Hib immunizations and the time elapsed since the last immunization [45]. The differences in international immunization schedules may result in differing carriage and disease patterns.
Genital tract colonization — NTHi can also colonize the female genital tract and cause locally invasive disease, such as endometritis, amnionitis, or Bartholin gland abscess, with or without accompanying bacteremia [3,46]. (See 'Nontypeable H. influenzae' below.)
Hib invasive disease — Universal immunization of infants against H. influenzae type b (Hib), which began in the early 1990s and is practiced in nearly all developed countries [47], has been associated with dramatic declines in the incidence of invasive Hib disease in children <5 years of age [48-50].
As the number of countries using Hib vaccines increased between 2000 and 2015, the estimated number of worldwide cases of severe Hib disease in children <5 years of age declined from >8 million to 340,000 [48,49]. Estimated Hib-related deaths among children <5 years of age also declined from 371,000 to <30,000.
Based on surveillance conducted in the United States, the incidence of invasive Hib disease in children <5 years of age declined from >20 cases per 100,000 children in the prevaccine era to ≤0.25 cases per 100,000 children during 2000 to 2012 (figure 1) [50]. In 2018, the reported incidence in children <5 years of age was 0.08 per 100,000 children [51]. Between 2009 and 2015, the incidence of invasive Hib disease in children ≥5 years of age and adults was <0.05 per 100,000 population [52].
Hia invasive disease — Recent surveillance data has demonstrated H. influenzae type a (Hia) has increased since 2008 by an average of 11.1 percent annually. Hia can cause invasive disease similar to Hib. The estimated annual incidence is 0.10 cases/100,000 persons per year, with the highest incidence among American Indian and Alaska Native children (8.29 cases/100,000 persons per year among those <5 years of age), with the highest incidence among Alaska Native children <1 year of age of 24.7 cases/100,000 persons per year. Currently, no vaccine against Hia exists [53].
Nontypeable H. influenzae and non-b encapsulated serotypes — Although the overall incidence of invasive disease due to NTHi and non-b encapsulated serotypes remains low, since 2000, there has been an increased recognition of invasive disease due to NTHi and non-b serotypes (eg, serotypes a, e, and f) in children and adults [52-63].
NTHi causes the majority of invasive H. influenzae infections in all age groups. During the period between 2009 and 2015, the incidence of invasive disease due to NTHi was 1.22 per 100,000 population and the incidence of invasive disease due to non-b serotypes was 0.45 per 100,000 population in the United States [52].
NTHi and non-b encapsulated serotype invasive disease predominantly occurs in the oldest and youngest age groups. During 2009 to 2015, the incidence of NTHi invasive disease was 4.99 per 100,000 adults ≥65 years of age and 5.63 per 100,000 infants <1 year of age; many of the cases in infants occurred in those who were <1 month of age, preterm, or low birth weight [52]. The incidence of non-b encapsulated serotype invasive disease was 1.27 per 100,000 adults ≥65 years and 2.53 per 100,000 infants <1 year of age.
Similar trends of increasing invasive disease due to NTHi and non-b serotypes have been noted in other countries [56,57,64]. It is unclear whether these changes are related to vaccine-mediated strain replacement, improved bacterial detection and serotyping, increased virulence of NTHi strains, or demographic changes [64].
Risk factors — Risk factors for invasive Hib infection include [50,65]:
●Age <5 years and incomplete Hib immunization
●Functional or anatomic asplenia, including sickle cell disease
●HIV infection
●Immunoglobulin deficiency and other deficits in humoral immunity (see "Primary humoral immunodeficiencies: An overview")
●Early component complement deficiency
●Hematopoietic cell transplant recipient
●Chemotherapy or radiation therapy for malignancy [65]
Native American children (including Alaska Native children, Indigenous (Aboriginal) children in Canada, and Aboriginal Australian children) appear to be at increased risk for invasive H. influenzae disease compared with the general population [52,66-68].
In adults, typeable and nontypeable H. influenzae disease has been associated with underlying conditions such as structural lung disease (eg, cystic fibrosis, chronic obstructive pulmonary disease, bronchiectasis), smoking, alcoholism, pregnancy, and older age [52,69-72]. Socioeconomic factors that increase the risk of H. influenzae disease include crowding, incomplete Hib immunization, and daycare attendance [6].
CLINICAL MANIFESTATIONS
Hib and non-b encapsulated serotypes — In the post-H. influenzae type b (Hib) conjugate vaccine era, serious Hib infections are rare [73,74]. Invasive disease occurs predominantly in infants and young children who are unimmunized or incompletely immunized against Hib and in older children and adults with immune-compromising conditions [50,75].
Hib can cause a number of clinical syndromes, including [5,76,77]:
●Meningitis
●Bacteremia
●Otitis media
●Epiglottitis
●Uvulitis
●Community-acquired pneumonia and empyema
●Exacerbations of chronic obstructive pulmonary disease (COPD)
●Pericarditis
●Septic arthritis
●Cellulitis, including buccal, preseptal, and orbital cellulitis
Less common manifestations include endocarditis, endophthalmitis, osteomyelitis, peritonitis, and necrotizing soft tissue infections [5].
Non-b serotypes can cause the same clinical syndromes as Hib [55,78-83]. In population- and laboratory-based surveillance of invasive disease caused by serotype a from eight sites in the United States, meningitis was the most common manifestation in children <1 year old, whereas bacteremic pneumonia was the most common manifestation in adults ≥50 years old [78].
Although infections due to invasive Hib and non-b serotypes are rare, they are associated with substantial mortality. In United States surveillance between 2009 and 2015, the case-fatality rate was 4 percent for invasive Hib disease and 11 percent for non-b serotype invasive disease.
Nontypeable H. influenzae — Nontypeable H. influenzae (NTHi) strains typically cause noninvasive mucosal infections in older children and adults, usually as a result of local spread of organisms from the nasopharynx [64,84]. It is an important cause of sinusitis, acute otitis media, conjunctivitis, chronic obstructive pulmonary disease exacerbations, and community-acquired pneumonia in children and adults [34,85-87].
Rarely, NTHi causes locally invasive genital tract infections (eg, endometritis, amnionitis, Bartholin gland abscess) with or without accompanying bacteremia [46].
In the post-Hib conjugate vaccine era, NTHi has also been identified as a cause of invasive infections (eg, bacteremia, meningitis, sepsis), particularly in older adults and young infants [34,50,52]. Among pregnant women, infection with NTHi has been associated with preterm birth, fetal loss, and neonatal sepsis [70,88,89].
Invasive NTHi infection is associated with increased mortality. In United States surveillance between 2009 and 2015, the case-fatality rate for invasive NTHi infection was 16 percent [52].
DIAGNOSIS
Approach to testing
Respiratory infections — For most respiratory infections caused by H. influenzae (typeable and nontypeable), a diagnosis is usually made based on the characteristic signs and symptoms of the particular syndrome (eg, acute otitis media, conjunctivitis, exacerbation of chronic obstructive pulmonary disease).
An etiologic diagnosis usually is not sought in uncomplicated noninvasive respiratory tract infections because empiric antimicrobial therapy typically includes activity against H. influenzae and isolation of H. influenzae from respiratory tract specimens does not differentiate colonization from infection. (See 'Empiric treatment' below and 'Colonization' above.)
Invasive infections — For patients with invasive disease (eg, bacteremia, meningitis, septic arthritis), the diagnosis of H. influenzae infection is confirmed by detection of H. influenzae through traditional culture or polymerase chain reaction (PCR)-based assays [90,91].
●Culture – Culture is highly specific for H. influenzae but may have poor sensitivity in patients who have received antibiotics or if specimens have not been handled properly [90]. Culture permits testing of isolates for beta-lactamase activity as a predictor of ampicillin resistance; in addition, isolates may be examined for resistance to other antimicrobials of potential clinical use. If necessary for epidemiologic investigations or decisions regarding chemoprophylaxis for Hib, isolates can be sent to a public health laboratory for serotyping.
If available, matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry is another method for identifying and typing H. influenzae with high sensitivity and specificity [90,91]. Turn-around time is shorter than for traditional serotyping methods. MALDI-TOF cannot differentiate between typeable and nontypeable H. influenzae and does not permit susceptibility testing.
Culture of specimens for specific clinical syndromes is discussed in the topic reviews related to those syndrome (eg, meningitis, bacteremia, septic arthritis, complicated pneumonia). Examples of appropriate specimens include cerebrospinal fluid, blood, and synovial fluid [91]. The microbiologic characteristics and growth requirements for H. influenzae are described above. (See 'Pathogen' above.)
●PCR-based assays – PCR-based assays have high sensitivity and specificity and rapid turn-around time and can be used in patients who received antibiotics before the specimen was obtained [90]. Some PCR assays can differentiate between serotypes, but they do not permit testing for antimicrobial resistance.
Commercial multiplex PCR assays are available for bloodstream, respiratory tract, and central nervous system (CNS) infections. Most of these assays do not identify serotype.
When H. influenzae is identified by PCR, laboratories should perform a culture or send a sample to a state lab for culture to determine serotype and antimicrobial susceptibility and to allow for more accurate surveillance [92].
Molecular testing for CNS infections is discussed separately. (See "Molecular diagnosis of central nervous system infections".)
Susceptibility testing — Most clinical laboratories perform a rapid assay for beta-lactamase production, which is the main mechanism of antimicrobial resistance. When the assay is positive, isolates can be considered to be resistant to ampicillin, amoxicillin, penicillin, and first-generation cephalosporins but susceptible to combination beta-lactam-beta-lactamase inhibitors (eg, amoxicillin-clavulanate, ampicillin-sulbactam, piperacillin-tazobactam), extended-spectrum cephalosporins, and carbapenems. A negative beta-lactamase assay indicates that the isolate is likely susceptible to ampicillin but does not fully exclude the possibility of ampicillin resistance, which is less commonly mediated by other mechanisms (eg, alterations in cell-wall penicillin-binding proteins). Additional susceptibility testing is not widely available but is generally unnecessary because antimicrobial resistance patterns are predictable.
TREATMENT
Empiric treatment — Most infections caused by H. influenzae are treated empirically. In general, empiric regimens are designed to include an antibiotic that treats H. influenzae. Antibiotics that have activity against H. influenzae include beta-lactams (eg, amoxicillin, amoxicillin-clavulanate, or second- and third-generation cephalosporins), fluoroquinolones, macrolides, and tetracyclines.
Beta-lactams are generally preferred. Amoxicillin-clavulanate is a commonly used empiric treatment option for localized and non-life-threatening infections, such as otitis media, sinusitis, and acute exacerbations of chronic obstructive pulmonary disease. In patients with systemic infections, such as bacteremia or meningitis, ceftriaxone is the treatment of choice. (See 'Ampicillin resistance' below.)
Empiric regimens for specific syndromes caused by H. influenzae are discussed separately:
●Community-acquired pneumonia in adults (see "Treatment of community-acquired pneumonia in adults in the outpatient setting" and "Treatment of community-acquired pneumonia in adults who require hospitalization")
●Community-acquired pneumonia in children (see "Community-acquired pneumonia in children: Outpatient treatment" and "Pneumonia in children: Inpatient treatment")
●Bacterial meningitis (see "Initial therapy and prognosis of community-acquired bacterial meningitis in adults")
●Epiglottitis (see "Epiglottitis (supraglottitis): Management", section on 'Antimicrobial therapy')
●Chronic obstructive pulmonary disease exacerbation (see "Management of infection in exacerbations of chronic obstructive pulmonary disease", section on 'Empiric antibacterial treatment')
●Sinusitis (see "Uncomplicated acute sinusitis and rhinosinusitis in adults: Treatment", section on 'Antibiotics' and "Acute bacterial rhinosinusitis in children: Microbiology and management", section on 'Empiric antibiotics')
Directed treatment — For patients with microbiologically diagnosed H. influenzae infections, antibiotic selection depends on the site and severity of infection and, when available, the results of laboratory susceptibility tests:
●For patients with mild to moderate infections treated in the outpatient setting (eg, chronic obstructive pulmonary disease exacerbations, pneumonia), we generally use an oral beta-lactam (such as amoxicillin-clavulanate) or an oral second- or third-generation cephalosporin (such as cefuroxime, cefdinir, cefixime, or cefpodoxime).
●For patients with severe infections (eg, meningitis, epiglottitis, bacteremia, or other respiratory tract infections requiring hospitalization), we typically use an intravenous third-generation cephalosporin such as ceftriaxone or cefotaxime. Because of the severity of such infections, we avoid treatment with ampicillin unless the infecting pathogen has been shown to be beta-lactamase negative.
For children with known or suspected H. influenzae meningitis, giving adjunctive dexamethasone at the time antibiotics are started (or just before) appears to improve outcomes. (See "Bacterial meningitis in children: Dexamethasone and other measures to prevent neurologic complications".)
Because antimicrobial susceptibility patterns vary regionally and susceptibility testing is not routinely available, modifications to this approach may be needed, particularly in areas where ampicillin resistance is high. (See 'Ampicillin resistance' below.)
Alternative options to cephalosporins include fluoroquinolones, tetracyclines, and carbapenems.
Ampicillin resistance — The production of a beta-lactamase, which confers resistance to ampicillin, amoxicillin, and penicillin, is the major mechanism of antimicrobial resistance among typeable and nontypeable H. influenzae strains. In the United States, approximately 25 to 28 percent of H. influenzae strains are estimated to produce beta-lactamase [93,94]. Beta-lactamase-producing strains typically remain susceptible to beta-lactam-beta-lactamase inhibitor combinations (ie, amoxicillin-clavulanate, ampicillin-sulbactam), second- and third-generation cephalosporins, and carbapenems.
Infrequently, resistance to ampicillin can be mediated by mechanisms other than beta-lactamase production (eg, alterations in penicillin-binding proteins) [95]. Isolates with this resistance pattern are termed beta-lactamase negative ampicillin resistant (BLNAR). Such isolates have been most commonly described in Asia [57,95-101]. While their clinical significance is unknown, most reported BLNAR isolates appear to be susceptible to ceftriaxone [101].
Resistance rates to most other antibiotics (ie, fluoroquinolones, tetracyclines) are generally low (ie, approximately 1 to 5 percent) [93,96,102-105]. Trimethoprim and trimethoprim-sulfamethoxazole may be exceptions [93]; H. influenzae are not reliably susceptible to these agents; thus, they are not used for treatment.
PREVENTION — Because H. influenzae is transmitted by respiratory droplets and direct contact with secretions, respiratory and hand hygiene are key to preventing spread. The United States Centers for Disease Control and Prevention recommend both standard and droplet precautions for hospitalized patients with invasive H. influenzae infections (ie, pneumonia in children, meningitis, epiglottitis) [106]. These precautions can generally be discontinued 24 hours after effective therapy has been given.
Postexposure chemoprophylaxis for at-risk patients and H. influenzae type b vaccination are discussed separately. (See "Prevention of Haemophilus influenzae type b infection".)
SUMMARY AND RECOMMENDATIONS
●Microbiology – Haemophilus influenzae are pleomorphic gram-negative bacilli that commonly colonize and infect the respiratory tract. Humans are the only known reservoir, and H. influenzae are primarily spread from person to person via airborne droplets or by direct contact with respiratory secretions. (See 'Introduction' above and 'Transmission' above.)
●Encapsulated and unencapsulated strains – The H. influenzae species is divided into typeable (encapsulated) and nontypeable (unencapsulated) strains. Among typeable strains, H. influenzae type b (Hib) is the most virulent. (See 'Microbiology' above.)
●Incidence – In the post-Hib conjugate vaccine era, invasive Hib disease in children <5 years of age is rare. Although the overall incidence of invasive disease due to nontypeable H. influenzae (NTHi) and non-b serotypes remains low, there has been an increase in the identification of invasive disease due to NTHi and non-b serotypes in children and adults, predominantly affecting adults ≥65 years and infants <1 month of age. (See 'Hib invasive disease' above and 'Nontypeable H. influenzae and non-b encapsulated serotypes' above.)
●Risk factors – Risk factors for invasive Hib infection include age <5 years and incomplete Hib immunization, functional or anatomic asplenia (including sickle cell disease), HIV infection, immunoglobulin deficiency and other deficits in humoral immunity, early component complement deficiency, hematopoietic cell transplant recipient, and chemotherapy or radiation therapy for malignancy. In adults, typeable and nontypeable H. influenzae disease has been associated with underlying conditions such as structural lung disease (eg, cystic fibrosis, chronic obstructive pulmonary disease [COPD], bronchiectasis), smoking, alcoholism, pregnancy, and older age. (See 'Risk factors' above.)
●Clinical manifestations
•Encapsulated strains – Clinical manifestations of Hib and non-b serotypes include meningitis, bacteremia, otitis media, epiglottitis, community-acquired pneumonia and empyema, pericarditis, septic arthritis, and cellulitis. Invasive Hib and non-b serotype disease is associated with increased mortality. (See 'Hib and non-b encapsulated serotypes' above.)
•Unencapsulated strains – NTHi typically causes noninvasive mucosal infections in older children and adults. It is an important cause of sinusitis, acute otitis media, conjunctivitis, COPD exacerbations, and community-acquired pneumonia in children and adults. In the post-Hib conjugate vaccine era, NTHi has also been identified as a cause of invasive infections (eg, bacteremia, meningitis, sepsis). Invasive NTHi infection is associated with increased mortality. (See 'Nontypeable H. influenzae' above.)
●Diagnosis – For most respiratory infections caused by H. influenzae, a diagnosis is usually made clinically; an etiologic diagnosis usually is not sought because empiric antimicrobial therapy typically includes activity against H. influenzae. For patients with invasive disease, the diagnosis of H. influenzae is confirmed by detection of H. influenzae through traditional culture or polymerase chain reaction-based assays. (See 'Diagnosis' above.)
●Antibiotic treatment
•Beta-lactams preferred – Beta-lactam antibiotics (ie, amoxicillin, amoxicillin-clavulanate, or second- and third-generation cephalosporins) are preferred for treatment. Other antibiotics with activity against H. influenzae include fluoroquinolones, tetracyclines, and carbapenems. (See 'Treatment' above.)
•Severe infections and ampicillin resistance – Because of potential ampicillin resistance, we generally use intravenous third-generation cephalosporins (eg, ceftriaxone, cefotaxime) when treating severe infections such as meningitis, epiglottitis, and bacteremia. (See 'Directed treatment' above and 'Ampicillin resistance' above.)
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