Haemophilus influenzae (H. influenzae) is a Gram-negative coccobacillus, commonly associated with human disease in both children and adults. While asymptomatic colonisation begins in the upper airways, it can spread through the respiratory tract, and potentially lead to invasive infections[1].
H. influenzae consists of capsulated strains (serotypes a to f), and non-capsulated strains designated as non-typeable (NTHi). The capsulated H. influenzae type b (Hib) was the predominating disease-causing serotype, with a high incidence of invasive Hib disease including meningitis and sepsis, until the introduction of the efficient polysaccharide capsule vaccine in the late 1980s/early 1990s, which has driven its almost complete disappearance in countries with established child immunisation programs[2], but it promoted the emergence of NTHi strains and non-b serotypes, as the main cause of H. influenzae associated invasive disease cases nowadays[3].
NTHi is a common coloniser of the upper airways in healthy individuals, responsible for multiple acute and chronic infections of the respiratory tract, including otitis media, conjunctivitis, sinusitis and lower respiratory infections in children; exacerbations of chronic obstructive pulmonary disease and cystic fibrosis in adults; and sepsis in neonates, immunocompromised adults, and the elderly[2, 4].
On a genomic basis, encapsulated types of H. influenzae constitute a limited set of clonal populations, while NTHi strains have revealed enormous genomic diversity, mainly due to their intrinsic transformable nature and to the high rate of recombination events they can undergo. NTHi could be divided into six clades[5]. The most common NTHi clade was V (ST3, ST14, ST103, and ST139) followed by clade VI and II, while clades I, III and IV were rarely observed. Virulence and colonization factors are important determinants of disease caused by H. influenzae. Haemophilus adhesion and penetration protein (Hap), high molecular weight proteins 1 and 2 (HMW1/HMW), H. influenzae adhesin/Haemophilus surface fibrils (Hia/hsf), and the pili proteins Hif participate in cell adherence. The hmg locus, encoding a sialylated four-sugar unit that enhances resistance to host immune killing, was associated with clades II, III, IV, and VI. The lpt3 gene, required for phase variable expression of a phosphoethanolamine linked to the Lipooligosaccharide inner core that alters bacterial serum resistance, was associated with clade V[6].
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[1] Bennett J E, Dolin R, Blaser M J. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases E-Book: 2-Volume Set[M]. Elsevier health sciences, 2019.
[2] Jalalvand F, Riesbeck K. Update on non-typeable Haemophilus influenzae-mediated disease and vaccine development[J]. Expert Rev Vaccines, 2018, 17(6): 503-512.
[3] Tsang R S W, Ulanova M. The changing epidemiology of invasive Haemophilus influenzae disease: Emergence and global presence of serotype a strains that may require a new vaccine for control[J]. Vaccine, 2017, 35(33): 4270-4275.
[4] Su Y C, Jalalvand F, Thegerström J, et al. The Interplay Between Immune Response and Bacterial Infection in COPD: Focus Upon Non-typeable Haemophilus influenzae[J]. Front Immunol, 2018, 9: 2530.
[5] De Chiara M, Hood D, Muzzi A, et al. Genome sequencing of disease and carriage isolates of nontypeable Haemophilus influenzae identifies discrete population structure[J]. Proc Natl Acad Sci U S A, 2014, 111(14): 5439-44.
[6] Carrera-Salinas A, González-Díaz A, Calatayud L, et al. Epidemiology and population structure of Haemophilus influenzae causing invasive disease[J]. Microb Genom, 2021, 7(12): 000723.