Sandbox hemophillus

Pathophysiology

Transmission is by direct contact or by inhalation of respiratory tract droplets.
Neonates can acquire infection by aspiration of amniotic fluid or contact with genital tract secretions containing the bacteria.

Incubation period of Hemophilus influenza infection is variable.

The colonizing bacteria invade the mucosa and enter the bloodstream.
Eustachian tube dysfunction, antecedent viral upper respiratory tract infection (URTI), foreign bodies, and mucosal irritants, including smoking, can promote infection.
In patients with underlying chronic obstructive pulmonary disease (COPD) or cystic fibrosis (CF), NTHi frequently colonizes the lower respiratory tract and can exacerbate the disease.

The antiphagocytic nature of the Hib capsule and the absence of the anticapsular antibody lead to increasing bacterial proliferation.
When the bacterial concentration exceeds a critical level, it can disseminate to various sites, including meninges, subcutaneous tissue, joints, pleura, pericardia, and lungs.
The antibody to the Hib capsule plays the primary role in conferring immunity.
Newborns have a low risk of infection, likely because of acquired maternal antibodies.
When these transplacental antibodies to the PRP antigen wane, infants are at high risk of developing invasive H influenzae disease, and their immune responses are low even after the disease.
Therefore, they are at high risk of repeat infections since prior episodes of H influenzae do not confer immunity. By age 5 years, most children have naturally acquired antibodies.
The Hib conjugate vaccine induces protection by inducing antibodies against the PRP capsule.
The Hib conjugate vaccine does not provide protection against NTHi strains. Since the widespread use of the Hib conjugate vaccine, NTHi has become more of a pathogen.