Chapter 128. Pneumococcal Infections (Part 2) pptx

Pneumococcal Infections Part 2 Nonimmunologic Mechanisms Nonimmunologic mechanisms that protect against pneumonia include filtration of air as it passes through the nasopharynx, the gl

Chapter 128 Pneumococcal Infections

(Part 2)

Nonimmunologic Mechanisms

Nonimmunologic mechanisms that protect against pneumonia include

filtration of air as it passes through the nasopharynx, the glottal reflex, laryngeal

closure, the cough reflex, clearance of organisms from the lower airways by

ciliated cells, and ingestion by pulmonary macrophages and PMNs of small

bacterial inocula that manage to reach alveolar spaces Respiratory virus infection,

chronic pulmonary disease, or heart failure compromises these mechanisms,

predisposing to the development of pneumococcal pneumonia

Immunologic Mechanisms

Innate Immunity

Innate immune mechanisms participate in clearance of pneumococci from

the nasopharynx as well as in phagocytosis by PMNs and macrophages via the

microbial pattern recognition receptor Toll-like receptor 2 (TLR2)

Humoral Immunity

Immunologically specific humoral mechanisms provide the best protection

against pneumococcal infection Most healthy adults have antibody to constituents

of S pneumoniae, such as PspA, PsaA, and the cell wall; however, there is no

convincing evidence for an opsonic role of these antibodies, especially at their

usual concentrations Most healthy adults lack IgG antibody to the majority of

pneumococcal capsular polysaccharides Antibody appears after colonization,

infection, or vaccination In the first few weeks after colonization, nonspecific

mechanisms probably protect the host from infection Thereafter, newly developed

anticapsular antibody provides a high degree of specific protection Adults who

are at risk of aspirating pharyngeal contents and/or who have diminished

mechanisms of lower airway clearance are at risk of developing pneumonia before

antibody is produced Persons with a diminished capacity to form antibody

probably remain susceptible as long as they are colonized

The risk of serious pneumococcal infection is greatly increased in persons

with conditions that compromise IgG synthesis and/or the phagocytic function of

PMNs and macrophages Most patients hospitalized for pneumococcal pneumonia

have one or more of these conditions (Table 128-1) Once a pneumococcal

infection has been initiated, the absence of a spleen predisposes to fulminant

disease The liver can remove opsonized (antibody-coated) pneumococci from the

circulation; in the absence of antibody, however, only the slow passage of blood

through the splenic sinuses and prolonged contact with reticuloendothelial cells in

the cords of Billroth can result in bacterial clearance Patients without spleens tend

to develop overwhelming pneumococcal disease that rapidly progresses to death

Table 128-1 Conditions that Commonly Predispose to Pneumococcal Infection

Increased risk of exposure

Day-care centers

Military training camps

Prisons

Shelters for the homeless

Respiratory infection, inflammation

Influenza, other viral respiratory

infections

Air pollution

Allergies

Defective complement

function

Defective bacterial

clearancea

Congenital asplenia,

hyposplenia

Splenectomy

Sickle cell disease

Multifactorial conditions

Infancy and aging

Cigarette smoking

Chronic obstructive pulmonary disease

Other causes of chronic pulmonary

inflammation or obstruction

Anatomical disruption of meninges

(dural tear)

Defective antibody formation

Common variable

hypogammaglobulinemia

Selective IgG subclass deficiency

Multiple myeloma

Chronic lymphocytic leukemia

Lymphoma

Chronic disease

Alcoholism

Prior hospitalization

Malnutrition

HIV infection

Chronic lung disease

Glucocorticoid treatment

Cirrhosis of the liver

Renal insufficiency

Diabetes mellitus

Anemia

Coronary artery disease

Fatigue, stress, and/or

exposure to cold

The absence of a spleen predisposes to more fulminant infection (see text)