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Persons who have recovered from pneumococcal pneumonia respond initially to vaccination, but no longer have detectable levantibody at 6 months.

The Immunization Practices Advisory Committee of the Centers for Disease Control and Prevention (CDC) now recommends PPV23 for: All persons over the age of 2 years who are at substantially increased risk of developing pneumococcal infection and/or a serious complication of such an infection. General categories included within these recommendations are those persons who: (1) are over the age of 65 years; (2) have anatomic or functional asplenia, CSF leak, diabetes mellitus, alcoholism, cirrhosis, chronic renal insufficiency, chronic pulmonary disease (including asthma), or advanced cardiovascular disease; (3) have an immune compromised condition that is associated with increased risk of pneumococcal disease, such as multiple myeloma, lymphoma, Hodgkin disease, HIV infection, organ transplantation, or chronic use of glucocorticosteroids; (4) are genetically at increased risk, such as Alaskan and American buy amoxicillin 250mg Natives(5) who live in special environments where outbreaks may occur, such as nursing homes. Recommendations regarding revaccination seem to be somewhat inconsistent because the committee advocates a single revaccination in persons over the age of 65 years as well as most others. Since antibody levels decline and there is no anamnestic response, it seems more reasonable simply to recommend: Revaccination at 5 to 7 year intervals, particularly in adults over the age of 65 years, who will have a minimal local reaction.

Hyporesponsiveness (the failure to make antibody to a second vaccination when given soon after a first vaccination) is not seen 5 years after prior vaccination.

Revaccination every 5 years for persons who are at highest risk of recurring pneumococcal infection—those who have undergone splenectomy or have a CSF leak.

Infants and young children do not make antibody after vaccination with pure polysaccharide antigens.

However, when pneumococcal capsular polysaccharides have been covalently conjugated to carrier proteins, the resulting antigens are recognized as T-cell dependent; they stimulate good antibody responses in children under the age of 2 years and induce immunologic memory. In a field trial involving 38,000 infants and toddlers, vaccination with PCV7 produced a brilliant response, being followed by a 90% decrease in pneumococcal meningitis. Widespread introduction of PCV7 in the pediatric population in 2000 decreased disease due to vaccine serotypes by ?90%, both in vaccinated and nonvaccinated subjects.

The decrease in incidence in unvaccinated persons is called the “herd effect;” it occurs because PCV immunizes against colonization as well as against infection, and that effect reduces the prevalence of vaccine-type pneumococci in the population at large.

An untoward result of widespread vaccination has been the appearance of new strains that are not contained in the vaccine; these are called replacement strains.

The principal one, type 19A, has become the predominant cause of pneumococcal disease in all age groups in the United States. This serotype is included in PCV13 which was put into widespread use in 2010. Hopes that protein conjugation would greatly enhance antibody responses have not been fulfilled. A comparison cvs amoxicillin over the counter of antibody levels and opsonic effect after vaccination with PPV23 versus PCV showed remarkably few differences or modestly higher antibody levels after PCV. On the other hand, some congenital nonresponders to PPV23 do respond to PCV, and two large studies in African patients with acquired immune deficiency syndrome (AIDS) showed no protection from PPV23 vs.

excellent protection in the year following PCV7, respectively. A large field trial of PCV13 has shown that PPV23 protects adults against pneumococcal pneumonia and IPD.

In June, 2012, the Advisory Council on Immunization Practices of the CDC recommended that: (1) adults aged 19 years or older with immunocompromising conditions, functional or anatomic asplenia, CSF leaks, or cochlear implants, and who have not previously received PCV13 or PPSV23 receive a single dose of PCV13 followed by a dose of PPSV23 at least 8 weeks later. (2) adults aged 19 years or older with immunocompromising conditions, functional or anatomic asplenia, CSF leaks or cochlear implants, and who have previously received one or more doses of PPSV23 receive a dose of PCV13 one or more years after the last PPSV 23 dose was received.

For those that require additional doses of PPSV23, the first such dose should be given no sooner than 8 weeks after PCV13 and at least 5 penicillin and amoxicillin together years since the most recent dose of PPSV23. The lack of convincing differences in responses to the two vaccine preparations and the fact that widespread use of PCV13 in children is expected to be followed by disappearance from the population of vaccine strains suggests to some authorities that routine vaccination of adults with PCV13 in the United States will be of little benefit.

Vaccines utilizing conserved protein antigens might bypass the problems relating to polysaccharide vaccines.

pneumoniae and can, when inoculated intratracheally into experimental animals, cause pulmonary infiltration. A pneumolysoid vaccine is currently in development.

Antibody to certain surface expressed proteins such as PspA (pneumococcal surface protein A) or the Pht (pneumococcal histidine triad) proteins has been shown to be protective in experimental animals, and these are also under study as vaccine candidates.

pneumoniae was the first organism to be shown to behave as what is now regarded as an extracellular bacterial pathogen.

The principal defense against infection is ingestion by dendritic and phagocytic cells; in the absence of antibody, it resists phagocytosis and replicates extracellularly in mammalian tissues. The polysaccharide capsule is chiefly responsible for resistance to ingestion and killing by host phagocytic cells.

Except for strains that cause conjunctivitis, nearly all pneumococci that cause disease in humans are encapsulated.

A total of 91 different pneumococcal capsular polysaccharides have been recognized; these form the basis for the common identification system.

It is important to the clinician to be familiar with the concept of capsular types because of their importance in new formulations of pneumococcal vaccine (see later in this chapter). Antibody to capsule is the principal defense mechanism against infection due to pneumococcus, but antibody to pneumolysin (the only recognized important toxin of S. pneumoniae) and to surface expressed proteins will become increasingly important, as will be mentioned during the consideration of pneumococcal vaccine.

Once nasopharyngeal colonization has taken place, infection may result if the organisms are carried into cavities from which they are not readily cleared.

Under normal circumstances, when bacteria find their way into the Eustachian tubes, sinuses, or bronchi, clearance mechanisms, chiefly ciliary action, lead to their rapid removal.

If conditions such as coexisting viral infection, exposure to pollutants, or an allergic condition cause edema that obstructs the opening of the Eustachian tube into the pharynx or the ostium of a paranasal sinus, clinically recognizable infection may result. Similarly, glottal and cough reflexes and ciliary activity of bronchial epithelial cells prevent pneumococci from infecting the lower airways.

Damage to ciliated bronchial cells or increased production of mucus, whether chronic (for example, from cigarette smoking or occupational exposure) or acute (from influenza or some other viral infection), may prevent the clearance of inhaled or aspirated organisms,

predisposing

Bacteria are certainly less well cleared from the airways because of viral-induced fleming amoxicillin clavulanic acid damage.

Pneumococcal disease is greatly increased in people with altered pulmonary clearance, such as those who have chronic bronchitis, asthma, or chronic obstructive pulmonary disease.

Only in the past few years has evidence clearly associated cigarette smoking with susceptibility to pneumonia. It is an interesting sign of the times that Heffron’s classical treatise on pneumococcus published in 1939 had a section on inhalation of “noxious substances” yet did not mention cigarette smoking. Defective antibody formation, whether congenital or acquired, has the greatest impact on susceptibility to pneumococcal infection.

Bruton’s original description of congenital agammaglobulinemia stressed the prominence of S.

Pneumococcus is also a major cause of serious infection in acquired agammaglobulinemia (common variable immunodeficiency) and perhaps in IgG subclass deficiency as well.

Diseases characterized by an inability to make IgG, such as multiple myeloma, lymphoma, and HIV infection, all predispose to pneumococcal infection. The increase in susceptibility in such persons may be of a staggering magnitude.

Multiple myeloma is often first recognized when an affected person develops pneumococcal pneumonia. The incidence of invasive pneumococcal disease in patients with AIDS is increased nearly 100-fold over an age-matched non-HIV infected population. Defective function of polymorphonuclear leukocytes (PMNs) is also highly associated with pneumococcal infection. Examples include renal insufficiency and diabetes mellitus.

The predisposition from alcoholism and chronic liver disease is in part due to the adverse effect on PMNs but is also multifactorial. The susceptibility of aged persons to pneumococcal pneumonia is multifactorial, reflecting senescence of the immune system because of diminished production of Igs (or production of poorly functional ones), impaired response to cytokines, and general debilitation caused by weakening of the gag reflex, malnutrition, and the presence of other diseases. The incidence of alcohol abuse in pneumococcal disease has been shown to be high since the first part of the twentieth century. The effect of alcoholism is multifactorial, involving lifestyle (such as cold exposure and malnutrition), suppression of the gag reflex, and possibly deleterious effects on PMN function. Anemia may also predispose to pneumococcal pneumonia by uncertain mechanisms. A wintertime increase in pneumococcal pneumonia adults

has

Splenectomy is often mentioned as a factor that predisposes to pneumococcal infection; this concept is only partly true. In the absence of anticapsular antibody, the spleen is the principal organ that clears pneumococci from the blood stream.

Persons who have had splenectomy or who have dysfunctional spleens (for example those with sickle cell disease) are not necessarily likely to have more frequent pneumococcal infections, but when they are infected, they are susceptible to rapidly progressive, overwhelming pneumococcal disease.

The heralding event in an outbreak of pneumococcal pneumonia in a metropolitan prison was the rapid, septic death of two prisoners, both of whom had previously undergone splenectomy. Pneumococcal disease progressed so rapidly in these cases that pneumonia was not initially detectable clinically or even with certainty by chest radiographs, although it was seen at autopsy.

What are the clinical manifestations of infection with this organism? pneumoniae causes infection of the middle ear, sinuses, trachea, bronchi, and lungs by direct spread of organisms from the nasopharyngeal site of colonization and causes infection of the CNS, heart valves, bones, and joints by hematogenous spread; the peritoneal cavity may be infected by local extension along the female genital tract or hematogenously. Infection of the pleura or peritoneal cavity and also of the CNS may occur by direct extension or by hematogenous spread; in any individual case, the route of infection can usually not be determined. Of 136 cases of invasive pneumococcal infection at the Houston Veterans Affairs Medical Center seen during a 9-year period, 116 patients (85%) had pneumonia, of whom three also had empyema.

Seven had bacteremia with no apparent source, five had meningitis, five had spontaneous bacterial peritonitis, three had septic arthritis, two had endocarditis, and individual patients had osteomyelitis and/or localized abscesses. Multiple areas of involvement were seen in nine patients. Bacteremia that occurs without an apparent source or focus of infection is called primary bacteremia. In a recent population-based study of bacteremic pneumococcal disease in adults in Israel, pneumonia was present in 71% of cases, meningitis was present in 8%, and otitis media or sinusitis in 4%; bacteremia was regarded as primary in 18%.

Primary bacteremia has always been more common in children than adults; when therapy has not initially been given, a focus of infection

has

pneumoniae has historically been the most common isolate, being identified in about 40 to 50% of cases in which an etiologic agent is isolated or in 30 to 40% of all cases. influenzae, historically the next most common organism, is more likely to predominate in highly vaccinated populations. Pneumococcus is the most prevalent pathogen in otitis media in adults as well.

As noted above, prior infection by a respiratory virus, allergy, or air pollutants contribute to pathogenesis by causing inflammation and blocking the opening to the Eustachian tube, thereby trapping bacteria in the middle ear.