Amoxicillin 875 mg pink

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

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

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 the patient to infection. Respiratory viral infection, especially that due to influenza virus, plays a prominent role in predisposing the patient to pneumococcal pneumonia. Upregulation of surface receptors during viral infection may enhance pneumococcal adherence and invasion.

Bacteria are certainly less well cleared from the airways because of viral-induced 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

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 long been noted, perhaps associated with viral infections. Pneumococcal pneumonia is greatly increased in the 6 months following hospitalization for any cause.

Other factors such as cold exposure, stress, and fatigue may predispose to pneumococcal pneumonia by unknown mechanisms. The death rate in the first year or two after pneumococcal pneumonia is also very high.

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 amoxicillin & clavulanic acid an outbreak of pneumococcal pneumonia in a metropolitan prison was the rapid, septic death of two prisoners,

both

previously

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

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 often become apparent.

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.

The diagnosis is made by the presence of pain and fever, with redness and bulging of the tympanic membrane that fails to respond to positive air pressure.

Pneumococcal mastoiditis has been only a rare complication of otitis media in the antibiotic era.

Acute purulent sinusitis is caused by the same organisms as acute otitis media; thus, S. The pathogenesis of infection is also similar, with a prominent predisposing role for congestion of the mucosal membranes. Accumulation of fluid in the paranasal sinus cavities, even during simple colds, provides a medium for bacterial proliferation and subsequent infection. This condition has been shown to be greatly overdiagnosed. Often the condition is biphasic, with an initial upper respiratory infection that appears to be viral, followed by a worsening, with the appearance of purulent secretions, malaise, fever, tenderness over one or more sinuses and or pain in a tooth. Diagnosis depends upon these clinical features; computed tomography scans of sinuses regularly show fluid in patients who have harmless, presumably viral upper respiratory infections without symptoms of sinusitis, so this finding does not indicate the presence of bacterial sinusitis. In persons who do not have chronic underlying bronchopulmonary disease, acute bronchitis is thought to be nearly always due to viral infection. Acute exacerbations of bronchitis in patients with chronic bronchitis, asthma, or obstructive lung disease may be caused by S.

A clinically recognizable exacerbation of the chronic disease is highly associated with acquisition of a new pneumococcal strain.

Pneumonia results when nonimmunologic and immunologic mechanisms fail to prevent access of pneumococci to the alveoli and their subsequent replication.

Most patients who develop pneumococcal pneumonia have one or more of the predisposing conditions that are summarized above, such as a preceding viral respiratory infection, cigarette smoking, chronic obstructive pulmonary disease, alcohol abuse, neurological disease (cerebrovascular accidents, seizures, and dementia), malignancy, liver disease (hepatitis and/or cirrhosis), congestive heart failure, diabetes mellitus, or HIV infection. Cough, fatigue, fever, chills, sweats, and shortness of breath are the most frequent symptoms of pneumonia; these are all more prominent in younger than in older patients.

Patients usually appear ill and have a grayish, anxious appearance that differs from that of persons with viral or mycoplasmal pneumonia. Temperature may be elevated to 102 o F, the pulse to greater than or equal to 110 beats per minute, and the respiratory rate to greater than 20 per minute. Elderly patients may have only a slight temperature elevation or be afebrile but are more likely to have an elevated respiratory rate. The sudden onset of shaking chills followed by the appearance of cough and rusty sputum has been called a “classical presentation” of pneumococcal pneumonia, but is uncommon. Occasionally reveals diminished respiratory excursion on the affected side.

Increased fremitus is often overlooked but is very useful in diagnosing pneumonia.

Dullness to percussion is present in approximately 50% of cases.

Crackles on careful auscultation are heard in nearly all cases but, in patients with chronic lung disease, it is often difficult to be certain that such sounds signify the presence of pneumonia.

Bronchial or tubular breath sounds may be heard if consolidation is present. Flatness to percussion at the lung base and an inability to detect the expected degree of diaphragmatic motion with deep inspiration suggest the presence of pleural fluid. Unless all the vital signs are normal, which substantially reduces the likelihood of pneumonia, no set of physical findings can reliably replace the chest X-ray in diagnosing the presence or absence of pneumonia. The finding of a heart murmur raises concern about endocarditis, a rare but serious complication.

Confusion, obtundation, or particularly neck stiffness suggest the presence of meningitis. In most cases of pneumococcal pneumonia, chest radiography reveals: An area of infiltration involving one or more segments

within

A thick-walled lung abscess is distinctly rare, and its finding raises the likelihood of other etiologic agents.

Although careful prospective study may reveal pleural effusion in up to 40% of patients with pneumococcal pneumonia, only 10% have sufficient amounts of fluid to aspirate, and in only a minority of these, perhaps 2% of the total, is empyema present. 25% of patients with pneumococcal pneumonia have a hemoglobin level of less than or equal to 11g/dL.

The majority of patients have leukocytosis (a white blood cell count [WBC] of >12,000/mm 3 ), But 25% may have normal WBC counts, at least at the time of admission.

A WBC count less than 6,000/mm 3 occurs in 5 to 10% of persons hospitalized for pneumococcal pneumonia and indicates a very poor prognosis. A low serum albumin level may reflect malnutrition—and therefore indicates a predisposing condition, or may appear as a manifestation of sepsis. Serum bilirubin may be increased to 3 to 4mg/dL; the pathogenesis of this abnormality is multifactorial, with hypoxia, hepatic inflammation, and breakdown of red blood cells in the lung all thought to contribute.

Complications.Empyema, the most common infectious complication of pneumococcal pneumonia, occurs in approximately 2% of cases.

Persistence of fever, even if only low grade, and leukocytosis after 4 to 5 days of appropriate antibiotic treatment of pneumococcal pneumonia is suggestive of empyema, and this diagnosis is even more likely if the radiograph shows persistence of any pleural fluid.

Under such conditions, attempts should be undertaken to drain the fluid completely. (As a general matter, drainage is indicated if pleural fluid is present at the time of diagnosis of pneumococcal pneumonia.) The presence of frank pus in the pleural space, a positive Gram stain or fluid with a pH of less than or equal to 7.1 is an indication for aggressive and complete drainage with repeated needle aspiration or prompt insertion of a chest tube.

If no response is seen, immediate removal of infected material by pleuroscopy or open thoracotomy is then indicated. Acute cardiac events have recently been recognized as important noninfectious complications of pneumococcal pneumonia.

In a recently reported series, of 170 veterans hospitalized for this disease: 33 (19.4%) had at least one major cardiac complication including: 12 (7%) with acute myocardial infarction (of whom two also had arrhythmia and five had new-onset or worsening congestive heart failure [CHF]).

Eight (5%) with new-onset atrial fibrillation or ventricular tachycardia that was transient in every case.