Infections Due To Gram Positive Cocci

Explanation
Pneumococci produce IgA protease, which cleaves the secretory immunoglobulin IgA1. IgA protease may be partly responsible for the high carrier rate and the respiratory tract pathogenicity of these bacteria. The organisms do not provoke an inflammatory response or cause clinical illness in the nasopharynx. Host defense mechanisms prevent penetration into more vulnerable areas, such as the paranasal sinuses, middle ear, and pulmonary alveoli. Examples of these defenses include the cough, gag, and sneeze reflexes; the viscous mucus that lines the respiratory epithelium and traps bacteria; and ciliary action, which expels trapped particles. Pneumococcal infection often follows influenza or other viral infections of the upper respiratory tract, which impair host defenses by increasing the volume and decreasing the viscosity of secretions. Other factors that predispose to pneumococcal infection include dementia, seizure disorders, alcoholism, stupor, and other conditions that increase the likelihood that oropharyngeal contents will be aspirated into the lungs. Air pollution, cigarette smoking, heart failure, chronic obstructive pulmonary disease (COPD), and HIV infection increase the risk of pneumococcal infection, but diabetes does not.
Pneumococcal pneumonia begins with aspiration of small quantities of oropharyngeal secretions containing pneumococci. Normally, alveolar macrophages ingest and kill such bacteria, but in the absence of type-specific immunity, strains of pneumococci are protected from ingestion.

Explanation
There are five major clinical manifestations of acute renal failure (ARF): carditis, polyarthritis, chorea, subcutaneous nodules, and erythema marginatum. Carditis develops in about 60% of patients; it involves the endocardium, myocardium, and pericardium. The typical manifestations of rheumatic carditis are sinus tachycardia (sometimes with first-degree heart block), mitral regurgitation, a pericardial friction rub, and cardiomegaly; congestive heart failure indicates severe carditis. Although most cases of carditis resolve within 3 months, patients with moderate to severe carditis or recurrent ARF are at risk for the late manifestation of mitral valve or aortic valve scarring. Polyarthritis develops in about 70% of patients with ARF. It is characteristically a migratory arthritis involving the large joints of the extremities; it resolves without sequelae in days to weeks. On rare occasions, adults may develop a persistent arthropathy of the hands and feet. Chorea, subcutaneous nodules, and erythema marginatum are all self-limited; each occurs in fewer than 10% of children with ARF and only very rarely in adults.

The minor manifestations of ARF are fever, arthralgias, and inflammation. The inflammation in such cases is evidenced by elevated erythrocyte sedimentation rates and C-reactive protein levels. The diagnosis of ARF is made on the basis of clinical features. The classic Jones criteria include the presence of either two major manifestations or one major and two minor manifestations, as well as laboratory evidence of a recent streptococcal infection (e.g., a positive throat culture or rising antistreptococcal antibody levels).

Treatment of ARF focuses on eradication of streptococcal pharyngitis and reduction of inflammation. Most clinicians recommend a course of penicillin or, as an alternative, other antistreptococcal antibiotics, even if the throat culture is negative at the time ARF is diagnosed. Antiinflammatory therapy includes aspirin and bed rest until inflammatory symptoms resolve; corticosteroids may have a role for patients with severe carditis.

ARF can be prevented by adequate treatment of streptococcal pharyngitis, even if antibiotics are delayed for up to 9 days after the onset of pharyngitis. Patients with a history of ARF are particularly vulnerable to recurrent attacks. Consequently, they should receive continuous prophylaxis for at least 5 years with daily oral penicillin (250 mg twice a day) or monthly injections of 1.2 million units of benzathine penicillin G. Prophylaxis can be discontinued when young patients who are at low risk for recurrence reach adulthood or when small children are no longer in the household.

Explanation
Changing resistance patterns will necessitate changes in antibiotic therapy for patients with enterococcal infections. Traditionally, ampicillin has been the drug of choice for enterococcal urinary tract infections, largely because of the high concentrations of drug excreted in the urine. In penicillin-allergic patients, nitrofurantoin, a fluoroquinolone, or trimethoprim-sulfamethoxazole may be effective for the treatment of simple urinary tract infections; however, because in vitro susceptibility testing of enterococci is often misleading and because resistance to these agents may rapidly emerge, patients should be continually evaluated through assessment of their clinical response and by use of follow-up cultures.

Infections caused by strains that are highly resistant to aminoglycosides can be treated with vancomycin. Infections caused by vancomycin-resistant strains are the most difficult to treat; linezolid has been particularly helpful, and quinupristin-dalfopristin is also effective. Doxycycline, chloramphenicol, and, for urinary tract infections, nitrofurantoin have also been used. In all cases, removal of infected indwelling catheters and foreign bodies and drainage of septic foci are essential. It is also essential to limit the spread of vancomycin-resistant Enterococcus by intensive surveillance, infection control measures, and prudent use of vancomycin and other antibiotics.

Explanation
Staphylococcal TSS was first reported in 1978; by 1990, more than 3,300 cases had been reported in the United States, 90% of which occurred during menstruation in women who were using tampons. The incidence of staphylococcal TSS declined precipitously after superabsorbent tampons were withdrawn from the market. Most cases are now nosocomially acquired, often as a result of postoperative staphylococcal wound infections, particularly those associated with nasal packing after rhinoplasty. Staphylococcal TSS caused by toxin-producing strains of methicillin-resistant Staphylococcus aureus has been reported in the United States and Japan.

TSS is a multisystem disease with diverse clinical manifestations. Leukocytosis and thrombocytopenia (< 100,000 platelets/μL) are common findings. Urinalysis may show mild pyuria and, occasionally, microscopic hematuria. Blood urea nitrogen and creatinine levels are elevated in more than 50% of patients. Serum bilirubin and hepatic enzyme levels are elevated in about half of patients. Serum creatine kinase levels are high in more than one third of patients, and myoglobinuria has developed in some patients. Blood cultures show no growth in almost all cases. Group A streptococci can produce a severe form of TSS that resembles staphylococcal TSS; in streptococcal TSS, however, bacteremia is common, necrotizing fasciitis may be present, and mortality is much higher (30 to 70%). The management of staphylococcal TSS calls for immediate correction of hypotension and shock with vigorous fluid replacement, attention to the site of S. aureus colonization or infection (e.g., removal of the tampon and drainage of any abscess), and systemic antimicrobial therapy with an antistaphylococcal agent.

Explanation
Patients with staphylococcal bacteremia have generally been treated with parenteral antibiotics for 4 to 6 weeks. This recommendation was made on the basis of the results of a study conducted from 1940 to 1954 in which endocarditis developed in 64% of 55 patients with staphylococcal bacteremia. Subsequent investigations suggested that patients with a removable or treatable primary focus of infection (most often infected IV devices) who have no clinical evidence of endocarditis can be treated safely with only 10 to 21 days of IV antibiotics. Other studies, however, reported development of endocarditis in 22 to 38% of patients with a primary focus of bacteremia. Therefore, the possibility of endocarditis should not be ignored, even if a primary focus is present. Moreover, major complications, including shock, acute respiratory distress syndrome, and metastatic infection, can occur even in the absence of endocarditis.

Controlled trials are necessary to determine the safety and efficacy of short-term therapy for staphylococcal bacteremia. It may therefore be prudent to treat patients with staphylococcal bacteremia as though they have endocarditis, unless all of the following features are present: clear evidence of only a transient bacteremia; a removable primary focus of infection; a benign clinical course; an absence of echocardiographically demonstrable valvular abnormalities and metastatic infection; and intact host defenses. Negative titers of teichoic acid antibodies would bolster the decision to shorten the IV antibiotic therapy, which should, in any case, be continued for at least 10 to 15 days.