The clinical significance of resistant uropathogens in ambulatory urinary tract infections in women.
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Biomedical subjects
Publications and source records attributed to B A Cunha.
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The most common atypical pneumonias are caused by three zoonotic pathogens, Chlamydia psittaci (psittacosis), Francisella tularensis (tularemia), and Coxiella burnetii (Q fever), and three nonzoonotic pathogens, Chlamydia pneumoniae, Mycoplasma pneumoniae, and Legionella. These atypical agents, unlike the typical pathogens, often cause extrapulmonary manifestations. Atypical CAPs are systemic infectious diseases with a pulmonary component and may be differentiated clinically from typical CAPs by the pattern of extrapulmonary organ involvement which is characteristic for each atypical CAP. Zoonotic pneumonias may be eliminated from diagnostic consideration with a negative contact history. The commonest clinical problem is to differentiate legionnaire's disease from typical CAP as well as from C. pneumoniae or M. pneumonia infection. Legionella is the most important atypical pathogen in terms of severity. It may be clinically differentiated from typical CAP and other atypical pathogens by the use of a weighted point system of syndromic diagnosis based on the characteristic pattern of extrapulmonary features. Because legionnaire's disease often presents as severe CAP, a presumptive diagnosis of Legionella should prompt specific testing and empirical anti-Legionella therapy such as the Winthrop-University Hospital Infectious Disease Division's weighted point score system. Most atypical pathogens are difficult or dangerous to isolate and a definitive laboratory diagnosis is usually based on indirect, i.e., direct flourescent antibody (DFA), indirect flourescent antibody (IFA). Atypical CAP is virtually always monomicrobial; increased IFA IgG tests indicate past exposure and not concurrent infection. Anti-Legionella antibiotics include macrolides, doxycycline, rifampin, quinolones, and telithromycin. The drugs with the highest level of anti-Legionella activity are quinolones and telithromycin. Therapy is usually continued for 2 weeks if potent anti-Legionella drugs are used. In adults, M. pneumoniae and C. pneumoniae may exacerbate or cause asthma. The importance of the atypical pneumonias is not related to their frequency (approximately 15% of CAPs), but to difficulties in their diagnosis, and their nonresponsiveness to beta-lactam therapy. Because of the potential role of C. pneumoniae in coronary artery disease and multiple sclerosis (MS), and the role of M. pneumoniae and C. pneumoniae in causing or exacerbating asthma, atypical CAPs also have public health importance.
Bacteremias in inpatient chronic HD units have been described, but there is little information on bacteremias in ambulatory HD units. To determine the frequency of bacteremia and pathogen distribution in ambulatory chronic HD units, we retrospectively reviewed our experience with 107 bacteremias in 5 chronic ambulatory HD units over a 3 year period. The object of the study was twofold. The first objective was to determine if bacteremias in ambulatory HD setting were substantially different in frequency or type than in the inpatient HD setting. Secondly, febrile patients suspected of having bacteremia in chronic HD patients are often empirically treated with vancomycin and gentamicin. Chronic HD patients require repeated and frequent venous access for HD. Bacteremias are common in chronic HD patients and may be primary or secondary and are often related to venous access site infections. The distributions of bacteremia pathogens in chronic HD patients are predominantly reflective of skin flora, i.e., staphylococci and to lesser extent aerobic Gram-negative bacilli. After S. aureus (MSRA/MSSA) and coagulase-negative staphylococcus (CoNS), enterococci are the next most important Gram-positive pathogens in bacteremic HD patients. Most strains of E. faecalis are sensitive to vancomycin and for practical purposes should be considered as vancomycin sensitive enterococci (VSE). In contrast, most strains of E. faecium are resistant to vancomycin and should be considered as vancomycin resistant enterococci (VRE). We retrospectively reviewed 107 patients on chronic ambulatory HD to determine the adequacy of empiric vancomycin and gentamicin prophylaxis. We found amikacin is preferred to gentamicin and that meropenem is an effective alternate substitution for gentamicin and vancomycin combination therapy.
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Methicillin-resistant Staphylococcus aureus (MRSA) is a common skin coloniser and less commonly causes infection. MRSA colonisation should be contained by infection control measures and not treated. MRSA infections cause the same spectrum of infection as MSSA infections, i.e., skin/soft tissue infections, bone/joint infections, central IV line infections, and acute bacterial endocarditis (native valve/prosthetic valve). There is a discrepancy between in-vitro sensitivity and in-vivo effectiveness with MRSA. To treat MRSA infections, clinicians should select an MRSA drug with proven in-vivo effectiveness, i.e., daptomycin. Linezolid, quinupristin/dalfopristin, minocycline, or vancomycin, and not rely on in-vitro susceptibility data. For MRSA, doxycycline cannot be substituted for minocycline. Linezolid and minocycline are available for oral administration and both are also effective in treating MRSA CNS infections. Vancomycin is being used less due to side effects, (increasing MICs/resistance, VISA/VRSA), and increased VRE prevalence. The most potent anti-MRSA drug at the present time is daptomycin. Daptomycin is useful when rapid/effective therapy of MRSA bacteraemia/endocarditis is necessary. Daptomycin is also useful to treat persistent MRSA bacteraemias/MRSA treatment failures with other drugs, i.e., vancomycin. There is no difference in virulence between MSSA and MRSA infections if treatment is started early and with an agent that has in-vivo effectiveness.
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The global spread of antibacterial resistance has important implications for the current and future management of bacterial respiratory tract infections in children. Data suggest that emerging resistance to commonly prescribed antibacterials, such as macrolides and trimethoprim-sulfamethoxazole, is beginning to impact the treatment of these infections, which include acute otitis media, tonsillitis/pharyngitis and community-acquired pneumonia. There is, therefore, a need for additional agents that are active against common respiratory tract pathogens, including resistant strains and are suitable for use in children. Infection control measures to curb the clonal spread of antibacterial resistance are also extremely important.
West Nile encephalitis (WNE) presents clinically as aseptic meningitis, meningoencephalitis, encephalitis, or acute flaccid paralysis. Non-specific laboratory findings, e.g., leukopenia and thrombocytopenia, accompany WNE. Lymphopenia is marked and prolonged with WNE. Three patients with WNE were found to have elevated serum ferritin levels. Severity seemed to be directly related to serum ferritin levels. Although preliminary, the results suggested that serum ferritin levels >or= 500 ng/mL (normal range 5-187 ng/mL) occur late with WNE, and not in a control group of patients with viral meningitis or encephalitis.
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Bioterrorism has become a potential diagnostic consideration in infectious diseases. This article reviews the clinical presentation and differential diagnosis of potential bioterrorist agents when first presenting to the hospital in the emergency room setting. The characteristic clinical features of inhalation anthrax, tularemic pneumonia, plague pneumonia, including laboratory and radiographic finding, are discussed. Ebola vieus and smallpox are also discussed as potential bioterrorist-transmitted infections from the clinical and epidemiologic standpoint. In addition to the clinical features of the infectious diseases mentioned, the article discusses the infectious disease control and epidemiologic implications of these agents when employed as bioterrorist agents. The review concludes with suggestions for postexposure prophylaxis and therapy.
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Acute bacterial endocarditis is commonly caused by Staphylococcus aureus. Acute bacterial endocarditis due to S. aureus is often complicated by metastatic infection to distant organs, i.e. the central nervous system, the heart, lungs, kidneys and joints. However, metastatic lymph node involvement has not been reported. This is a case report of S. aureus acute bacterial endocarditis complicated by metastatic suppurative lymphadenitis of retroperitoneal lymph nodes. We believe this is the first reported case of suppurative lymphadenitis of the mesenteric lymph nodes secondary to S. aureus acute bacterial endocarditis.
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Optimal empiric therapy of CAP is with appropriate monotherapy (e.g., doxycycline, levofloxacin). Combination therapy is problematic because of potential side effects and high cost. Empiric coverage should have a high degree of activity against both typical and atypical pathogens. The antibiotic selected should have an excellent side-effect profile and be relatively inexpensive. Clinicians should be selective in their choice of antibiotic for CAP and choose an antimicrobial that has little or no resistance potential, is relatively inexpensive, and permits i.v.-to-PO switch monotherapy.
Many patients with presumed nosocomial pneumonia probably have infiltrates on the chest radiograph, fever, and leukocytosis resulting from noninfectious causes. Because of the high mortality and morbidity associated with nosocomial pneumonias, however, most clinicians treat such patients with a 2-week empiric trial of antibiotics. Before therapy is initiated, the clinician should rule out other causes of pulmonary infiltrates, fever, and leukocytosis that mimic a nosocomial pneumonia (e.g., pre-existing interstitial lung disease, primary or metastatic lung carcinomas, pulmonary emboli, pulmonary drug reactions, pulmonary hemorrhage, collagen vascular disease affecting the lungs, or congestive heart failure). If these disorders can be eliminated from diagnostic consideration, a 2-week trial of empiric monotherapy is indicated. The clinician should treat cases of presumed nosocomial pneumonia as if P. aeruginosa were the pathogen. Although P. aeruginosa is not the most common cause of nosocomial pneumonia, it is the most virulent pulmonary pathogen associated with nosocomial pneumonia. Coverage directed against P. aeruginosa is effective against all other aerobic gram-negative bacillary pathogens causing hospital-acquired pneumonia. The clinician should select an antibiotic for empiric monotherapy that is highly effective against P. aeruginosa, has a good side-effect profile, has a low resistance potential, and is relatively inexpensive in terms of its cost to the institution. The preferred agents for empiric monotherapy for nosocomial pneumonia are cefepime, meropenem, and piperacillin. Single organisms are responsible for nosocomial pneumonia, not multiple pathogens. S. aureus rarely, if ever, causes nosocomial pneumonia but is mentioned frequently in studies based on cultures of respiratory tract secretions. S. aureus, unless accompanied by a necrotizing pneumonia with rapid cavitation within 72 hours, in the sputum indicates colonization rather than infection and should not be addressed therapeutically. Antibiotics associated with a high resistance potential should not be used as monotherapy or included in combination therapy regimens (i.e., ceftazidime, ciprofloxacin, imipenem, or gentamicin). Combination therapy is more expensive than monotherapy and is indicated only when P. aeruginosa is extremely likely, based on its characteristic clinical presentation, or is proved by tissue biopsy. Therapy should not be based on respiratory secretion cultures regardless of technique. Optimal combination regimens include cefepime or meropenem plus levofloxacin or piperacillin or aztreonam or amikacin. Nosocomial pneumonias usually are treated for 14 days. Lack of radiographic or clinical response to appropriate empiric nosocomial pneumonia monotherapy after 14 days suggests an alternate diagnosis. In these patients, a tissue biopsy specimen should be obtained to determine the cause of the persistence of pulmonary infiltrates unresponsive to appropriate antimicrobial therapy.
Despite the development of extended-spectrum penicillins, cephalosporins, and quinolones, the older antimicrobial agents, doxycycline, minocycline, TMP-SMX, clindamycin, and metronidazole, still play an important role in the treatment of infectious diseases. All of these older drugs are well absorbed by the oral route, attaining serum levels equivalent to those achieved by parenteral administration. The availability of generic forms of the older drugs reduces their cost. Besides traditional uses, some older drugs have become the preferred therapy for newly recognized infectious diseases. Doxycycline is the preferred drug for rickettsial tickborne diseases, ehrlichiosis and early Lyme disease. TMP-SMX is the preferred drug for I. belli and Cyclospora. Minocycline has been used to treat MRSA and MRSE infections. Clindamycin or metronidazole combined with a quinolone is an excellent oral regimen for polymicrobial infections. [table: see text]