Paul E. Schoch

Diagnostic Importance of Relative Lymphopenia as a Marker of Swine Influenza (H1N1) in Adults

NOTE. The rapid influenza test was QuickS Influ A/B kit (Denka Seiken). Among patients with complete blood counts, 25 adults and 16 children tested positive for influenza A, and 3 adults and 2 children tested positive for influenza B. in HIV-infected patients with tuberculosis. Clin Infect Dis 2007; 44:141–4. 10. Manosuthi W, Tantanathip P, Prasithisirikul W, Likanonsakul S, Sungkanuparph S. Durability of stavudine, lamivudine and nevirapine among advanced HIV-1 infected patients with/without prior co-administration of rifampicin: a 144-week prospective study. BMC Infect Dis 2008; 8:136.

Intravenous line infection due to Ochrobactrum anthropi (CDC Group Vd) in a normal host

Ochrobactrum anthropi, formerly known as Achromobacter species (CDC group Vd), is an aerobic, gram-negative bacillus widely distributed in aquatic environments. Most important, it has been implicated as a cause of intravenous line infection in immunocompromised hosts with solid tumors or hematologic malignancies. Trimethoprim-sulfamethoxazole and aminoglycosides are usually active against O. anthropi, but this organism is usually resistant to beta-lactam antibiotics. Because O. anthropi is a low-virulence organism, patients with intravenous-line infections have been cured without removal of the intravenous catheter. We describe a case of intravenous-line infection in a normal host that was successfully resolved alter catheter removal.

Proteus penneri urosepsis in a patient with diabetes mellitus

Proteus penneri has been isolated from many different clinical sources, including surgical wound infections, urine, and blood. We describe the first reported case of P. penneri nosocomial urosepsis in a patient with diabetes. P. penneri was subsequently isolated from bronchoalveolar lavage fluid and a pulmonary artery catheter tip.

Nitrofurantoin: Preferred Empiric Therapy for Community-Acquired Lower Urinary Tract Infections

To the Editor: I read with great interest the article on nitrofurantoin for uncomplicated urinary tract infections (UTIs) by McKinnell et al.1 Although their study primarily focused on pharmacoeconomics, comparing nitrofurantoin to trimethoprim/sulfamethoxazole (TMP-SMX) and fluoroquinolones, it has important clinical implications. Nitrofurantoin is an underused antimicrobial for empiric therapy for community-acquired and nosocomial lower UTIs. Among susceptible uropathogens after extensive use worldwide for more than 50 years, there has been virtually no acquired resistance to nitrofurantoin.2,3 Most physicians are acquainted with the adverse effects of nitrofurantoin but are unfamiliar with its virtues. Nitrofurantoin has a unique mechanism of action by interfering with bacterial growth at 3 different locations in the Kreb’s cycle. Although approximately 25% of nitrofurantoin is excreted renally, some is eliminated via the gastrointestinal tract. Unlike “high resistance potential” antibiotics, nitrofurantoin does not predispose to resistance.4 Pharmacokinetically, nitrofurantoin reabsorption is pH dependent and at normal urinary pH (approximately 5.5 pH); nitrofurantoin is preferentially excreted into the lower urinary tract, ie, bladder urine, making it is useful to treat lower UTIs.3,5-7 Nitrofurantoin is active against most common uropathogens, but most Proteus species, Serratia marcescens, and Pseudomonas aeruginosa are naturally resistant.4,8 Nitrofurantoin is useful against Escherichia coli and Enterococci, the most frequent causes of nosocomial lower UTIs, ie, catheter-associated bacteriuria. Nitrofurantoin is also active against most strains of multidrug-resistant gram-negative bacilli, including most extended spectrum β lactamase-producing strains.8 Nitrofurantoin is also active against vancomycin-sensitive enterococci and vancomycin-resistant enterococci.3,7,8 During the past 3 decades, I have had extensive experience with nitrofurantoin therapy for nosocomial and community-acquired lower UTIs. Nitrofurantoin, 100 mg orally every 12 hours is well tolerated. The adverse effects of nitrofurantoin are relatively uncommon and benign.4,8 Occasional nausea may occur but is uncommon with macrocrystalline formulations. In patients with intact renal function, nitrofurantoin urinary concentrations are 50 to 300 mg/mL.8 With creatinine clearances lower than 30 mL/min, therapeutic urinary concentrations are unlikely to be obtained, and therapeutic failure may result.4,8 For this reason, nitrofurantoin should be avoided in patients with a creatinine clearance lower than 30 mL/min.7,8 Acute toxicity is limited to acute/reversible migratory pulmonary infiltrates/eosinophilia. Long-term nitrofurantoin toxicity includes peripheral neuropathy, interstitial lung disease, or hepatotoxicity, which may occur in patients treated long term who have chronic renal insufficiency.6,8 Nitrofurantoin has advantages over TMP-SMX and fluoroquinolones for initial empiric therapy of community-acquired and nosocomial lower UTIs. Against gram-negative bacilli uropathogens, nitrofurantoin has a “low resistance potential” vs the “high resistance potential” of TMP-SMX and ciprofloxacin. Unlike TMP-SMX and fluoroquinolones, nitrofurantoin has activity against vancomycin-resistant enterococci3,8 (Table). TABLE. Antibiotic Activities Against Selected Gram-Negative and Gram-Positive Uropathogensa In my experience-based opinion, nitrofurantoin should be the preferred empiric therapy for community-acquired and nosocomial lower UTIs. Nitrofurantoin has remained effective after more than 50 years of extensive use worldwide with essentially no resistance, and for initial empiric therapy for uncomplicated community-acquired or nosocomial UTIs, nitrofurantoin is an ideal antibiotic. If urine cultures are positive for Proteus species, S marcescens, or P aeruginosa, an alternate agent should be selected. I agree with the authors that nitrofurantoin should be the preferred antibiotic for the initial empiric treatment of community-acquired lower UTIs.

Oral therapy of catheter-associated bacteriuria (CAB) in the era of antibiotic resistance: nitrofurantoin revisited

Nosocomial catheter-related urinary tract infections, i.e. catheter-associated bacteriuria (CAB), is common in hospitalized patients with urinary catheters. The most common uropathogens in CAB are Escherichia coli and vancomycin sensitive enterococci (VSE). Other common uropathogens in patients with CAB include other aerobic Gram-negative bacilli and vancomycin-resistant enterococci (VRE). In patients with nosocomial CAB, infection control measures are important to prevent transmitting Gram-negative bacilli and enterococci to other patients. IDSA guidelines state that antimicrobial therapy of CAB is not necessary. In practice, nosocomial CAB in patients with impaired host defences, are often empirically treated. Since patients with nosocomial CAB are afebrile, are not bacteremic, and do not have upper tract disease, if nosocomial CAB is treated, an oral antibiotic is preferred. In the present era of antibiotic resistance, particularly among uropathogens, oral therapeutic options to treat nosocomial CAB are limited. While some oral antibiotics used to treat nosocomial CAB may be active against some uropathogens, their use may induce subsequent resistance in the patient’s fecal flora. Resistance is a common problem with oral antibiotic treatment of nosocomial CAB. Often antibiotic treatment only replaces one pathogen with another more highly resistant pathogen. Since there are relatively few oral antibiotics active against common nosocomial CAB pathogens, therapeutic options are limited. Nitrofurantoin is an underutilized often overlooked antibiotic for CAB used extensively worldwide for over 60 years, and is one of the few oral antibiotics active against E. coli, most strains of Klebsiella sp. as well as both VSE and VRE. The lack of resistance associated with prolonged nitrofurantoin use over the years is explained by its unique antibacterial mechanism of action, i.e. nitrofurantoin blocks carbohydrate metabolism in three different locations in the Krebs’s cycle in bacterial cells of susceptible organisms. Because nitrofurantoin is excreted primarily via the urine, relatively small amounts are excreted in the fecal flora and nitrofurantoin does not affect the fecal flora. Nitrofurantoin’s spectrum includes most aerobic uropathogens except Proteus sp., Serratia marcescens, and Pseudomonas aeruginosa. Fortunately, these three organisms are relatively uncommon causes of nosocomial CAB. Clinicians should be aware of the difference between in vitro susceptibility and in vivo effectiveness. In vivo effectiveness is also dependent on antibiotic concentration at the site of infection. In lower urinary tract infections, urinary concentrations of renally eliminated antibiotics may exceed brothderived susceptibility breakpoints. Susceptibility breakpoints with nitrofurantoin are expressed as susceptible, intermediate, or resistant. In adults with intact renal function, the urinary concentrations of nitrofurantoin are 50–300 mcg/ml. Nitrofurantoin susceptibility breakpoints are: ,64 mcg/ml5susceptible, 64 mcg/ml5intermediate susceptibility, and .64 mcg/ml5resistant. Since relative resistance/intermediate susceptibility is concentration dependent, susceptibility to nitrofurantoin at achievable urinary concentrations may be greater than is apparent from in vitro susceptibility data. With E. coli nosocomial CAB, if an E. coli strain has an MIC of 1 : 128 to nitrofurantoin, the strain may be eradicated if the urinary concentrations are .128 mcg/ml. Since susceptibility is, in part, concentration dependent, it is reasonable to combine susceptible with intermediate susceptibility data to achieve a more accurate prediction of susceptibility. The clinically effective urinary spectrum of an antibiotic is determined by its concentration in the urine, urinary antibacterial substances, and urinary pH. The antimicrobial activity of nitrofurantoin is optimal when the urinary pH is y5.5. In addition, the tubular reabsorption of nitrofurantoin is pH dependent Correspondence to: B A Cunha, Infectious Disease Division, WinthropUniversity Hospital, Mineola, NY 11501, USA and State University of New York School of Medicine, Stony Brook, NY, USA. Email: bacunha@ windthrop.org

Viridans streptococcal (Streptococcus mitis) biosynthetic aortic prosthetic valve endocarditis (PVE) complicated by complete heart block and paravalvular abscess

Prosthetic valve endocarditis (PVE) may be classified clinically as early (<60 days) or late (>60 days) post-valve replacement PVE. The pathogens of early versus late PVE differ in type and virulence. Early PVE pathogens are virulent, for example, Pseudomonas aeruginosa and Staphylococcus aureus. Late PVE pathogens resemble those of subacute bacterial endocarditis and are due to relatively avirulent and noninvasive organisms, for example, viridans streptococci. Viridans streptococci vary in their invasiveness and abscess potential. Myocardial abscess and complete heart block are rare complications of late PVE due to viridans streptococci. We present an unusual case of Streptococcus mitis late aortic PVE complicated by aortic root abscess, myocardial abscess, and complete heart block.

Pseudomonas pseudoalcaligenes Peritoneal Dialysis-Associated Peritonitis

1. Collado L, Figueras MJ. Taxonomy, epidemiology, and clinical relevance of the genus arcobacter. clin microbiol rev 2011; 24:174–92. 2. Fera MT, Maugeri TL, Giannone M, Gugliandolo C, La Camera E, Blandino G, et al. In vitro susceptibility of arcobacter butzleri and arcobacter cryaerophilus to different antimicrobial agents. Int J antimicrob agents 2003; 21:488–91. 3. Lau SK, Woo PC, Teng JL, Leung KW, Yuen KY. Identification of 16S ribosomal RNA gene sequencing of arcobacter butzleri bacteraemia in a patient with gangrenous appendicitis. mol Pathol 2002; 55:182–5. doi:10.3747/pdi.2012.00114