Jean E. Hage

Transthoracic echocardiography (TTE): Sufficiently sensitive screening test for native valve infective endocarditis (IE)

We recently reviewed our experience with paired transthoracic echocardiogram (TTE) and transesophageal echocardiogram (TEE) studies for the diagnosis of native valve infective endocarditis. In patients with normal heart valves, we demonstrated that a normal TTE effectively rules out infective endocarditis and a TTE is unnecessary. In patients with abnormal heart valves, a TEE did not enhance the diagnostic yield in most patients (12/15). We reviewed 87 paired TTEs and TEEs, that is, TEE with a preceding TTE performed for the evaluation of native valve IE. Of 87 paired echocardiograms, 72 of 87 had normal TTEs and TEEs, with no evidence of a vegetation indicative of infective endocarditis. A total of 15 of 87 TTEs had thickened/calcified valves without a definite vegetation. Of these, only 3 of 15 were subsequently shown to have a vegetation indicative of endocarditis by TEE. In patients with possible native valve infective endocarditis, before blood culture results are known, a negative TTE was sufficiently specific to rule out native valve infective endocarditis. Our data showed that the negative predictive value of a normal TTE in the evaluation of possible native valve endocarditis is 90% or greater. In those with some valve abnormality (ie, thickened/calcified heart valves), subsequent TTE did not materially increase vegetation detection.

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

Respiratory syncytial virus (RSV) community-acquired pneumonia (CAP) in a hospitalized adult with human immunodeficiency virus (HIV) mimicking influenza A and Pneumocystis (carinii) jiroveci pneumonia (PCP).

BACKGROUND Respiratory syncytial virus (RSV) is an important cause of lower respiratory tract infections in young children, the elderly, and immunocompromised hosts, but RSV is a rare cause of community-acquired pneumonia (CAP) in hospitalized adults with human immunodeficiency virus (HIV). In patients with HIV, CAP is most frequently attributable to the usual bacterial respiratory pathogens that cause CAP in immunocompetent hosts, eg, Streptococcuspneumoniae or Hemophilus influenzae. Adults with HIV are also predisposed to intracellular CAP pathogens, ie, Mycoplasmatuberculosis, Salmonella spp., Pneumocystis (carinii) jiroveci (PCP), cytomegalovirus, and Legionella spp. This year, co-circulating in the community during influenza season were strains of human seasonal influenza A (H3N2) and swine influenza A (H1N1). During the influenza season, in adults hospitalized with HIV, the diagnostic possibilities should include influenza-like illnesses, eg, human parainfluenza virus types 3 and 4, human metapneumovirus, and pertussis. CASE REPORT We present an adult with HIV, hospitalized for an influenza-like illness during influenza season. The differential diagnosis of CAP in this patient included influenza A and PCP. CONCLUSION We report on an adult patient with HIV with CAP that mimicked influenza and PCP, and was attributable to RSV.

Legionella pneumophila community-acquired pneumonia (CAP) in a post-splenectomy patient with myelodysplastic syndrome (MDS).

Legionnaires disease is a cause of community-acquired pneumonia (CAP) in normal hosts, but those with impaired cell-mediated immunity (CMI) and T-lymphocyte function are particularly predisposed to Legionella species CAP. Myelodysplastic syndrome (MDS) is a disorder of the elderly that is associated with impaired CMI. Cases of MDS or Legionella species CAP are rare. Splenectomized patients primarily have impaired humoral immunity and B-lymphocyte function, and, to a lesser extent, some decrease in CMI. For this reason, Legionnaires disease has rarely been reported in splenectomized patients. We believe this to be the first reported case of Legionella pneumophila CAP in an asplenic patient with MDS.

Fever of unknown origin (FUO) in an immunocompetent adult due to cytomegalovirus (CMV) with polyclonal gammopathy

Fever of unknown origin (FUO) may be due to infection, malignancy, collagen vascular/inflammatory disorders, or other causes. Cytomegalovirus (CMV) infection is a rare cause of FUO in immunocompetent adults. We present a case of FUO due to CMV in an immunocompetent adult with polyclonal gammopathy on serum protein electrophoresis (SPEP).

Are ESR/CRP ratios helpful in differentiating West Nile encephalitis from non-West Nile virus meningitis/encephalitis?

Abstract West Nile encephalitis (WNE) may mimic other acute central nervous system infections in endemic areas. The laboratory diagnosis of WNE often takes several days. We review our recent experience of WNE to determine if the erythrocyte sedimentation rate/C-reaction protein ratio would be helpful in the early/presumptive diagnosis of WNE in hospitalized adults.

Pseudomonas pseudoalcaligenes Peritoneal Dialysis-Associated Peritonitis

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Ehrlichia chaffeensis human monocytic ehrlichiosis with pancytopenia

Ehrlichia are rickettsial-like organisms and are obligate intracellular parasites that affect the white blood cells (WBCs), i.e., macrophages, granulocytes, and lymphocytes. Clinically, ehrlichiosis is a tick-borne infectious disease resembling rocky mountain spotted fever (RMSF) in most of its clinical manifestations. With RMSF, a petechial rash on the wrists/ ankles 3 – 5 days after the onset of infection is characteristic, while a rash in ehrlichiosis is unusual. Accordingly, ehrlichiosis has been termed ‘ spotless RMSF ’ . The peak incidence of ehrlichiosis occurs in the summer months, coinciding with peak human tick exposure. Patients with ehrlichiosis have usually been exposed to ticks, but only a minority report a tick bite. Unlike RMSF, which is transmitted primarily by Dermacentor sp. ticks, Ehrlichia is transmitted by Amblyomma americanum ticks [1 – 3]. Because tick-borne disease may be due to Babesia (babesiosis), Borrelia (Lyme disease), or Ehrlichia (ehrlichiosis), the diagnosis may be perplexing [4]. Lyme disease usually presents with headache, sore throat and/or mild meningismus and/or erythema migrans rash. Non-specifi c laboratory tests are usually unremarkable, but serum transaminases may be minimally/transiently elevated. The WBC count, platelet count, and erythrocyte sedimentation rate (ESR) are usually normal in Lyme disease. Serum transaminases may be elevated. In contrast, babesiosis is a malarialike illness, with headache and haemolytic anaemia, and usually a highly elevated lactate dehydrogenase (LDH). Pancytopenia has been reported with babesiosis, and also erythrophagocytosis [1,5,6]. In the absence of rash, ehrlichiosis has few clinical fi ndings. An enlarged liver or spleen is unusual with ehrlichiosis, and hepatosplenomegaly should suggest an alternate diagnosis. Ehrlichiosis presents a problem in the differential diagnosis as the clinical and laboratory fi ndings are non-specifi c. The clinical triad leukopenia, thrombocytopenia, and elevated serum transaminases in a patient without a rash should suggest ehrlichiosis [1,2,7]. Fever and fatigue are features of ehrlichiosis, but chills are infrequent and are not a prominent part of the clinical presentation. However, pancytopenia in the absence of splenomegaly or haemophagocytosis is rare in babesiosis. Pancytopenia occurs commonly with canine ehrlichiosis, but human ehrlichiosis-associated pancytopenias have only been reported rarely [3,7 – 10]. We present a case of human monocytic ehrlichiosis (HME) with pancytopenia.

Ehrlichia chaffeensis presenting with bilateral anterior thigh pain (Louria's sign).

Bilateral anterior thigh pain may indicate bacteremia (Lourias Sign). We present a case of Ehrlichiosis due to Ehrlichia chaffeensis whose predominant presenting symptom was localized bilateral anterior thigh pain.

Cryptococcal pneumonia in a patient with presumptive sarcoidosis and selective immunoglobulin A deficiency

Sarcoidosis is a multisystem granulomatous disease of unknown cause associated with impaired T-lymphocyte function and impaired cell-mediated immunity. Decreased cell-mediated immunity predisposes one to intracellular pathogens (eg, cryptococci).