Yu Shia Lin

Antibody response to inactivated influenza A (H1N1) 2009 monovalent vaccine in patients with and without HIV.

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Does Alkaline Colonic pH Predispose to Clostridium difficile Infection

Objectives Clostridium difficile caused nearly 500,000 infections and was associated with approximately 29,000 deaths in 2011, according to data from the Centers for Disease Control and Prevention. C. difficile is a bacterium that causes diarrhea and, often, severe illness in healthcare facilities, as well as the community. Our objective was to determine whether alkaline colonic pH predisposes to colonization and infection with C. difficile. Methods A total of 228 patients with diarrhea and/or abdominal pain, leukocytosis, and fever were included. Stool pH was measured, and C. difficile antigen and toxin in stool were detected. Results Of 228 patients, 30 (13.2%) tested positive for C. difficile (antigen+/toxin+) and 171 (75%) were C. difficile negative (antigen−/toxin−). Of 171 patients who tested negative, 93 (54.4%) had stool pH >7.0 and 78 (45.6%) had pH ⩽7.0. Among the 30 patients who tested positive, 26 (86.7%) had stool pH >7.0 (P = 0.002). Among the 27 colonized patients (antigen+/toxin−), 12 (44.4%) had stool pH >7.0 (P = 0.34). For all patients with stool pH ⩽7.0, 96% tested negative for C. difficile infection (P = 0.002). Conclusions A strong association between C. difficile infection and alkaline stool pH was found.

Case report on pulmonary disease due to coinfection of Mycobacterium tuberculosis and Mycobacterium abscessus: Difficulty in diagnosis

Mycobacterium abscessus, which is ubiquitous environmental organism, is more likely to cause pulmonary infection in the presence underlying lung disease and immunosuppression. We report a case of pulmonary disease due to coinfection of Mycobacterium tuberculosis (MTB) and Mycobacterium abscessus (M. abscessus) in an immunocompetent patient without underlying lung disease. Healthcare professionals should be aware of co-infection with MTB and M. abscessus, and treatment should be based on clinical suspicion and/or epidemiological circumstances.

Artesunate-related fever and delayed hemolysis in a returning traveler

Malaria is a serious and sometimes fatal disease caused by an intraerythrocytic parasite, and is commonly seen in developing countries. Approximately 1500 cases of malaria are diagnosed in the United States each year, mostly in travelers and immigrants returning from endemic areas [1]. There are many different regimens used to treat malaria, some of which are not approved in the USA. The side effects of these medications may not be familiar to physicians in the USA. We report a case of a returning traveler from Nigeria presenting with fever and hemolytic anemia caused by a delayed response to artesunate given 3 weeks earlier while in Nigeria. To our knowledge, there are few cases reported in the United States of hemolytic anemia secondary to artesunate therapy [2].

Staphylococcus lugdunensis endocarditis with destruction of the ventricular septum and multiple native valves.

Staphylococcus lugdunensis (S. lugdunensis) is a coagulase negative staphylococcus (CoNS) that can cause destructive infective endocarditis. S. lugdunensis, unlike other CoNS, should be considered to be a pathogen. We report the first case of S. lugdunensis endocarditis causing ventricular septal defect and destruction of the aortic and mitral valves. A 53-year-old male with morbid obesity and COPD presented with intermittent fever and progressive shortness of breath for 2 weeks. Chest examination showed bilateral basal crepitations, and a grade 2 systolic murmur along the right sternal border. The leukocyte count was 26,000 cells/μl with 89% neutrophils. He was treated with intravenous vancomycin and ceftriaxone. Blood cultures grew Staphylococcus lugdunensis. Transthoracic echocardiogram, which was limited by body habitus, showed no definite valvular vegetations. Repeat transthoracic echocardiogram performed one week later revealed a large aortic valve vegetation Vancomycin was switched to daptomycin on day 4 because of difficulty achieving therapeutic levels of vancomycin and the development of renal insufficiency. Open heart surgery on day 10 revealed aortic valve and mitral valve vegetations with destruction, left ventricular outflow tract (LVOT) septal abscess and ventricular septal defect (VSD). Bio-prosthetic aortic and mitral valve replacement, LVOT and VSD repair were done. Intraoperative cultures grew Staphylococcus lugdunensis. The patient was discharged home with daptomycin to complete 6 weeks of treatment. S. lugdunensis can cause rapidly progressive endocarditis with valve and septal destruction. Early diagnosis and therapy are essential, with consideration of valve replacement.

Pacemaker-Associated Infective Endocarditis Caused by Staphylococcus schleiferi: A Case Report and Review of the Literature

AbstractStaphylococcus schleiferi is a relatively newly discovered coagulase-negative Staphylococcus that has been associated with wound infections, bacteremia, hip prosthesis infections, and vascular device infections. Despite being a coagulase-negative Staphylococcus, there are some shared characteristics with coagulase-positive Staphylococcus aureus that make this bacterium unique among its class. S. schleiferi seems to play a significant role in the colonization and infection of implanted devices and should be regarded as an important opportunistic pathogen. We report the case of a 67-year-old male with a persistent pacemaker-related endocarditis caused by S. schleiferi.

Recurrent Isosporiasis in a Patient With Human T-cell Lymphotropic Virus 1 Infection

AbstractInfection with Isospora belli is a well-known cause of chronic diarrhea in patients with human immunodeficiency virus/acquired immunodeficiency syndrome. Recurrent isosporiasis, causing chronic diarrhea in human immunodeficiency virus–seronegative individuals, should lead to a search for other causes of immunosuppression, including human T-cell lymphotropic virus 1 infection.

Pneumothorax in a Young Man in Brooklyn, New York

Diagnosis: Pneumothorax from Rupture of a Coccidioidal Pulmonary Cavity Biopsy specimens (Figures 1 and 2) showed necrotizing granulomata containing 30to 40-lm thick-walled, nonbudding spherules revealed on Gomori methenamine silver stain (Figure 2). Results of stains for acid-fast bacilli were negative. Coccidioides immunoglobulin G (IgG) antibody was detected by means of immunodiffusion. Liposomal amphotericin B (AmBisome, Astellas Pharma) 5 mg/kg/day was given. On day 9 of the treatment, the patient developed right upper quadrant tenderness and elevated serum levels of transaminases. Sonogram of the liver was unremarkable, and viral hepatitis serological test results were negative. Liposomal amphotericin B was discontinued, and fluconazole 800 mg daily was started. Liver enzyme levels began to improve 2 days after discontinuation of amphotericin and were normal after 6 weeks.