Kunatum Prasidthrathsint

Severe influenza in 33 US hospitals, 2013–2014: Complications and risk factors for death in 507 patients

BACKGROUND Influenza A (H1N1) pdm09 became the predominant circulating strain in the United States during the 2013-2014 influenza season. Little is known about the epidemiology of severe influenza during this season. METHODS A retrospective cohort study of severely ill patients with influenza infection in intensive care units in 33 US hospitals from September 1, 2013, through April 1, 2014, was conducted to determine risk factors for mortality present on intensive care unit admission and to describe patient characteristics, spectrum of disease, management, and outcomes. RESULTS A total of 444 adults and 63 children were admitted to an intensive care unit in a study hospital; 93 adults (20.9%) and 4 children (6.3%) died. By logistic regression analysis, the following factors were significantly associated with mortality among adult patients: older age (>65 years, odds ratio, 3.1 [95% CI, 1.4-6.9], P=.006 and 50-64 years, 2.5 [1.3-4.9], P=.007; reference age 18-49 years), male sex (1.9 [1.1-3.3], P=.031), history of malignant tumor with chemotherapy administered within the prior 6 months (12.1 [3.9-37.0], P<.001), and a higher Sequential Organ Failure Assessment score (for each increase by 1 in score, 1.3 [1.2-1.4], P<.001). CONCLUSION Risk factors for death among US patients with severe influenza during the 2013-2014 season, when influenza A (H1N1) pdm09 was the predominant circulating strain type, shifted in the first postpandemic season in which it predominated toward those of a more typical epidemic influenza season.

Bacterial and viral co-infections complicating severe influenza: Incidence and impact among 507 U.S. patients, 2013–14

Abstract Background Influenza acts synergistically with bacterial co-pathogens. Few studies have described co-infection in a large cohort with severe influenza infection. Objectives To describe the spectrum and clinical impact of co-infections. Study design Retrospective cohort study of patients with severe influenza infection from September 2013 through April 2014 in intensive care units at 33 U.S. hospitals comparing characteristics of cases with and without co-infection in bivariable and multivariable analysis. Results Of 507 adult and pediatric patients, 114 (22.5%) developed bacterial co-infection and 23 (4.5%) developed viral co-infection. Staphylococcus aureus was the most common cause of co-infection, isolated in 47 (9.3%) patients. Characteristics independently associated with the development of bacterial co-infection of adult patients in a logistic regression model included the absence of cardiovascular disease (OR 0.41 [0.23–0.73], p=0.003), leukocytosis (>11K/μl, OR 3.7 [2.2–6.2], p<0.001; reference: normal WBC 3.5–11K/μl) at ICU admission and a higher ICU admission SOFA score (for each increase by 1 in SOFA score, OR 1.1 [1.0–1.2], p=0.001). Bacterial co-infections (OR 2.2 [1.4–3.6], p=0.001) and viral co-infections (OR 3.1 [1.3–7.4], p=0.010) were both associated with death in bivariable analysis. Patients with a bacterial co-infection had a longer hospital stay, a longer ICU stay and were likely to have had a greater delay in the initiation of antiviral administration than patients without co-infection (p<0.05) in bivariable analysis. Conclusions Bacterial co-infections were common, resulted in delay of antiviral therapy and were associated with increased resource allocation and higher mortality.

Pulmonary blastomycosis: a new endemic area in New York state

We describe three cases of pulmonary blastomycosis in patients from central New York State (NYS). Two of these cases occurred in 2012, and in patients who resided in the same county. Moreover, two of these cases manifested with acute respiratory distress syndrome and survived. Interestingly, one of the two received corticosteroids and was extubated within 1 week. To the best of our knowledge, these are the first cases of human blastomycosis to be reported from NYS and we propose that corticosteroids administration might reduce hospitalisation time and ventilator‐associated complications, even though it is not currently recommended in standard treatment.

Haemophilus influenzae serotype f as a rare cause of septic arthritis.

Non-type B Haemophilus influenzae emerges as a new pathogen in the post H. influenzae serotype b vaccine era. We describe a case of polyarticular septic arthritis caused by H. influenzae serotype f in an adult. The patient was successfully treated with surgical debridement and antibiotic. To the best of our knowledge, this is the fourth reported case of H. influenzae serotype f septic arthritis in adults.

Antimicrobial Susceptibility Patterns among a Large, Nationwide Cohort of Abiotrophia and Granulicatella Clinical Isolates

ABSTRACT Antimicrobial susceptibility patterns from 599 A. defectiva, G. adiacens, and G. elegans clinical isolates were determined by broth microdilution. We observed significant differences in susceptibility across species, particularly to penicillin and ceftriaxone, and across geographical regions. A. defectiva was the least susceptible species overall to penicillin. All isolates were susceptible to vancomycin and >90% were susceptible to levofloxacin.

Association of Q fever with Autoimmune Hepatitis

Human infection by Coxiella burnetii, a zoonosis, is associated with the development of autoantibodies, though the clinical significance of these is unclear. We describe two patients with high-titer Q fever antibodies associated with autoimmune hepatitis (AIH) as demonstrated on biopsy and supported by autoantibody results. For one, the chronology of serologic results uniquely demonstrates the development of autoantibodies after Q fever antibodies were detected, providing supportive evidence that Coxiella burnetii infection may have been a trigger for autoimmune hepatitis.

Clinical Implication of T2* Cardiac Magnetic Resonance Imaging in Cardiac Siderosis

A 55-year-old woman with a history of myelodysplastic syndrome status after multiple blood transfusions presented with a 2-week history of shortness of breath, decreased exercise tolerance, weight gain, and bilateral leg edema. Transthoracic echocardiography 1 week before revealed a left ventricular ejection fraction of 35%. With the concern for iron-overload syndrome and new-onset heart failure, the patient was admitted for further evaluation. The patient had an irregularly irregular tachycardic rhythm with normal blood pressure and pulse oximetry on room air. Pertinent physical findings included jugular venous distention, bibasilar rales, and edematous lower extremities. Laboratory results revealed an anemia, mildly elevated transaminase levels, a ferritin level of 7300 ng/mL, and a negative troponin. Electrocardiogram showed atrial fibrillation with a ventricular rate of 130 beats/min without ST-T changes. Chest x-ray showed mild cardiomegaly with minimal perihilar vascular congestion. Transthoracic echocardiogram demonstrated moderate left atrial enlargement and left ventricular global hypokinesis with an ejection fraction of 20%. Cardiovascular magnetic resonance imaging revealed a decreased signal in both the heart and the liver with a myocardial T2* of 7.2 ms (Figure 1). Magnetic resonance imaging of the abdomen showed a decreased signal on T2weighted imaging consistent with iron deposition in the liver, spleen, and pancreas. A diagnosis of iron overload syndrome with cardiac siderosis was made, and intravenous deferoxamine therapy was initiated. The hospital course was uneventful, and the patient was discharged with intravenous deferoxamine and oral deferiprone. Cardiac siderosis resulting in cardiomyopathy is a serious complication of chronic transfusion therapy. Diagnosis of this condition can be challenging. Although history and physical examination can provide clinical clues, to quantify myocardial iron deposition requires further diagnostic evaluation. Serum ferritin level and

Warfarin-related nephropathy can be mimicked by an interaction between sulfonamide derivatives and vitamin K antagonists

To the Editor: We thank Brodsky et al.1 for their excellent study on warfarin-related nephropathy (WRN). The authors analyzed data and risk factors of WRN in patients with and without chronic kidney disease. However, an interesting topic that the authors did not mention is concurrent treatment of warfarin with antimicrobial agents, especially sulfonamide derivatives. Interaction between trimethoprim/sulfamethoxazole and warfarin can mimic WRN by causing both elevation of international normalized ratio (INR) level and serum creatinine, without the mechanism of WRN. Sulfamethoxazole inhibits CYP2C9, the main enzyme responsible for metabolizing (S)-warfarin (60–70% of warfarins activity), in the liver.2 This antimicrobial agent can cause elevated INR levels with concurrent warfarin treatment. At the same time, trimethoprim is known to decrease the tubular secretion of creatinine and lead to increases in serum creatinine with intact glomerular filtration rate (GFR),3 unlike the case in WRN, which decreases GFR. Moreover, not mentioned in their paper are the large numbers of medications that can acutely increase INR in warfarin-treated patients, and therefore are risk factors for WRN.

The Brief Case: Angiostrongylus cantonensis Eosinophilic Meningitis in a Returned Traveler

CASE A22-year-old male without significant prior medical history presented to the hospital with headache and double vision of 1 month’s duration. He reported a trip to the island of Hawaii 1.5 months prior, where he spent time on the beach, including in the ocean, and ate various types of seafood, including sushi, crab, mahimahi, and shrimp. No other close contacts from his travel became ill. His symptoms began 2 weeks after his return, with headaches, malaise, red eyes, and ear pain. All of these symptoms resolved with a short course of oral antibiotics except the headache and malaise. Approximately a week from his initial symptoms, he developed fevers, and a lumbar puncture was performed, showing 270 white blood cells (WBC)/ l, 2 red blood cells (RBC)/ l, 85% mononuclear cells, 12% eosinophils, and 3% polymorphonuclear cells (PMN). Cerebral spinal fluid (CSF), bacterial culture, and Epstein-Barr virus (EBV) and herpes simplex virus (HSV) real-time PCRs were all negative, and he was assigned a presumptive diagnosis of viral meningitis. Two weeks later, he developed double vision. He was referred to ophthalmology, where an ophthalmologic exam revealed papilledema and bilateral cranial nerve 6 palsy. A noncontrasted brain computed tomography was performed, which was normal. Magnetic resonance imaging of the brain showed a markedly abnormal appearance of the brain and optic nerves, with a T2 hyperintense signal and enhancement in the bilateral optic nerves suggestive of acute inflammation. Additionally, scattered cerebral cortex-based nodular foci of enhancement with a T2 signal abnormality were seen. Lumbar puncture was repeated, with an opening pressure of 28 cm H2O, 588 WBC/ l, no RBC, 61% eosinophils, 29% lymphocytes, 9% monocytes, 1% PMN, protein of 343 mg/dl, and glucose at 36 mg/dl. CSF was tested by PCR for HSV and varicella-zoster virus (VZV), and direct staining and culture were performed for aerobic organisms, fungi, and acid-fast bacillus; all were negative. Serum HIV testing was also negative. CSF flow cytometry showed marked acute inflammation with abundant eosinophils. No malignant cells were identified. A CSF cysticercosis IgG enzyme-linked immunosorbent assay (ELISA) was positive. A CSF sample was sent to the CDC for an Angiostrongylus cantonensis real-time PCR, which was positive. The patient was diagnosed with Angiostrongylus cantonensis eosinophilic meningitis with likely exposure from consumption of undercooked crab or shrimp in a known region of endemic Angiostrongylus cantonensis on the big island of Hawaii. He was started on prednisone and had several additional therapeutic lumbar punctures for treatment of increased intracranial pressure, with significant improvement in his clinical symptoms at the 2-month follow-up.