Uzma Syed

Winthrop-University Hospital Infectious Disease Division's swine influenza (H1N1) pneumonia diagnostic weighted point score system for hospitalized adults with influenza-like illnesses (ILIs) and negative rapid influenza diagnostic tests (RIDTs)

Background In spring 2009, a novel strain of influenza A originating in Veracruz, Mexico, quickly spread to the United States and throughout the world. This influenza A virus was the product of gene reassortment of 4 different genetic elements: human influenza, swine influenza, avian influenza, and Eurasian swine influenza. In the United States, New York was the epicenter of the swine influenza (H1N1) pandemic. Hospital emergency departments (EDs) were inundated with patients with influenza-like illnesses (ILIs) requesting screening for H1N1. Our ED screening, as well as many others, used a rapid screening test for influenza A (QuickVue A/B) because H1N1 was a variant of influenza A. The definitive laboratory test i.e., RT-PCR for H1N1 was developed by the Centers for Disease Control (Atlanta, GA) and subsequently distributed to health departments. Because of the extraordinary volume of test requests, health authorities restricted reverse transcription polymerase chain reaction (RT-PCR) testing. Hence most EDs, including our own, were dependent on rapid influenza diagnostic tests (RIDTs) for swine influenza. A positive rapid influenza A test was usually predictive of RT-PCR H1N1 positivity, but the rapid influenza A screening test (QuickVue A/B) was associated with 30% false negatives. The inability to rely on RIDTs for H1N1 diagnosis resulted in underdiagnosing H1N1. Confronted with adults admitted with ILIs, negative RIDTs, and restricted RT-PCR testing, there was a critical need to develop clinical criteria to diagnose probable swine influenza H1N1 pneumonia. Methods During the pandemic, the Infectious Disease Division at Winthrop-University Hospital developed clinical criteria for adult admitted patients with ILIs and negative RIDTs. Similar to the one developed for the clinical diagnosis of legionnaires disease. The Winthrop-University Hospital Infectious Disease Divisions diagnostic weighted point score system for swine influenza H1N1 pneumonia is based on key clinical and laboratory features. Results During the “herald” wave of the swine influenza H1N1 pandemic, the diagnostic weighted point score system accurately identified probable swine influenza H1N1 pneumonia and accurately differentiated swine influenza H1N1 pneumonia from ILIs and other viral and bacterial community-acquired pneumonias. Conclusion In hospitalized adults with ILIs and negative RIDTs, the diagnostic weighted diagnostic point score system, may be used to make a presumptive clinical diagnosis of swine influenza H1N1 pneumonia.

Severe swine influenza A (H1N1) versus severe human seasonal influenza A (H3N2): Clinical comparisons

At the beginning of the swine influenza (H1N1) pandemic in the spring of 2009, there were still stories of human seasonal influenza A circulating in the New York area. Adult patients admitted with influenza-like illnesses (ILIs) (fever > 102°F, dry cough, and myalgias) presented diagnostic problems. First, clinicians had to differentiate ILIs from influenza, and then differentiate human seasonal influenza A from H1N1 in hospitalized adults with ILIs and negative chest films (no focal segmental/lobar infiltrates). Human seasonal influenza A was diagnosed by rapid influenza diagnostic tests (RIDTs), but H1N1 was often RIDT negative. Reverse transcriptase-polymerase chain reaction for H1N1 was restricted or not available. The Winthrop-University Hospital Infectious Disease Division developed clinical diagnostic criteria (a diagnostic weighted point score system) to rapidly and clinically diagnose H1N1 in patients with negative RIDTs. The point score system was modified and shortened for ease of use, that is, the diagnostic H1N1 triad (any 3 of 4) (ILI, see above) plus thrombocytopenia, relative lymphopenia, elevated serum transaminases, or an elevated creatine phosphokinase. Our clinical experience during the pandemic allowed us to develop the swine diagnostic H1N1 triad. In the process, similarities and differences between human seasonal influenza A and H1N1 were noted. We present 2 illustrative cases of severe influenza, one due to human seasonal influenza A and one due to H1N1, for clinical consideration reflective of our experiences early in the H1N1 pandemic in 2009.

Swine influenza (H1N1) pneumonia: elevated serum procalcitonin levels not due to superimposed bacterial pneumonia

TCC 27853, which was between reference values [3]. For both eropenem and doripenem, the MIC90 (MIC for 90% of the organsms) of the collected strains was >64 mg/L. The MIC50 (MIC for 0% of the organisms) was also identical for the two antibitics tested (64 mg/L) (Table 1). None of the strains collected was ensitive according to CLSI criteria (susceptible ≤4 mg/L; resistant 8 mg/L) [3]. Only marginal differences in MICs of meropenem verus doripenem were found, with a maximal difference of only two ilutions (Table 1). In case of such high MICs, these differences were ot sufficient to consider treatment with doripenem in infections ith MDR Pseudomonas spp. We conclude that, as Fujimura et al. lso mentioned, although doripenem is one of the most potent and romising antipseudomonal drugs, in vitro results from our hospial suggest no role of doripenem in the treatment of infections with DR Pseudomonas spp.

Fulminant fatal swine influenza (H1N1): Myocarditis, myocardial infarction, or severe influenza pneumonia?

The swine influenza (H1N1) pandemic began in Mexico and rapidly spread worldwide. As is the case with pandemic influenza A, the majority of early deaths have been in young healthy adults. The complications of pandemic H1N1 have been reported from several centers. Noteworthy has been the relative rarity of bacterial coinfection in bacterial pneumonia in hospitalized adults with H1N1 pneumonia. Simultaneous bacterial community-acquired pneumonia due to methicillin-sensitive Staphylococcus aureus or community-acquired methicillin resistant S. aureus and subsequent bacterial community-acquired pneumonia due to S. pneumoniae or Haemophilus influenzae have been reportedly rare (0.4%-4% of well-documented cases). Cardiac complications of H1N1 infection have been uncommon. Young healthy adults without a cardiac history who have H1N1 and chest pain usually have either acute myocardial infarction or acute myocarditis. Cardiac symptomatology with H1N1 often overshadows pulmonary manifestations, that is, influenza pneumonia. With H1N1 pneumonia, clinicians should be alert for otherwise unexplained tachycardia or chest pain that may represent acute myocardial infarction or myocarditis. We present a case of rapidly fatal H1N1 in a young adult treated with oseltamivir and peramivir. He was initially tachycardic, thought to represent myocarditis. He subsequently became hypotensive and expired. At autopsy there was cardiomegaly present but there were no signs of acute myocardial infarction or myocarditis. Pathologically, he died of severe H1N1 pneumonia and not bacterial pneumonia.

Non-specific laboratory test indicators of severity in hospitalized adults with swine influenza (H1N1) pneumonia

New York was at the epicenter of the “herald wave” of the swine influenza (H1N1) pandemic in the spring of 2009 [1, 2]. Our hospital, Winthrop-University Hospital (WUH), like other hospitals in the area, were inundated with patients with influenza-like illnesses (ILIs) presenting themselves to our Emergency Department (ED) for testing and clinical evaluation. In the majority of patients, the swine influenza (H1N1) was a mild ILI not severe enough to warrant hospitalization. However, 25 adult patients were ill enough to be admitted with definite/probable swine influenza (H1N1) pneumonia during the “herald wave” of the pandemic.

Swine influenza (H1N1) pneumonia in hospitalized adults: chest film findings.

In patients with swine influenza (H1N1) pneumonia, the admission chest film is critical to rapidly detect simultaneous bacterial pneumonia due to Staphylococcus aureus or subsequent bacterial pneumonia due to Streptococcus pneumoniae or Haemophilus influenzae by the presence of focal infiltrates. Our objective was to characterize the chest film findings in 25 adults hospitalized with H1N1 pneumonia during the pandemic and detect focal infiltrates indicative of bacterial coinfection, that is, bacterial pneumonia. Chest films were obtained on admission, after 48 hours, and thereafter as indicated throughout hospitalization. Chest film findings were classified as no infiltrates, clear with accentuated bibasilar lung markings, or focal segmental/lobar infiltrates. The presence or absence of pleural effusion and cavitation was also noted. Admitted adults with H1N1 pneumonia had negative chest films or accentuated basilar lung markings. After 48 hours, 13% of patients developed patchy bilateral interstitial infiltrates. No patients had or subsequently developed focal segmental/lobar infiltrates indicative of bacterial community-acquired pneumonia during hospitalization. The most common chest film finding was no infiltrates or an accentuation of bibasilar lung markings in hospitalized adults with H1N1 pneumonia. No patients had focal segmental/lobar infiltrates indicative of superimposed bacterial community-acquired pneumonia.

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.

The gastrointestinal manifestations with swine influenza (H1N1) in hospitalized adults

It is well known that infl uenza may be accompanied by gastrointestinal symptoms, i.e., nausea, vomiting and diarrhoea [1]. Because of its gastrointestinal manifestations, infl uenza has even been termed ‘ intestinal fl u ’ . The swine infl uenza (H1N1) pandemic began in 2009 and spread from Mexico to the USA, subsequently spreading rapidly worldwide. Reports have noted that gastrointestinal symptoms may accompany swine infl uenza (H1N1) [2]. However, no published reports have described the frequency/duration of nausea, vomiting and diarrhoea in adults hospitalized with swine infl uenza (H1N1) [3 – 5]. To characterize the gastrointestinal manifestations of swine infl uenza (H1N1), we retrospectively reviewed the charts of 14 adults admitted during the ‘ fall ’ wave of the pandemic with confi rmed swine infl uenza (H1N1) by laboratory criteria, i.e., a positive rapid infl uenza A (Quick Vue) test and/or a positive H1N1 PCR test. Charts were reviewed for the frequency and duration of nausea, vomiting and diarrhoea. The presence of abdominal pain was also noted. None of the patients had positive stool studies for Clostridium diffi cile, enteric pathogens or ova/ parasites. To determine if gastrointestinal symptoms were related to severity of infection, intensive care unit admission was used as a marker for swine infl uenza (H1N1) severity. We found that 6/14 (43%) hospitalized adults with swine infl uenza (H1N1) had nausea before/on the day of admission. The duration of nausea in these patients ranged from 1 to 7 days. Vomiting, less frequent and present in 5/14 (36%) patients, occurred before/on the day of admission; the duration of vomiting was also 1 – 7 days. Watery diarrhoea occurred in 4/14 (29%) patients before/on the day of admission, and lasted 1 – 12 days (Table I). Nausea with vomiting was present in 5/14 (36%) patients, while nausea with diarrhoea was present in 2/14 (14%) patients. Vomiting with diarrhoea was least common and present in 1/14 (7%) patients. Nausea, vomiting and diarrhoea together occurred in only 1/14 (7%) patients. Abdominal pain was common and occurred in 3/14 (21%) patients. Nausea, vomiting or diarrhoea did not appear to be related to the severity of swine infl uenza (H1N1), since none of the intubated patients (0/2) had nausea with vomiting and only one (1/2) had diarrhoea. We conclude that gastrointestinal symptoms, i.e., nausea, vomiting and/or diarrhoea were common in hospitalized adults with swine infl uenza (H1N1). Nausea was the most common symptom, occurring in nearly half of the patients. Vomiting was next in frequency and diarrhoea was the least common gastrointestinal manifestation. Nausea, vomiting and diarrhoea together were very uncommon. Nausea, vomiting and diarrhoea were self-limited in all patients. Various reports describing the gastrointestinal manifestations of swine infl uenza (H1N1) have recorded the frequency of nausea or diarrhoea in ambulatory/hospitalized children/adults. However, this is the fi rst report to describe the frequency and duration of nausea, vomiting and diarrhoea in LETTER TO THE EDITOR

Legionella pneumophila community acquired pneumonia (CAP) presenting with myoclonus

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Nosocomial Escherichia coli pacemaker pocket infection.

To the Editor: Implantable electronic pacemakers and implantable cardiac comewith the riskof infection, including pocket infection, lead infection, bacteremia, and endocarditis. The incidence of pacemaker infections ranges from 0.13% to 19.9%, with a morbidity of 27%-66%. Pacemaker pocket infections result fromcontamination of thepacemakergenerator at the timeof implantation. The average time to presentation of infection is 8 days (range, 4-25 days). Common signs and symptoms of pacemaker pocket infections include erythema (34%), pain (32%), breakdown of overlying skin (23%), swelling (21%), warmth (11.5%), and/or drainage through the incision site. Localized pacemaker pocket infections occur with and without bacteremia. The most common pathogens in infected pacemaker pocket infections are coagulase-negative Staphylococcus epidermidis (CoNS) and S aureus. Infrequent pathogens include aerobic gram-negative bacilli (GNBs), such as Enterobacter cloacae, Pseudomonas aeruginosa, Klebsiella pneumoniae, Proteus mirabilis, and Acinetobacter baumannii. Less-virulent organisms usually have a more subacute/chronic clinical presentation. Pacemaker pocket infections can spread along the leads to the endocardium and electrode tip, exposing the mediastinum as well as the heart to infection. We present a rare case of nosocomial Escherichia coli pacemaker pocket infection complicated by bacteremia. The patient was a 68-year male who presented to the emergency department with fever and chills. His past medical history was significant for atrial fibrillation, coronary artery diseasewith stent placement 5 years earlier, andmyocardial infarction 2 weeks before admission. He developed bradycardia while on vacation, necessitating emergent pacemaker placement. In the week after pacemaker insertion, he noticed erythema and change at the site accompanied by fever and chills. On admission, the patient had a temperature of 102.28F, pulse rate of 61/minute, respiratory rate of 20/minute, and blood pressure of 112/72 mm Hg. The physical examination was unremarkable except for serosanguinous wound drainage and erythema at the lateral edge of the pacemaker site. Laboratory test results