No full-text available
To read the full-text of this research,
you can request a copy directly from the author.
Swine influenza (H1N1) pneumonia during the 'herald wave' of the pandemic: no increase in bacterial pneumonia without empirical antibiotics
... This case also merits comment from a antibiotic stewardship standpoint since without a definite diagnosis there was no clinical rationale for empirical antibiotics. 5,6 PCT is unhelpful in bacterial pneumonia diagnosis and may be elevated with renal insufficiency, as in this case. 7,8 There were no clinical findings to suggest bacterial coinfection/pneumonia. ...
Relation of Diagnostic Accuracy of Viral Respiratory Polymerase Chain Reaction to Specimen Number and Source in Severe Adenovirus Pneumonia: Antimicrobial Stewardship Implications - Volume 37 Issue 9 - Cheston B. Cunha
... [14][15][16] Like SARS and avian influenza (H 7 N 9 ), MERS has not been complicated by bacterial co-infections. 5,[28][29][30] Pandemic influenza, in contrast, which may be complicated by simultaneous bacterial co-infection, with S. aureus (MSSA or MRSA), or sequential co-infection in patients who improve ~1 wk who then may develop a secondary bacterial pneumonia due to Haemophilus influenzae or S. pneumoniae. 14,15 Since any patient, including MERS or influenza patients, that receive prolonged mechanical ventilation may develop late nosocomial bacterial pneumonia. ...
Coronaviruses have traditionally been associated with mild upper respiratory tract infections throughout the world. In the fall of 2002, a new coronavirus emerged in in Asia causing severe viral pneumonia, i.e., severe acute respiratory syndrome (SARS). Nearly a decade following the SARS epidemic, a new coronavirus causing severe viral pneumonia has emerged, i.e., middle east respiratory syndrome (MERS). Since the initial case of MERS-CoV occurred in June of 2012 in Saudi Arabia there have been 688 confirmed cases and 282 deaths in 20 countries.
Although both SARS and MERS are caused by coronaviruses, SARS was characterized by efficient human transmission and relatively low mortality rate. In contrast, MERS is relatively inefficiently transmitted to humans but has a high mortality rate. Given the potential overlap in presentation and manifestation, it is important to understand the clinical and epidemiologic differences between MERS, SARS and influenza.
Fecal Microbiota Therapy as Rescue Therapy for Life-Threatening Clostridium difficile Infection in the Critically Ill: A Small Case Series - Volume 37 Issue 9 - Sebastian Schulz-Stübner, Zoran Textor, Martin Anetseder
We studied the presence of extended spectrum beta lactamases (ESBLs) in 44 clinical isolates of Escherichia coli collected from out-patients in two university teaching hospitals in South-Eastern Nigeria. Species identification was performed by standard microbiology methods and re-confirmed by MALDI-TOF technology. Phenotypic characterization of ESBL enzymes was done by double disc synergy test and presence of ESBL genes was determined by specific PCR followed by sequencing. Transfer of plasmid DNA was carried out by transformation using E. coli DH5 as recipient strain. Phenotypic characterization identified all isolates to be ESBL positive. 77% of strains were from urine, 13.6% from vaginal swabs and 9.0% from wound swabs. 63.6% were from female patients, 68% were from outpatients and 95.5% from patients younger than 30 years. All ESBL producers were positive in a PCR for bla
CTX-M-1 cluster, in exemplary strains bla
CTX-M-15 was found by sequencing. In all strains ISEcp1 was found upstream and ORF477 downstream of bla
CTX-M. PCR for bla
TEM and bla
OXA-1 was positive in 93.1% of strains, whereas bla
SHV was not detected, aac(6′)-Ib-cr was found in 97.7% of strains. RAPD analysis revealed seven different clonal groups named A through G with the majority of the strains (65.9%) belonging to clone A. Transfer of an ESBL plasmid with co-resistance to gentamicin, kanamycin, tobramycin, doxycycline and trimethropim-sulfamethoxazole was successful in 19 (43.2%) strains. This study showed a high rate of CTX-M-1 cluster - ESBLs in South-Eastern Nigeria and further confirms the worldwide spread of CTX-M ESBL in clinical isolates.
Clin Microbiol Infect 2012; 18: E49–E51
Of 109 clinical Escherichia coli isolates from two major tertiary hospitals in Lagos (University Teaching Hospital and the National Orthopaedic Hospital Igbobi), 14 (12.8%) extended-spectrum beta-lactamse (ESBL) producers were characterized using PCR and sequencing, ERIC-PCR and multilocus sequence typing. All ESBL-producing isolates encoded only the CTX-M-15 gene. Clonal group ST131 (35.7%) was the predominant ST, followed by ST617 (28.6%). Isolated cases of other sequence types were also observed. Plasmid-mediated quinolone resistance genes qnrA, qnrB1 and aac-(6′)-lb-cr were detected among these ESBL isolates of different clonal groups. This is the first description of the clonality of CTX-M-15-producing E. coli from Nigeria. The presence of diverse clonal lineages shows the continuing potential for genetic diversification and emergence of new epidemic strains.
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.
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.
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.
The "herald wave" of the H1N1 pandemic spread from Mexico to the United States in spring 2009. Initially, the epicenter of H1N1 in the United States was in the New York area. Our hospital, like others, was inundated with large numbers of patients who presented at the Emergency Department (ED) with influenza-like illnesses (ILIs) for swine influenza testing and evaluation.
The Winthrop-University Hospital ED used rapid influenza (QuickVue A/B) tests to screen for H1N1 infection. Patients who were rapid influenza A test-positive were also reverse transcription-polymerase chain reaction (RT-PCR) positive for H1N1. In our ED, 30% of patients with ILIs and possible H1N1 pneumonia had negative rapid influenza A screening tests. Because H1N1 RT-PCR testing was restricted, there was no laboratory test to confirm or rule out H1N1. Other rapid influenza diagnostic tests (RIDTs), e.g., the respiratory fluorescent antibody (FA) viral panel test, were used to identify H1N1 patients with negative RIDTs.
Unfortunately, there was not a good correlation between RIDT results and RT-PCR results. There was a critical need to develop a clinical syndromic approach for diagnosing hospitalized adults with probable H1N1 pneumonia with negative RIDTs. Early in the pandemic, the Winthrop-University Hospital Infectious Disease Division developed a diagnostic weighted point score system to diagnose H1N1 pneumonia clinically in RIDT-negative adults. The point score system worked well, but was time-consuming. As the "herald wave" of the pandemic progressed, our ED staff needed a rapid, simplified method to diagnose probable H1N1 pneumonia in hospitalized adults with negative RIDTs. A rapid and simplified diagnosis was based on the diagnostic weighted point score system, which we simplified into a triad of key, nonspecific laboratory indicators. In adults hospitalized with an ILI, a fever >102 degrees F with severe myalgias, and a chest x-ray without focal segmental/lobar infiltrates, the presence of three indicators, i.e., otherwise unexplained relative lymphopenia, elevated serum transaminases, and an elevated creatinine phosphokinase, constituted the diagnostic swine influenza triad. The Infectious Disease Division's diagnostic swine flu triad was used effectively as the pandemic progressed, and was not only useful in correctly diagnosing probable H1N1 pneumonia in hospitalized adults with negative RIDTs, but was also in ruling out mimics of swine influenza, e.g., exacerbations of chronic bronchitis, asthma, or congestive heart failure, as well as bacterial community-acquired pneumonias (CAPs), e.g., legionnaire's disease.
Clinicians can use the Winthrop-University Hospital Infectious Disease Division's Diagnostic swine influenza triad to make a rapid clinical diagnosis of probable H1N1 pneumonia in hospitalized adult patients with negative RIDTs.
Pandemic influenza A(H1N1) emerged rapidly in California in April 2009. Preliminary comparisons with seasonal influenza suggest that pandemic 2009 influenza A(H1N1) disproportionately affects younger ages and causes generally mild disease.
To describe the clinical and epidemiologic features of pandemic 2009 influenza A(H1N1) cases that led to hospitalization or death.
Statewide enhanced public health surveillance of California residents who were hospitalized or died with laboratory evidence of pandemic 2009 influenza A(H1N1) infection reported to the California Department of Public Health between April 23 and August 11, 2009.
Characteristics of hospitalized and fatal cases.
During the study period there were 1088 cases of hospitalization or death due to pandemic 2009 influenza A(H1N1) infection reported in California. The median age was 27 years (range, <1-92 years) and 68% (741/1088) had risk factors for seasonal influenza complications. Sixty-six percent (547/833) of those with chest radiographs performed had infiltrates and 31% (340/1088) required intensive care. Rapid antigen tests were falsely negative in 34% (208/618) of cases evaluated. Secondary bacterial infection was identified in 4% (46/1088). Twenty-one percent (183/884) received no antiviral treatment. Overall fatality was 11% (118/1088) and was highest (18%-20%) in persons aged 50 years or older. The most common causes of death were viral pneumonia and acute respiratory distress syndrome.
In the first 16 weeks of the current pandemic, the median age of hospitalized infected cases was younger than is common with seasonal influenza. Infants had the highest hospitalization rates and persons aged 50 years or older had the highest mortality rates once hospitalized. Most cases had established risk factors for complications of seasonal influenza.
Between March and July 2009, the largest number of confirmed cases of 2009 influenza A(H1N1) infection occurred in North America.
To describe characteristics, treatment, and outcomes of critically ill patients in Canada with 2009 influenza A(H1N1) infection.
A prospective observational study of 168 critically ill patients with 2009 influenza A(H1N1) infection in 38 adult and pediatric intensive care units (ICUs) in Canada between April 16 and August 12, 2009.
The primary outcome measures were 28-day and 90-day mortality. Secondary outcomes included frequency and duration of mechanical ventilation and duration of ICU stay.
Critical illness occurred in 215 patients with confirmed (n = 162), probable (n = 6), or suspected (n = 47) community-acquired 2009 influenza A(H1N1) infection. Among the 168 patients with confirmed or probable 2009 influenza A(H1N1), the mean (SD) age was 32.3 (21.4) years; 113 were female (67.3%) and 50 were children (29.8%). Overall mortality among critically ill patients at 28 days was 14.3% (95% confidence interval, 9.5%-20.7%). There were 43 patients who were aboriginal Canadians (25.6%). The median time from symptom onset to hospital admission was 4 days (interquartile range [IQR], 2-7 days) and from hospitalization to ICU admission was 1 day (IQR, 0-2 days). Shock and nonpulmonary acute organ dysfunction was common (Sequential Organ Failure Assessment mean [SD] score of 6.8 [3.6] on day 1). Neuraminidase inhibitors were administered to 152 patients (90.5%). All patients were severely hypoxemic (mean [SD] ratio of Pao(2) to fraction of inspired oxygen [Fio(2)] of 147 [128] mm Hg) at ICU admission. Mechanical ventilation was received by 136 patients (81.0%). The median duration of ventilation was 12 days (IQR, 6-20 days) and ICU stay was 12 days (IQR, 5-20 days). Lung rescue therapies included neuromuscular blockade (28% of patients), inhaled nitric oxide (13.7%), high-frequency oscillatory ventilation (11.9%), extracorporeal membrane oxygenation (4.2%), and prone positioning ventilation (3.0%). Overall mortality among critically ill patients at 90 days was 17.3% (95% confidence interval, 12.0%-24.0%; n = 29).
Critical illness due to 2009 influenza A(H1N1) in Canada occurred rapidly after hospital admission, often in young adults, and was associated with severe hypoxemia, multisystem organ failure, a requirement for prolonged mechanical ventilation, and the frequent use of rescue therapies.
In March 2009, novel 2009 influenza A(H1N1) was first reported in the southwestern United States and Mexico. The population and health care system in Mexico City experienced the first and greatest early burden of critical illness.
To describe baseline characteristics, treatment, and outcomes of consecutive critically ill patients in Mexico hospitals that treated the majority of such patients with confirmed, probable, or suspected 2009 influenza A(H1N1).
Observational study of 58 critically ill patients with 2009 influenza A(H1N1) at 6 hospitals between March 24 and June 1, 2009. Demographic data, symptoms, comorbid conditions, illness progression, treatments, and clinical outcomes were collected using a piloted case report form.
The primary outcome measure was mortality. Secondary outcomes included rate of 2009 influenza (A)H1N1-related critical illness and mechanical ventilation as well as intensive care unit (ICU) and hospital length of stay.
Critical illness occurred in 58 of 899 patients (6.5%) admitted to the hospital with confirmed, probable, or suspected 2009 influenza (A)H1N1. Patients were young (median, 44.0 [range, 10-83] years); all presented with fever and all but 1 with respiratory symptoms. Few patients had comorbid respiratory disorders, but 21 (36%) were obese. Time from hospital to ICU admission was short (median, 1 day [interquartile range {IQR}, 0-3 days]), and all patients but 2 received mechanical ventilation for severe acute respiratory distress syndrome and refractory hypoxemia (median day 1 ratio of Pao(2) to fraction of inspired oxygen, 83 [IQR, 59-145] mm Hg). By 60 days, 24 patients had died (41.4%; 95% confidence interval, 28.9%-55.0%). Patients who died had greater initial severity of illness, worse hypoxemia, higher creatine kinase levels, higher creatinine levels, and ongoing organ dysfunction. After adjusting for a reduced opportunity of patients dying early to receive neuraminidase inhibitors, neuraminidase inhibitor treatment (vs no treatment) was associated with improved survival (odds ratio, 8.5; 95% confidence interval, 1.2-62.8).
Critical illness from 2009 influenza A(H1N1) in Mexico occurred in young individuals, was associated with severe acute respiratory distress syndrome and shock, and had a high case-fatality rate.
Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) co-infection has been described previously in association with respiratory tract infection caused by seasonal influenza A viruses, but not with swine origin influenza A (H1N1) virus (S-OIV). We report the clinical and pathological findings of the first death with fulminant co-infection by CA-MRSA. Since early empirical treatment with beta-lactam plus fluoroquinolone or macrolides is often initiated before specimen collections, bacterial co-infection in S-OIV may have been under-reported.