jugular ganglia, or centrally at the level of the brainstem.

We believe that our patient had a combination of both central and peripheral cough sensitization secondary to latanoprost therapy and gastroesophageal reflux. PGs, which were first isolated in 1935,4 are a group of lipids derived enzymatically from fatty acids. The cyclooxygenase pathway yields PGD, PGE, and PGF. Latanoprost is a PGF2- isopropyl ester analog and is a selective agonist of the prostanoid FP receptor. It is believed to reduce intraocular pressure by increasing the outflow of aqueous humor. PGF2- receptors are present in respiratory tract and uterine muscles. The functional effect of PGF2- on cough reflex sensitivity has been well characterized in experimental clinical studies. Nichol and colleagues5 found that PGF2- can augment cough reflex induced by capsaicin. Moreover, PGF2- has been shown6 to substantially enhance cough response in chloride and capsaicin challenges. These observations suggest that PGF2- may potentiate the cough reflex by acting at the nodose ganglion, brainstem, or intracellular level and not at the receptor level. This case reflects the clinical manifestation of the effect of a PG analog, latanoprost, on augmentation of the cough reflex. The patient had a clinical history compatible with gastroesophageal reflux,7 and because of increased sensitivity of the cough reflex by latanoprost, reflux became symptomatic; hence, the patient presented with cough. There seems to be a similar mechanism of cough induced by angiotensinconverting enzyme inhibitors, as we have shown8 that captopril can significantly shift the dose-response curve for capsaicin inhalation when compared with placebo. To our knowledge, there has not been any case reported in the literature of heightened cough reflex following the administration of latanoprost. However, a case series9 has been reported of chest tightness secondary to the topical application of latanoprost. Our case highlights the importance of recognizing the side effects of topical medications, as timolol therapy is a well-known cause of worsening bronchospasm in patients with asthma.10,11 In conclusion, this case illustrates the importance of considering the functional effects of topical medications as a possible cause of serious side effects.

5 Nichol G, Nix A, Barnes PJ, et al. Prostaglandin F2 enhancement of capsaicin induced cough in man: modulation by 2 adrenergic and anticholinergic drugs. Thorax 1990; 45:694 698 6 Stone R, Barnes PJ, Fuller RW. Contrasting effects of prostaglandins E2 and F2 on sensitivity of the human cough reflex. J Appl Physiol 1992; 73:649 653 7 Everett CF, Morice AH. Clinical history in gastroesophageal cough. Respir Med 2007; 101:345348 8 Morice AH, Lowry R, Brown MJ, et al. Angiotensin-converting enzyme and the cough reflex. Lancet 1987; 2:1116 1118 9 Rajan MS, Syam P, Liu C. Systemic side effects of topical latanoprost. Eye 2003; 17:442 444 10 Confalonieri M, Aiolfi S, Patrini G, et al. Severe bronchial spasm crises induced by topical administration of eyedrops with timolol base: a non-selective beta blocking agent. Recenti Prog Med 1991; 82:402 404 11 Inamizu T, Yoshikawa M, Murai H. A case of severe bronchial asthma following first use of timolol ophthalmic solution. Nihon Kyobu Shikkan Gakkai Zasshi 1993; 31:385389

Community-Acquired Methicillin-Resistant Staphylococcus aureus Pneumonia and ARDS

1-Year Follow-Up
Lena M. Napolitano, MD, FCCP; Melissa E. Brunsvold, MD; Raju C. Reddy, MD; and Robert C. Hyzy, MD, FCCP

Acknowledgments
Financial/nonfinancial disclosures: The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reported infections due to methicillin-resistant Staphylococcus aureus (MRSA) are increasing. Although most of these cases are skin and skin structure infections, necrotizing pneumonias also have been reported. Recently, reports of communityacquired MRSA (CA-MRSA) pneumonia have documented that it is a severe necrotizing pneumonia and often is fatal. To our knowledge, no previous reports have examined the long-term recovery of patients who have had this condition. We present a case of confirmed CA-MRSA necrotizing pneumonia with post-hospital discharge follow-up involving radiologic imaging and pulmonary function testing. (CHEST 2009; 136:14071412)
Manuscript received February 3, 2009; revision accepted June 30, 2009. Affiliations: From the Division of Acute Care Surgery, Department of Surgery (Drs. Napolitano and Brunsvold) and the Division of Pulmonary and Critical Care Medicine (Drs. Reddy and Hyzy), Department of Medicine, University of Michigan, Ann Arbor, MI. Correspondence to: Lena M. Napolitano, MD, FCCP, Department of Surgery, 1C421 University Hospital, Box 0033, 1500 E Medical Center Dr, Ann Arbor, MI 48109-0033; e-mail: lenan@umich.edu 2009 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/site/ misc/reprints.xhtml). DOI: 10.1378/chest.07-1511
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References
1 Morice AH, Kastelik JA, Thompson R. Cough challenge in the assessment of cough reflex. Br J Clin Pharmacol 2001; 52:365375 2 Mitchell JE, Campbell AP, New NE, et al. Expression and characterization of the intracellular vanilloid receptor (TRPV1) in bronchi from patients with chronic cough. Exp Lung Res 2005; 31:295306 3 Groneberg DA, Niimi A, Dinh QT, et al. Increased expression of transient receptor potential vanilloid-1 in airway nerves of chronic cough. Am J Respir Crit Care Med 2004; 170:1276 1280 4 Von Euler US. Uber die spezifische blutdrucksenkende Substanz des menschilchen Prostata- und Samenblasensekrets. Wien Klin Wochenschr 1935; 14:11821183
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Abbreviations: CA-MRSA community-acquired methicillinresistant Staphylococcus aureus; CAP community-acquired pneumonia; MRSA methicillin-resistant Staphylococcus aureus; PVL Panton-Valentine leukocidin

nfections with methicillin-resistant I reus (MRSA) were first reported Staphylococcus auin the 1960s, 1
1

decade after the release of methicillin. Methicillin resistance in patients with S aureus infection is defined as an oxacillin minimum inhibitory concentration of 4 g/mL. Previously, MRSA infections were largely nosocomial infections and a common cause of hospital-acquired pneumonia, ventilator-associated pneumonia, and bacteremia. Community-acquired MRSA (CA-MRSA) infection has emerged in patients who do not have established risk factors for MRSA, and is now a common and serious health problem.2 It is the most common identifiable cause of skin and soft-tissue infections among patients presenting to EDs in the United States3,4 and can cause necrotizing fasciitis.5 CA-MRSA isolates have been responsible for fatal, severe sepsis in children6,7 and necrotizing pneumonia deaths in children.8 Community-onset necrotizing pneumonia due to CA-MRSA is an emerging clinical entity, especially following a viral infection, with substantial morbidity and mortality.9 11 During the 2003 to 2004 influenza season, 17 cases of community-acquired pneumonia were reported12 from nine states, and MRSA was isolated in 15 cases (88%). The median age of the patients was 21 years, and the mortality rate was 29%. In January 2007, the Centers for Disease Control and Prevention13 received reports of 10 cases of severe MRSA community-acquired pneumonia (CAP) among previously healthy children and adults in Louisiana and Georgia between December 2006 and January 2007. The median age of the 10 patients was 17.5 years (age range, 4 months to 48 years), and 6 patients (60%) died. A report14 of 51 cases of S aureus CAP from 19 states during the 2006 to 2007 influenza season documented that 79% were due to MRSA. The mortality rate was 51%, and only 43% of the patients with MRSA received therapy with anti-MRSA empiric antimicrobial agents. Influenza was confirmed in 33% of these patients.14 Case reports of CA-MRSA pneumonia now span the globe, and the reported cases involve severe necrotizing pneumonia, which often is fatal.1522 The pneumonia often is rapidly progressive; bilateral; and with shock, cavitation of lung parenchyma, and pleural effusion. Although there are a growing number of cases of CAP due to MRSA, the longterm course and recovery of patients have not been reported. This case report describes the course of one patient with CA-MRSA necrotizing pneumonia from initial presentation through hospital management and outpatient follow-up.

Case Report
A 31-year-old woman presented 1 week prior to hospitalization complaining of a headache. She was afebrile, had a normal WBC count, and was sent home with symptomatic therapy. A few days later, productive cough, difficulty breathing, fevers, and chills developed, and the patient required hospitalization. Of note, two of her three children had recently had upper respiratory tract
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infections. The patients respiratory status gradually worsened, requiring intubation. She was treated with methylprednisolone, azithromycin, vancomycin, ceftriaxone, and cefepime. After endotracheal intubation, the patient had increasing ventilatory requirements due to severe hypoxemia and ARDS over the next day. Her antibiotic regimen was switched to azithromycin, ceftriaxone, and trimethoprim/sulfamethoxazole for the treatment of severe CAP, and she was resuscitated with 8 L of crystalloid for associated hypotension. No sputum Gram stain or culture was performed at the initial hospital admission. The patient was transported to the University of Michigan Medical Center (Ann Arbor, MI) for evaluation for possible extracorporeal membrane oxygenation for severe hypoxemia and ARDS. At the time of transfer, she was receiving a 100% fraction of inspired oxygen with positive end-expiratory pressure of 12 cm H2O and a Pao2 of 35 mm Hg. On arrival, pulmonary recruitment maneuvers were performed, arterial oxygen saturation improved to 90%. Initial WBC count was 2,500 cells/ L with 12% bands, and the platelet count was 188,000 cells/ L. Diagnostic flexible bronchoscopy was performed for quantitative BAL for culture and susceptibility, and purulent bronchial secretions were noted throughout. Vancomycin (1.5 g every 8 h; weight, 68 kg) was added as empiric antibiotic therapy, achieving vancomycin trough concentrations of 11.5 to 15.1 g/dL. Therapy with vasopressors was required for the treatment of septic shock. A chest radiograph (Fig 1, left) demonstrated multiple infiltrates in the right upper lobe and left lower lobe. The patient was switched to pressure-control ventilation and a regimen of recruitment maneuvers; prone positioning every 6 h was initiated. BAL results confirmed 10,000 colony forming units/mL MRSA, and a diagnosis of CA-MRSA necrotizing pneumonia was reached. The MRSA antimicrobial susceptibility results confirmed susceptibility to vancomycin, clindamycin, doxycycline, trimethoprim/sulfamethoxazole, and gentamicin, and resistance to penicillin, ampicillin, oxacillin, levofloxacin, and erythromycin by Kirby-Bauer in vitro testing performed in the hospital microbiology laboratory. The vancomycin minimum inhibitory concentration was 1.0 g/mL; the isolate was not tested for PantonValentine leukocidin (PVL) toxin. Inducible clindamycin resistance was confirmed by the D test. Viral BAL fluid cultures were negative. All other cultures were negative. A CT scan performed on hospital day 10 showed cystic cavitary changes consistent with multifocal necrotizing pneumonia (Fig 1, right). The patient was treated with IV vancomycin for CAMRSA necrotizing pneumonia, and diuresis, prone positioning, and recruitment maneuvers were continued for the treatment of severe hypoxemia. She subsequently improved, was switched to bilevel ventilation to allow spontaneous breathing, and was extubated 14 days after hospital admission. At extubation, the patient was switched to a 2-week course of therapy with linezolid. She was discharged from the hospital on hospital day 23. At hospital discharge, the patient required 1 L of oxygen by nasal cannula and was able to ambulate 30 to 40 feet before stopping, but she had intermittent arterial oxygen desaturations to 86%. At her follow-up visit 2 weeks after hospital discharge, the patient complained of a cough and was found to have leukocytosis (16,900 cells/ L). She was started on a course of trimethoprim/ sulfamethoxazole therapy for the treatment of presumed bronchitis. The patient underwent a screening hall-walk study in the clinic and was able to walk several hundred feet, with her oxygen saturation remaining at 91%. Fluticasone propionate was initiated for the treatment of possible underlying reactive airways disease. Two months after hospital discharge, the patient reported significant improvement in her cough and dyspnea. She underwent a 6-min pulmonary hall-walk study and was able to walk
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Figure 1. Left: chest radiograph from March 23, 2006. Multifocal patchy areas of airspace opacification are noted, bilaterally involving all lobes consistent with diffuse multifocal pneumonia. Right: high-resolution CT scan of the chest from March 23, 2006. Diffuse bilateral areas of airspace consolidation with cystic and cavitary changes are seen, with more severe changes seen on the right. The largest cavity is in the right apex, measuring approximately 8 4.5 cm (in anteroposterior by transverse dimensions). Elsewhere within the right lung are innumerable areas of cystic change, some of which contain soft-tissue attenuation structures involving all lobes on the right. On the left, the majority of the cystic changes are seen in the inferior portion of the left upper lobe. Findings are consistent with the given history of multifocal pneumonia, with pneumatocele and cavitary formation. No significant pneumothorax and no focal parenchymal fluid-containing structure to suggest the presence of an intraparenchymal abscess were found at this stage.

1,300 feet with no evidence of arterial oxygen desaturation. A high-resolution CT scan revealed significant interval resolution of her prior lung consolidation, and cystic and cavitary changes (Fig 2). Five months after hospital discharge, she reported continued improvement in her symptomatology, including cough and dyspnea. The patient was now walking 3 miles daily. At 11 months after hospital discharge, she demonstrated continued improvement as determined by spirometry and pulmonary function testing findings (Table 1). She complained of a chronic cough and some asthma symptoms. A repeat CT scan revealed significant interval improvement (Fig 2). The patient was discharged from the pulmonary clinic at that time.

Discussion
With the growing incidence of CA-MRSA as a pathogen in patients with severe CAP, clinicians must obtain pulmonary cultures to make a definitive diagnosis and provide prompt empiric antimicrobial therapy, including MRSA coverage. Although knowledge of specific risk factors for CA-MRSA, such as residence in endemic areas or past antibiotic exposure, is important, we now recognize that some patients with CA-MRSA and severe infections have no prior medical comorbidities and no specific MRSA risk factors, such as in the case of the
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patient presented here. Therefore, clinical cultures to make a definitive diagnosis of CA-MRSA pneumonia is of paramount importance. CA-MRSA pneumonia has been associated with the PVL toxin genes, among other virulence factors commonly found in patients with this condition. The PVL toxin causes tissue necrosis, and most of the cases of severe CA-MRSA necrotizing pneumonia have been attributed to PVL-positive CA-MRSA, especially when preceded by viral respiratory illness.23 Among the 10 cases reported by the Centers for Disease Control and Prevention13 in January 2007, all isolates were positive for PVL toxin genes by polymerase chain reaction. Similarly in the most recent report,14 all but one isolate contained genes for PVL toxin. One study24 documented that PVL, a pore-forming toxin secreted by strains epidemiologically associated with the current outbreak of CA-MRSA and with the often lethal necrotizing pneumonia, is sufficient to cause pneumonia in a murine model. Furthermore, the expression of the PVL toxin induces global changes in transcriptional levels of genes encoding secreted and cell-wall-anchored staphylococcal proteins, including the lung inflammatory factor staphylococcal protein A. This study documents that
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Figure 2. Left: follow-up chest radiograph from May 10, 2006. Right: high-resolution CT scan of the chest from May 10, 2006 (left) and from February 5, 2007 (right). Significant interval resolution of prior lung consolidation and cystic and cavitary changes are seen on the left. A thick-walled right-upper-lobe cavity is significantly smaller. In most of the lung, consolidation has been replaced by ground-glass opacity, and small focal areas of consolidation and cavitary changes remain in the right upper lobe. Significant interval improvement of abnormality is seen on the right. Two thin-walled cystic lesions are seen in the right upper lobe in addition to ill-defined areas of ground-glass opacity elsewhere in the lung. No focal consolidation is seen.

PVL toxin is a significant S aureus virulence factor and that PVL-positive strains can cause murine necrotizing pneumonia with manifestations that resemble those observed in humans. Importantly, the expression of the genes that encode PVL (lukS-PV and lukF-PV) or direct inoculation with native toxin was sufficient to induce pneumonia in mice. In other words, the toxin alone was enough to destroy lungs. This study also documented that PVL increased the expression of staphylococcal protein A, which activates a receptor on the surface of respiratory epithelial cells that normally binds to the proinflammatory cytokine tumor necrosis factor- . This triggers the recruitment of neutrophils to the lung, thus mimicking the effect of the cytokine. This current report underscores the importance of sputum cultures in diagnostic testing for causative pathogens of CAP in patients who present with severe CAP, particularly those with cavitary lesions evident on diagnostic imaging. The Infectious Diseases Society of America/ American Thoracic Society Consensus Guidelines on

the Management of Community-Acquired Pneumonia in Adults25 stated that patients with severe CAP should at least have blood samples drawn for culture, urinary antigen tests for Legionella pneumophila and Streptococcus pneumoniae performed, and expectorated sputum samples collected for culture. For intubated patients, an endotracheal aspirate sample should be obtained (Moderate recommendation; Level II evidence). The present report also documents the importance of considering empiric antibiotic coverage for MRSA infection in patients with severe CAP. The case reported herein had a delay of initiation of empiric antimicrobial therapy for possible MRSA until after transfer to our facility. The Infectious Diseases Society of America/American Thoracic Society25 guidelines address the issue of MRSA as a possible pathogen that warrants empiric antibiotic therapy for CAP in patients requiring inpatient ICU treatment and recommend the following: For community-acquired methicillin-resistant Staphylococcus aureus infection, add

Table 1Results of Interval Spirometry After Hospital Discharge

FEV1 Time After Hospital Discharge 2 wk 2 mo 6 mo 11 mo L 1.29 1.59 1.84 1.91 % Predicted 45 57 65 69 L 1.80 2.39 2.74 2.81 FVC % Predicted 50 68 78 80 DLCO mL/min/mm Hg 10.2 14.3 17.8 19.1 % Predicted 42 60 74 80 O2 Saturation Breathing Room Air, % 95 99 96 97

On 11-month follow-up, these spirometry values are consistent with a moderate obstructive ventilatory defect with normal gas transfer. DLCO diffusing capacity of the lung for carbon monoxide. 1410
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vancomycin or linezolid (Moderate recommendation; Level III evidence). Linezolid may have advantages over vancomycin for initial therapy of severe CA-MRSA pneumonia as it has been documented to suppress PVL toxin production in CA-MRSA.26 This severe necrotizing pneumonia carries a high mortality rate and requires aggressive management if the patient is to survive. The first important principle of management includes early diagnosis and appropriate empiric antibiotic therapy. Management of sepsis and optimal mechanical ventilatory support for acute respiratory failure, and in this case for severe ARDS, with prevention of ventilator-associated lung injury also is a necessary component of successful therapy. The necrotizing component often results in large cavitary lesions, resulting in increased dead space, hypoxemia, and hypercarbia. Transfer to a tertiary care hospital with expertise and equipment for advanced pulmonary support strategies, such as high-frequency oscillatory ventilation, extracorporeal membrane oxygenation, or other techniques, should be considered early in the course of illness.27 In addition, CA-MRSA pneumonia is frequently complicated by empyema, which requires drainage with tube thoracostomy and long-term management. The long-term recovery of patients with CA-MRSA necrotizing pneumonia has not been reported previously in the literature. Spirometry performed 2 weeks after hospital discharge in the patient reported on in this article revealed an FEV1 of 1.29 L (45% predicted), an FVC of 1.80 L (50% predicted), and a diffusing capacity of the lung for carbon monoxide of 10.2 mL/min/mm/Hg (42% predicted), reflecting a severe restrictive ventilatory defect with severely impaired gas transfer. The patient complained of severe dyspnea on exertion; thus, she required extensive pulmonary rehabilitation, including home supplemental oxygen therapy. Although the role for pulmonary rehabilitation has been well documented in patients with COPD, its efficacy in patients with CAP, hospital-acquired pneumonia, and health-care-associated pneumonia is assumed but has not been proven. Pulmonary rehabilitation generally consists of a regimen that includes an oxygen need assessment and therapy, patient education regarding the disease process, an exercise program, breathing training, chest physiotherapy, nutrition, and psychosocial support. The patient in this case report received supplemental home oxygen, education, an exercise program with breathing training, and chest physiotherapy. She showed interval improvement at each follow-up visit. The patients respiratory symptoms, evidenced by ongoing oxygen therapy requirements, persisted well after hospital discharge but resolved by her 6-month follow-up visit. As expected, this study represents a significantly worse overall course than patients with mild-to-moderatesevere CAP who generally had resolution of respiratory symptoms by 14 days.28 This patient had an ongoing supplemental oxygen requirement that lasted 6 months, and she continued to have a chronic cough even at 10 months after hospital discharge. Necrotizing pneumonia due to CA-MRSA is severe and often fatal. As a result, there has been no prior documentation (to our knowledge) of the recovery phase of this
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disease. This case of a patient with CA-MRSA necrotizing pneumonia documents the natural course of the disease, with prolonged pulmonary symptoms and hypoxemia requiring treatment, and may provide insight into additional future treatment strategies that may be of benefit to these patients. Further studies are needed to better characterize both the acute and the chronic phases of this important and frequently fatal disease entity.

Acknowledgments
Financial/nonfinancial disclosures: The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

References
1 Benner EJ, Kayser FH. Growing clinical significance of methicillin-resistant Staphylococcus aureus. Lancet 1968; 2:741 2 Fridkin SK, Hageman JC, Morrison M, et al. Methicillinresistant Staphylococcus aureus disease in three communities. N Engl J Med 2005; 352:1436 1444 3 Moran GJ, Krishnadasan A, Gorwitz RJ, et al. Methicillinresistant S aureus infections among patients in the emergency department. N Engl J Med 2006; 355:666 674 4 Kazakova SV, Hageman JC, Matava M, et al. A clone of methicillin-resistant Staphylococcus aureus among professional football players. N Engl J Med 2005; 352:468 475 5 Miller LG, Perdreau-Remington F, Rieg G, et al. Necrotizing fasciitis caused by community-associated methicillin-resistant Staphylococcus aureus in Los Angeles. N Engl J Med 2005; 352:14451453 6 Centers for Disease Control and Prevention. Four pediatric deaths from community acquired methicillin-resistant Staphylococcus aureus: Minnesota and North Dakota 19971999. JAMA 1999; 282:11231125 7 Herold BC, Immergluck LC, Maranan MC, et al. Communityacquired methicillin resistant Staphylococcus aureus in children with no identified predisposing risk. JAMA 1998; 279: 593598 8 Adern PV, Montgomery CP, Husain AN, et al. Staphylococcus aureus sepsis and the Waterhouse-Friderichsen syndrome in children. N Engl J Med 2005; 353:12451251 9 Niederman MS. Recent advances in community-acquired pneumonia: inpatient and outpatient. Chest 2007; 131:1205 1215 10 Francis JS, Doherty MC, Lopatin U, et al. Severe communityonset pneumonia in healthy adults caused by methicillin resistant Staphylococcus aureus carrying the Panton-Valentine leukocidin genes. Clin Infect Dis 2005; 40:100 107 11 Hidron A, Low CE, Honig EG, et al. Emergency of communityacquired methicillin-resistant Staphylococcus aureus strain USA 300 as a cause of necrotizing community-onset pneumonia. Lancet Infect Dis 2009; 9:384 392 12 Hageman JC, Uyeki TM, Francis JS, et al. Severe communityacquired pneumonia due to Staphylococcus aureus: 2003 04 influenza season. Emerg Infect Dis 2006; 12:894 899 13 Centers for Disease Control and Prevention. Severe methicillinresistant Staphylococcus aureus community-acquired pneumonia associated with influenza: Louisiana and Georgia, December 2006-January 2007. MMWR Morb Mortal Wkly Rep 2007; 56:325329
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14 Kallen AJ, Brunkard J, Moore Z, et al. Staphylococcus aureus community-acquired pneumonia during the 2006 2007 influenza season. Ann Emerg Med 2009; 53:358 365 15 Chua AP, Lee KH. Fatal bacteraemic pneumonia due to community-acquired methicillin-resistant Staphylococcus aureus. Singapore Med J 2006; 47:546 548 16 Torell E, Molin D, Tano E, et al. Community-acquired pneumonia and bacteraemia in a healthy young woman caused by methicillin-resistant Staphylococcus aureus (MRSA) carrying the genes encoding Panton-Valentine leukocidin (PVL). Scand J Infect Dis 2005; 37:902904 17 Francis JS, Doherty MC, Lopatin U, et al. Severe communityonset pneumonia in healthy adults caused by methicillinresistant Staphylococcus aureus carrying the Panton-Valentine leukocidin genes. Clin Infect Dis 2005; 40:100 107 18 Frazee BW, Salz TO, Lambert L, et al. Fatal communityassociated methicillin-resistant Staphylococcus aureus pneumonia in an immunocompetent young adult. Ann Emerg Med 2005; 46:401 404 19 Garnier F, Tristan A, Francois B, et al. Pneumonia and new methicillin-resistant Staphylococcus aureus clone. Emerg Infect Dis 2006; 12:498 500 20 Tseng MH, Wei BH, Lin WJ, et al. Fatal sepsis and necrotizing pneumonia in a child due to community-acquired methicillin-resistant Staphylococcus aureus: case report and literature review. Scand J Infect Dis 2005; 37:504 507 21 Soderquist B, Berglund C, Stralin K. Community-acquired pneumonia and bacteremia caused by an unusual methicillinresistant Staphylococcus aureus (MRSA) strain with sequence type 36, staphylococcal cassette chromosome mec type IV

22

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24 25

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and Panton-Valentine leukocidin genes. Eur J Clin Microbiol Infect Dis 2006; 25:604 606 Gerogianni I, Mpatavanis G, Gourgoulianis K, et al. Combination of staphylococcal chromosome cassette SCCmec type V and Panton-Valentine leukocidin genes in a methicillinresistant Staphylococcus aureus that caused necrotizing pneumonia in Greece. Diagn Microbiol Infect Dis 2006; 56:213 216 Cunha BA. Antimicrobial therapy of multidrug-resistant Streptococcus pneumoniae, vancomycin-resistant enterococci, and methicillin-resistant Staphylococcus aureus. Med Clin North Am 2006; 90:11651182 Labandeira-Rey M, Couzon F, Boisset S, et al. Staphylococcus aureus Panton-Valentine leukocidin causes necrotizing pneumonia. Science 2007; 315:1130 Mandell LA, Wunderink RG, Anzueto A, et al. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of communityacquired pneumonia in adults. Clin Infect Dis 2007; 44:S27 S72 Stevens DL, Ma Y, Salmi DB, et al. Impact of antibiotics on expression of virulence-associated exotoxin genes in methicillinsensitive and methicillin-resistant Staphylococcus aureus. J Infect Dis 2007; 195:202211 Hemmila MR, Napolitano LM. Severe respiratory failure: advanced treatment options. Crit Care Med 2006; 34(suppl): S278 S290 El Moussaoui R, Opmeer BC, de Borgie CA, et al. Long-term symptom recovery and health-related quality of life in patients with mild-to-moderate-severe community-acquired pneumonia. Chest 2006; 130:11651172

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