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jugular ganglia, or centrally at the level of the brainstem.We believe that our patient had a combination of bothcentral and peripheral cough sensitization secondary tolatanoprost therapy and gastroesophageal reflux.

PGs, which were first isolated in 1935,4 are a group oflipids derived enzymatically from fatty acids. The cycloox-

ygenase pathway yields PGD, PGE, and PGF. Latano-prost is a PGF2- isopropyl ester analog and is a selective

agonist of the prostanoid FP receptor. It is believed toreduce intraocular pressure by increasing the outflow ofaqueous humor. PGF2- receptors are present in respi-ratory tract and uterine muscles. The functional effect ofPGF2- on cough reflex sensitivity has been well character-ized in experimental clinical studies. Nichol and colleagues5

found that PGF2- can augment cough reflex induced bycapsaicin. Moreover, PGF2- has been shown6 to substan-tially enhance cough response in chloride and capsaicinchallenges. These observations suggest that PGF2- maypotentiate 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 coughreflex. The patient had a clinical history compatible withgastroesophageal reflux,7 and because of increased sensitivityof the cough reflex by latanoprost, reflux became symptom-atic; hence, the patient presented with cough. There seems tobe a similar mechanism of cough induced by angiotensin-converting enzyme inhibitors, as we have shown8 that capto-pril can significantly shift the dose-response curve for capsa-icin inhalation when compared with placebo.

To our knowledge, there has not been any case reportedin the literature of heightened cough reflex following theadministration of latanoprost. However, a case series9 hasbeen reported of chest tightness secondary to the topical

application of latanoprost. Our case highlights the impor-tance of recognizing the side effects of topical medications,as timolol therapy is a well-known cause of worsening broncho-spasm in patients with asthma.10,11 In conclusion, this caseillustrates the importance of considering the functional effects oftopical medications as a possible cause of serious side effects.

Acknowledgments

Financial/nonfinancial disclosures: The authors have re-ported to the ACCP that no significant conflicts of interest exist

with any companies/organizations whose products or servicesmay be discussed in this article.

References

1 Morice AH, Kastelik JA, Thompson R. Cough challenge inthe assessment of cough reflex. Br J Clin Pharmacol 2001;52:365375

2 Mitchell JE, Campbell AP, New NE, et al. Expression andcharacterization of the intracellular vanilloid receptor(TRPV1) in bronchi from patients with chronic cough. ExpLung Res 2005; 31:295306

3 Groneberg DA, Niimi A, Dinh QT, et al. Increased expression oftransient receptor potential vanilloid-1 in airway nerves of chroniccough. Am J Respir Crit Care Med 2004; 170:12761280

4 Von Euler US. Uber die spezifische blutdrucksenkende Sub-stanz des menschilchen Prostata- und Samenblasensekrets.

Wien Klin Wochenschr 1935; 14:11821183

5 Nichol G, Nix A, Barnes PJ, et al. Prostaglandin F2 enhance-ment of capsaicin induced cough in man: modulation by 2adrenergic and anticholinergic drugs. Thorax 1990; 45:694698

6 Stone R, Barnes PJ, Fuller RW. Contrasting effects ofprostaglandins E2 and F2 on sensitivity of the human coughreflex. J Appl Physiol 1992; 73:649653

7 Everett CF, Morice AH. Clinical history in gastroesophagealcough. Respir Med 2007; 101:345348

8 Morice AH, Lowry R, Brown MJ, et al. Angiotensin-converting

enzyme and the cough reflex. Lancet 1987; 2:111611189 Rajan MS, Syam P, Liu C. Systemic side effects of topical

latanoprost. Eye 2003; 17:44244410 Confalonieri M, Aiolfi S, Patrini G, et al. Severe bronchial spasm

crises induced by topical administration of eyedrops with timololbase: a non-selective beta blocking agent. Recenti Prog Med1991; 82:402404

11 Inamizu T, Yoshikawa M, Murai H. A case of severe bronchialasthma following first use of timolol ophthalmic solution. NihonKyobu Shikkan Gakkai Zasshi 1993; 31:385389

Community-AcquiredMethicillin-ResistantStaphylococcus aureusPneumonia 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

Reported infections due to methicillin-resistantStaphylococcus aureus (MRSA) are increasing. Al-

though most of these cases are skin and skin struc-ture infections, necrotizing pneumonias also havebeen reported. Recently, reports of community-acquired MRSA (CA-MRSA) pneumonia have docu-mented that it is a severe necrotizing pneumonia andoften is fatal. To our knowledge, no previous reportshave examined the long-term recovery of patients

who have had this condition. We present a case ofconfirmed CA-MRSA necrotizing pneumonia withpost-hospital discharge follow-up involving radio-logic imaging and pulmonary function testing.

(CHEST 2009; 136:14071412)

Manuscript received February 3, 2009; revision accepted June30, 2009.

Affiliations: From the Division of Acute Care Surgery, Depart-ment of Surgery (Drs. Napolitano and Brunsvold) and the Divisionof 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, Depart-ment of Surgery, 1C421 University Hospital, Box 0033, 1500 EMedical Center Dr, Ann Arbor, MI 48109-0033; e-mail:[email protected] 2009 American College of Chest Physicians. Reproductionof this article is prohibited without written permission from theAmerican College of Chest Physicians (www.chestjournal.org/site/misc/reprints.xhtml).DOI: 10.1378/chest.07-1511

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Abbreviations: CA-MRSA community-acquired methicillin-resistant Staphylococcus aureus; CAP community-acquiredpneumonia; MRSA methicillin-resistant Staphylococcus au-reus; PVL Panton-Valentine leukocidin

Infections with methicillin-resistant Staphylococcus au-reus (MRSA) were first reported1 in the 1960s, 1

decade after the release of methicillin. Methicillin resis-tance in patients with S aureus infection is defined as an

oxacillin minimum inhibitory concentration of 4 g/mL.Previously, MRSA infections were largely nosocomial in-fections and a common cause of hospital-acquired pneu-monia, ventilator-associated pneumonia, and bacteremia.

Community-acquired MRSA (CA-MRSA) infection hasemerged in patients who do not have established riskfactors for MRSA, and is now a common and serioushealth problem.2 It is the most common identifiable causeof skin and soft-tissue infections among patients present-ing to EDs in the United States3,4 and can cause necro-tizing fasciitis.5 CA-MRSA isolates have been responsiblefor fatal, severe sepsis in children6,7 and necrotizing

pneumonia deaths in children.8

Community-onset necrotizing pneumonia due toCA-MRSA is an emerging clinical entity, especially follow-ing a viral infection, with substantial morbidity and mor-tality.911 During the 2003 to 2004 influenza season, 17cases 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, andthe mortality rate was 29%. In January 2007, the Centersfor Disease Control and Prevention13 received reports of10 cases of severe MRSA community-acquired pneumonia(CAP) among previously healthy children and adults inLouisiana and Georgia between December 2006 and

January 2007. The median age of the 10 patients was17.5 years (age range, 4 months to 48 years), and 6patients (60%) died. A report14 of 51 cases of S aureusCAP from 19 states during the 2006 to 2007 influenzaseason documented that 79% were due to MRSA. Themortality rate was 51%, and only 43% of the patients

with MRSA received therapy with anti-MRSA empiricantimicrobial agents. Influenza was confirmed in 33%of these patients.14

Case reports of CA-MRSA pneumonia now span theglobe, and the reported cases involve severe necrotizingpneumonia, which often is fatal.1522 The pneumonia often israpidly progressive; bilateral; and with shock, cavitation oflung parenchyma, and pleural effusion. Although there are agrowing number of cases of CAP due to MRSA, the long-term course and recovery of patients have not been reported.This case report describes the course of one patient withCA-MRSA necrotizing pneumonia from initial presentationthrough hospital management and outpatient follow-up.

Case Report

A 31-year-old woman presented 1 week prior to hospitalizationcomplaining of a headache. She was afebrile, had a normal WBCcount, and was sent home with symptomatic therapy. A few dayslater, productive cough, difficulty breathing, fevers, and chillsdeveloped, and the patient required hospitalization. Of note, twoof her three children had recently had upper respiratory tract

infections. The patients respiratory status gradually worsened,requiring intubation. She was treated with methylprednisolone,azithromycin, vancomycin, ceftriaxone, and cefepime. After en-dotracheal intubation, the patient had increasing ventilatoryrequirements due to severe hypoxemia and ARDS over the nextday. Her antibiotic regimen was switched to azithromycin, ceftri-axone, and trimethoprim/sulfamethoxazole for the treatment ofsevere CAP, and she was resuscitated with 8 L of crystalloid forassociated 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 possibleextracorporeal membrane oxygenation for severe hypoxemia andARDS. At the time of transfer, she was receiving a 100% fractionof inspired oxygen with positive end-expiratory pressure of 12 cmH2O and a Pao2 of 35 mm Hg. On arrival, pulmonary recruit-ment maneuvers were performed, arterial oxygen saturationimproved to 90%. Initial WBC count was 2,500 cells/L with12% bands, and the platelet count was 188,000 cells/L.

Diagnostic flexible bronchoscopy was performed for quantita-tive BAL for culture and susceptibility, and purulent bronchialsecretions 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. Ther-apy with vasopressors was required for the treatment of septicshock. A chest radiograph (Fig 1, left) demonstrated multipleinfiltrates in the right upper lobe and left lower lobe. The patient

was switched to pressure-control ventilation and a regimen ofrecruitment maneuvers; prone positioning every 6 h was initiated.

BAL results confirmed 10,000 colony forming units/mLMRSA, and a diagnosis of CA-MRSA necrotizing pneumonia wasreached. The MRSA antimicrobial susceptibility results con-firmed susceptibility to vancomycin, clindamycin, doxycycline,trimethoprim/sulfamethoxazole, and gentamicin, and resistanceto penicillin, ampicillin, oxacillin, levofloxacin, and erythromycinby Kirby-Bauer in vitro testing performed in the hospital micro-biology laboratory. The vancomycin minimum inhibitory concen-

tration was 1.0 g/mL; the isolate was not tested for Panton-Valentine leukocidin (PVL) toxin. Inducible clindamycinresistance 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 CA-MRSA necrotizing pneumonia, and diuresis, prone positioning,and recruitment maneuvers were continued for the treatment ofsevere hypoxemia. She subsequently improved, was switched tobilevel ventilation to allow spontaneous breathing, and wasextubated 14 days after hospital admission. At extubation, thepatient was switched to a 2-week course of therapy with linezolid.She was discharged from the hospital on hospital day 23. Athospital discharge, the patient required 1 L of oxygen by nasalcannula 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, thepatient 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 bron-chitis. The patient underwent a screening hall-walk study in theclinic and was able to walk several hundred feet, with her oxygensaturation remaining at 91%. Fluticasone propionate wasinitiated for the treatment of possible underlying reactive airwaysdisease.

Two months after hospital discharge, the patient reportedsignificant improvement in her cough and dyspnea. She under-

went a 6-min pulmonary hall-walk study and was able to walk

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1,300 feet with no evidence of arterial oxygen desaturation. Ahigh-resolution CT scan revealed significant interval resolution ofher prior lung consolidation, and cystic and cavitary changes (Fig2). Five months after hospital discharge, she reported continuedimprovement in her symptomatology, including cough and dys-pnea. The patient was now walking 3 miles daily. At 11 monthsafter hospital discharge, she demonstrated continued improve-ment as determined by spirometry and pulmonary functiontesting findings (Table 1). She complained of a chronic cough andsome asthma symptoms. A repeat CT scan revealed significantinterval improvement (Fig 2). The patient was discharged from

the pulmonary clinic at that time.

Discussion

With the growing incidence of CA-MRSA as a patho-gen in patients with severe CAP, clinicians must obtainpulmonary cultures to make a definitive diagnosis andprovide prompt empiric antimicrobial therapy, includ-ing MRSA coverage. Although knowledge of specificrisk factors for CA-MRSA, such as residence in endemicareas or past antibiotic exposure, is important, we nowrecognize that some patients with CA-MRSA and severeinfections have no prior medical comorbidities and nospecific MRSA risk factors, such as in the case of the

patient presented here. Therefore, clinical cultures tomake a definitive diagnosis of CA-MRSA pneumonia isof paramount importance.

CA-MRSA pneumonia has been associated with thePVL toxin genes, among other virulence factors commonlyfound in patients with this condition. The PVL toxincauses tissue necrosis, and most of the cases of severeCA-MRSA necrotizing pneumonia have been attributed toPVL-positive CA-MRSA, especially when preceded by

viral respiratory illness.23 Among the 10 cases reported by

the Centers for Disease Control and Prevention13 inJanuary 2007, all isolates were positive for PVL toxin genesby polymerase chain reaction. Similarly in the most recentreport,14 all but one isolate contained genes for PVL toxin.

One study24 documented that PVL, a pore-formingtoxin secreted by strains epidemiologically associated withthe current outbreak of CA-MRSA and with the oftenlethal necrotizing pneumonia, is sufficient to cause pneu-monia in a murine model. Furthermore, the expression ofthe PVL toxin induces global changes in transcriptionallevels of genes encoding secreted and cell-wall-anchoredstaphylococcal proteins, including the lung inflammatoryfactor staphylococcal protein A. This study documents that

Figure 1. Left: chest radiograph from March 23, 2006. Multifocal patchy areas of airspaceopacification 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 airspaceconsolidation 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 bytransverse dimensions). Elsewhere within the right lung are innumerable areas of cystic change, someof which contain soft-tissue attenuation structures involving all lobes on the right. On the left, themajority of the cystic changes are seen in the inferior portion of the left upper lobe. Findings areconsistent with the given history of multifocal pneumonia, with pneumatocele and cavitary formation.No significant pneumothorax and no focal parenchymal fluid-containing structure to suggest thepresence of an intraparenchymal abscess were found at this stage.



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PVL toxin is a significant S aureus virulence factor and thatPVL-positive strains can cause murine necrotizing pneu-monia with manifestations that resemble those observed inhumans. Importantly, the expression of the genes thatencode 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 expres-sion of staphylococcal protein A, which activates a receptoron the surface of respiratory epithelial cells that normallybinds to the proinflammatory cytokine tumor necrosis fac-tor-. This triggers the recruitment of neutrophils tothe lung, thus mimicking the effect of the cytokine.

This current report underscores the importance ofsputum cultures in diagnostic testing for causative patho-gens of CAP in patients who present with severe CAP,particularly those with cavitary lesions evident on diagnos-tic imaging. The Infectious Diseases Society of America/American Thoracic Society Consensus Guidelines on

the Management of Community-Acquired Pneumonia inAdults25 stated that patients with severe CAP should atleast have blood samples drawn for culture, urinary anti-gen tests for Legionella pneumophila and Streptococcus

pneumoniae performed, and expectorated sputum samplescollected for culture. For intubated patients, an endotra-cheal aspirate sample should be obtained (Moderate rec-ommendation; Level II evidence).

The present report also documents the importance ofconsidering empiric antibiotic coverage for MRSA infec-tion in patients with severe CAP. The case reported hereinhad a delay of initiation of empiric antimicrobial therapyfor possible MRSA until after transfer to our facility. TheInfectious Diseases Society of America/American ThoracicSociety25 guidelines address the issue of MRSA as apossible pathogen that warrants empiric antibiotic therapyfor CAP in patients requiring inpatient ICU treatment andrecommend the following: For community-acquiredmethicillin-resistant Staphylococcus aureus infection, add

Figure 2. Left: follow-up chest radiograph from May 10, 2006. Right: high-resolution CT scan of thechest 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-lobecavity is significantly smaller. In most of the lung, consolidation has been replaced by ground-glassopacity, 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 areseen in the right upper lobe in addition to ill-defined areas of ground-glass opacity elsewhere in thelung. No focal consolidation is seen.

Table 1Results of Interval Spirometry After Hospital Discharge

Time After Hospital Discharge

FEV1 FVC DLCOO2 Saturation Breathing

Room Air, %L % Predicted L % Predicted mL/min/mm Hg % Predicted

2 wk 1.29 45 1.80 50 10.2 42 952 mo 1.59 57 2.39 68 14.3 60 996 mo 1.84 65 2.74 78 17.8 74 96

11 mo 1.91 69 2.81 80 19.1 80 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.



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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 pneu-monia as it has been documented to suppress PVL toxinproduction in CA-MRSA.26

This severe necrotizing pneumonia carries a high mor-tality rate and requires aggressive management if thepatient is to survive. The first important principle of

management includes early diagnosis and appropriateempiric antibiotic therapy. Management of sepsis andoptimal mechanical ventilatory support for acute respira-tory failure, and in this case for severe ARDS, withprevention of ventilator-associated lung injury also is anecessary component of successful therapy. The necrotiz-ing component often results in large cavitary lesions,resulting in increased dead space, hypoxemia, and hyper-carbia. Transfer to a tertiary care hospital with expertiseand equipment for advanced pulmonary support strate-gies, such as high-frequency oscillatory ventilation, extra-corporeal membrane oxygenation, or other techniques,should be considered early in the course of illness.27 Inaddition, CA-MRSA pneumonia is frequently complicatedby empyema, which requires drainage with tube thoracos-tomy and long-term management.

The long-term recovery of patients with CA-MRSAnecrotizing pneumonia has not been reported previouslyin the literature. Spirometry performed 2 weeks afterhospital discharge in the patient reported on in this articlerevealed an FEV1 of 1.29 L (45% predicted), an FVC of1.80 L (50% predicted), and a diffusing capacity of the lungfor carbon monoxide of 10.2 mL/min/mm/Hg (42% pre-dicted), reflecting a severe restrictive ventilatory defect withseverely impaired gas transfer. The patient complained ofsevere dyspnea on exertion; thus, she required extensivepulmonary rehabilitation, including home supplemental oxy-gen therapy.

Although the role for pulmonary rehabilitation has beenwell documented in patients with COPD, its efficacy inpatients with CAP, hospital-acquired pneumonia, andhealth-care-associated pneumonia is assumed but has notbeen proven. Pulmonary rehabilitation generally consistsof a regimen that includes an oxygen need assessment andtherapy, patient education regarding the disease process,an exercise program, breathing training, chest physiother-apy, nutrition, and psychosocial support. The patient inthis case report received supplemental home oxygen,education, an exercise program with breathing training,and chest physiotherapy. She showed interval improve-ment at each follow-up visit. The patients respiratorysymptoms, evidenced by ongoing oxygen therapy require-ments, persisted well after hospital discharge but resolvedby her 6-month follow-up visit. As expected, this studyrepresents a significantly worse overall course than pa-tients with mild-to-moderatesevere CAP who generallyhad resolution of respiratory symptoms by 14 days.28 Thispatient had an ongoing supplemental oxygen requirementthat lasted 6 months, and she continued to have a chroniccough even at 10 months after hospital discharge.

Necrotizing pneumonia due to CA-MRSA is severe andoften fatal. As a result, there has been no prior documen-tation (to our knowledge) of the recovery phase of this

disease. This case of a patient with CA-MRSA necrotizingpneumonia documents the natural course of the disease,

with prolonged pulmonary symptoms and hypoxemia re-quiring treatment, and may provide insight into additionalfuture treatment strategies that may be of benefit to thesepatients. Further studies are needed to better characterizeboth the acute and the chronic phases of this importantand frequently fatal disease entity.

Acknowledgments

Financial/nonfinancial disclosures: The authors have re-ported to the ACCP that no significant conflicts of interest exist

with any companies/organizations whose products or servicesmay be discussed in this article.

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