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   Table of Contents     
LETTER TO EDITOR  
Year : 2015  |  Volume : 7  |  Issue : 3  |  Page : 119-120
A red flag for community-acquired pneumonia in the elderly


1 Department of Pulmonary, Allergy and Critical Care Medicine, Respiratory Institute, Cleveland, Ohio, USA
2 Pathology and Laboratory Medicine Institute, Cleveland Clinic, Cleveland, Ohio, USA
3 Department of Infectious Disease, Medicine Institute, Cleveland Clinic, Cleveland, Ohio, USA

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Date of Web Publication18-Aug-2015
 

How to cite this article:
Panchabhai TS, Bandyopadhyay D, Arrossi V, Brizendine KD, Ahmad M. A red flag for community-acquired pneumonia in the elderly. J Global Infect Dis 2015;7:119-20

How to cite this URL:
Panchabhai TS, Bandyopadhyay D, Arrossi V, Brizendine KD, Ahmad M. A red flag for community-acquired pneumonia in the elderly. J Global Infect Dis [serial online] 2015 [cited 2019 Aug 21];7:119-20. Available from: http://www.jgid.org/text.asp?2015/7/3/119/146383


Sir,

Advanced age is associated with defects in innate and adaptive immunity, called immunosenescence. [1] As a result, apparently immunocompetent patients become susceptible to many opportunistic infections. [2] The clinical features of sepsis are distinct in elderly individuals. We describe an elderly female patient who presented with community-acquired pneumonia, which posed a considerable diagnostic challenge, leading to significant delay in appropriate intervention.

An 84-year-old Caucasian female presented with nonproductive cough, decreased appetite, and malaise of 2 months' duration. She was initially diagnosed as right middle lobe pneumonia and had received three courses of antibiotics. However, her symptoms continued to worsen and she required 5 liters oxygen via nasal cannula. She had no history of fevers, chills, night sweats, weight loss, or skin rash. She had past history of hypertension, hyperlipidemia, and chronic atrial fibrillation.

Initial laboratory data demonstrated elevated calcium with 1,25-dihydroxyvitamin D 3 , parathyroid hormone, parathyroid-related peptide, serum M-protein, and angiotensin-converting enzyme level. All primary relevant microbiology evaluations were normal. A computerized tomography (CT) scan of the chest showed partial collapse and consolidation of the right middle lobe, and a 15-mm cavitary lesion situated inferiorly [Figure 1].
Figure 1: CT scan of chest at admission showing consolidative lesion in right middle lobe

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The patient underwent bronchoscopy with normal airway examination, and bronchoalveolar lavage (BAL) and transbronchial biopsies (TBBx) were performed from the right middle and lower lobes, respectively. The BAL cultures were negative. The TBBx demonstrated interstitial pneumonitis with histiocytic infiltrates and vaguely formed non-necrotizing granulomas [Figure 2]a and b. The hematoxylin-andeosin (H&E) and Gomori's methenamine-silver (GMS) stains showed several yeasts morphologically consistent with Histoplasma species within the cytoplasm of the infiltrating histiocytes [Figure 3]a and b. The patient's serum fungal battery for histoplasma antibody and urinary histoplasma antigen were later reported as positive. Therapy with intraconazole was initiated for the diagnosis of acute diffuse histoplasmosis. Her symptoms improved remarkably, and her oxygen was weaned down. A follow-up chest X-ray at 8 weeks showed complete resolution of the lesion.
Figure 2: (a) Transbronchial biopsy showing focal interstitial pneumonitis(black arrow), H&E, 4× (b) Infi ltrating histiocytes with vague non-necrotizing granuloma formation with a multinucleated giant cell (arrow)shown H&E, 10×

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Figure 3: (a) Transbronchial biopsy showing foamy histiocytes (black arrow) in association with the interstitial pneumonitis and ill-formed non-necrotizing granulomas, H&E, 20× (b) Histoplasma yeasts within the macrophages (black arrow), GMS stain, 20×

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Histoplasma capsulatum is the most common endemic mycosis in the US. [3] The lungs provide a portal of entry for this fungus. Acute histoplasmosis is often self-limited, and the symptoms are usually mild in immunocompetent hosts. Ledke et al. noted certain age-related differences in the characteristics of histoplasmosis. [4] The asymptomatic presentation, acute histoplasmosis, chronic cavitary lesion similar to mycobacterial tuberculosis, and absence of hilar lymphadenopathy are more common in the elderly population. [4] Chronic progressive histoplasmosis, also commonly described in the elderly population, manifests with minimal symptoms but electrolyte abnormalities. Histoplasmosis characteristically causes necrotizing granulomatous inflammation, leading to hypercalcemia, which is less likely to occur in immunocompromised individuals.

Treatment is indicated in the elderly with acute pulmonary histoplasmosis if symptoms persist for longer than a month or in case of a severe disease burden. [5] This infection is commonly treated with itraconazole in the elderly and not amphotericin, given the risk of nephrotoxicity. [4],[5] Chronic progressive pulmonary histoplasmosis should be treated, even if it is minimally symptomatic.

The clinical outcome of fungal infections is also likely to be worse in elderly patients because they are less able to cope with the burden of endemic mycosis, owing to age-related changes in innate and adaptive immunity. A high index of suspicion should be harbored for acute pulmonary histoplasmosis in elderly patients presenting with atypical features of community-acquired pneumonia.

 
   References Top

1.
Grubeck-Loebenstein B, Wick G. The aging of the immune system. Adv Immunol 2002;80:243-84.  Back to cited text no. 1
    
2.
Kauffman CA. Endemic mycoses in older adults. Infect Dis Clin Pract 1995;4:41-5.  Back to cited text no. 2
    
3.
Kauffman CA. Endemic mycoses: Blastomycosis, histoplasmosis, and sporotrichosis. Infect Dis Clin North Am 2006;20:645-62.  Back to cited text no. 3
    
4.
Ledtke C, Tomford JW, Jain A, Isada CM, van Duin D. Clinical presentation and management of histoplasmosis in older adults. J Am Geriatr Soc 2012;60:265-70.  Back to cited text no. 4
    
5.
Kennedy CC, Limper AH. Redefining the clinical spectrum of chronic pulmonary histoplasmosis: A retrospective case series of 46 patients. Medicine (Baltimore) 2007;86:252-8.  Back to cited text no. 5
    

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Correspondence Address:
Tanmay S Panchabhai
Department of Pulmonary, Allergy and Critical Care Medicine, Respiratory Institute, Cleveland, Ohio
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-777X.146383

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2008 Journal of Global Infectious Diseases | Published by Wolters Kluwer - Medknow
Online since 10th December, 2008