Hi, colleage!
I understand you are a pulmonologist. I saw this on Medscape. You may find it interesting.
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From
Infections in Mediciner
Granulomatous Pneumonia in an AIDS Patient
Authors: Leonardo A. Palau, MD, Ochsner Foundation Hospital; Newton E. Hyslop, Jr., MD, Tulane University School of Medicine; George A. Pankey, MD, Ochsner Foundation Hospital
[Infect Med 14(11):846-848, 1997. c 1997 SCP Communications, Inc.]
Introduction
A 31-year-old homosexual male presented to his primary care physician with a 2-week history of fever to 39.4øC (103øF) and a nonproductive cough. A chest x-ray revealed bilateral pulmonary infiltrates. As part of his initial work-up, HIV testing was undertaken, which revealed a positive ELISA and Western blot. The CD4+ count was 89/mm3, and HIV viral load in blood yielded a concentration of 354,000/mL. The patient was started on zidovudine, lamivudine (3TC), oral trimethoprim/sulfamethoxazole (TMP/SMX) as treatment for possible Pneumocystis carinii pneumonia (PCP), and azithromycin 1200mg/week for disseminated Mycobacterium avium complex prophylaxis. Four weeks after the initial visit he returned because of persistent fever, a worsening cough, and increased difficulty in breathing. Three days prior to admission, he developed a maculopapular rash and the TMP/SMX was discontinued. A repeat chest x-ray demonstrated progression of the pulmonary changes, and the patient was admitted to the hospital.
Additional medical history was positive only for recurrent seborrheic dermatitis. The patient smoked one-half pack of cigarettes per day but denied alcohol abuse or the use of intravenous recreational drugs. He worked as a waiter at a restaurant in the French Quarter of New Orleans.
On physical examination, the patient had a temperature of 38.4øC (101.2øF), pulse of 120 beats/min, blood pressure 110/70mm Hg, and respiratory rate of 20 breaths/min. There was no significant adenopathy. Auscultation of the lungs revealed bilateral wheezing and coarse breath sounds. The rest of his physical examination was noncontributory.
Laboratory data included a WBC count of 2200/mm3 with 47% segmented neutrophils, 33% lymphocytes, 7% monocytes, and 13% eosinophils. Hemoglobin had dropped to 8.8g/dL (normal, 13.5-17.5) and hematocrit down to 25.8% (normal, 41%-53%). Serum sodium declined to 127mEq/L (normal, 136-143), while the remaining electrolytes were within normal limits. Liver function tests were normal, and pulse oximitry was 97% on room air.
Chest x-ray demonstrated multiple areas of parenchymal consolidation with air bronchograms (Fig. 1). A CT scan of the chest revealed multiple nodules, particularly affecting the upper and middle lobes of the right lung. The lower lobes appeared relatively spared. Mediastinal lymphadenopathy was also noted. Bronchoscopy with transbronchial biopsy of the right middle lobe nodule yielded interstitial granulomatous inflammatory changes characterized by non-necrotizing granulomatous tubercles.
Figure 1. (click here to zoom) Chest x-ray showed nodular opacities in upper lung zones, bilaterally and in right middle lobe.
Differential Diagnosis
Dr. Newton Hyslop: We have an AIDS patient with worsening pulmonary infiltrates. I would be interested to know his travel history and where he was born, since additional epidemiologic data may help with our differential. It appears on the CT scan of the chest that cavitation is occurring, and there are multiple bronchopneumonic sites. His rash had resolved by the time he was admitted. He is neutropenic, anemic, and thrombocytopenic. If the TMP/SMX had been stopped only 3 days ago, presumably his blood count decline is related to drug hypersensitivity or drug toxicity. In any case, this process has probably disseminated.
The findings on bronchoscopy indicate a granulomatous process with associated mediastinal lymph-adenopathy. The 3 leading causes are attributed to an Actinomyces family organism, a fungus, and mycobacteria.
Since the patient is a waiter in the densely populated tourist section of downtown New Orleans, the French Quarter, I would say that the leading organism is probably Mycobacterium tuberculosis. Other organisms that present in this fashion include Cryptococcus, which is pretty easy to diagnose with serum antigen determination, and blastomycosis, which is endemic in southern Louisiana and continues to be an important pathogen in association with HIV disease.
Histoplasmosis is not an uncommon process in this setting, producing the same chest x-ray changes as TB, cryptococcosis, and blastomycosis. Aspergillosis is an opportunistic infection associated with HIV disease that should be considered; it causes pulmonary changes that can be similar to those caused by other fungal agents. Nocardia is also certainly able to produce the clinical picture described here.
In summary, I would say that TB is the most likely etiology for this population of patients. I would obtain an open biopsy specimen to identify the organism and to guide appropriate therapy.
Hospital Course
A Grocutt-Gomori methenamine-silver (GMS) stain revealed multiple P carinii organisms inside the granulomas (Fig. 2). Cultures for bacteria, fungi, and acid-fast bacilli were negative. Because of the history of rash while taking TMP/SMX and possible failure with this drug, the patient was started on clindamycin 900mg IV q8h and primaquine 15mg daily as well as prednisone.
Figure 2. (click here to zoom) Grocutt-Gomori methenamine-silver stain showed Pneumocystis carinii organisms within granulomas in lung tissue.
His symptoms slowly resolved during the next 2 weeks, and he was discharged from the hospital, although his radiograph changes persisted for several weeks. He completed 21 days of treatment with clindamycin/primaquine followed by 2 more weeks of atovaquone. At completion of treatment his anemia had resolved and the LDH level was normal. He is currently on monthly aerosolized pentamidine and has been observed for 6 months without any signs of recurrence.
Final Diagnosis
Granulomatous PCP
Discussion
P carinii is the most frequent manifestation of AIDS. It presents radiologically as diffuse bilateral, "fluffy," alveolar infiltrates beginning in the perihilar areas and progressing to diffuse involvement. Chest radiographs are occasionally normal or demonstrate atypical changes such as unilateral infiltrates, nodules, cavities, pneumatoceles, lymphadenopathy, or pleural effusions. Typical histologic findings in routine hematoxylin-eosin stained sections include a foamy, acellular eosinophilic intraalveolar exudate with a mild interstitial infiltrate of plasma cells, lymphocytes, and occasional histiocytes. The cysts of the organisms are demonstrated with GMS within the alveolar exudate.
Granulomatous PCP is a very rare presentation.[1-5] Fewer than 20 cases have been described in the English literature. In one study, granulomatous inflammation occurred in 5% (6 of 123) of cases of PCP in HIV-infected patients.[4] Pulmonary nodules with granuloma formation are even more unusual; only a few cases have been described.[3] Histopathology reveals scattered giant cells and noncaseating granulomas, mostly present in the alveolar space. However, cavitation and calcifications with granulomas have been described. True granulomas are rarely seen in AIDS patients, even in the presence of mycobacterial infection.[4] This is probably due to the patients' defective T-cell function. PCP must be considered in the differential diagnosis of patients with AIDS with nodular pulmonary infiltrates and granulomatous reaction.
About the Authors
Dr. Palau is a Fellow in Infectious Diseases, Department of Medicine, Ochsner Foundation Hospital, New Orleans, La. Dr. Hyslop is Professor, Department of Medicine, Tulane University School of Medicine, New Orleans. Dr. Pankey is Staff Physician, Department of Medicine, Ochsner Foundation Hospital, New Orleans. Associate Editors: Joseph R. Dalovisio, MD, Ochsner Foundation Hospital; Newton E. Hyslop, MD, Tulane University School of Medicine; David H. Martin, MD, LSU School of Medicine; Russell vanDyke, MD, Tulane University Combined LSU/Tulane Pediatric Disease Program. This series is edited by Dr. Steele, Professor and Vice Chairman, Division Head Infectious Diseases, Louisiana State University School of Medicine, New Orleans.
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Drugs Mentioned in This Article
Atovaquone Mepron
Azithromycin Zithromax
Clindamycin Cleocin, generic
Lamivudine (3TC) Epivir
Pentamidine NebuPent, Pentacarinat, Pentam, generic
Prednisone Generic
Primaquine Generic
Trimethoprim/sulfamethoxazole Bactrim, Cotrim, Septra, Sulfatrim, generic
Zidovudine (AZT) Retrovir
References
Travis W: Atypical pathologic manifestations of Pneumocystis carinii pneumonia in the acquired immune deficiency syndrome. Am J Surg Pathol 14:615-625, 1990.
Bleiweiss I: Granulomatous Pneumocystis carinii pneumonia in three patients with the acquired immune deficiency syndrome. Chest 94:580-583, 1988.
Flannery MT, Quiroz E, Grundy LS, et al: Pneumocystis carinii pneumonia with atypical granulomatous response. South Med J 89:409-410, 1996.
Kadakia J, Kiyabu M, Sharma OP, et al: Granulomatous response to Pneumocystis carinii in patients infected with HIV. Sarcoidosis 10:44-49, 1993.
Moran CA, Angritt P: Granulomatous Pneumocystis carinii in AIDS patients. Mil Med 158:633-635, 1993. New Orleans Citywide Rounds
Column Index
Contents
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Introduction
Differential Diagnosis
Hospital Course
Final Diagnosis
Discussion
Drugs Mentioned in This Article
References
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