The immunosuppressive properties of corticosteroids are well established and cause a depression of pulmonary defense mechanisms. We report the case of a patient treated with short-term corticosteroids for an exacerbation of chronic obstructive lung disease who developed a multiple organism pneumonia

Haapaniemi, John R.

Popovich, John, Jr.

Henry Ford Health System Scholarly Commons

Henry Ford Hospital Medical Journal Volume 32 Number 1 Article 11 3-1984 Polymicrobal Pneumonia in a Corticosteroid-Treated Patient with Chronic Obstructive Lung Disease John R. Haapaniemi John Popovich Jr. Follow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournal  Part of the Life Sciences Commons, Medical Specialties Commons, and the Public Health Commons Recommended Citation Haapaniemi, John R. and Popovich, John Jr. (1984) "Polymicrobal Pneumonia in a Corticosteroid-Treated Patient with Chronic Obstructive Lung Disease," Henry Ford Hospital Medical Journal : Vol. 32 : No. 1 , 49-52. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol32/iss1/11 This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Henry Ford Hosp Med J Vol 32, No 1,1984 Polymicrobal Pneumonia in a Corticosteroid-Treated Patient with Chronic Obstructive Lung Disease John R. Haapaniemi, DO"** and John Popovich, Jr, MD'^ The immunosuppressive properties of corticosteroids are well established and cause a depression of pul-monary defense mechanisms. We report the case of a patient treated with short-term corticosteroids for an exacerbation of chronic obstructive lung disease who developed a multiple organism pneumonia. I he immunosuppressive properties of corticosteroids are well established and cause a depression of pu l -monary defense mechanisms (1). The clinical conse-quence of these depressed defense mechanisms is infect ions, f requent ly manifested by infect ion wi th organisms of low pathogenicity or increased severity of infection with common pathogens (2). Such disease may be caused by several organisms and may be dif f icult to diagnose by conventional diagnostic techniques (2-6). We report the case of a patient treated with short-term corticosteroids for an exacerbation of chronic obstruc-tive lung disease who developed a mult iple organism pneumonia. Case Report A 71-year-old black man wi th a long history of coal worker's pneumonoconiosis and chronic obstructive pulmonary disease was admitted with increased cough, sputum product ion, and shortness of breath. Initial chest radiograph revealed no pneumatic infi l trates but evidence of chronic pulmonary disease. Sputum on admission revealed normal respiratory flora. He was treated for an acute purulent bronchitis and exacer-bation of obstructive disease by means of oxygen, intravenous antibiotics (cefazolin), bronchodilators, and methylprednisolone (160 mg/day). His hospital course was complicated by an upper gastrointestinal hemorr-hage, which was noted on endoscopy to be due to diffuse gastritis. Treatment included 15 days of intra-venous therapy and nasogastric intubation, transfusion of six units of packed red blood cells, cimetidine, and antacids. Progressive malnourishment was noted. Due to the patient's persistent bronchospasm, initial bronchodilator and methylprednisolone therapy was cont inued from admission through the f i f th week of hospitalization, when he developed increasing short-ness of breath and fever to 38.5°C. Diffuse expiratory wheezing was heard. Recentsputum cultures had grown numerous Pseudomonas aeruginosa. The patient was started on tobramycin and ticarcill in and moved to the intensive care unit. He progressed to respiratory failure and shock. With in 24 hours he died. Postmortem blood and urine cultures were reported as negative. The rapidity of the patient's death precluded the use of other d i agnos t i c t e c h n i q u e s to o b t a i n m i c r o b i o l o g i c specimens. An antero-posterior chest radiograph taken on the day of death (Fig. 1) demonstrated large bullae at the left base with f ibrot ic changes in both upper lobes and perihilar region. The f i lm was interpreted as being "basically unchanged" f rom numerous radiographs obtained over the previous month. Autopsy revealed bilateral consolidative changes in the lungs. Microscopic sections are shown in Fig. 2. Pneumo-cystis carinii was demonstrated by hematoxylin and eosin, as well as by Grocott stains of sections f rom the right lower lobe. Another distinct area o f the right lower lobe showed purulent pneumonia on hematoxylin and eosin stain, consistent wi th Gram negative bacillary infection. Postmortem cultures grew Pseudomonas aeru-ginosa. The left upper lobe revealed encapsulated budding yeasts consistent wi th cryptococcus by hema-toxylin and eosin and PAS stains f rom the left lower lobe. Silicotic nodules and emphysema were also demon-strated histologically. Submit ted for pub l ica t ion : August 23,1983 Accepted for pub l ica t ion : October 24,1983 •Depar tment of Med ic ine , Division of Pulmonary and Crit ical Care Med ic ine , Henry Ford Hospital, Address repr int requests to Dr, Popovich, Henry Ford Hospital , 2799 W Grand Blvd, Detro i t , M l 48202, 49 Haapaniemi and Popovich, Jr Discussion High doses of corticosteroids are known to cause immuno-supression, and infection is a well known complication (1). Steroid therapy affects the immune system in many ways. Migrat ion of phagocytes is decreased, release of inflammatory mediators is inhibi ted, and available num-bersof lymphocytes are reduced. Infection isthecl inical consequence of these depressed pulmonary defense mechanisms, frequently manifested as opportunistic infection by organisms of low pathogenicity or increased severity of infection with common pathogens. Decreased, delayed hypersensitivity is in turn associated with each of the organisms found in this patient (2). This specific combinat ion of organisms (cytomegalovirus, Pneumocystis carinii, cryptococcus, and Gram negative bacterial infection) has been described in patients with Hodgkins disease or lymphosarcoma and pulmonary infect ion (7). Patients are f requent ly infected wi th mult iple organisms. Other factors that may have contr ibuted to this patient's immunosuppression are malnutrit ion, coal worker's pneu-monoconiosis, and the cytomegaloviral infection itself. It is felt that corticosteroids must have played the major role in this immunosuppression given the patient's previous state of health and the clinical course. On many occasions, more than one organism is present in pu lmonary in fect ions of i m m u n o c o m p r o m i s e d patients (2-4). Ramsey reviewed 227 renal transplant patients to evaluate those with fever and pulmonary infiltrates (5). In these immunosuppressed patients cyto-megalovirus (CMV) was the most common virus to infect the lungs. Frequently, patients were superinfected with one or more other organisms, including Pneumocystis carinii and Pseudomonas aeruginosa. In 100 cancer patients with febrile pneumonit is, Rubin noted that 14% had mixed infections (6). Particular combinations likely to be present included CMV, Gram negative bacilli or fung i . He also noted that pneumonias caused by mult iple superinfected organisms were usually not demonstrated until autopsy material was evaluated. Several authors have noted the association of cyto-megalovirus wi th Pneumocystis carinii pneumonia, including many recent reports of acquired immuno-deficiency syndrome (AIDS) in homosexual men (8-10). The relationship between CMV infection and impaired, cel l -mediated immun i ty , specif ically, the altered T lymphocyte funct ion and numbers, is presently an area of active investigation (11). The diff iculty in diagnosing such cases before the patient dies is clear. Chest radiographs often do not reveal the extent of disease or are nondiagnostic (12). Our patient had an unchanged radiograph from the t ime of ad-Fig. 1 Antero-poster ior chest radiograph taken on day of death demon-strating large bullae at the (eft base wi th f ibrot ic changes in both upper lobes and the left perihi lar region. mission unt i l death despite widespread pulmonary infection. Noninvasive measures, such as sputum exami-nation or serologic testing, are potentially unreliable, or results are delayed (13). Invasive measures, such as open lung biopsy or sterile bronchoscopic brushing, have significant limitations because of sampling error pro-duced by sampling localized segmental or lobar regions. The potential of sampling error is exemplif ied by the discrete bilateral involvement in this patient. Obviously, single location sampling by either procedure could have resulted in missed diagnosis of some of the in-fecting organisms. In summary, we report the case of a patient with chronic obstructive lung disease and coal worker's pneumocon-iosis who was treated with corticosteroids for an exacer-bation of chronic obstructive lung disease and devel-oped a mult iple organism pneumonia. The short-term use of corticosteroids can produce significant immuno-suppression and lead to the development of such opportunistic and mixed infections. Furthermore, the i n te rp re ta t i on of bac ter io log ic data ob ta ined by localized techniques, such as open lung biopsy or single locat ion, sheathed bronchoscopic brushing, should consider the potential for missed diagnosis because of sampling error. 50 Fig. 2 Correlation of histology and area of biopsy with chest radiograph. A. Demonstration of Pneumocystis carinii on hematoxylin and eosin and Grocott stains; B. Demonstration of crytococcus on hematoxylin and eosin and PAS stains; C. Purulent pneumonia, postmortem cultures grew Pseudomonas aeruginosa; D. Giant inclusion bodies indicative of cytomegaloviral pneumonia demonstrated by hematoxylin and eosin stain. ^^^^ sMP Haapaniemi and Popovich, Jr References 1, Green C M , Jakob GC, Low RB, et al. Defense mechanisms of the respiratory membrane. Am Rev Respir Dis 1977;115:479-514, 2, Will iams D M , Kirk JA, Remington JS, Pulmonary infect ion in the compromised host. Am Rev Respir Dis 1976;119:359-94, 593-627, 3, Fantze CH, Pennington JE, Fever and new lung infiltrates in the immunocompromised host, Clin Chest M e d 1981;2:19-39, 4, Editorial, Pulmonary problems in the immunocompromised patient, Br M e d J 1981;282:2077, 5, Ramsey PG, Rubin RH,Tolkof f -Rubin NE, e ta l . The renal transplant patient wi th fever and pulmonary infi l trates; et iology, clinical manifestations, and management. Medic ine 1980;59:206-22, 6, Remington JS, Schwartz MA, The cancer patient wi th fever and pulmonary infiltrates; et iology and diagnostic approach, by R,H, Rubin, M D , In: Current clinical topics in infectious disease - 1 , New York: McGraw-Hi l l Book Company, 1980, 7, Bode FR, Pare JAP, Fraser RG, Pulmonary diseases in the com-promised host; A review of clinical and roentgenographic manifest-ations in patients wi th impaired host defense mechanisms. Medic ine 1974;53:255-93, 8, Walzer PD, Perl DP, Krogstad, et al, Pneumocystis carinii pneu-monia in the Uni ted States; epidemiologic, diagnostic, and clinical features, Ann Intern M e d 1974;80:83. 9. Wang NS, Huang SN, Thurlbeck W M , Combined Pneumocystis carinii and cytomegalovirus infect ion. Arch Pathol 1970;90:559, 10, Follansbee SE, Busch DF, Wofsy CB, et al. An outbreak of Pneumocystis carinii pneumonia in homosexual men, Ann Intern M e d 1982;95:705-13, 11, Mi ldvan D, Mathur U, Enlow RW, et al. Oppor tun is t ic infections and immune deficiency in homosexual men, Ann Intern M e d 1982;96:700-4, 12, Singer C, Armstrong D, Rosen PP, et al. Diffuse pulmonary inf i l -trates in immunosuppressed patients: Prospective study of 80 cases. A m J M e d 1979;66:110-20. 13, Valdivieso M , Gil-Extremera, B, Zornoza J, et al. Gram-negative baci l lary pneumon ia in the compromised host. Med i c i ne 1977;56:241-54, 52 

Polymicrobal Pneumonia in a Corticosteroid-Treated Patient with Chronic Obstructive Lung Disease

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