Pleurisy

(CHEST 2001; 119:1266-1269)

A 29-year-old male physician presented with pleuritic chest pain and fever of 5 days' duration. He was in excellent general health and ran 6 to 8 miles daily. Two weeks previously, he had a 1-day viral syndrome, with fatigue, headache, rhinorrhea, and fever. He recovered fully; however, 6 days prior to hospital admission, he developed a temperature to 38.9 [degrees] C, chills, and diffuse myalgias. He was awakened the next morning by severe right pleuritic chest pain. He saw his primary-care physician the same day. Findings on chest examination and a chest radiograph were normal. The total WBC count was 6.6 x [10.sup.3]/[micro]L. Erythromycin was prescribed but was not taken. Over the next 3 days, the fever and chest pain progressed and the patient returned to his physician. At that time, he was tachypneic with severe splinting of the right chest. A chest radiograph showed a small right pleural effusion (Fig 1). He was treated with oral erythromycin and analgesics. The chest pain worsened over the next 6 h, and he was admitted to hospital. The patient was initially treated for community-acquired pneumonia with cefuroxime and erythromycin, and he received opiates for analgesia.

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His medical history was remarkable only for mild exercise-related asthma. There was no history of smoking, IV drug use, tuberculosis, or prior episodes of pneumonia.

Physical Examination

The patient's temperature was 37.1 [degrees] C; pulse, 100 beats/min; respiratory rate, 24 breaths/min; and BP, 112/68 mm Hg. Examination of the head, eyes, ears, nose, and throat was normal. The patient was splinting his right chest. Chest examination showed decreased breath sounds with dullness to percussion and rales over the lower right chest. There was moderate tenderness on palpation of the right upper quadrant. The spleen was not palpable. There was no lymphadenopathy or rash. The remainder of the physical examination was normal.

Laboratory Findings

Admission laboratory findings included the following: total WBC count, 17.5 x [10.sup.3]/[micro]L, with 5% band forms and toxic granulations; hematocrit, 40%. The serum sodium concentration was 132 mEq/L, lactate dehydrogenase level was 321 IU/L, and [Gamma]-glutamyl transpeptidase level was 93 IU/L. Total serum protein concentration was 6.7 g/dL. Serum aspartate and alanine aminotransferase and total bilirubin levels were normal. Westergren erythrocyte sedimentation rate was 85 mm/h. A serum antistreptolysin O titer was 163 IU/mL (normal range, 0 to 180 IU/mL). A repeat chest radiograph 8 h after hospital admission showed right basilar infiltrates and increased pleural effusion (Fig 2). An arterial blood gas analysis on 4 L/min of oxygen by nasal cannula following analgesia showed a pH of 7.35; Pa[CO.sub.2], 52 mm Hg; and Pa[O.sub.2], 76 mm Hg.

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A diagnostic procedure was performed.

What is the expected diagnosis?

Diagnosis: Group A [Beta]-hemolytic streptococcal pneumonia with empyema

Thoracocentesis yielded cloudy yellow fluid with a pH of 6.89; WBC count, 9,500/[micro]L (91% granulocytes); RBC count, 240/[micro]L; glucose, 14 mg/dL; total protein, 5.5 g/dL; and lactate dehydrogenase, 1,005 IU/L. Gram's stain of a slide centrifuge preparation (Cytospin; Shandon; Pittsburgh, PA) of the pleural fluid showed rare intracellular Gram-positive cocci in chains.

The patient was initially treated with erythromycin and cefuroxime plus vancomycin to cover for possible penicillin-resistant pneumococci and methicillin-resistant Staphylococcus aureus. Following thoracocentesis, two chest tubes were placed that drained [is less than] 200 mL of sanguineous fluid (Fig 3, top). A chest CT scan was performed showing severe consolidation and loculated effusion (Fig 3, bottom). Right thoracotomy and decortication were performed on the morning of the third hospital day. A pleural peel was removed from the lung, and 800 mL of bloody fluid was drained. Pleural fluid cultures from the initial thoracocentesis grew group A [Beta]-hemolytic Streptococcus pyogenes that was sensitive to penicillin. Antibiotic treatment was switched to penicillin G, 4 million IU IV every 4 h. The patient steadily improved and was discharged on the ninth hospital day.

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DISCUSSION

Group A [Beta]-hemolytic streptococcal pneumonia is an uncommon cause of community-acquired pneumonia in the antibiotic era. Lancefield group A streptococci are the most frequent causes of pneumonia; however, groups B, E, F, K, and O streptococci also have been reported to cause lower-respiratory-tract infection. The main virulence factor of the group A streptococci is the cell wall M protein that inhibits complement activation and decreases phagocytosis. Group A streptococci also produce exotoxins. These exotoxins are superantigens capable of direct T-cell activation without antigen processing by antigen-presenting cells. Exotoxins mediate fever and rash and the streptococcal toxic shock syndrome seen in some patients with invasive group A streptococcal infection.

[Beta]-Hemolytic streptococcal pneumonia usually occurs as a secondary pneumonia following other respiratory infections, including influenza, pertussis, varicella, measles, and in patients with COPD. Outbreaks of streptococcal pneumonia have been reported in institutional settings such as military recruit training barracks and nursing homes. Sporadic cases also occur in otherwise healthy individuals. Most cases occur during the winter months in temperate climates. Streptococcal pneumonia infrequently follows streptococcal pharyngitis. In one large series of 95 patients, one third of the patients reported sore throat, and positive cultures were only seen in 17% of 51 patients with pharyngitis. Entry of the organism into the lung usually results from inhalation or microaspiration. Rarely, streptococcal pneumonia is due to hematogenous seeding from other infected sites.

The clinical presentation of streptococcal pneumonia is similar to pneumococcal pneumonia, with the abrupt onset of fever, productive cough, and rigors. The sputum is usually purulent and frequently blood tinged. Pleuritic chest pain occurs in 75% of patients. On examination, patients are toxic with fever, tachypnea, and tachycardia. Splinting of the chest wall is frequent.

In one series of 95 patients, the total WBC count was between 10 x [10.sup.3]/[micro]L and 20 x [10.sup.3]/[micro]L in one half of the patients and [is greater than] 20 x [10.sup.3]/[micro]L in one fourth of patients. The chest radiograph usually shows patchy or homogeneous consolidation, usually in the lower lobes. Cavitation can appear several days later. Bilateral infiltrates also may be seen. Isolation of the organism from blood or pleural fluid cultures is diagnostic in the appropriate clinical setting. Blood cultures are positive in 2 to 15% of patients. Group A [Beta]-hemolytic streptococci frequently colonize the oropharynx, and a positive sputum culture may reflect only colonization. An acute serum antistreptolysin O titer [is greater than] 250 Todd units or a fourfold increase comparing acute and convalescent sera obtained several weeks after diagnosis is useful supportive information.

An important feature of streptococcal pneumonia is the high frequency of pleurisy and pleural effusion that rapidly progress to loculated empyema--so-called "explosive pleuritis." This process can occur over a period of hours. Pathologically severe serosanguineous pleural effusion, hemorrhagic edema of consolidated areas of the lung, and dilated lymphatics in the intralobular septa are present. Pleural effusions occur in 55 to 95% of patients with streptococcal pneumonia, with positive pleural fluid cultures in 30 to 40%.

Other complications, including pneumatocele, pneumothorax, bronchopleural fistula, pericarditis, and acute glomerulonephritis, occur in [is less than] 5% of cases. Chronic pleural thickening as a sequelae of parapneumonic effusions and empyema occurs in 44%.

The course of streptococcal pneumonia frequently is prolonged. Even with appropriate antibiotic therapy, fever persisted in 60% of patients for up to 1 week in one large series and was frequently associated with empyema. Empyemata should be drained urgently by chest tubes. Some patients will require early decortication for control of pleural sepsis.

CLINICAL PEARLS

1. Pneumonia due to group A [Beta]-hemolytic streptococci should be suspected in patients with lower-lobe pneumonia, severe pleurisy, and rapidly evolving pleural effusions.

2. Effusions in group A streptococcal pneumonia can rapidly loculate. Prompt pleural space drainage is indicated either by tube thoracostomy or decortication, depending upon the pleural space anatomy.

3. The antibiotic therapy of choice is high-dose IV penicillin G.

4. Fever is often prolonged in streptococcal pneumonia, and antibiotic therapy should not be altered if the patient is improving otherwise clinically.

SUGGESTED READINGS

Barnham M, Weightman N, Anderson A, et al. Review of 17 cases of pneumonia caused by Streptococcus pyogenes. Eur J Clin Microbiol Infect Dis 1999; 18:506-509

Basiliere JL, Bistrong HW, Spence WF. Streptococcal pneumonia: recent outbreaks in military recruit populations. Am J Med 1968; 44:580-589

Braman SS, Donat WE. Explosive pleuritis: manifestation of group A [Beta]-hemolytic streptococcal infection. Am J Med 1986; 81:723-726

Lerner AM, Jankauskas K. The classical bacterial pneumonias. Dis Mon 1975:1-46

Ruben FL, Norden CW, Heisler B, et al. An outbreak of Streptococcus pyogenes infections in a nursing home. Ann Intern Med 1984; 101:494-496

Welch CC, Tombridge TL, Baker WJ, et al. [Beta]-Hemolytic streptococcal pneumonia: report of an outbreak in a military population. Am J Med Sci 1961; 242:157-165

(*) From the Division of Infectious Diseases, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, OH.

Manuscript received June 26, 2000; revision accepted August 11, 2000.

Correspondence to: John L. Johnson, MD, FCCP, Associate Professor of Medicine, Case Western Reserve University, School of Medicine, Room E-202, Tuberculosis Research Unit, 10900 Euclid Ave, Cleveland, OH 44106-4984; e-mail: jlj@po.cwru.edu

COPYRIGHT 2001 American College of Chest Physicians
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