- Email: [email protected]
Adult Respiratory Distress Syndrome in Babesiosis
seleCled reports -----+~IIIIi.....-------------======-
-====::
Adult Respiratory Distress Syndrome in Babesiosis· Shale Gordon, M.D.; Ricardo A Cordon, M.D.; Edward]. Mazdzer, M.D.;]on M. Valigorsky, M.D.; Noel A Blagg, M.D.; and Susan] Barnes, M.D.
A patient is described who contracted transfusion-induced babesiosis, and later developed acute respiratory distress syndrome (ARDS) as a fatal complication. ARDS has been reported in patients with Plasmodium falciparum malaria, but to our knowledge has not been observed as a complication of babesiosis.
B
abesiosis, a tick-borne protozoal disease, formerly considered a rarity in humans, has been described in an increasing number of patients. This was emphasized during an epidemic on Nantucket Island in 1975. 1 Symptoms associated with the infection due to Babesia microti are extremely variable. Respiratory complaints, however, are rarely noted, and to our knowledge, acute respiratory distress syndrome (ARDS) as a complication of babesiosis has not previously been described. This report describes a patient who contracted Babesia microti and ARDS, in whom a cardiac cause for pulmonary edema was excluded by right heart catheterization. The pathophysiologic mechanisms involved in the production of this complication is unclear, but may be similar to ARDS observed in P [alciparum malaria, which is often abrupt in onset, refractory to therapy, and frequently fatal. 2 CASE REPORT
A 79-year-old woman was admitted to a hospital in western Massachusetts with a four-day history of fever, chills, nausea, arthralgia and lethargy, occurring sixweeks after sigmoidectomy and drainage of an abdominal abscess secondary to perforated diverticulitis. She had received 2 units of packed RBCs during surgery. On admission, her blood pressure was 12ono mm Hg, pulse rate was 100 beats per minute; temperature, 38.3 0 C; respirations, 24 per minute and slightly labored. The lungs were clear; an S4 gallop was noted, and there was right lower quadrant tenderness with rebound. The remainder of the physical examination was within normal limits. Laboratory studies showed hemoglobin; 10.2 g/dl, leukocytes; 5,700/cu mrn, with 56 percent neutrophils, 14 percent bands, 2 percent eosinophils, 18 percent lymphocytes, 4 percent atypical lymphocytes, and 6 percent monocytes. Reticulocyte count was 4.8 percent; SCm: 62 IU/L (normal 8-33 lUlL); LDH, 633 lUlL (normal 100-190 lUlL). At Flo2 of 21 percent, pH was 7.57; Pa02, 61 mm Hg; PaC02, 29 mm Hg. Ao abdominal abscess was suspected and the patient was treated with cephalexin monohydrate, clindamycin and gentamicin sulfate for three days. Her condition failed to improve. On the fourth day of hospitalization the laboratory reported parasitemia (10percent) with *From the Division of Pulmonary Medicine, Department of Medicine, Department of Pathology, Berkshire Medical Center, Pittsfield, Massachusetts. Reprint requests: Dr: Gordon, Berkshire Medical Center, 725North Street, Pittsfield, MA 01201
ringed-shaped intraerythrocytic organisms. Transfusion-induced malaria (Plasmodiumfalciparum) was suspected and she was treated with quinine, pyrimethanine and sulfadiazine. Three days later, the organisms were morphologically identified as Babesia microti. Therapy was changed to chloroquine phosphate, 1 g orally, followed by 500 mg six hours later, then 500 mg daily, which continued through the remainder of her clinical course. Transfusion-induced babesiosis was suspected. Her serum had an indirect fluorescent antibody (IFA)against B microti of 1:4,096. One blood donor, a 34year-old man, had camped on Cape Cod, MA for two weeks, returning to Pittsfield seven days before donating blood. Serum from this donor had an IFA titer against B microti of -1:4,096 and less than 1:16for Plasmodium species. On the ninth hospital day the patient became acutely dyspneic and hypoxic. Arterial blood pH was 7.50; Pa02, 45 mm Hg; PaC02, 35 mm Hg, on 28 percent oxygen. Physical examination revealed a blood pressure ofBO/60 mm Hg, pulse rate no beats per minute, and scattered rales at the bases of both lung fields. Chest roentgenogram disclosed diffuse bilateral pulmonary infiltrates. The patient required intubation and mechanical ventilation. On an Flo, of 60 percent, Pa02 was 60 mm Hg. A Swan-Ganz catheter was inserted. Initial pressures and cardiac output were normal. With an Flo, 60 percent and PEEP of 14 cm H 20, Pa02 was maintained between 60-70 mm Hg. Her chest roentgenogram demonstrated progressive worsening of the consolidative process in both lungs. On the 15th hospital day her cardiopulmonary status suddenly deteriorated and she died. At postmortem examination, the most prominent lesions were in the lungs and reticuloendothelial system. The lungs were congested and consolidated. Peritracheal, hilar, mesenteric and periaortic lymph nodes were enlarged, congested and deep reddish-purple. Microscopically the lungs demonstrated marked hyperplasia of type II pneumocytes, interstitial edema and focal hyaline membrane formation. The heart showed only rare fociof interstitial fibrosis and no evidence of interstitial cellular infiltrates. The 345-g spleen had a thick yellow capsule, was deep reddish-purple, and contained several small subcapsular infarcts. The liver weighed 1,350 g and demonstrated moderate to marked passive congestion and reticuloendothelial hyperplasia. DISCUSSION
Babesia are intraerythrocytic parasites that are widely distributed in nature and are transmitted primarily by the bites of various tick species. Inadvertent transmission by blood transfusion has been reported. 3 The clinical expression of infection with B micron is extremely variable. Many patients have few, ifany, symptoms while others experience prolonged illness characterized by fever, chills, malaise, myalgias and marked weakness. Because the symptoms of babesiosis may resemble malaria, and as some babesia are small ring-shaped trophozoites which occasionally take up a peripheral position within the erythrocyte, they have often been mistaken for Plasmodium falciparum. Most of the early cases were reported from Europe and occurred in previously splenectomized patients who died of fulminant disease." Cases reported from the United States have occurred, with few exceptions, in nonsplenectomized patients, many ofwhom were asymptomatic; CHEST / 86 / 4 / OClOBER, 1984
633
most recovered completely. 1.5 Previous reports have not emphasized respiratory symptoms as a manifestation of babesia infection. However, it has been described with P falciparom malaria and may range from minimal upper airway complaints to fatal ARDS. 2.6 Two forms of ARDS in malaria have been described. One is secondary to volume overload following aggressive fluid replacement," while the other appears to be related to increased capillary permeability.'" The patient described developed acute pulmonary edema in the presence of normal pulmonary capillary wedge pressure and cardiac index, suggesting that the cause of the pulmonary edema was secondary to an increase in capillary membrane permeability similar to patients with malaria and ARDS. The causal mechanisms for ARDS in both malaria and babesiosis remain speculative. It has been suggested that the increased vascular permeability may be secondary to microemboli, disseminated intravascular coagulation and immune complex disease," Experimentally, the effects of babesiosis have been likened to those of endotoxin shock, and injury to vascular endothelium has been demonstrated. 8 Except for its presence in red blood cells within the pulmonary vasculature, direct infestation of the parasite in lung tissue or pleural fluid does not seem to playa role. l .s In summary, this case presents a previously undescribed complication of infection with Babesiamicroti, acute respiratory failure due to noncardiogenic pulmonary edema. For most patients, babesiosis is a self-limiting febrile illness of varying severity. In splenectomized patients, however, the illness can be acute and more fulminant. Although our patient had an intact spleen, she appears to have fallen into this latter group. As awareness of this disease increases, the number of patients diagnosed with babesiosis will probably increase. This case emphasizes the need for careful monitoring of chest roentgenograms, arterial blood gases and, if indicated, pulmonary artery wedge pressure measurement in patients with symptomatic infection due to B microti. REFERENCES 1 Ruebush TK II, Cassaday PB, Marsh HJ, Lisker SA, Voorhees DB, Mahoney EB, et ale Human babesiosis on Nantucket Island: clinical features. Ann Intern Med 1977; 86:6-9 2 Brooks MH, Keil FW, Sheehy lW, Barry KG. Acute pulmonary edema in Falciparum malaria: a clinical-pathological correlation. N Engl J Med 1968; 279:732-37 3 Marcus LC, Valigorsky JM, Fanning WL, Joseph 1: Glick B. A case report of transfusion-induced babesiosis. JAMA 1982; 248: 465-67 4 Fitzpatrick JE, Kennedy CC, McGeown MG. Further details of third recorded case of redwater (babesiosis) in man. Br Med J 1969; 4:770-72. 5 Ruebush TK II, Juranek DD, Chisholm ES, Snow PC, Healy GR, Sulzer AJ. Human babesiosis on Nantucket Island: Evidence for self-limited and subclinical infections. N Engl J Med 1977; 297:825-27 6 Fein lA, Rackow EL, Shapiro L. Acute pulmonary edema in Plasmodium faldparum malaria. Am Rev Respir Dis 1978; 118:425-29 7 Hall A~ The treatment of malaria. Br Med J 1976; 1:323-25 8 Clark IA. Does endotoxin cause both the disease and parasite death in acute malaria and babesiosis? Lancet 1978; 2:75-7 9 Cayea PD, Rubin E, Texidor HS. Atypical pulmonary malaria. AJR 1981; 137:51-5
834
Lymphomatoid Granulomatosis Presenting as Central Neurogenic Hyperventllatlon* Ettayapuram ~ Sunderrajan, M.D., Paul M. Passamonfe, M.D. t
F:C.C.~t
and
A patient with lymphomatoid granulomatosis and
focal
transformation to lymphoma limited to the central nervous system presented with severe central neurogenic hyperventilation. The hyperventilation resolved as the underlying pathologic condition was treated with prednisone and cyclophosphamide.
C
ntral neurogenic hyperventilation (CNH) has been defined by Plum and Swanson! as a syndrome comprising normal arterial oxygen tension (PaOJ, decreased arterial carbon dioxide tension (PaCOJ, and respiratory alkalosis in the absence of cardiac or pulmonary abnormalities that would stimulate a compensatory hyperpnea. We report here an awake patient with CNH associated with lymphomatoid granulomatosis (LG) confined to the central nervous system.
CASE REPORT A 41-year-old white male electrician presented to his local hospital with a three-day history of uncontrollable rapid breathing. His past medical history revealed a grand mal seizure one year prior to this admission which was not evaluated. At the outside hospital, the patient was awake and alert. Arterial blood gas levels obtained breathing room air revealed pH, 7.62; PaOs, 120 mm Hg; PaCO •• 7 mm Hg with a bicarbonate of 12 mEq/L. His white blood cell (WBC) count was 26,600/cu mm with a hemoglobin of17.1 g/dl, The patient underwent a lumbar puncture which revealed glucose 52 mg/dl, protein, 90 mgldl, and 15 cells (87 percent lymphocytes). Computerized tomography (CIj of the brain revealed multiple small contrast enhancing lesions. He was treated with chloramphenicol and tobramycin. Three days later, the patient was found to be confused and his mentation was slow. He was transferred to the University Medical Center for further evaluation. Physical examination revealed a temperature of 36. T'C with a pulse rate of85 beatsper minute and a blood pressure ofll0l70 mm Hg. The patient was found to be breathing rapidly with a respiratory rate of26 per minute. He was awake and alert but had a flat affect. He was oriented to person. but he had a decrease in immediate memory. His coordination was poor. The reflexes were all intact and four plus bilaterally. His plantar reflexes were flexor bilaterally. His admission chest roentgenogram was normal. Arterial blood gaslevels breathing room air revealed pH, 7.55, PaO•• 113 mm Hg, and PaCO t , 16 mm Hg. A repeat spinal fluid examination revealed 10WBCs (100percent lymphocytes), protein, 109 mg/dl, glucose, 44 mg/dl, and a negative VDRL. Sedation with morphine sulfate failed to control the hyperventilation. Repeat blood gasvalues obtained 24 hours later revealed pH, 7.67; PaO., 124 mm Hg; PaCO•• 6 mm Hg; bicarbonate. 7 mEqlL; and the anion gap was 11 mEqlL. Repeat chest roentgenogram was normal. Because of the severe alkalosis, the patient was intubated, mechanically ventilated, and paralyzed with pancuronium bromide. A CT scan of the brain revealed decreased left frontal density with diffuse irregular contrast enhancement of both hemispheres that was greatest in the frontal areas (Fig 1). No mass *From the Department of Internal Medicine, University of Missouri, Columbia. t Assistant Professor of Medicine. Reprint requests: Dr. Sunderrajan, PulmonaryMedicine, 800 Hospital Drive, Columbia, MO 65201 Lymphomatoid Granulomatoels (Sunderrajan, Pauamonte)
-====::
Adult Respiratory Distress Syndrome in Babesiosis· Shale Gordon, M.D.; Ricardo A Cordon, M.D.; Edward]. Mazdzer, M.D.;]on M. Valigorsky, M.D.; Noel A Blagg, M.D.; and Susan] Barnes, M.D.
A patient is described who contracted transfusion-induced babesiosis, and later developed acute respiratory distress syndrome (ARDS) as a fatal complication. ARDS has been reported in patients with Plasmodium falciparum malaria, but to our knowledge has not been observed as a complication of babesiosis.
B
abesiosis, a tick-borne protozoal disease, formerly considered a rarity in humans, has been described in an increasing number of patients. This was emphasized during an epidemic on Nantucket Island in 1975. 1 Symptoms associated with the infection due to Babesia microti are extremely variable. Respiratory complaints, however, are rarely noted, and to our knowledge, acute respiratory distress syndrome (ARDS) as a complication of babesiosis has not previously been described. This report describes a patient who contracted Babesia microti and ARDS, in whom a cardiac cause for pulmonary edema was excluded by right heart catheterization. The pathophysiologic mechanisms involved in the production of this complication is unclear, but may be similar to ARDS observed in P [alciparum malaria, which is often abrupt in onset, refractory to therapy, and frequently fatal. 2 CASE REPORT
A 79-year-old woman was admitted to a hospital in western Massachusetts with a four-day history of fever, chills, nausea, arthralgia and lethargy, occurring sixweeks after sigmoidectomy and drainage of an abdominal abscess secondary to perforated diverticulitis. She had received 2 units of packed RBCs during surgery. On admission, her blood pressure was 12ono mm Hg, pulse rate was 100 beats per minute; temperature, 38.3 0 C; respirations, 24 per minute and slightly labored. The lungs were clear; an S4 gallop was noted, and there was right lower quadrant tenderness with rebound. The remainder of the physical examination was within normal limits. Laboratory studies showed hemoglobin; 10.2 g/dl, leukocytes; 5,700/cu mrn, with 56 percent neutrophils, 14 percent bands, 2 percent eosinophils, 18 percent lymphocytes, 4 percent atypical lymphocytes, and 6 percent monocytes. Reticulocyte count was 4.8 percent; SCm: 62 IU/L (normal 8-33 lUlL); LDH, 633 lUlL (normal 100-190 lUlL). At Flo2 of 21 percent, pH was 7.57; Pa02, 61 mm Hg; PaC02, 29 mm Hg. Ao abdominal abscess was suspected and the patient was treated with cephalexin monohydrate, clindamycin and gentamicin sulfate for three days. Her condition failed to improve. On the fourth day of hospitalization the laboratory reported parasitemia (10percent) with *From the Division of Pulmonary Medicine, Department of Medicine, Department of Pathology, Berkshire Medical Center, Pittsfield, Massachusetts. Reprint requests: Dr: Gordon, Berkshire Medical Center, 725North Street, Pittsfield, MA 01201
ringed-shaped intraerythrocytic organisms. Transfusion-induced malaria (Plasmodiumfalciparum) was suspected and she was treated with quinine, pyrimethanine and sulfadiazine. Three days later, the organisms were morphologically identified as Babesia microti. Therapy was changed to chloroquine phosphate, 1 g orally, followed by 500 mg six hours later, then 500 mg daily, which continued through the remainder of her clinical course. Transfusion-induced babesiosis was suspected. Her serum had an indirect fluorescent antibody (IFA)against B microti of 1:4,096. One blood donor, a 34year-old man, had camped on Cape Cod, MA for two weeks, returning to Pittsfield seven days before donating blood. Serum from this donor had an IFA titer against B microti of -1:4,096 and less than 1:16for Plasmodium species. On the ninth hospital day the patient became acutely dyspneic and hypoxic. Arterial blood pH was 7.50; Pa02, 45 mm Hg; PaC02, 35 mm Hg, on 28 percent oxygen. Physical examination revealed a blood pressure ofBO/60 mm Hg, pulse rate no beats per minute, and scattered rales at the bases of both lung fields. Chest roentgenogram disclosed diffuse bilateral pulmonary infiltrates. The patient required intubation and mechanical ventilation. On an Flo, of 60 percent, Pa02 was 60 mm Hg. A Swan-Ganz catheter was inserted. Initial pressures and cardiac output were normal. With an Flo, 60 percent and PEEP of 14 cm H 20, Pa02 was maintained between 60-70 mm Hg. Her chest roentgenogram demonstrated progressive worsening of the consolidative process in both lungs. On the 15th hospital day her cardiopulmonary status suddenly deteriorated and she died. At postmortem examination, the most prominent lesions were in the lungs and reticuloendothelial system. The lungs were congested and consolidated. Peritracheal, hilar, mesenteric and periaortic lymph nodes were enlarged, congested and deep reddish-purple. Microscopically the lungs demonstrated marked hyperplasia of type II pneumocytes, interstitial edema and focal hyaline membrane formation. The heart showed only rare fociof interstitial fibrosis and no evidence of interstitial cellular infiltrates. The 345-g spleen had a thick yellow capsule, was deep reddish-purple, and contained several small subcapsular infarcts. The liver weighed 1,350 g and demonstrated moderate to marked passive congestion and reticuloendothelial hyperplasia. DISCUSSION
Babesia are intraerythrocytic parasites that are widely distributed in nature and are transmitted primarily by the bites of various tick species. Inadvertent transmission by blood transfusion has been reported. 3 The clinical expression of infection with B micron is extremely variable. Many patients have few, ifany, symptoms while others experience prolonged illness characterized by fever, chills, malaise, myalgias and marked weakness. Because the symptoms of babesiosis may resemble malaria, and as some babesia are small ring-shaped trophozoites which occasionally take up a peripheral position within the erythrocyte, they have often been mistaken for Plasmodium falciparum. Most of the early cases were reported from Europe and occurred in previously splenectomized patients who died of fulminant disease." Cases reported from the United States have occurred, with few exceptions, in nonsplenectomized patients, many ofwhom were asymptomatic; CHEST / 86 / 4 / OClOBER, 1984
633
most recovered completely. 1.5 Previous reports have not emphasized respiratory symptoms as a manifestation of babesia infection. However, it has been described with P falciparom malaria and may range from minimal upper airway complaints to fatal ARDS. 2.6 Two forms of ARDS in malaria have been described. One is secondary to volume overload following aggressive fluid replacement," while the other appears to be related to increased capillary permeability.'" The patient described developed acute pulmonary edema in the presence of normal pulmonary capillary wedge pressure and cardiac index, suggesting that the cause of the pulmonary edema was secondary to an increase in capillary membrane permeability similar to patients with malaria and ARDS. The causal mechanisms for ARDS in both malaria and babesiosis remain speculative. It has been suggested that the increased vascular permeability may be secondary to microemboli, disseminated intravascular coagulation and immune complex disease," Experimentally, the effects of babesiosis have been likened to those of endotoxin shock, and injury to vascular endothelium has been demonstrated. 8 Except for its presence in red blood cells within the pulmonary vasculature, direct infestation of the parasite in lung tissue or pleural fluid does not seem to playa role. l .s In summary, this case presents a previously undescribed complication of infection with Babesiamicroti, acute respiratory failure due to noncardiogenic pulmonary edema. For most patients, babesiosis is a self-limiting febrile illness of varying severity. In splenectomized patients, however, the illness can be acute and more fulminant. Although our patient had an intact spleen, she appears to have fallen into this latter group. As awareness of this disease increases, the number of patients diagnosed with babesiosis will probably increase. This case emphasizes the need for careful monitoring of chest roentgenograms, arterial blood gases and, if indicated, pulmonary artery wedge pressure measurement in patients with symptomatic infection due to B microti. REFERENCES 1 Ruebush TK II, Cassaday PB, Marsh HJ, Lisker SA, Voorhees DB, Mahoney EB, et ale Human babesiosis on Nantucket Island: clinical features. Ann Intern Med 1977; 86:6-9 2 Brooks MH, Keil FW, Sheehy lW, Barry KG. Acute pulmonary edema in Falciparum malaria: a clinical-pathological correlation. N Engl J Med 1968; 279:732-37 3 Marcus LC, Valigorsky JM, Fanning WL, Joseph 1: Glick B. A case report of transfusion-induced babesiosis. JAMA 1982; 248: 465-67 4 Fitzpatrick JE, Kennedy CC, McGeown MG. Further details of third recorded case of redwater (babesiosis) in man. Br Med J 1969; 4:770-72. 5 Ruebush TK II, Juranek DD, Chisholm ES, Snow PC, Healy GR, Sulzer AJ. Human babesiosis on Nantucket Island: Evidence for self-limited and subclinical infections. N Engl J Med 1977; 297:825-27 6 Fein lA, Rackow EL, Shapiro L. Acute pulmonary edema in Plasmodium faldparum malaria. Am Rev Respir Dis 1978; 118:425-29 7 Hall A~ The treatment of malaria. Br Med J 1976; 1:323-25 8 Clark IA. Does endotoxin cause both the disease and parasite death in acute malaria and babesiosis? Lancet 1978; 2:75-7 9 Cayea PD, Rubin E, Texidor HS. Atypical pulmonary malaria. AJR 1981; 137:51-5
834
Lymphomatoid Granulomatosis Presenting as Central Neurogenic Hyperventllatlon* Ettayapuram ~ Sunderrajan, M.D., Paul M. Passamonfe, M.D. t
F:C.C.~t
and
A patient with lymphomatoid granulomatosis and
focal
transformation to lymphoma limited to the central nervous system presented with severe central neurogenic hyperventilation. The hyperventilation resolved as the underlying pathologic condition was treated with prednisone and cyclophosphamide.
C
ntral neurogenic hyperventilation (CNH) has been defined by Plum and Swanson! as a syndrome comprising normal arterial oxygen tension (PaOJ, decreased arterial carbon dioxide tension (PaCOJ, and respiratory alkalosis in the absence of cardiac or pulmonary abnormalities that would stimulate a compensatory hyperpnea. We report here an awake patient with CNH associated with lymphomatoid granulomatosis (LG) confined to the central nervous system.
CASE REPORT A 41-year-old white male electrician presented to his local hospital with a three-day history of uncontrollable rapid breathing. His past medical history revealed a grand mal seizure one year prior to this admission which was not evaluated. At the outside hospital, the patient was awake and alert. Arterial blood gas levels obtained breathing room air revealed pH, 7.62; PaOs, 120 mm Hg; PaCO •• 7 mm Hg with a bicarbonate of 12 mEq/L. His white blood cell (WBC) count was 26,600/cu mm with a hemoglobin of17.1 g/dl, The patient underwent a lumbar puncture which revealed glucose 52 mg/dl, protein, 90 mgldl, and 15 cells (87 percent lymphocytes). Computerized tomography (CIj of the brain revealed multiple small contrast enhancing lesions. He was treated with chloramphenicol and tobramycin. Three days later, the patient was found to be confused and his mentation was slow. He was transferred to the University Medical Center for further evaluation. Physical examination revealed a temperature of 36. T'C with a pulse rate of85 beatsper minute and a blood pressure ofll0l70 mm Hg. The patient was found to be breathing rapidly with a respiratory rate of26 per minute. He was awake and alert but had a flat affect. He was oriented to person. but he had a decrease in immediate memory. His coordination was poor. The reflexes were all intact and four plus bilaterally. His plantar reflexes were flexor bilaterally. His admission chest roentgenogram was normal. Arterial blood gaslevels breathing room air revealed pH, 7.55, PaO•• 113 mm Hg, and PaCO t , 16 mm Hg. A repeat spinal fluid examination revealed 10WBCs (100percent lymphocytes), protein, 109 mg/dl, glucose, 44 mg/dl, and a negative VDRL. Sedation with morphine sulfate failed to control the hyperventilation. Repeat blood gasvalues obtained 24 hours later revealed pH, 7.67; PaO., 124 mm Hg; PaCO•• 6 mm Hg; bicarbonate. 7 mEqlL; and the anion gap was 11 mEqlL. Repeat chest roentgenogram was normal. Because of the severe alkalosis, the patient was intubated, mechanically ventilated, and paralyzed with pancuronium bromide. A CT scan of the brain revealed decreased left frontal density with diffuse irregular contrast enhancement of both hemispheres that was greatest in the frontal areas (Fig 1). No mass *From the Department of Internal Medicine, University of Missouri, Columbia. t Assistant Professor of Medicine. Reprint requests: Dr. Sunderrajan, PulmonaryMedicine, 800 Hospital Drive, Columbia, MO 65201 Lymphomatoid Granulomatoels (Sunderrajan, Pauamonte)