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Mycoplasma pneumoniae associated with hemolytic anemia, cold agglutinins, and recurrent arterial thrombosis.

Abstract: A 40-year-old white male developed Mycoplasma pneumoniae pneumonia (IgM titer 1:256) as well as autoimmune hemolytic anemia due to cold agglutinins (titer of 1:512). Four days after admission to the hospital, he developed an acute superior mesenteric artery (SMA) thrombosis. Four feet of ischemic small bowel were resected. A follow-up angiogram again showed SMA thrombosis and a left popliteal artery thrombosis. The patient was returned to the operating room and underwent thrombectomy of the affected arteries. The following day, he again developed a left popliteal artery thrombosis requiring thrombectomy. Plasmapheresis, Coumadin and prednisone were implemented. No further thrombotic events occurred. Hypercoagulability workup was negative. Pathology samples revealed vasculitis. Based on a negative hypercoagulability workup, nonrecurrence of thrombotic events after treatment, and in the absence of any structural abnormalities of the affected arteries, an autoimmune phenomenon with damage to the endothelium was thought to have played a role in the mechanism of thrombosis.

Key Words: Mycoplasma pneumoniae, hemolytic anemia, cold agglutinins, arterial thrombosis, pneumonia


Mycoplasma pneumoniae represents between 7 to 20% of the causes of community-acquired pneumonia in the United States. (1,2) As many as 25% of patients develop extrapulmonary complications, (3,4) and approximately 25% develop a clinically significant dermatological manifestation. Nonspecific myalgias and arthralgias occur in around 14% of the patients. (5) Cardiac involvement has been reported at rates from 1 to 8.5%. (6,7) Hemolytic anemia associated with multiple vascular thromboses is a rare but severe complication of Mycoplasma pneumoniae. Our search revealed only one case reported in the literature. (8)

Case Report

A 40-year-old white male presented to the emergency department with a 2-week history of dyspnea, cough productive of green sputum, fever and malaise. He had been taking ibuprofen 800 mg every 4 hours to reduce his fever. No family history of hypercoagulability was present. His review of systems was negative for hypercoagulability, skin, musculoskeletal or nervous system abnormalities. Physical findings revealed a blood pressure of 130/70, pulse 108, temperature 100.7[degrees]F and a pulse oximetry of 96%. He was ill appearing, diaphoretic and mildly icteric. His respiratory examination showed diminished breath sounds in the right lower lung field and bilateral rhonchi. The rest of the physical examination was otherwise unremarkable. Initial laboratory investigations revealed increased values for the white blood cell count (WBC 33,000 [10.sup.3][micro]l), lactate dehydrogenase (LDH 760 IU/L) and cold agglutinin titer of 1:128. A total bilirubin, predominantly direct, (2.8 mg/dL) also revealed decreased values for hemoglobin (Hb 7.6 g/dL) and haptoglobin (<6 mg/dL).

His initial chest x-ray (Fig. 1), showed a right lower lobe infiltrate consistent with pneumonia.

In the presence of pneumonia associated with hemolytic changes, Mycoplasma pneumoniae was suspected; serology was performed revealing an IgM titer of 1:256. At this point, the diagnosis was confirmed and the patient was started on azithromycin. He was also transfused with two units of packed red blood cells. Once the patient's anemia stabilized and acute bleeding was ruled out, he was begun on enoxaparin prophylactically. Four days after admission, the patient began to complain of severe abdominal pain requiring a surgery consult. The patient's abdominal examination revealed tenderness of the right upper quadrant to palpation. No rebound or peritoneal signs were evident. A contrast-enhanced CT of the abdomen and pelvis showed no evidence of intra-abdominal pathology. He then developed a Raynaud phenomenon of the lower extremities. Distal pulses were present and there were no complaints of pain from the patient. The Raynaud phenomenon was thought to be secondary to cold agglutinins. High-dose steroids were started. Six days after admission, the patient developed an acute abdomen and was brought to the operating room for an exploratory laparotomy (Fig. 2). The superior mesenteric artery (SMA) was noted to have palpable pulses. A second-look operation revealed no ongoing ischemia and a palpable SMA pulse. A follow-up angiogram was performed, demonstrating an SMA thrombus (Fig. 3) and a left popliteal artery thrombus (Fig. 4). The patient was returned to the operating room and underwent a SMA and popliteal thrombectomy. Completion angiogram demonstrated adequate flow in both vessels. The following day, he developed a cold, pulseless left foot which required repeat thrombectomy of his left popliteal artery without any other complications. Following these unexpected complications, it was decided to initiate plasmapheresis. He was started on 1.5 plasma volume exchange daily for three days, followed by every other day. The patient was also begun on warfarin. A follow-up cold agglutinin titer was 1:512. As before, the patient was continued on prednisone at 1 mg/kg/d. Following the initiation of plasmapheresis, the patient's hospital course began to improve, with no further thrombotic events. He was evaluated for an underlying coagulation disorder. Other than an expected slightly below-normal protein C level, all other laboratory studies, including protein S, factor V Leiden, homocysteine, prothrombin G, fibrinogen, antiphospholipid antibody, lupus anticoagulant and anti-cardiolipin antibody, were all within normal limits. Subsequent protein C levels were normal. Pathology samples revealed a superior mesenteric artery and left popliteal artery vasculitis. No other abnormalities were noted. Subsequently, his thrombotic events ceased. The patient recovered fully with no long-term sequelae.


The formation of thrombi in the human arterial system is regulated by three principle factors. (9). These include damage to the vessel wall, alterations in blood flow, and increased coagulability of the blood. Initial test results indicated that there was no increased likelihood that this patient had a hypercoagulable state. The patient was also taking very large doses of ibuprofen before admission, as well as being treated with enoxaparin while hospitalized. An alteration in blood flow did not seem to play a significant role in thrombi formation. There were no atherosclerotic plaques, structural abnormalities or evidence of trauma in the affected arteries at either the time of surgery or in the pathology samples. This leaves only the possibility of endothelial damage as the source of clot formation.

There are only a limited number of possible causes for this type of vessel damage. Autoimmune vasculitis or immune-mediated inflammation of the arterial wall is a well-known documented cause of this kind of injury. It is interesting that in pathology samples of the popliteal artery and the superior mesenteric artery, vasculitis was noted. Although vasculitis is not a well-described complication of Mycoplasma pneumoniae, a recent search of the journal literature reveals several cases of cutaneous vasculitis as well as one case of cerebral vasculitis with associated Mycoplasma pneumoniae infection. (10,11) Successful treatment of this patient with high-dose steroids and plasmapheresis also lends credence to this hypothesis. The etiology of the extrapulmonary sequelae of Mycoplasma pneumoniae remains poorly understood. Mycoplasma pneumoniae causes disease either by direct cytotoxicity or by triggering an autoimmune response. These manifestations of Mycoplasma pneumoniae can present a diagnostic and treatment challenge of which clinicians need to be aware.






The authors wish to acknowledge Mrs. Debbie Wells for helping to prepare the manuscript.


1. Bartlett JG, Mundy LM. Community-acquired pneumonia. N Engl J Med 1995;333:1618-1624.

2. Hammerschlag MR. Mycoplasma pneumoniae infections. Curr Opin Infect Dis 2001;14:181-186.

3. Mansel JK, Rosenow EC III, Smith TF, et al. Mycoplasma pneumoniae pneumonia. Chest 1989;95:639-646.

4. Waites KB, Talkington DF. Mycoplasma pneumoniae and its role as a human pathogen. Clin Microbiol Rev 2004;17:697-728.

5. Ali NJ, Sillis M, Andrews BE, et al. The clinical spectrum and diagnosis of Mycoplasma pneumoniae infection. Q J Med 1986;58:241-251.

6. Meseguer MA, Perez-Molina JA, Fernandez-Bustamante J, et al. Mycoplasma pneumoniae pericarditis and cardiac tamponade in a ten-year-old girl. Pediatr Infect Dis J 1996;15:829-831.

7. Ponka A. Carditis associated with mycoplasma pneumoniae infection. Acta Med Scand 1979;206:77-86.

8. Frappaz D, Rigal D, Valla JS, et al. [Multiple vascular thromboses in severe acute autoimmune hemolytic anemia with Mycoplasma pneumoniae serology treated by plasma exchange and immunosuppressive agents]. Pediatrie 1983;38:411-419.

9. Van Cott EM, Laposata M, Prins MH, et al. Laboratory evaluation of hypercoagulability with venous or arterial thrombosis. Arch Pathol Lab Med 2002;126:1281-1295.

10. Orlandini V, Dega H, Dubertret L, Cutaneous vasculitis revealing a Mycoplasma pneumonia infection. Presse Med 2004:1365-1366.

11. Oventchkine P, Brugieres P, Seradj A, et al. An 8-year-old boy with acute stroke and radiological signs of cerebral vasculitis after recent Mycoplasma pneumoniae infection. Scand J Infect Dis 2002;34:307-309.

Michelle L. Wilson, DO, FACP, FABHP, Eduardo Menjivar, MD, Viswanath Kalapatapu, MD, Alfred P. Hand, MD, James Garber, MD, and Michael A. Ruiz, MD

From the Department of Internal Medicine, Education, Memorial Health University Medical Center, Savannah, GA.

Reprint requests to Michelle L. Wilson, DO, FACP, FABHP, Pooler Parkway Internal Medicine, LLC, 143 Canal Street, Suite 100, Pooler, GA 31322. Email:

Accepted August 22, 2006.


* Mycoplasma pneumoniae represents between 7 to 20% of the causes of community-acquired pneumonia in the United States.

* Twenty-five percent of the patients develop extrapulmonary complications. Hemolytic anemia associated with multiple vascular thrombosis is a rare but severe complication of Mycoplasma pneumoniae.

* Mycoplasma pneumoniae causes disease either by direct cytotoxicity or by triggering an autoimmune response.

* An autoimmune phenomenon causing vasculitis with damage to the endothelium may have played the underlying mechanism for thrombosis.
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Article Details
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Author:Wilson, Michelle L.; Menjivar, Eduardo; Kalapatapu, Viswanath; Hand, Alfred P.; Garber, James; Ruiz,
Publication:Southern Medical Journal
Article Type:Clinical report
Geographic Code:1USA
Date:Feb 1, 2007
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