Final Diagnosis -- Middle-aged man with Streptococcus pneumoniae psoas abscess and recurrent pneumococcal bacteremia as the initial presentation of a monoclonal gammopathy


FINAL DIAGNOSIS: Streptococcus pneumoniae psoas abscess and recurrent pneumococcal bacteremia as initial presentation of a monoclonal gammopathy.

(Note: the exact nature of this patient's monoclonal gammopathy is currently under investigation. Once finalized, this web case will be updated.)

DISCUSSION:

Pyogenic abscess of the psoas muscle was first described by Herman Mynter in 1881. It is a relatively rare but well described condition that generally presents with fever and pain in the lumbar region extending down the thigh [2]. Psoas muscle abscess can be either primary (via direct inoculation or hematogenous spread subsequent to trauma) or secondary (dissemination from adjacent structures). The treatment of choice is surgical drainage and antibiotic treatment. The prognosis is generally good [2, 3].

Historically the majority of primary psoas abscess were a manifestation of extra-pulmonary tuberculosis. Today, over 80% of cases of primary psoas abscess are caused by Staphylococcus aureus. There are only 14 reported cases of Streptococcus pneumoniae primary psoas abscess [4-7].

S. pneumoniae is better known as the major cause of community-acquired pneumonia, as well as the most common cause of bacterial meningitis in adults. Infrequently, it may cause endocarditis, peritonitis, septic arthritis, and pelvic infections. It is a recognized, albeit rare, cause of soft tissue infections such as cellulitis, fasciitis, rhabdomyolysis, and abscesses. The vast majority of these types of cases occur in patients with underlying conditions, such as end-stage renal disease, rheumatoid arthritis or connective tissue disorders, HIV infection, complement deficiencies, lymphomas and leukemias, and plasma cell dyscrasias [1].

Plasma cell dyscrasias, categorized in the table below, are disorders that involve neoplastic proliferation of plasma cells and excess production of immunoglobulin.

    Condition

    Non-IgM monoclonal proteins

    IgM monoclonal proteins

    Premalignant/ undetermined

    Monoclonal gammopathy of undetermined significance (MGUS) (IgG, IgA, other)

    MGUS (IgM)

     

     

    Other lymphoproliferations

    Intermediate

    Smoldering multiple myeloma

    Smoldering macroglobulinemia

    Malignant

    Active multiple myeloma

    Waldenstrom macroglobulinemia

     

    Plasma cell leukemia

    Other

     

    Solitary plasmacytoma

     

Proper categorization is essential for treatment, as those patients with MGUS are followed clinically, while those with multiple myeloma (and usually smoldering myeloma) are treated. As noted above, the clinical manifestations of plasma cell dyscrasias range from benign and of uncertain significance to highly malignant. Multiple myeloma, the most severe case of these diseases, generally presents with bone pain due to lytic lesions, renal failure, hypercalcemia, anemia, and susceptibility to bacterial infections, especially of encapsulated organisms [8]. The susceptibility to infection is due to defects of both the primary and secondary antibody responses, with the insufficient synthesis of polyclonal immunoglobulins as probably the most significant contribution to risk. Pneumococcal bacteremia has been described a presenting sign of multiple myeloma [9]

This patient had a Streptococcus pneumoniae psoas abscess and recurrent pneumococcal bacteremia as the initial presentation of a monoclonal gammopathy, with a final categorization of the monoclonal gammopathy to be determined. The most likely explanation for his recurrent pneumococcal bacteremia is the immune dysregulation due to a monoclonal gammopathy, with subsequent seeding of his trauma site leading to the psoas abscess. The patient's presenting symptoms, as well as his laboratory data available so far, are highly suggestive of a plasma cell dyscrasia. He did have a bone survey that did not reveal lytic lesions, as well as flow cytometry of peripheral blood that was non-diagnostic. To date, however, the bone marrow biopsy that is crucial for final diagnosis and appropriate treatment has not been performed. Of the 14 case reports of pneumococcal psoas infection, one patient had an underlying multiple myeloma [10]. Thus, while pneumococcal infections are known to be associated with multiple myelomas, this patient's pneumococcal infection of the psoas muscle in association with a monoclonal gammopathy has only been reported in one other case.

REFERENCES

  1. Koneman EW, Allen SD, Janda WM, et al. Color Atlas and Textbook of Diagnostic Microbiology. 5 ed. 1997, Philadelphia: Lippincott. 591.
  2. Ricci MA, Rose FB, and Meyer KK. Pyogenic psoas abscess: worldwide variations in etiology. World Journal of Surgery, 1986. 10: 834-843.
  3. Mandell GL, Bennett JE, and Dolin R. Mandell, Douglas and Bennett's principles and practice of infectious diseases. 5 ed. 2000, Philadelphia: Churchill Livingstone. 1063.
  4. Giladi M, Sada MJ, Spotkov J, et al. Pneumococcal psoas abscess: report of a case and review of the world literature. Israel Journal of Medical Science, 1996. 32: 771-774.
  5. Nakazato T, Kitahara M, Watanabe K, et al. Pneumococcal psoas abscess. Internal Medicine, 1999. 38(1): 63-66.
  6. Oliver A, Saban J, Pujol I, et al. Pneumococcal psoas abscess: report of two cases. Clin Microbiol Infect, 2000. 6(3): 168-169.
  7. Tuerlinckx D, Bodart E, de Bilderling G, et al. Pneumococcal psoas pyomyositis associated with complement deficiency. Pediatric Infectious Disease Journal, 2004. 23(4): 371-373.
  8. Greer JP, Foerster J, and Lukens JN. Wintrobe's Clinical Hematology. 11 ed. 2003: Lippincott Williams & Wilkins. 2555-2564.
  9. Gregersen H, Gitte P, Svendsen N, et al. Multiple myeloma following an episode of community-acquired pneumococcal bacteremia or meningitis. Acta Pathologica, Microbiologica et Immunologica Scandinavica, 2001. 109(11): 797-800.
  10. Bernstein I and Schmidt J. Iatrogenic psoas abscess. Scandinavian Journal of Urologic Nephrology, 1991. 25(1): 85-86.

Contributed by Melina Flanagan, MD, MSPH, Casmiar Nwaigwe, MD, and William Pasculle, ScD




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