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Correspondence

Lymphangitis after Self-Administration of Lipopolysaccharide

N Engl J Med 2005; 352:944-945March 3, 2005

Article

To the Editor:

Acute lymphangitis is caused most often by Streptococcus pyogenes and occasionally by a range of other bacteria.1 We describe a patient in whom acute lymphangitis developed, with no evidence of infection.

The patient was a 27-year-old medical student who was working in the laboratory and was resuspending membranes isolated from lysed Escherichia coli when he accidentally stabbed his left index finger with a contaminated needle. Within an hour, he noted pain and swelling in his left hand. Over the next several hours, tenderness in his left arm and axilla developed, and then red streaks extending from the site of puncture to the axilla. After evaluation at the student health center, he received a dose of oral cefuroxime and was referred to the emergency department, where he was found to be afebrile and had moderate swelling of his index and middle fingers, decreased range of motion of the index and middle metacarpophalangeal joints, and erythematous streaking of the hand and arm (Figure 1Figure 1Photographs of the Patient's Left Hand and Left Upper Arm at the Time of Presentation to the Emergency Department.).

Blood was collected for cultures, and he was admitted to the hospital and treated with intravenous antibiotics. Two days later, he had minimal residual swelling and streaking and was discharged home with instructions to complete a short course of oral antibiotics. His blood cultures were negative, and a culture of the sample coating the needle with which he had stuck himself was also negative. A month after his illness, antistreptolysin O and anti–DNase B titers were obtained and were in the normal range. Considering the history, physical examination, and laboratory evaluation, we conclude that the patient had acute lymphangitis that probably resulted from the lipopolysaccharide present in E. coli membranes.

Investigation has established that eukaryotes have a conserved system of toll-like receptors (TLRs) for recognizing so-called pathogen-associated microbial patterns (e.g., lipopolysaccharide, peptidoglycan, and lipoteichoic acid).2 Activation of TLRs by the appropriate ligand leads to up-regulation of many cytokines, including tumor necrosis factor α and interleukin-6.3 The endothelium of lymphatic vessels has been shown to express TLRs.4 Given this information, it is possible that the TLR system is involved in recognition of bacteria within lymphatic vessels and is responsible, in part, for the clinical manifestations of lymphangitis.

This case highlights the possibility that lipopolysaccharide and other pathogen-associated microbial patterns present in bacterial membranes may play a key role in the pathogenesis of lymphangitis by activating the TLR pathway, perhaps explaining the stereotypical manifestations of lymphangitis despite the diversity of organisms that are capable of causing it.

Neeraj K. Surana, B.S.
Joseph W. St. Geme, M.D.
Washington University School of Medicine, St. Louis, MO 63110

4 References
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    Mandell GL, Bennett JE, Dolin R, eds. Principles and practice of infectious diseases. Vol. 1. Philadelphia: Churchill Livingstone, 2000:1072-5.

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    Medzhitov R, Preston-Hurlburt P, Janeway CA Jr. A human homologue of the Drosophila Toll protein signals activation of adaptive immunity. Nature 1997;388:394-397
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    Akira S, Takeda K. Toll-like receptor signalling. Nat Rev Immunol 2004;4:499-511
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    Kuroshima S, Sawa Y, Kawamoto T, et al. Expression of Toll-like receptors 2 and 4 on human intestinal lymphatic vessels. Microvasc Res 2004;67:90-95
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  1. 1

    R. Sura, J.-F. Colombel, H. J. Van Kruiningen. (2011) Lymphatics, tertiary lymphoid organs and the granulomas of Crohn’s disease: an immunohistochemical study. Alimentary Pharmacology & Therapeutics 33:8, 930-939
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  2. 2

    Gregory J. Brunn, Jeffrey L. Platt. (2006) The etiology of sepsis: turned inside out. Trends in Molecular Medicine 12:1, 10-16
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