—  SPECIALTY CONFERENCE  —

Infectious Disease Pathology

Case 1 - Chlamydial Epididymitis

Peter McEvoy
Armed Forces Institute of Pathology
Washington, DC


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Clinical History:
Marine, 21 years old with right testicular mass for several months. No laboratory abnormalities or pertinent travel history. Orchiectomy performed for possible neoplasm.

Diagnosis: Chlamydial epididymitis


Case 1 - Figure A

Case 1 - Figure B

Case 1 - Figure C

Histologic findings:
The epididymal ducts are distended by acute inflammation, coalescing to form larger abscesses focally. Most of the ducts are surrounded by chronic inflammation comprising lymphocytes, plasmacytoid lymphocytes, and histiocytes. Some of the ducts appear to have squamous metaplastic changes. At the interface of the duct cells with the lumen, occasional vacuolated cells are noted, containing fine bodies (0.3 nm) that often line the wall of the vacuole. Although visible on H and E and B-H tissue gram stains, they are much more apparent on W-S silver stain. Free elementary bodies can also be identified on the W-S stain. Some spermatic granulomas can be identified.

Discussion:
Chlamydiae are nonmotile, obligate intracellular gram-negative bacteria. They have a unique developmental cycle, which differentiates them from all other microorganisms. Chlamydiae have cell walls similar to gram-negative bacteria, have prokaryotic ribosomes and are able to synthesize proteins. Unlike most bacteria, these organisms cannot replicate outside host cells or synthesize ATP. The developmental cycle comprises two forms of the organism: the elementary body, which is relatively inert, resistant to environmental degradation, and the infectious form of the organism; and the reticulate body, the metabolically active, dividing form which resides within the host cell. The three major species causing human disease are Chlamydia trachomatis, Chlamydia psittaci, and Chlamydia pneumoniae. A proposed fourth species, Chlamydia pecorum, has recently been described; its role as a pathogen is unclear. Chlamydia psittaci causes psittacosis (Ornithosis or parrot fever), and results from inhalation of the organism from birds, which shed the organisms in feces; Chlamydia pneumoniae seems to be an exclusive human pathogen also spread by the respiratory route, and causes a mild pneumonitis which is frequently unrecognized. It has been implicated in vascular disease, and may play a role in atherogenesis, a controversial topic currently under investigation.

Chlamydia trachomatis
causes trachoma (serovars A, B, Ba, C), genital disease and neonatal inclusion conjunctivitis (serovars D-K), and lymphogranuloma venereum (L1, L2, L3). Although some of the trachoma strains can be associated with genital infections, they do not require a genital reservoir, and can be transmitted by flies, fomites, or direct contact.

Genital infections by chlamydia may be asymptomatic in men and women. Usual manifestations include urethritis in men and mucopurulent cervicitis in women. Sequelae (men and/or women) include epididymitis, Reiter syndrome, infertility, salpingitis, pelvic inflammatory disease, proctitis, and premature rupture of membranes during pregnancy. LGV strains are associated with more invasive disease involving the inguinal lymph nodes, with resultant elephantiasis, strictures, fistulae, etc. Diagnosis of genital chlamydial infections is usually made by demonstration of the agent with immunofluorescent methodology, enzyme immunoassays, or molecular probes. Serology can be used for more invasive, longstanding infections with LGV strains. The surgical pathologist can play a role in recognizing the less common manifestations of chlamydial infection, for example epididymal inflammatory 'tumors'. While rarely recognized, they have specific histopathological features that allow for unequivocal diagnosis. There is not very much information in the surgical pathology literature on recognition of chlamydial infections. In one study 1 which compared features of chlamydial and bacterial (i.e. E coli) epididymitis, six cases of chlamydial epididymitis were identified on review of 31 resection specimens showing acute/chronic epididymitis by use of chlamydial immunohistochemistry. Apparently all six presented as indolent tumors, although this was not elaborated upon. The histopathological changes appeared characteristic enough (in retrospect) to recognize on H and E examination. The major changes were dense periductal infiltration of lymphocytes, plasma cells, and nonfoamy histiocytes, reactive epithelial proliferation (sometimes with formation of lymphoepithelial complexes), small microabscesses, and granular material within vacuoles of the duct epithelial cells (which corresponded with the chlamydial immunostain). Although these investigators felt that destructive macroabscesses were more characteristic of E coli epididymitis, the case we present contains macroabscesses. A study from the AFIP (2) described similar histological findings in 12 patients with suppurative inguinal lymphadenitis (i.e. LGV). Here, however, the organisms were found in macrophages, and stained with W-S silver stains and Brown-Hopps gram stain. In both studies and in the case presented, organisms can be discerned on careful H and E examination.

Excellent recent chapters on chlamydial infections are available.3,4,5 

References

  1. Histological differentiation between chlamydial and bacterial epididymitis: Nondestructive and proliferative versus destructive and abscess forming- immunohistochemical and clinicopathological findings. Hori S and Tsutsumi Y.1995. Hum Pathol 26:402-7.
  2. Demonstration of Chlamydia trachomatis in inguinal lymphadenitis of lymphogranuloma venereum: A light microscopy, electron microscopy and polymerase chain reaction study. Hadfield TL, Lamy Y, and Wear DJ. Mod Pathol.1995 Dec;8(9):924-9.
  3. Pathology of Infectious Diseases. Connor D et al, eds. Chapter 51. Appleton and Lange, 1997.
  4. Manual of Clinical Microbiology. 7th edition, Murray et al, eds. Chapter 57. ASM Press, Washington DC 1999.
  5. Principles and Practice of Infectious Diseases. 5th edition. Mandell et al, eds. Chapters 167-170. Churchill-Livingstone 2000.