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Gut. 2007 October; 56(10): 1476–1477.
PMCID: PMC2000237

Lymphogranuloma venereum proctocolitis: mucosal T cell immunity of the rectum associated with chlamydial clearance and clinical recovery

Lymphogranuloma venereum (LGV) is a sexually transmitted disease caused by Chlamydia trachomatis serovars L1 to L3. At present there is an epidemic of LGV proctitis in the Western world among men who have sex with men. HIV seropositivity and other sexual transmitted infections are the main risk factors.1 Moreover, a concurrent HIV infection seems to be associated with a more severe course of LGV proctitis, indicating that LGV may behave as an opportunistic infection.2,3 Animal studies have shown a predominant role of CD4 lymphocytes in clearing chlamydial infection, including LGV proctitis, but knowledge of the human rectal immune response in LGV is limited.4,5,6 This is the first report of a patient with T cell immunodeficiency describing the rectal immunopathological response during prolonged LGV proctocolitis.

In April 2005, a 33 year old man was referred to our clinic because of resistant Crohn's disease despite treatment with sulfasalazine, corticosteroids, and azathioprine. The patient was known to have sex with men and he assured that HIV serology was recently performed and was negative. Endoscopy revealed deep aphthoid and linear discontinuous ulcers from rectum to sigmoid (fig 11).). Histology showed indeterminate colitis. Other infections (Treponema pallidum, Neisseria gonorrhoeae, herpes simplex virus, cytomegalovirus, Mycobacterium sp, Clostridium difficile, Entamoeba histolytica, and common enteric bacterial pathogens) were excluded by culture or polymerase chain reaction (PCR). Crohn's disease was additionally treated with the anti‐TNFα agent infliximab. Three months later the colitis deteriorated and the possibility of HIV infection was reconsidered. At this time, and retrospectively until at least 1 year before the onset of intestinal symptoms (July 2002), HIV serology was positive. The CD4 count was 69×106/l and the HIV‐RNA load was 229 000 copies/ml plasma. All available rectal biopsy specimens were reviewed and PCR was carried out for Ctrachomatis detection and typing, as described previously.7,8 L‐type Ctrachomatis was present in all specimens, confirming the diagnosis of LGV proctocolitis (fig 22).). The diagnosis of Crohn's disease was rejected, and mesalazine, azathioprine, and infliximab were stopped while prednisone was tapered off. The LGV was treated with a four week course of azithromycin (1 g loading dose followed by 250 mg daily) as tetracyclines were contraindicated. In September 2005 a subsequent rectal biopsy specimen remained positive for Ctrachomatis DNA (serovar L2 by RFLP genotyping). By two months, the clinical symptoms improved and highly active antiretroviral therapy (HAART: tenofovir, lamivudine, and nevirapine) was started. Endoscopy in January 2006 showed normal mucosa of the left colon except for some superficial ulcers and submucosal scarring in the rectosigmoid. Ctrachomatis PCR on rectal biopsy specimen was negative. HAART resulted in well suppressed HIV replication (HIV‐RNA load, <50 copies/ml) and an increase in the CD4 count (406×106/l). Histological examination of all rectal biopsy specimens stained with immunohistochemical markers showed that CD4 lymphocytes (fig 22,, A, B) and macrophages (fig 22,, E, F) appeared during immune reconstitution and clinical recovery while CD8 lymphocytes disappeared (fig 22,, C, D).

figure gt128264.f1
Figure 1 Endoscopy of the rectosigmoid showing multiple deep linear discontinuous ulcerations.
figure gt128264.f2
Figure 2 Immunohistochemistry of rectal biopsy specimens concurrent with treatment and lymphogranuloma venereum detection over time. The presence of lymphocytic cells was scored semiquantitatively using the percentage of positive cells (scale: ...

HIV causes a rapid depletion of most CD4 lymphocytes in gastrointestinal mucosal surfaces.9 This might explain the particular susceptibility of HIV infected people to the development of LGV proctocolitis. As is illustrated by this case, the close association over time between the appearance of CD4 lymphocytes and macrophages and chlamydial clearance strongly suggests that the immunological recovery was the underlying key in controlling rectal chlamydial infection, as antibiotic treatment alone was not sufficient.

In conclusion, rectal CD4 lymphocytes and macrophages seem to play a significant role in mucosal host defence against LGV proctitis. It is possible therefore that the vulnerability of HIV infected people to developing LGV proctitis is not only explained by sexual behaviour but also by mucosal T cell immunodeficiency of the rectum. This may contribute to the development of chronic symptomatic LGV proctocolitis which can be indistinguishable from resistant Crohn's disease.


We thank J Spaargaren and J Merks (Public Health Laboratory, Municipal Health Service of Amsterdam, and The Netherlands) for undertaking RFLP genotyping.

The study was presented in part at the 46th Interscience Conference on Antimicrobial Agents and Chemotherapy, abstract L2‐1235, San Francisco, California, USA, 2006.


Conflict of interest: none declared.


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