Colonoscopy was performed to evaluate the extent of his disease. This confirmed the presence of a posterior anal fissure with severe inflammation of the rectum to the recto-sigmoid. There was patchy inflammation of the descending, transverse, ascending colon and caecum. No further biopsies were taken at this time, and the diagnosis of Crohn's disease remained unchanged.

Four months later with continued symptoms he presented to the Courtyard Clinic at St George's Hospital requesting a HIV test. The patient was diagnosed with advanced HIV infection with a CD4 count of 25 cells/mm³ (4%) and viral load of 159 000 copies/ml. A full sexual health screen was performed, and the patient was admitted for further investigation of his symptoms.

The rectum was markedly tender during proctoscopy, the rectal mucosa was erythematous with contact bleeding. A positive Chlamydia nucleic acid amplification test (NAAT) was reported by the laboratory within 24 h. This was subsequently genotyped in a reference laboratory (HPA Colindale, London, UK) and confirmed as LGV infection (figure 1A,B).

The symptoms and signs of infection in MSM such as proctitis presenting as severe rectal pain, mucoid and/or haemorrhagic rectal discharge, tenesmus, constipation and other features of lower gastrointestinal inflammation¹; have led to incorrect diagnosis of IBD. This misdiagnosis has been described in case reports previously,^3–5 the new surge in cases this year suggests that we need to raise awareness of LGV infection to ensure patients are managed appropriately.

Further analyses of reported cases has identified a pattern of LGV infection among white MSM, the vast majority of whom were HIV positive and co-infected with hepatitis C infection.^{1 2} While sexual behaviour may account for this finding, the ulcerative nature of LGV infection is likely to increase the transmission risk of HIV and other bloodborne viruses, in the same way as with other ulcerative sexually transmitted infections such as genital herpes.

Classical LGV infection follows three clinical stages – primary, secondary and tertiary. It occurs at the site of the infection (mouth, anus, or any part of male or female genitalia). The primary lesion presents as a painless sore which may go unnoticed, and the incubation period ranges over 3–30 days. The secondary stage follows the primary lesion by 10–30 days and typically causes systemic symptoms and lymphadenopathy. C trachomatis serovars L1–L3 are lymphotropic, and cause disease by thrombolymphangitis and perilymphangitis. The LGV infection therefore manifests itself with inflammation and swelling of lymph nodes and surrounding tissue. Thus clinically, patients present with tender inguinal and/or femoral lymphadenopathy which may ulcerate and discharge pus from multiple points, creating chronic fistulae. The tertiary stage of the infection has also been referred to as the genito-anorectal syndrome. This describes a few patients who do not recover following the secondary stage of infection. In these patients C trachomatis infection persists and causes a chronic inflammatory response, leading to destruction of involved tissues. Patients can present with proctitis, acute proctocolitis, rectal bleeding, fistulae, strictures and chronic destruction of the vulva. Lymphoedema of the genitals with persistent suppuration and pyoderma may result secondary to the destruction of lymph nodes.^{1 2}

Diagnosis of LGV infection requires a rectal swab for Chlamydia (NAAT). Positive rectal Chlamydia results are subsequently genotyped in a reference laboratory for LGV infection. Rectal swabs are currently performed in genitourinary clinics for all cases of rectal sexual exposure with symptoms. National guidelines are set to change to ensure all UK genitourinary clinics offer rectal Chlamydia testing for all MSM reporting rectal exposure. Clinicians should have a low index of suspicion for an infective cause of rectal or bowel symptoms, and LGV infection should be excluded in all patients.

In addition, routine HIV testing will continue to identify a large number of patients with otherwise undiagnosed HIV infection, and we are actively trying to normalise this recommendation.⁶ HIV infection itself can cause bowel symptoms in over 50% of patients at some time during their illness, the most common infective causes are summarised in table 1. In this case, misdiagnosis led to inappropriate treatment being initiated in a severely immunocompromised individual highlighting the importance of always considering a wide number of differential diagnoses.