Monkeypox-associated proctitis and rectal wall perforation

Background

Monkeypox is a zoonotic infection caused by monkeypox virus, a member of the Orthopoxvirus genus and close relative of the variola virus which causes smallpox. The infection is characterised by an initial prodrome of fever and lymphandenopathy (1–5 days), followed by the emergence of a characteristic centrifugal rash.1 Although most cases are self-limiting, severe secondary infections including pneumonia, encephalitis, keratitis and sepsis may occur. Recent reports of rectal involvement (perianal lesions, proctitis) have led the Centre for Disease Control and Prevention (CDC) to acknowledge these as additional symptoms of monkeypox but little is known about this atypical presentation.2–4 Here, we present a case of monkeypox-associated proctitis and rectal perforation in the UK.

Case presentation

A man in his 40s with confirmed monkeypox presented to the emergency department with a 9-day history of fever, rash and rectal pain. The illness began with fatigue and joint pain primarily affecting the hips and shoulders. Two days later, the patient developed high grade fevers (up to 40°C), rectal pain and discharge and tenesmus. He subsequently presented to a sexual health clinic and was noted to have pustules in his mouth, around the anus and scalp. Diagnosis of monkeypox was suspected, rectal swabs were obtained and the patient was instructed to self-isolate at home pending results. High grade fevers, with associated rigours and night sweats, persisted for 3 days. On the fifth day, the patient reported a sore throat, headache and pruritic maculopapular rash on his upper limbs which subsequently spread to his legs and then to his torso (figure 1). He also noted painful lymphadenopathy in the neck and groin. Diagnosis of monkeypox (by PCR of rectal, throat and skin swabs and urine) was confirmed on day 6 of symptoms. Rectal pain and tenesmus became more severe over the next 3 days and was associated with constipation. No genital involvement was reported. Additionally, the patient described suprapubic pain during urination and hesitancy during the 2 days before presenting to hospital.

Medical history was notable for HIV, diagnosed 21 years prior, with good virologic control on antiretroviral therapy with biktarvy (viral load undetectable since 2011). Patient reported previous infections with Neisseria gonorrhoeae, Chlamydia trachomatis, Treponema pallidum and herpes simplex virus. There was no history of proctitis and no previous abdominal surgery. There was no recent travel history, no recent attendance at large events and no animal exposure. He reported exposure to monkeypox through his partner with whom he shared a house, who had returned from Mainland Europe, developed fever and rash and tested positive for the virus 1 day prior to the patient’s onset of symptoms. The patient reported sharing drinks, bedding and a single episode of unprotected receptive anal sexual intercourse 5 days before onset of symptoms. No oral sexual intercourse and no other recent sexual partners were reported. As contact tracing of partner revealed recent exposure to gonorrhoea, the patient had been prescribed a 7-day course of doxycycline as sexually transmitted infection (STI) prophylaxis (unlicensed use) at his prior visit to the sexual health clinic.

On initial presentation, the patient was not febrile, tachycardic, tachypnoeic, hypotensive or hypoxic on room air. Physical examination revealed widespread vesicular rash (>100 lesions) (figure 1), papular rash with white exudate in the oral cavity, cervical lymphadenopathy and tenderness in the lower abdomen and inguinal region. A cluster of five perianal papules, marked rectal tenderness and boggy prostate were noted on digital rectal examination. No penile lesions were seen. Cardiovascular and respiratory examination were unremarkable.

Investigations and differential diagnosis

Initial work up revealed mildly raised C-reactive protein of 41 mg/L with normal white cell, lymphocyte and neutrophil counts. Renal function was abnormal with a creatinine of 133 µmol/L and estimated glomerular filtration rate (eGFR) of 50 mL/min, but this was similar to baseline renal function (creatinine of 123 µmol/L and eGFR of 55 mL/min in March 2022). Liver profile and coagulation was unremarkable (table 1).

Given the patient’s rectal symptoms and contact history, Chlamydia trachomatis and Neisseria gonorrhoeae co-infections were differentials. Pharyngeal, penile and rectal swabs collected for nucleic acid amplification tests were negative for bacteria (table 2). Midstream urine sample for cytometry and culture was also negative. Serology for Treponema pallidum was positive but rapid plasma reagin was negative indicating past infection only. Rectal, skin, urine and throat swabs were PCR-positive for monkeypox.

Due to the finding of an exquisitely tender and boggy prostate on examination, the medical team requested MRI for the investigation of prostatitis and prostatic or rectal abscess. As there is limited capacity of MRI scanning over the weekend at our facility and the patient was clinically stable and receiving empirical antimicrobial therapy, MRI was performed 5 days after admission. The imaging revealed inflammation affecting the mid to lower rectum with mural thickening, surrounding oedema and extensive reactive nodal changes within the mesorectum (figures 2–4). Adjacent to a 3.1 mm defect in the lower left rectal wall, there was a 3.5 cm presumed cavity which likely represented an area of localised perforation. Reactive nodal changes were also noted along the pelvic sidewalls and inguinal regions. The prostatic appearance was within normal limits. Features suggested active proctitis with perforation and associated collection. Immediate surgical review was requested.

Treatment

On admission, the patient was initiated on oral co-amoxiclav (1.2 g three times per day) with rationale documented as rectal abscess, a decision which is not supported by local antimicrobial guidelines. Doxycycline (100 mg once a day), prescribed by his community sexual health team for prophylaxis of STIs given significant exposure history, was continued until negative pharyngeal, penile and rectal swabs for chlamydia and gonorrhoea were obtained. The use of doxycycline as STI prophylaxis is a practice which is not endorsed by the British Association for Sexual Health and HIV or the UK Health Security Agency due to concerns regarding the emergence of antimicrobial resistance (AMR).5 Aciclovir (400 mg four times per day) was briefly started to cover herpes simplex virus, but ceased after senior review as no clinical suspicion. When prostatitic involvement was suspected on the day after admission, co-amoxiclav was ceased and switched to ciprofloxacin (500 mg two times per day). Although ciprofloxacin is recommended by the National Institute for Health and Care Excellence for empirical treatment of prostatitis, local hospital guidelines instead recommend ofloxacin.6 On the same day, the decision was made to commence tecovirimat, a novel antiviral licensed for treatment of smallpox. The patient received 600 mg two times per day for a total of 14 days. After MRI pelvis revealed proctitis and localised perforation, ciprofloxacin was ceased and replaced with intravenous cefuroxime and oral metronidazole to prevent secondary bacterial infection and sepsis secondary to rectal perforation, which is in line with local guidelines. Intravenous cefuroxime and metronidazole were stepped down to oral co-amoxiclav at discharge as per local guidance.6 Analgesia including oral paracetamol and morphine sulfate liquid, laxatives and instillagel (for rectal use) were administered for symptom control. As the patient remained clinically stable, with soft abdomen and normal biochemistry, surgical intervention was not indicated.

Outcome and follow-up

The patient was isolated and reviewed by the infectious disease and surgical teams daily. After remaining clinically stable throughout admission, he was discharged home on day 9 of hospitalisation with a 7-day course of oral co-amoxiclav and instructions to self-isolate until all skin lesions resolved. Flexible sigmoidoscopy was arranged for 3 months after discharge to confirm no underlying lesion. A follow-up telephone call revealed ongoing watery diarrhoea in the 3 days since discharge. The patient was advised to stop laxatives and the diarrhoea subsequently resolved. Pain in the rectum, most severe on defecation, persisted for 2–3 weeks after discharge. The patient reported low mood due to acquiring the infection from his partner and long period of self-isolation (over 4 weeks) and was allocated a trauma therapist. Follow-up MRI pelvis at 3 months revealed persistent nodular signal abnormality within the mesorectum abutting the lower rectum, corresponding to site of previous perforation. No drainable collection and no features of ongoing proctitis. By 3 months, patient’s symptoms had completely resolved with no rectal pain and regular bowel movements.