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Infectious diseases

Ophthalmology Letters 18 September 2017 Free

Invasive Neisseria gonorrhoeae producing pre-septal cellulitis and keratoconjunctivitis: diagnosis and management

To the Editor: A 53-year-old woman experienced rapid onset of left eyelid pain, swelling and purulent discharge (Box 1). She presented to our eye hospital 3 days later and, on assessment, the lids were exquisitely tender, inflamed and difficult to open. There was chemosis, microcystic corneal oedema with Descemet membrane folds and moderate inflammation in the anterior chamber. Visual acuity was 6/24 in the left eye and 6/9 in the right eye. Ocular motility appeared normal. The severe inflammation and visual impairment raised concerns for post-septal orbital cellulitis. A computed tomography scan showed severe pre-septal stranding only (Box 2). A diagnosis of left pre-septal cellulitis and keratoconjunctivitis was made. She was given intravenous ceftriaxone 2 g daily, intravenous flucloxacillin 2 g four times a day, topical chloramphenicol 0.5% four times a day and regular eye washings. Microscopy found gram-negative diplococci, and polymerase chain reaction testing was positive for Neisseria gonorrhoeae. The patient denied history of sexually transmissible infection. A urine and serum sexually transmissible infection screen for N. gonorrhoeae, Chlamydia trachomatis and blood-borne viruses was negative. Treatment was rationalised to intravenous ceftriaxone 1 g daily, with a single 1 g dose of oral azithromycin. The patient had dramatic improvement over 4 days, and visual acuity improved to 6/7.5 at discharge (Box 3). One week later, the infection had predominately resolved. N. gonorrhoeae typically produces a hyperacute unilateral conjunctivitis. While the source of infection in this patient is unclear, in most cases infection is acquired via sexual transmission and reaches the conjunctiva through hand–eye auto-inoculation.1,2 The bacteria can invade the corneal epithelium, producing keratitis and corneal melting necessitating therapeutic keratoplasty.1,2 Gonococcal periorbital infection is rare, with only three cases of pre-septal cellulitis and two cases of post-septal cellulitis reported.3 All patients were successfully treated with parenteral antibiotics. N. gonorrhoeae has increasing antimicrobial resistance, creating a therapeutic challenge. The Australian Gonococcal Surveillance Programme has shown an emerging resistance to ceftriaxone — the antibiotic of choice — from 0.6% in 2006 to 5.4% in 2014.4 Azithromycin resistance occurs in 2.4% of strains.4 The Australian Therapeutic Guidelines recommend treatment of N. gonorrhoeae with parenteral ceftriaxone and oral azithromycin, for bactericidal synergy and cotreatment for C. trachomatis. When presented with pre-septal cellulitis and purulent keratoconjunctivitis, the clinician should be vigilant for a sight-threatening N. gonorrhoeae infection. Box 1 – Lid inflammation and purulent discharge at onset, 3 days before presentation Box 2 – Contrast-enhanced computed tomography scan showing significant pre-septal subcutaneous stranding (blue arrow) and severe conjunctival chemosis (yellow arrow) Box 3 – Marked improvement in periorbital inflammation after 3 days of antibiotic therapy, with residual conjunctival injection

Shivesh Varma · Nathan Wong · Jwu Jin Khong

Australian transplant recipients are at risk of chronic hepatitis E

To the Editor:Hepatitis E virus (HEV) genotype 3, the most common genotype in high income countries, is transmitted by ingestion of high risk food — including pork, deer and shellfish — and by blood transfusion. Rural residence, travel to hyperendemic areas (eg, southern Europe) and animal exposure are other risk factors.1 Both de novo and reactivated HEV infection can lead to chronic infection in up to 60% of immunocompromised patients, particularly in solid organ transplant (SOT) recipients.1,2 Moreover, 10% of patients who are chronically infected develop cirrhosis.1 In a 2013 study, the seroprevalence of HEV in Australian blood donors was 5.99%.3 Autochthonous transmission in Australia, including one patient who was a liver transplant recipient, is well documented.4,5 However, the seroprevalence and rate of chronic HEV infection in SOT recipients in Australia are unknown. We carried out a study to investigate this in an Australian tertiary hospital. In phase 1 of our study, we recruited renal transplant recipients attending routine outpatient follow-up in 2014–15; phase 2 was limited to seropositive participants from phase 1. The study was approved by the Northern Sydney Local Health District Human Research Ethics Committee (LNR/14/HAWKE/300). Seventy-four patients consented to participate in phase 1, and post-transplant stored serum was tested for HEV IgG. Six participants were HEV IgG positive. One seropositive participant died of invasive fungal infection before phase 2. The remaining five participants who were seropositive consented to phase 2, of whom one was HEV IgM positive. We tested plasma for HEV RNA and no phase 2 participants had evidence of ongoing chronic infection. While our study had limitations and we did not identify any participant with chronic infection, it is important to note that Australian SOT recipients are exposed to HEV and are at risk of chronic infection. Effective therapy for chronic HEV is available; therefore, we recommend that SOT recipients who have abnormal liver function tests should be tested for HEV RNA in blood to maximise early diagnosis. In addition, with respect to risk mitigation, previous Australian research supports a link between local pork consumption and HEV infection,4 and French guidelines suggest that SOT recipients should avoid consuming food containing pork liver.6 We believe that similar advice should be given to SOT recipients in Australia. Moreover, consideration should be given to screening donated blood in Australia for HEV RNA, as done in France and the United Kingdom, with experts calling for such screening across the European Union.7,8 The Australian Red Cross Blood Service has undertaken a large scale screening study of donated plasma for HEV RNA to estimate the local risk of HEV transmission by blood transfusion, with results currently pending.9

James P Newcombe · Stella McGinn · Bruce Wong · Archie Darbar · George Kotsiou

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