Enteric fever in a UK regional infectious diseases unit: A 10 year retrospective review
Introduction
Enteric fever is caused by infection with Salmonella enterica serotype Typhi (S. Typhi) or Salmonella enterica serotype Paratyphi (S. Paratyphi). Globally, up to 27 million infections occur annually, with over 200,000 attributable deaths per year, predominantly among children under 5 years old.1, 2 Enteric fever is endemic throughout the developing world with an especially high incidence in some parts of Southern Asia.
In the developed world, enteric fever is uncommon and predominantly a disease of returning travellers. Around 500 cases of enteric fever were reported to the UK Health Protection Agency (HPA) in 2006–2007 as part of an enhanced national surveillance programme, principally among returning travellers from the Indian Subcontinent.3 Travel to this region has been associated with a high risk of contracting enteric fever in subjects returning to the USA, France, Germany and Israel.4, 5, 6, 7 If diagnosed promptly and adequately treated, enteric fever is generally a mild illness characterised by fever and gastrointestinal symptoms. However complications including disseminated infection, relapse and death can occur, especially if appropriate antimicrobial therapy is delayed.
Fluroquinolones became the first-line antimicrobial therapy following their introduction in the 1980s, and were initially associated with rapid fever clearance times, and low rates of relapse and chronic fecal carriage.8 However, reduced ciprofloxacin sensitivity (Mean Inhibitory Concentration [MIC] of 0.125–1 mg/L) has become increasingly prevalent and is associated with high rates of clinical and microbiological failure.9, 10, 11, 12, 13 Reduced ciprofloxacin sensitivity is not detected by standard ciprofloxacin disc diffusion testing, but nalidixic acid resistance (detected by disc diffusion testing) can been used as a surrogate marker, although it does not detect all cases.12, 13 In the UK, over 90% of S. Typhi and S. Paratyphi isolates acquired in India during 2006–2007 were nalidixic acid resistant.3 Therefore, alternative antimicrobials including third generation cephalosporins and azithromycin are increasingly used as first-line therapy.14, 15, 16
We reviewed all cases of laboratory confirmed enteric fever diagnosed in University Hospitals of Leicester NHS Trust during 1999–2009. Our aims were to define the epidemiology, clinical and laboratory features, treatment and clinical outcomes of adult patients over this period.
Section snippets
Study design
We conducted a retrospective descriptive study of all microbiologically confirmed cases of enteric fever at University Hospitals Leicester NHS trust between 1st January 1999 and 30th April 2009. Our 1100 bed teaching hospital serves an ethnically diverse population; the UK National Census of 2001 showed that Leicester had the highest proportion (26%) of Indian-born residents of any local authority area in England and Wales.17 The Infectious Disease Unit manages all adult patients with confirmed
Microbiology
During the study period, 100 subjects (76 adult and 24 paediatric respectively) were identified as having culture-confirmed enteric fever; 48 of 100 [48%] S. Typhi and 52 [52%] S. Paratyphi A. There were no cases of S. Paratyphi B or C. The numbers of culture-confirmed cases per year increased over the study period, with a mean of 6 cases per year (95% confidence interval [CI], 4.4–7.4) during 1999–2003, and 13.2 (95% CI, 11.3–15.1) cases per year during 2004–2008. All 100 cases were notified
Discussion
We conducted a 10 year retrospective review of patients with enteric fever presenting to a large teaching hospital in the United Kingdom. We identified an increasing number of confirmed cases per year during the study period and, in keeping with international experience, reducing antimicrobial susceptibility to quinolones requiring adaptation of local treatment guidelines.
The annual rise in cases of enteric fever diagnosed in Leicester is consistent with national trends over the last ten years.3
Conflict of interest
None declared.
Funding source
None.
Writing assistance used
None.
Acknowledgements
We would like to recognise and thank the staff of the UHL microbiology laboratory and all the clinical staff involved in the care of the patients. In particular we thank Dr David Jenkins, Consultant microbiologist for his role in data collection.
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