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Final Issue: Volume 16 Number 51

Published on: 21 December 2006

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News Archives 26 January 2006

Last updated: Volume 16, No 4 (PDF file, 331 KB)

Archives | News Archives 2006: Page 1| News 26 January 2006

News Archives: | 2006 | 2005 | 2004 | 2003

 

A case of diphtheria caused by toxigenic Corynebacterium ulcerans

 

On 17 January 2006 a diphtheria toxin producing strain of Corynebacterium ulcerans was confirmed in a woman from Cheshire. This was confirmed by the Health Protection Agency Respiratory and Systemic Infection Laboratory (RSIL), Centre for Infections, (WHO Collaborating Centre for Diphtheria) from throat swabs and clinical samples.

The woman had been recently hospitalised with a two day history of malaise, sore throat and a change in the sound of her voice. She also reported feeling that her throat was closing, causing difficulty in breathing. On examination she had a swollen neck and post pharyngeal area, cervical lymphadenopathy, and a sero-sanguinous nasal discharge. She had started angiotensin-converting enzyme (ACE) Inhibitors in the previous six months and treatment with antihistamines and steroids for a presumed diagnosis of angioneurotic oedema.

The patient’s condition deteriorated over the next two days and a tracheostomy was carried out. During the procedure a grayish-white membrane was seen covering the pharynx and this, linked to an elevated white blood cell count and other features of the clinical presentation, raised the possibility of diphtheria.

Based on the clinical diagnosis, antibiotics and antitoxin were given and the consultant in communicable disease control (CCDC) convened an outbreak control meeting. Given the strong probability that this could be a toxigenic strain of diphtheria it was decided to instigate control measures while laboratory confirmation was being sought. Close hospital and community contacts were identified and nose and throat swabs taken. Close contacts were offered both oral erythromycin to clear carriage, and booster Td/IPV vaccine (where appropriate).

Efforts to trace the source of the infection are continuing. There is no history of foreign travel and swabs from close contacts have proved negative. Samples of unpasteurised milk and swabs from domestic animals are being taken on the farm where the case had recently stayed with her family. The patient remains unwell in the intensive care unit.

UK Epidemiology of C. Ulcerans
C. ulcerans produces exactly the same toxin as C. diphtheriae and infection may present as full-blown diphtheria, as seen in this case. During the period 2000 to 2005, 18 cases of toxigenic
C. ulcerans have been documented in the UK. There was one death in an elderly female in 2000, due to toxigenic C. ulcerans. Although exposure to raw dairy products is the most widely recognised risk factor, most cases, including the fatal case, have had no association with a farming community or through the consumption of raw dairy products. From 2002 to date, the organism has also been isolated from several domestic cats and one dog with respiratory discharges within the United Kingdom and other European countries suggesting a possible novel reservoir for this organism. Molecular typing studies on a large collection of isolates have revealed a predominant genotype circulating within Europe, with strains isolated from SOME domestic cats exhibiting the same type as observed among strains causing human infections (1).


References
1. De Zoysa A, Hawkey PM, Engler K, George R, Mann G, Reilly W, et al. Characterisation of toxigenic Corynebacterium ulcerans from humans and domestic cats. J Clin Microbiol; 2005; 43:4377-81.

Variant Creutzfeldt-Jakob disease in the United Kingdom and elsewhere: situation at the end of 2005

A cumulative total of 159 cases of variant Creutzfeldt-Jakob disease (vCJD) had been reported in the UK by the end of December 2005, of whom 153 had died. Outside the UK, the numbers remain small with 15 cases in France, four in the Republic of Ireland, two in the United States, and one each in Canada, Italy, Japan, the Netherlands, Portugal, Saudi Arabia, and Spain (1).

Recent data published by the National CJD surveillance unit shows that, in the United Kingdom (UK), a total of five deaths from vCJD were reported in 2005, four less than the previous year’s total of nine (2). Results from modelling the incidence of deaths indicate that the current epidemic wave reached a peak of 28 deaths in 2000, and has since declined (figure). Extrapolating this trend gives an estimate of two deaths in the next 12 months (95% prediction interval 0 to 5). With six cases alive at the end of 2005, however, a prediction of two deaths is likely to be an underestimate.

Figure vCJD deaths by year and fitted quadratic model for the incidence trend

Figure vCJD deaths by year and fitted quadratic model for the incidence trend

 

It is important to note that, to date, all vCJD cases have been methionine homozygote at codon 129 of the prion protein gene. Preclinical vCJD infection has, however, been reported in a heterozygous patient after blood transfusion from a donor who subsequently developed vCJD (3). Although the initial epidemic wave is now in decline, it is possible that there will be further epidemics of cases in other genetic groups. There is also the possibility of continuing person-to-person transmission through certain forms of healthcare (for instance, in relation to surgery, blood transfusion, or treatment with plasma products). It is essential, therefore, to maintain and promote active surveillance of CJD to investigate these possibilities.

 

References

1. The European and Allied Countries Collaborative Study Group of CJD (EUROCJD) [online].The European and allied countries collaborative study group of cjd (eurocjd). [cited 26 Janaury 2006]. Available at: <http://www.eurocjd.ed.ac.uk/EUROINDEX.htm>.

2.The National CJD surveillance unit [online]. Incidence Of variant Creutzfeldt-Jakob Disease onsets and deaths in the UK - January 1994 – December 2005. Available at:
<http://www.cjd.ed.ac.uk/vcjdqdec05.htm>.

3. Peden AH, Head MW, Ritchie DL, Bell JE, Ironside JW. Preclinical vCJD after blood transfusion in a PRNP codon 129 heterozygous patient. Lancet 2004; 364:527-9.