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Volume 3 No 46; 20 November 2009

Pandemic influenza: UK situation at 19 November 2009



The Health Protection Agency's Weekly National Influenza Report of 19 November (week 47) [1] described the UK (and international) situation as follows:

  • Pandemic influenza activity was variable across the UK;
  • In week 46 (ending 15 November), for the second week running the weekly influenza/influenza-like illness (ILI) consultation rates were stable or decreased, although they remained above the winter baseline thresholds in all UK schemes;
  • The National Pandemic Flu Service (NPFS) continued to issue antiviral drugs to people in England but the number of assessments and antiviral collections decreased slightly over the past week;
  • Interpretation of data to produce estimates on the number of new cases continued to be subject to a considerable amount of uncertainty with the move to NPFS. HPA modelling gave an estimate of 53,000 (range 26,000 - 114,000) new cases in England in week 46. The estimated number of new cases decreased in most regions and age groups;
  • The main influenza virus circulating in the UK continued to be the pandemic (H1N1) 2009 strain, with few influenza H1 (non-pandemic), H3 and B viruses detected. Twelve of 3569 pandemic viruses tested have been confirmed to carry a mutation which confers resistance to the antiviral drug oseltamivir; three are phenotypically resistant to the drug but retain sensitivity to zanamivir (see also below);
  • The majority of pandemic influenza cases continued to be mild. The cumulative number of deaths reported due to pandemic (H1N1) 2009 in the UK was 214. There was a total of 1483 new patients hospitalised with suspected pandemic influenza in the week from 5 to 11 November, an increase from 1355 in the previous week. The hospitalisation rates have increased in the under-5-year age group but have decreased in most other age groups recently;
  • The UK pandemic influenza vaccination programme continues in people at high risk for severe disease and in health-care workers. For further information see the Department of Health website;
  • According to the European Centre for Disease Prevention and Control (ECDC), by 16 November, 7051 deaths due to pandemic influenza had been reported globally; according to the World Health Organisation (13 November), in Europe, and in central and eastern Asia, influenza transmission continues to intensify. Pandemic influenza activity may have peaked in parts of the USA; however Canada and Mexico continue to experience significant influenza activity. A number of African countries are reporting their first confirmed cases since the first wave.

Vaccination programme extended to all under-fives

The Department of Health's swine flu vaccination programme was extended to offer all children over six months and under five protection against the virus [2].

HPA statement on possible transmission of oseltamivir-resistant influenza

The HPA is working with Public Health Service of Wales to investigate a number of possible cases of person-to-person transmission of oseltamivir-resistant swine flu, including among patients in a hospital ward in Wales [3].

References

1. HPA. Weekly National Influenza Report: week 47 (19 November2009, PDF 402 KB), HPA website: www.hpa.org.uk/swineflu/surveillance&epidemiology.
2. "Children over six months and under five years will be offered vaccine", DH news distribution service, 19 November 2009.
3. HPA press release, 20 November 2009.

HSE consultation on artificial optical radiation regulations

The Health and Safety Executive has published a consultation document outlining how it plans to transpose EU directive 2006/25/EC on the protection of workers from hazardous sources of artificial optical radiation [1] into UK law.

The directive aims to achieve harmonised controls across the EU on the exposures to intense sources of artificial optical radiation in the workplace. Particularly UV radiation and powerful laser beams, which can harm the eyes and skin. It lays down statutory exposure limit values and includes provisions relating to the determination of exposure and the assessment of risks, the avoidance or reduction of risks, worker information and training and health surveillance.

The proposed control of artificial optical radiation at work regulations would not cover x-rays, gamma rays, electromagnetic fields or natural sources such as sunlight, but would have implications for a diverse range of processes – ranging from ultraviolet A and C fluorescence in scientific research and engineering, and phototherapy in medicine and opthalmoscopy, to glass furnaces and forgery detection processes used in the retail industry – involving ultraviolet, visible and infrared parts of the spectrum.

A report on the implications of the directive in the draft stage was prepared by the then National Radiological Protection Board (now the HPA Radiation Protection Division) in 2003 [2]. The Radiation protection Division was contracted by the European Commission to produce the draft non-binding guide to the Directive [3], which was aimed at small and medium sized enterprises.

The HPA Radiation Protection Division (RPD) runs a one-day course on the provisions of the directive and the non-binding guide. The guide gives practical advice on the actions to be taken, lists trivial sources for which there is no need for further actions (eg display screen equipment, photocopiers, indicator LEDs, photographic flashlamps) and includes worked examples and other guidance on the risk assessment process for other potentially hazardous sources [4].

The UK has until 27 April 2010 to implement the requirements of the directive and HSE aims to introduce the regulations before that date. Interested parties and businesses are invited to comment on the draft regulations by February 5, 2010.

References

1. A consultative document on legislation to implement the Physical Agents (Artificial Optical Radiation) Directive (cd 227), Health and Safety Executive. Downloadable at: http://www.hse.gov.uk/consult/condocs/cd227.htm.
2. NRPB (2003). Occupational exposure to optical radiation in the context of a possible EU proposal for a directive on optical radiation. Downloadable at: http://www.hpa.org.uk/webc/HPAwebFile/HPAweb_C/1194947312809.
3. See HPA website: http://www.hpa.org.uk/webw/HPAweb&HPAwebStandard/HPAweb_C/1204286177417?p=115893460776
4.“Non-ionising radiation - artificial optical radiation - a guide to your duties” (Training course direct involving the authors of the EU Artificial Optical Radiation Guide). HPA website: Home › Events & Professional Training › Radiation Training & Events › Radiation Training Courses ›Non-ionising radiation - Artificial Optical Radiation.

Two cases of infant botulism associated with consumption of honey

In two (unlinked) cases of the rare disease infant botulism recently reported in the UK, there was a history of the infants having been fed honey, which is known to be a risk factor for the disease. In one of the cases, C. botulinum was found to be present in the honey fed to the affected infant before onset of illness, the toxin type being the same as that isolated from the affected infant. Since 1996 jars or containers of commercial honey sold in the UK have contained a health warning stating that honey should not be fed to infants less than one year old. It is evident, however, that this advice is not always being heeded.

Background

Infant botulism is a rare disease in the UK with only 10 reported cases from 1976 to the present time. The disease is a toxico-infection due to the ingestion of Clostridium botulinum spores and their germination, multiplication and production of botulinum neurotoxin (BoNT) in the colon of infants less than one year of age [1]. BoNT is absorbed in the intestine and binds to peripheral cholinergic synapses resulting in flaccid paralysis. Whilst there is a spectrum of disease severity, to date, all reported cases in the UK have required hospitalisation. Early signs of infant botulism may include lethargy, listlessness, poor feeding and a decrease in the number of bowel movements with increasing generalised weakness over several days being the feature that brings the infant to medical attention. Clinically symptoms range from mild hypotonia to severe flaccid paralysis with an absence of cranial reflexes. Typically an infant will present with an expressionless face, a feeble cry, poor head control, loss of suck and gag reflex and as being afebrile: characteristically there is usually a history of constipation. The differential diagnosis of infant botulism includes sepsis, meningitis, myasthenia gravis and Guillain Barré syndrome. However, due to its rarity infant botulism may not be considered initially as a diagnosis.

Specific therapy for infant botulism is now available in the form of human derived botulinum immunoglobulin ("baby-BIG") which can be obtained from the Californian Infant Botulism Treatment and Prevention programme [2]. To be effective, treatment needs to be initiated early in the onset of disease in order to stop further progression by blocking binding of toxin at the neuromuscular junction. Infants with botulism also require meticulous supportive care particularly with regard to respiration and nutrition. Antimicrobial therapy is not usually advised and may results in lysis of C. botulinum cells releasing more BoNT in the intestinal lumen. The recovery period may be long as it requires resprouting of nerve terminals. The use of baby-BIG has been shown to improve recovery of infants and reduce the length of hospital stay [3].

The source of C. botulinum is unknown in most cases of infant botulism. The consumption of honey is the only dietary reservoir to have been definitively linked to cases by both laboratory and epidemiological evidence [1]. C. botulinum spores are naturally found in soil and dust and infant botulism is also thought to be acquired by swallowing spores from the environment. Perturbation of the immature gut flora induced by changing infant breast to formula milk, through weaning or via antimicrobial therapy, is thought to provide a window of opportunity for ingested spores to germinate and multiply.

Two UK cases in 2009

In the second half of 2009 there have been two unlinked cases of infant botulism in the UK. The first case occurred in an eight-week-old female infant admitted to a London hospital with a history of poor feeding, profound constipation and floppiness. The infant was transferred to the paediatric intensive care unit (PICU) at a specialist children's hospital on 10 August 2009 where she was treated empirically for meningitis. The infant continued to deteriorate and underwent respiratory arrest requiring mechanical ventilation. The infant had been fed a mixture of breast milk and formula milk and had also consumed honey. Rectal wash-out and a one-day cooked meat enrichment broth containing rectal wash out were received by the HPA Foodborne Pathogens Reference Unit (FPRU), at the HPA Centre for Infections, on 11 August for testing and C. botulinum type A neurotoxin genes were detected by PCR in the enrichment broth on the same day with C. botulinum type A being isolated subsequently. C. botulinum type A toxin was detected in the infant's rectal wash-out specimen the following day by mouse bioassay. Two types of powdered formula milk (from the same manufacturer) and commercial honey consumed by the infant were examined for the presence of C. botulinum but none was detected in any of the samples. The infant received baby-BIG and began to show gradual signs of clinical progress such as improved limb movement, regaining swallowing reflex by the end of August. The infant was subsequently discharged to a local hospital before being sufficiently recovered to return home.

The second case was the first infant botulism case to be reported in Scotland. An eight-week-old male infant was admitted to PICU at a specialist children's hospital in Edinburgh on the 19 September 2009, after attending a local hospital in Fife the previous day with a 4-5 day history of poor feeding and generalised weakness but no clinical record of constipation. On admission the infant was breathing normally but pupils were sluggish and differential diagnoses of myopathy, encephalopathy, sepsis or metabolic disorder were considered. The infant was treated empirically with antibiotics for 4-5 days and despite initial improvement he gradually but progressively deteriorated over the next four weeks, eventually requiring invasive ventilatory support. An electroencephalogram was normal, a tensilon test ruled out a myasthenic process, and an initial electromyogram (EMG) was not suggestive of botulism. However, a second EMG performed when the infant was in PICU was strongly suggestive of botulism and a clinical diagnosis of infant botulism was, therefore, considered. A faecal specimen was received for testing at the FPRU on 29 October; C. botulinum type A neurotoxin genes were detected by PCR on the following day and the organism subsequently isolated. A decision not to treat the infant with baby-BIG was taken following advice from clinicians in California regarding the date of onset symptoms and the recent clinical improvement in the infant. The infant had been exclusively breast fed but honey had been administered to the infant on it's dummy. The original container of honey was sent to the FPRU for testing and C. botulinum type A, ie the same type as isolated from the infant, was detected in enrichment cultures by PCR. Further work is currently underway to isolate the organism from the honey and type both the infant and honey strains to determine if they are the same. This is the first occasion in the UK on which C. botulinum of the same type as that isolated from a case of infant botulism has been isolated from honey known to have been consumed by the case.

Whilst infant botulism is an uncommon illness in the UK, there have been four reported cases in the last two years compared with a total of six cases between 1976 and 2007. It is intriguing that all four cases developed symptoms in either August or September. Two of the cases, one in 2007 and the other in 2009 were diagnosed at the same specialist childrens's hospital in London and thus the second case may represent increased awareness of disease. The specialist children's hospital in Edinburgh also has previous experience of dealing with infant botulism as one of the 2007 cases was transferred from PICU in London to Edinburgh as the infant's parents were in the process of relocating to Scotland when the infant became ill.

References

1. Arnon SS (2004). Infant botulism. In: Textbook of Paediatric Diseases (chapter 153), pp1758-1766, (eds: Feigin MD, Cherry JD, Demmler GJ and Kaplan SL) 5 th ed. Philadelphia, Pa, Saunders.
2. http://www.infantbotulism.org.
3. Fox K, Keet CA and Strober JB (2005). Recent advances in infant botulism, Pediatr Neurol. 32: 149-154.