E.coli outbreak resistant to antibiotics

Scientists have identified ‘an entirely new super-toxic’ strain of E.coli which has infected more than 1,600 people worldwide, including seven in the UK.

Chinese and German researchers have been working round the clock to identify the strain, which has struck people in 10 countries and killed at least 16.

A statement from the Beijing Genomics Institute, which has been working on sequencing the strain, said it contained several genes that were resistant to antibiotics.

Analysis shows the bacterium is an enterohemorrhagic E.coli (EHEC) O104 strain, but is a ‘new serotype’ – not previously involved in any E.coli outbreaks.

More than 90 per cent of the bacterium is the same as a virulent strain that causes serious diarrhoea, but the new strain has ‘also acquired specific sequences’, the statement said.

These are similar to those involved in hemorrhagic colitis and haemolytic uraemic syndrome (HUS) – a deadly complication of E.coli.

Earlier today, Hilde Kruse, a food safety expert at the World Health Organisation (WHO), told the Associated Press the strain was ‘unique’ and ‘has never been isolated from patients before’.

E.coli bacteria
E.coli bacteria

She said the new strain had ‘various characteristics that make it more virulent and toxin-producing’, although it is not uncommon for bacteria to continually evolve and swap genes.

The most severe E.coli cases are usually seen in children and the elderly, but all age groups are currently affected.

So far, seven people in the UK have been affected by the strain, including three Britons and four German nationals.

According to the Health Protection Agency (HPA), all the UK cases caught the infection in Germany, where the outbreak began, with three now being treated for HUS.

It has issued a warning urging people travelling to Germany to avoid eating raw tomatoes, cucumbers and leafy salad, including lettuce, while experts try to find the source of the outbreak.

Anyone returning from Germany with an illness, including bloody diarrhoea, is also urged to seek medical attention.

Victims can require hospital treatment because HUS affects the blood, kidneys and, in severe cases, the central nervous system.

Dr Dilys Morgan, head of the gastrointestinal, emerging and zoonotic infections department at the HPA, said: ‘The HPA continues to actively monitor the situation very carefully and we are working with the authorities in Germany and with our counterparts across Europe as to the cause of the outbreak.

E.coli bacteria
E.coli bacteria

‘We have alerted health professionals to the situation and advised them to urgently investigate and report suspected cases with a travel history to Germany.’

Cases of HUS and EHEC have continued to rise in Germany in recent days.

Nine patients in Germany have died of HUS and another six of EHEC. One person has also died in Sweden, bringing the total number of deaths to 16, according to WHO.

There are unconfirmed reports of at least one more death.

Many more patients are in hospital, with several needing intensive care, including dialysis.

All cases except two are among people who had recently visited northern Germany. In one case, the person had contact with a visitor from northern Germany.

Professor Brendan Wren, from the London School of Hygiene and Tropical Medicine, said EHEC was usually caught from the consumption of meat products, particularly beef.

EHEC is found in the gut microflora of humans and livestock, he added.

‘Improper water/sewage disposal and slurry procedures can contaminate fresh produce, which isn’t cooked, so therefore does not kill adherent bacteria.’

Prof Wren said whole genome DNA sequencing could identify what sparked the outbreak, but ‘as in many food borne disease outbreaks, the real culprit may never be identified and the epidemic just fades away’.

Anthony Hilton, reader in microbiology at Aston University, said: ‘The pattern of infection in this outbreak is unusual in the proportion of adults presenting with HUS, which is normally observed in children, and the bias towards females.

‘If the current strain is indeed a novel virulent type, it will be important to determine if this is simply surface contamination of vegetables or if the organism has developed a mechanism of intracellular invasion and persistence, as that will greatly influence the effectiveness of the simple washing of vegetables intended to be eaten raw as a means of reducing the risk of infection.’

Douglas Noble, lecturer in the centre for primary care and public health at Queen Mary, University of London, said: ‘This is obviously a very serious outbreak of a rare strain of E.coli with the exact source of contamination remaining undetermined.

‘The UK has in recent years been very strong in its response to such threats to human health, and this episode particularly highlights the need for a joined-up public health response across Europe.’

Russia has extended its ban on vegetables to the entire European Union – a move described as disproportionate by EU officials.

Meanwhile, Spain’s prime minister has demanded an explanation from Germany for suggesting Spain’s produce was a possible source of the outbreak.

High fat cholesterol diet damages brain

Research from the Laboratory of Psychiatry and Experimental Alzheimers Research at the Medical University Innsbruck (Austria) demonstrated that chronic high fat cholesterol diet in rats exhibited pathologies similar to Alzheimer’s disease.

The results were published in Molecular Cellular Neuroscience with lead author Dr. Christian Humpel. The study was co-authored by PhD students, Celine Ullrich and Michael Pirchl, from the same Laboratory.

Alzheimer’s disease is a severe neurodegenerative disorder of the brain that is characterized by loss of memory and cognitive decline. The majority of Alzheimer’s disease cases are sporadic (risk age >60 years), and only <2.5% have a genetic disposition. It is estimated that in 2050, approximately 80 million people will suffer from Alzheimer's disease worldwide. The major pathological hallmarks of Alzheimer's disease are extracellular aggregates (plaques) of the small peptide beta-amyloid, hyperphosphorylation of the protein tau and subsequent formation of intracellular neurofibrillary tangles, degeneration of neurons secreting the neurotransmitter acetylcholine, inflammation, and cerebrovascular dysfunction. [caption id="attachment_1797" align="alignnone" width="300" caption="Alzheimer\'s"]Alzheimer's[/caption]

The causes for Alzheimer’s disease are not known, but dysregulation of amyloid-precursor protein expression and beta-amyloid clearance is hypothesized (beta-amyloid cascade). Alternatively, a pathological cascade of events may trigger hyper-phosphorylation of tau, putting the tau-hypothesis into the center. A third hypothesis suggests that chronic long-lasting mild cerebrovascular damage, including inflammatory processes and oxidative stress, may cause Alzheimer’s disease. It has been suggested that Alzheimer’s disease starts 20-30 years before first symptoms appear and recent studies have shown, that high cholesterol levels are linked to the pathology of this disease.

The aim of the study led by Humpel was to study the effects of hypercholesterolemia in adult rats. Male 6 months old Sprague Dawley rats were fed with normal food (controls) or with a special 5% cholesterol-enriched diet (hypercholesterolemia). After 5 months animals were tested for behavioral impairments and pathological markers similar to those found in the brains of patients with Alzheimer’s disease. The results showed that chronic hypercholesterolemia caused memory impairment, cholinergic dysfunction, inflammation, enhanced cortical beta-amyloid and tau and induced microbleedings, all indications, which resemble an Alzheimer’s disease-like pathology.

Thus the data are in line with earlier studies showing that high fat lipids, including cholesterol, may participate in the development of sporadic Alzheimer’s disease. However, since Alzheimer’s disease is a complex heterogenous disease, these data do not allow the conclusion that cholesterol alone is responsible for the disease. It can be speculated that chronic mild cerebrovascular damage caused and potentiated by different vascular risk factors (including cholesterol) may contribute to these pathologies. It needs to be determined in future studies how mild chronic microvascular bleedings, silent strokes and mild blood-brain barrier damage over decades may play a role in the development of this disease. Indeed several data (Ladecola, Nat.Rev.Neurosci. 5, 347-360, 2004) support the view that Alzheimer’s disease can be considered as a vascular disease and that a dysfunctional clearance of beta-amyloid from brain to blood and vice versa may be a secondary important step in the cascade of initiation of the disease.

This study was supported by the Austrian Science Funds (P19122-B05).