Cheese and disease

Cheese and disease

IJM cheeses
According to an eyewitness account, the pre-Christmas queue for the Stockbridge branch of cheesemonger IJ Mellis stretched out of the shop and down the street. Cheese, with crackers and dried fruit, has become a popular alternative to Christmas pudding in family dinners. The gnome wonders if there’s a belief that cheese is a solution to our annual season of over-indulgence. True: the enormous variety of specialty cheeses provides a decent choice of tasty nibbles to round off the Christmas feast. But it is not all plain sailing with water biscuits. Cheese has its association with a range of diseases.

Cheese and infection

Granada cheeses
Reliance on bacterial culture for the form, taste and texture of cheese introduces a potential risk of infection from cheese-borne species like Listeria monocytogenes, Salmonella enterica and Shigella-like toxin producing Escherichia coli. These infections are uncommon in the overall scheme of things. But changes in industrial cheese production in the 1970s and 1980s were associated with an increase in Listeria infections, generally attributed to low acidity, high moisture content (soft) cheese [1]. Since then there have been improvements in food standards, reducing the risk to cheese consumers. A recent American study showed that there were differences in the pattern of cheese-associated infection outbreaks between unpasteurised and pasteurised cheeses [2]. Mexican style soft white cheese (queso fresco) was the commonest unpasteurised source, while cheese made with pasteurised milk was a commoner source of infection when poor food hygiene practice resulted in contamination after cheese production. Some countries, such as Canada have introduced a short heating step to reduce pathogenic bacteria and spoilage organisms without losing the species that contribute taste and texture [3]. While some disease-causing bacteria can theoretically survive cheese manufacture, it appears that others including Campylobacter, Clostridium and Yersinia species do not last the entire production process which may explain their absence from cheese associated infectious outbreaks.

Cheese and non-infectious diseases
Cheese has been blamed for various ailments in some circles. But the news is not all bad. Cheese is one of the full fat dairy foods associated with better cardiac health in the long-running Luxembourg study [4]. For those interested in a possible explanation the French, who currently hold the world record for consumption of blue-veined cheese, may be reducing their risk of arteriosclerosis by consumption of an inhibitor of Chlamydia pneumoniae propagation [5]. More good news: the risk of pancreatic cancer does not appear to be influenced by consumption of any full fat dairy product including cheese [6]. But before the cheese lovers reach for another cracker, there are rumours that cheese consumption may be linked with a small increase in Parkinson’s Disease risk [7]. Clearly, this is a possibility that needs lengthy discussion during the final stages of dinner. Try talking with a mouthful of oatcake crumbs.

Cheese spoilage
Starter cultures for cheese production are usually pure lactic acid bacteria. Some strains are poor acid producers and are known as non-starter lactic acid bacteria. These may be important to the taste and texture of a finished cheese, but can contribute to increased acid, excess gas production or unpleasant flavour, and thus spoil the cheese. Foodborne infection attributed to cheese and cheese spoilage are not the same thing. But the two phenomena overlap, at least in the sense that spoilage can indicate poor hygiene during the production process. Cheese spoilage is important in its own right as a contributor to loss of taste, texture and consequent wastage. Greater reliance on refrigeration of milk before use in cheese production contributes to the presence of cold-tolerant bacteria that can cause discolouring of the cheese surface, unpleasant smells, a bitter or rancid taste. Pseudomonas species in particular can discolour cheese as in the blue mozzarella event of 2010 [8], interfere with ripening and increase the moisture content so that it becomes runny. Coliform bacteria (Escherichia, Klebsiella and other species) can cause an unpleasant or even putrid smell, or excessive gas. Could you pass the cheese, please?

TEL cheese

References
1 Lopez-Valladares G et al. 2014. Human isolates of Listeria monocytogenes in Sweden during half a century (1958-2010). Epidemiol Infect 142: 2251-60.
2 Gould LH et al. 2014. Outbreaks attributed to cheese: differences between outbreaks caused by unpasteurized and pasteurized dairy products, United States, 1998-2011. Foodborne Pathog Dis 11:545-51.
3 D’Amico DJ. 2014. Adventitious microbes can affect the safety and quality of cheese. Microbe 9: 99-104.
4 Crichton GE, Alkerwi A. 2014. Dairy food intake is positively associated with cardiovascular health: findings from observation of cardiovascular risk frequency in Luxembourg study. 34: 1036-44.
5 Petyaev IM et al. 2013. Roquefort cheese proteins inhibit Chlamydia pneumoniae propagation and LPS-inducted leukocyte migration. ScienceWorld J 140591.
6 Genkinger et al. 2014. Dairy products and pancreatic cancer risk: pooled analysis of 14 cohort studies. Ann Oncol 25: 1106-15.
7 Jiang W et al. 2014. Dairy food intake and risk of Parkinson’s Disease: a dose response meta-analysis of prospective cohort studies. Eur J Epid 29:613-9.
8 Nogarol C et al. 2013 Continue reading

New STEC in Europe

New STEC in Europe

E.coli O104:H4,  Germany

LATEST NEWS:

  • 49 deaths, 852 HUS cases, > 4000 infections, fewer new cases

PREVIOUSLY:

  • first take on the genetic origins of the new STEC in Europe
  • interest in bean sprouts persists following latest food test results
  • bean sprouts notconsumed by all victims of European STEC outbreak (details from Robert Koch Institute, translated courtesy CIDRAP). Further epidemiological survey analysis neededmap of HUS case distribution
  • de novo assembly of genome sequence announced by Beijing Genomics Institute collaboration with University Medical Centre Hamburg-Eppendorf
  • 27 deaths, 757 cases of HUS,  2142 infected, new cases diminishing. HUS peaked 21-MAY-11
  • EU agriculture ministers consider 150m Euro compensation bill for European farmers, though damage to industry estimated at twice that sum
  • Australian beef ruled out as cause of Japanese outbreak
  • first round of STEC environmental tests negative from farm near Hamburg, Germany. Other results pending.
  • reports that outbreak has been traced organic bean shoots from Germany
  • update on the new STEC in Europe from the Centers for Disease Control
  •  

E.coli O157:H7 on SMAC agar

Reports of a European cluster of haemorrhagic uraemic syndrome (HUS) caused a stir in late May. European surveillance groups reported that this was caused by a verotoxin-bearing E.coli strain with the designation O 104:H4 that also had entero-aggregating and antibiotic resistance features. This combination of virulence and resistance is a genuinely new and potentially worrying development. Other notable differences with this infection are the predominance of adult female cases,  subtle neurological complications and a longer than usual incubation period of 7-12 days. Australia is now on the lookout for cases closer to home, though none have been confirmed so far.

 

Non-STEC E.coli on SMAC agar

So far over 2000 cases, over 600 of which have had HUS and 22 deaths have been attributed to the infection in 11 countries, which was initially blamed on Spanish cucumbers and other vegetables including tomatoes and lettuce. More recent claims have been made that bean sprouts were the likely source. Further afield in Japan, Australian beef was blamed for similar infections following cooking in Korean barbecues though the MicroGnome has yet to learn of any convincing evidence.

Meanwhile, additional details come to light as a result of more discriminating laboratory tests, food investigations and heightened surveillance. The Centers for Disease Control reported infection in US citizens and the European CDC has started to regularly update the earlier data.

  1. The process of outbreak investigation is a complex one, requiring the assembly of different types of data from different sources gathered according to differing time lines. The preliminary stage gathers data from clinical cases and pathology laboratories, molecular biology tests, epidemiological surveillance and environmental health investigations. The overlap from these three main sources of data is critical to understanding the disease event. We refer to this as level 1 evidence, or congruence.
  2. When a similarly well-defined pattern of patient-microorganism-disease occurs at another time or location and not by simple extension of the original event, the evidence for causation strengthens to level 2, or consistency.
  3. Level 3 evidence  concerns the decomposition of the patient-microorganism-disease process into is constituent parts at progressive levels of biological organisation i.e. molecular, cellular, tissue biology, organs & organ systems, whole patient, patient groups and the localisation of specific aspects of that process in order to establish a mechanistic understanding of disease outcomes. This level of evidence for causation is known as cumulative dissonance.
  4. The final level of evidence is curtailment. This concerns the use of specific interventions targeting one or more potential vulnerable stages in the progressive escalation of an infectious disease process, and highlights the aetiological significance of practical objectives to physicians and public health authorities.

The current data on the E.coli O104:H4 case cluster consists of strong but incomplete level 1 evidence, possible level 2 and 3, but a lack of level 4 evidence. That does not mean that curtailment of a potentially fatal food-borne infection has to wait until  development of a full description of E.coli O104:H4’s actions at every level of biological organisation.

Clearly, identification of a specific contaminated food as the critical element in the genesis of this outbreak should lead to prompt introduction of control measures. Subsequent disappearance of the infection after these measures have been introduced establishes the food as a sufficient, but not as a necessary cause. Only when the evidence for causality has been strengthened by the missing items from levels 1, 2 and 3 will it be possible to fully understand the sequence of events that conspired to end in these sad consequences.

Further information

MicroGnome, 5-JUN-11


Wedding fever

Wedding fever: a cautionary tale

No this is not another blog about a happy British couple who tied the knot recently, the thousands of people who camped out in the streets to see a bit of pomp & circumstance, or the frenzied attempts of a swarm of journalists saying something their colleagues hadn’t already said. Nor is it an allusion to the early clinical presentation of honeymoon cystitis. This is a sad and sorry tale of how what should have been a happy event for many becomes a torrid affair for a few.

A wedding breakfast was held in Louisiana in May, 1960. Shortly after the event a series of guests needed medical attention. By the time the Health Board began their investigation, 20 people were under treatment for typhoid. A further 11 cases were discovered, bringing the total to 31 wedding guests. Investigations implicated chicken salad sandwiches, prepared by one particular food handler. As there were 88 guests, the attack rate was 35% overall, and was as high as 50% of those 15yr and younger. Full account via PubMED.

There’ a catalogue of biological agents awaiting the unsuspecting wedding guest, most of which are food-borne and pack either an emetic or diarrhoeagenic punch, or both.

Revellers take care, wedding planners beware:

From a party-pooping MicroGnome, 29-APR-11