Whether beer is best avoided by patients receiving treatment with MOAI has been subject to some debate (Tailor et al., 1993; Izquierdo-Pulido et al., 1996b; Shulman et al., 1997). Although the consensus is to minimise the risk by susceptible individuals not consuming beer, it is clear that this view is driven by the unpredictability of biogenic amine concentration in some beers. For example, in the study of Tailor et al. (1994) canned and bottled beers were universally low in tyramine (0-3.2mgl *), whereas four of 49 draught beers had elevated 'dangerous' levels of tyramine (26-133mgl *). Similarly, a survey (see Table 8.4) of biogenic amines in 195 European canned or bottled beers showed the widest fluctuations in the 'indicator' amines -tyramine, histamine and cadaverine (Izquierdo-Pulido et al., 1996b). The fermentation style is also important with the more complex, less controlled approaches (Iambic, gueze, kriek and Wiessbier) tending toward elevated levels of these amines. Collectively, these observations are in keeping with the view that elevated levels of these amines reflect either unwanted or intentional microbial contamination or complexity. However, it is bacteria not yeast that have been implicated in the formation of biogenic amines through the decarboxylation of amino acids present in wort and beer. The presence of lactic acid bacteria, specifically Pediococcus (Izquierdo-Pulido et al., 1996a) and Lactobacillus species (Donhauser et al., 1993), has been shown to correlate with elevated levels of tyramine and, to a lesser extent, other biogenic amines. However, it remains unclear whether poor hygiene in the brewery or in trade dispense is the major factor in determining the level of biogenic amines in beer. Although Donhauser et al. (1993) implicate wort spoilage in the brewery, it might be argued that the more potent threat originates from poor or infrequent line cleaning and associated unhygienic operations in trade outlets - a view, which is in agreement with the survey of Tailor et al. (1993) that elevated levels of tyramine in beer were exclusive to draught products.
188.8.131.52 Pathogens. It is generally accepted that pathogenic bacteria cannot grow in beer. Indeed, the whole issue is somewhat academic, as food pathogens have not been associated with either raw materials or the brewing process. Two studies (Bunker, 1955; Sheth et al., 1988) have inoculated beer with low (c. 200ml 1 and high (2-20 x 106ml *) concentrations of enteric Gram-negative pathogens (Shigella, Salmonella and Escherichia coli). Irrespective of challenge, all three pathogens were unable to grow in beer, and over time died. Sheth et al. (1988), showed that for E. coli, an initial loading of 2 x 106ml 1 was reduced to 5cfuml 1 over 48 hours. Bunker (1955) reported similar kill kinetics for E. coli when four beers were challenged with 200cfuml 1. However when challenged with 20 x 106ml \ E. coli could still be detected after 14, and in two cases 21, days.
The consensus is that a combination of low pH and ethanol protect alcoholic beverages from threat by pathogenic bacteria. Indeed, in the experiments reported by Sheth et al. (1998), E. coli was killed within 4 hours of inoculation into wine. However, the 'success' of pathogenic isolates of E. coli (e.g. 0157:H7) has been attributed to their acid resistance such that survival at pH 3 has been reported (Jordan et al., 1999). Fortunately, the presence of ethanol (5% v/v) overcomes the resistance of pathogenic E. coli to low pH resulting in rapid cell death.
Although not viewed as being a threat to the brewing industry, it is perhaps wise to maintain a 'watching brief on developments in the wider area of pathogens in food safety. The appearance of more robust pathogens (e.g. acid resistant E. coli 0157:H7) together with the well documented ability of E. coli to survive in beer suggest that it would be foolhardy to ignore a possible future threat to product safety.
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