P. van Netten

Lactic acid decontamination of fresh pork carcasses: a pilot plant study

Lactic acid decontamination (LAD) was carried out in an abattoir on pork carcasses, artificially contaminated with Salmonella typhimurium in faeces suspensions. The surface contamination with S. typhimurium ranged from 1-2 log10 cfu/cm2. Before cold and hot LAD was undertaken, the inoculum was allowed to adhere to the meat surface for 20 min. Cold LAD consisted of treatment for 60 s with 2% (pH 2.3) or 5% (pH 1.9) lactic acid (LA); for hot LAD the exposure times were 30, 60, 90 and 120 s. The spray nozzle temperatures were 11 degrees C and 55 degrees C, and that of the treated meat surface 16-18 degrees C and 36-38 degrees C, respectively. Treatment with cold 2% and 5% LA for 60 s eliminated S. typhimurium from pork carcasses inoculated with ca. 1 log10 cfu/cm2, but not from those inoculated at ca. 2 log10 cfu/cm2. However, this could be achieved by hot 2% and 5% LA sprayed for 60-120 s. Also exposures of at least 30 s using these hot LA solutions eliminated S. typhimurium consistently from carcasses inoculated with ca. 1 log10 cfu/cm2. Rinsing-off contributed only marginally to contamination reduction. Application of 2% or 5% LA for 120 s led to an unacceptable deterioration of the organoleptic qualities of the meat. Addition of nicotinic and ascorbic acid as colour stabilizers to the spraying solutions reduced these changes to just acceptable levels when 2% LA was used.

The survival and growth of acid-adapted mesophilic pathogens that contaminate meat after lactic acid decontamination

Lactic acid decontamination (LAD) may adapt pathogens to lactic acid. Such organisms may have an increased resistance to acid and can contaminate meat after LAD. The survival and growth of acid adapted Campylobacter jejuni, Salmonella typhimurium. Escherichia coli O157 : H7 and Staphylococcus aureus inoculated on skin surface of still warm pork belly cuts 2 h after LAD was examined during chilled (4 °C) storage and refrigeration abuse equivalent to 12·5 °C. Lactic acid decontamination included dipping in 1, 2 or 5% lactic acid solutions at 55 °C for 120 s. Lactic acid decontamination brought sharp reductions in meat surface pH, but these recovered with time after LAD at approximately 1–1·5 pH units below that of water‐treated controls. A sharp decrease in the number of cfu of pathogens occurred on chilled 2–5% lactic acid treated pork belly cuts when the skin surface was less than pH 4·8–5·2. The reductions ranged from 0·1–0·3 log10 cfu cm−2 for E. coli O157 : H7 to over 1·7–2·4 log10 cfu cm−2 for Camp. jejuni, respectively. Increase in storage temperature from 4 to 12·5 °C reduced delayed decrease in numbers of all pathogens except Camp. jejuni by a factor of two. Deaths in Camp. jejuni at 12·5 °C slightly exceeded those at 4 °C. After the initial sharp decline, the number of cfu of mesophilic pathogens decreased gradually at a rate similar to that on water‐treated controls. Growth of all mesophilic pathogens except Camp. jejuni on 2–5% LAD meat occurred during storage at 12·5 °C when the meat surface pH exceeded 4·8–5·2, and was slower than on water‐treated controls. Low temperature and acid‐adapted E. coli O157 : H7, Salm. typhimurium and Staph. aureus, and acid adapted Camp. jejuni that contaminate skin surface after hot 2–5% LAD, did not cause an increased health hazard, although microbiota and intrinsic parameters (lactic acid content, pH) were created that could advantage their survival and growth.

Fate of low temperature and acid-adapted Yersinia enterocolitica and Listeria monocytogenes that contaminate lactic acid decontaminated meat during chill storage

Pathogens found in the environment of abattoirs may become adapted to lactic acid used to decontaminate meat. Such organisms are more acid tolerant than non‐adapted parents and can contaminate meat after lactic acid decontamination (LAD). The fate of acid‐adapted Yersinia enterocolitica and Listeria monocytogenes, inoculated on skin surface of pork bellies 2 h after LAD, was examined during chilled storage. LAD included dipping in 1%, 2% or 5% lactic acid solutions at 55°C for 120 s. LAD brought about sharp reductions in meat surface pH, but these recovered with time after LAD at ≈1–1·5 pH units below that of water‐treated controls. Growth permitting pH at 4·8–5·2 was reached after 1% LAD in less than 0·5 d (pH 4·8–5·0), 2% LAD within 1·5 d (pH 4·9–5·1) and after 5% LAD (pH 5·0–5·2) within 4 d. During the lag on 2% LAD meat Y. enterocolitica counts decreased by 0·9 log10 cfu per cm2 and on 5% LAD the reduction was more than 1·4 log10 cfu per cm2. The reductions in L. monocytogenes were about a third of those in Y. enterocolitica. On 1% LAD the counts of both pathogens did not decrease significantly. The generation times of Y. enterocolitica and L. monocytogenes on 2–5% LAD meats were by up to twofold longer than on water‐treated controls and on 1% LAD‐treated meat they were similar to those on water‐treated controls. Low temperature and acid‐adapted L. monocytogenes and Y. enterocolitica that contaminate skin surface after hot 2–5% LAD did not cause an increased health hazard, although the number of Gram‐negative spoilage organisms were drastically reduced by hot 2–5% LAD and intrinsic (lactic acid content, pH) conditions were created that may benefit the survival and the growth of acid‐adapted organisms.