by attacking cell membranes it produces local tissue disruption in the
wound and its absorption into the circulation causes a serious toxaemia. It
does not however have any role in the food poisoning syndrome.
C. perfringenstype C which producesaandbtoxins causes enteritis
necroticans, a more severe, but far more rare, enteric disease in which the
btoxin damages the intestinal mucosa causing necrosis. Illness is pre-
ventable by active immunization against thebtoxin. Outbreaks were
reported in Germany in 1946 and 1949, but it is nowadays particularly
associated with Papua New Guinea where it is known as pigbel. Symp-
toms of abdominal pain and bloody diarrhoea develop several days after
a high-protein meal, often pork consumed on festive occasions. Low
levels of intestinal proteases are a predisposing factor in victims. This
could arise from a poor diet low in protein, as with the European
outbreaks after the Second World War, and may be compounded in
Papua New Guinea by protease inhibitors consumed with other foods in
the diet such as sweet potatoes.
C. perfringenstype A ranks belowSalmonellaas a cause of outbreaks
of bacterial food poisoning in the UK. Total cases numbered less than
one-tenth the number of salmonella cases between 1980 and 2005.
Reported outbreaks ofC. perfringensfood poisoning have declined in
recent years from an average total of 28 per year in the period 1992-1998
to an average of 9 p.a. in the period 1999-2005. The total numbers of
people made ill in these outbreaks are shown in Figure 7.5. These do not
include sporadic cases which the Infectious Intestinal Disease Study in
England recognised as being ‘‘quite common’’.
0100200300400500600700800Numbers ill in
general outbreaks1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005
YearClostridium perfringens food poisoning in England and WalesFigure 7.5 Clostridium perfringensfood poisoning in England and Wales
210 Bacterial Agents of Foodborne Illness