486 Chapter 28
England, 100,000 turkeys died of unknown
causes, and the disease was called Turkey X
disease. After much work, the contaminant
was found to have originated from peanut
meal from Brazil. The organisms responsible
for producing the toxic compounds were
identifi ed as A. fl avus. Later, A. parasiticus
was also found to be able to produce the
toxin. Recently, A. nomius has also been
added to the list of cultures producing the
afl atoxin. The mold can grow between 7.5 ° C
and 43 ° C, with optimal temperatures at 24 °
to 28 ° C. The minimal water activity for
growth is 0.82 and the optimal is 0.99. The
pH range for growth is from 2 to near 11.
Production of the toxins generally parallels
the growth of the organisms. Research data
from the author ’ s laboratory suggested that
sporulation of the cultures seems to be a pre-
requisite for toxin production. In 1 to 3 days
of growth, the organism can produce the
toxins. The primary toxins are B 1 , B 2 , G 1 , and
G 2. B and G indicate that the toxins fl uoresce
blue or green under ultraviolet light, respec-
tively. When cows consume B 1 and B 2 toxins,
they can modify the toxins and excrete the
toxins as M 1 and M 2 in milk.
Spores of these molds are ubiquitous; the
organisms have been found to grow in rice,
sorghum, peanut, corn, wheat, and soybean
crops, as well as animal feed. Human food
shown to support growth and toxin produc-
tion of this mold include peanuts, peanut
butter, pecans, beans, dried fruits, fi sh, and
even cheese. Because the toxins are carcino-
genic, they are under strict government scru-
tiny, since the Delaney Clause of 1958
prohibits the presence of carcinogenic com-
pounds in U.S. foods. Currently, the allowed
limit is 20 ppb for animal feed and all foods,
except milk, which has an action level of 0.5
afl atoxin M 1. Although no direct food - related
afl atoxin cases have been reported in the
United States, there are concerns that
afl atoxin can affect the immune systems
of patients. Afl atoxin fatality cases were
reported in Southeast Asia when people con-intoxication due to the heat - stable toxins in
the food. Several years ago in the United
States, imported canned mushrooms caused
a great deal of concern. No live S. aureus
were found in the canned mushrooms, yet the
preformed enterotoxins in the mushrooms
caused many cases of food intoxication.
The value of monitoring live S. aureus is
to ascertain the hygienic quality of the food
and the potential of the live organisms to
grow and produce the enterotoxins in foods.
Detection of staphylococcal enterotoxins has
been a subject of much research in the past
35 years. Monkeys, cats, and other animals
have been used to detect toxins, but using
these animals is not practical for routine
testing. Immunological methods such as
ELISA test, Latex agglutination tests, and gel
diffusion tests are used to detect the toxin in
foods. The commercial kits can detect entero-
toxin A, B, C, D, and/or E. either singularly
or in combination.
Fortunately, the organism is not a good
competitor compared with other spoilage
organisms (e.g., Pseudomonas ) in raw foods
such as ground beef and fi sh. However, in the
absence of competitors, such as in salty food
(e.g., ham) or processed foods (e.g., pro-
cessed cheese), the organism can grow and
produce the heat - stable toxins. They can
produce enough toxins in 4 hours at room
temperature to cause a problem. That is the
reason why this intoxication is called picnic
food poisoning because during a picnic, food
may be left nonrefrigerated for hours before
consumption by partygoers. It is, therefore,
essential to use proper refrigeration (4 ° C) to
prevent S. aureus from growing in the food
or by keeping hot food hot (60 ° C). This
advice is applicable to all subsequent discus-
sions on food intoxication and infections.
Aspergillus
Aspergillus fl avus and A. parasiticus are
molds that can produce a group of carcino-
genic toxins called afl atoxins. In 1960 in