Staphylococcal Gastroenteritis 557
exponential growth phase and at the beginning of the stationary phase.
82 SEC 1 was detected after
10 hours (2 ng/ml) at an S. aureus population of 8.3 × 10
7 cfu/ml, while TNase was detected after
5 hours with a cell count of 1.3 × 10
4 cfu/ml. SEC 2 and TNase first appeared after 7 hours with a
cell population of 10
7 cfu/ml.
82 With both enterotoxins, TNase production ceased before enterotoxin
production.
In regard to quantities of enterotoxins produced, levels of 375 and 60 µg/ml or more of SEB
and SEC, respectively, have been recorded.
91 In a protein hydrolysate medium, up to 500 µg/ml\l
[Author: Please check the unit “µg/ml/l” here]of SEB may be produced.
14 Employing a sac culture
assay method, 289 ng/ml of SEA were produced by S. haemolyticus, 213 ng/ml of SEC by S. aureus,
and 779 ng/ml of SED, also by S. aureus.
9 Chitin has been shown to enhance SEA production. With
0.5% crude chitin in BIH broth, SEA production increased by around 52%.
4 SEA thermostability was
also increased, but cell growth was apparently not affected. The production of SEH was favored by
aeration and controlled pH with about 275 ng/ml having been produced in a fermentor at pH 7.0 with
aeration at 300 ml/minute.
102 Around 5 µg/ml of SEG and SEI have been reported.
76
SEB production in unbuffered media has been found to be repressed by excess glucose in the
medium.
74 Streptomycin, actinomycin D, acriflavine, Tween 80, and other compounds have been
found to inhibit SEB synthesis in broth.
38 SEB production is inhibited by 2-deoxyglucose, and the
inhibition is not restored by glucose, indicating that this toxin, at least, is not under catabolite control.
55
While actinomycin D has been shown to inhibit SEB synthesis in strain S-6, the inhibition occurred
about 1 hour after cellular synthesis ceased. The latter was immediately and completely inhibited. A
possible conclusion from this finding is that the messenger RNA (mRNA) responsible for enterotoxin
synthesis is more stable than that for cellular synthesis.
62
The lowest number of cells of S. aureus required to produce the minimum level of enterotoxin
considered necessary to cause the gastroenteritis syndrome in humans (1 ng/g) appears to differ for
substrates and for the particular enterotoxin. Detectable SEA has been found with as few as ∼10
4
cfu/g.
48 In milk, SEA and SED were detected with counts of 10
7 but not below this level.
77 Employing
a strain of S. aureus that produces SEA, SEB, and SED, SEB and SED were detected when the count
reached 6 × 10
6 /ml and the enterotoxin level was 1 ng/ml, while SEA at a level of 4 ng/ml was
detected with a count of 3 × 10
7 cfu/ml.
78 In imitation cheese with pH of 5.56–5.90 and a w of 0.94–
0.97, enterotoxins were first detected at the following counts: SEA at 4 × 10
6 /g; SEC at 1 × 10
8 ; SED
at 3 × 10
6 ; SEE at 5 × 10
6 ; and SEC and SEE at 3 × 10
6 /g.
12 In precooked bacon, SEA was produced
by strain A100 with cells >10
6 /g.
95 In meat products and vanilla custard, SEA was produced with
≥log 10 7.2 cells/g, but in certain vegetable products SEA production was delayed and detected only
when numbers of cells were ≥log 10 8.9/g.
80 In the latter study, no SE could be detected in spinach
and french beans after 72 hours at 22
◦ C when cell numbers were log 10 6.7–8.7/g. All staphylococcal
enterotoxins are resistant to pepsin (see exception in previous section).
Mode of Action
All staphylococcal enterotoxins, along with the toxic shock syndrome toxin (TSST), are bacterial
superantigens (pyrogenic toxin superantigens—PTSags) relative to in vivo antigen recognition in
contrast to conventional antigens. With the latter, a CD4 T cell facilitates contact between T cell
antigen receptors and major histocompatibility complex (MHC) class II molecules. Staphylococcal
superantigens bind directly to T cell receptor β chains without processing. Once bound to MHC
class II molecules, SEs stimulate helper T cells to produce cytokines such as the interleukins (IL),
exponential growth phase and at the beginning of the stationary phase.
82 SEC 1 was detected after
10 hours (2 ng/ml) at an S. aureus population of 8.3 × 10
7 cfu/ml, while TNase was detected after
5 hours with a cell count of 1.3 × 10
4 cfu/ml. SEC 2 and TNase first appeared after 7 hours with a
cell population of 10
7 cfu/ml.
82 With both enterotoxins, TNase production ceased before enterotoxin
production.
In regard to quantities of enterotoxins produced, levels of 375 and 60 µg/ml or more of SEB
and SEC, respectively, have been recorded.
91 In a protein hydrolysate medium, up to 500 µg/ml\l
[Author: Please check the unit “µg/ml/l” here]of SEB may be produced.
14 Employing a sac culture
assay method, 289 ng/ml of SEA were produced by S. haemolyticus, 213 ng/ml of SEC by S. aureus,
and 779 ng/ml of SED, also by S. aureus.
9 Chitin has been shown to enhance SEA production. With
0.5% crude chitin in BIH broth, SEA production increased by around 52%.
4 SEA thermostability was
also increased, but cell growth was apparently not affected. The production of SEH was favored by
aeration and controlled pH with about 275 ng/ml having been produced in a fermentor at pH 7.0 with
aeration at 300 ml/minute.
102 Around 5 µg/ml of SEG and SEI have been reported.
76
SEB production in unbuffered media has been found to be repressed by excess glucose in the
medium.
74 Streptomycin, actinomycin D, acriflavine, Tween 80, and other compounds have been
found to inhibit SEB synthesis in broth.
38 SEB production is inhibited by 2-deoxyglucose, and the
inhibition is not restored by glucose, indicating that this toxin, at least, is not under catabolite control.
55
While actinomycin D has been shown to inhibit SEB synthesis in strain S-6, the inhibition occurred
about 1 hour after cellular synthesis ceased. The latter was immediately and completely inhibited. A
possible conclusion from this finding is that the messenger RNA (mRNA) responsible for enterotoxin
synthesis is more stable than that for cellular synthesis.
62
The lowest number of cells of S. aureus required to produce the minimum level of enterotoxin
considered necessary to cause the gastroenteritis syndrome in humans (1 ng/g) appears to differ for
substrates and for the particular enterotoxin. Detectable SEA has been found with as few as ∼10
4
cfu/g.
48 In milk, SEA and SED were detected with counts of 10
7 but not below this level.
77 Employing
a strain of S. aureus that produces SEA, SEB, and SED, SEB and SED were detected when the count
reached 6 × 10
6 /ml and the enterotoxin level was 1 ng/ml, while SEA at a level of 4 ng/ml was
detected with a count of 3 × 10
7 cfu/ml.
78 In imitation cheese with pH of 5.56–5.90 and a w of 0.94–
0.97, enterotoxins were first detected at the following counts: SEA at 4 × 10
6 /g; SEC at 1 × 10
8 ; SED
at 3 × 10
6 ; SEE at 5 × 10
6 ; and SEC and SEE at 3 × 10
6 /g.
12 In precooked bacon, SEA was produced
by strain A100 with cells >10
6 /g.
95 In meat products and vanilla custard, SEA was produced with
≥log 10 7.2 cells/g, but in certain vegetable products SEA production was delayed and detected only
when numbers of cells were ≥log 10 8.9/g.
80 In the latter study, no SE could be detected in spinach
and french beans after 72 hours at 22
◦ C when cell numbers were log 10 6.7–8.7/g. All staphylococcal
enterotoxins are resistant to pepsin (see exception in previous section).
Mode of Action
All staphylococcal enterotoxins, along with the toxic shock syndrome toxin (TSST), are bacterial
superantigens (pyrogenic toxin superantigens—PTSags) relative to in vivo antigen recognition in
contrast to conventional antigens. With the latter, a CD4 T cell facilitates contact between T cell
antigen receptors and major histocompatibility complex (MHC) class II molecules. Staphylococcal
superantigens bind directly to T cell receptor β chains without processing. Once bound to MHC
class II molecules, SEs stimulate helper T cells to produce cytokines such as the interleukins (IL),