684 Modern Food Microbiology
10–200 µm in diameter, and the bradyzoites are smaller in size than the more active tachyzoites.
Bradyzoites may persist in the body for the lifetime of an individual, but if the cysts are mechanically
broken or break down under immunosuppression, bradyzoites are freed and begin to multiply rapidly
as tachyzoites and thus bring on another active infection. The development of a cyst wall around
bradyzoites coincides with the development of permanent host immunity. The cysts are normally
intracellular in host cells. T. gondii infections are asymptomatic in the vast majority of human cases
(immunocompetents), but in congenital infections and in immunocompromised hosts, such as patients
with acquired immunodeficiency syndrome (AIDS), the disease is much more severe. In pregnant
mothers with newly contracted toxoplasmosis, the tachyzoites are reported to cross the placenta about
45% of the time.
Unlike certain other intestinal protozoal diseases, toxoplasmosis cannot be diagnosed by demonstrating oocysts in stools, as these forms occur only in cat feces. Various serological methods are widely
used to diagnose acute infection. A fourfold rise in immunoglobulin G (IgG) antibody titer between
acute and convalescent serum specimens is indicative of acute infection. A more rapid confirmation
of acute infection can be made by the detection of immunoglobulin M (IgM) antibodies, which appear
during the first week of infection and peak during the second to fourth weeks.
80 Among other diagnostic methods are the methylene blue dye test, indirect hemagglutination, indirect immunofluorescence,
and immunoelectrophoresis. With the indirect hemagglutination test, antibody titers above 1:256 are
generally indicative of active infection.
Although toxoplasma infection induces protective immunity, it is, in part, cell mediated. In many
bacterial infections where phagocytes ingest the cells, their internal granules release enzymes that
destroy the bacteria. During this process, aerobic respiration gives way to anaerobic glycolysis, which
results in the formation of lactic acid and the consequent lowering of pH. The latter contributes to
the destruction of the ingested bacteria along with the production of superoxide, which, at the acid
pH, yields singlet oxygen (
1 O 2 ). The latter is quite toxic. T. gondii tachyzoites are unusual in that
once they are phagocytosed, the production of H 2 O 2 is not triggered, and neither do the acid pH
nor the singlet oxygen events occur. Also, they reside in vacuoles of phagocytes that do not fuse
with preexisting secondary lysosomes. Thus, it appears that their mode of pathogenicity involves
an alteration of phagocyte membranes in such a way that they fail to fuse with other endocytic
or biosynthetic organelles, in addition to the other events noted.
55 T cells play a role in immunity
to T. gondii, and this has been demonstrated by use of nude rats, where T cells from T. gondiiinfected normal rats conferred to nude rats the ability to resist infection by a highly virulent strain of
T. gondii.
29
Antimicrobial therapy for toxoplasmosis consists of sulfonamides, pyrimethamine, pyrimethamine
plus clindamycin, or fluconazole. Pyrimethamine is a folic acid antagonist that inhibits dihydrofolate
reductase.
Distribution of T. gondii
Toxoplasmosis is regarded as a universal infection, with the incidence being higher in the tropics
and lower in colder climes. It is estimated that 50% of Americans have circulating antibodies to T.
gondii by the time of adulthood.
80 In a study of U.S. Army recruits, 13% were positive for toxoplasma
antibodies.
36 In the United States, it is estimated that over 3000 babies are infected each year with T.
gondii because their mothers acquire the infection during pregnancy.
33 Fetal infections occur in 17%
of first-trimester and 65% of third-trimester cases, with the first-trimester cases being more severe.
80
Among 3000 pregnant women tested for T. gondii antibodies, 32.8% were positive.
58
10–200 µm in diameter, and the bradyzoites are smaller in size than the more active tachyzoites.
Bradyzoites may persist in the body for the lifetime of an individual, but if the cysts are mechanically
broken or break down under immunosuppression, bradyzoites are freed and begin to multiply rapidly
as tachyzoites and thus bring on another active infection. The development of a cyst wall around
bradyzoites coincides with the development of permanent host immunity. The cysts are normally
intracellular in host cells. T. gondii infections are asymptomatic in the vast majority of human cases
(immunocompetents), but in congenital infections and in immunocompromised hosts, such as patients
with acquired immunodeficiency syndrome (AIDS), the disease is much more severe. In pregnant
mothers with newly contracted toxoplasmosis, the tachyzoites are reported to cross the placenta about
45% of the time.
Unlike certain other intestinal protozoal diseases, toxoplasmosis cannot be diagnosed by demonstrating oocysts in stools, as these forms occur only in cat feces. Various serological methods are widely
used to diagnose acute infection. A fourfold rise in immunoglobulin G (IgG) antibody titer between
acute and convalescent serum specimens is indicative of acute infection. A more rapid confirmation
of acute infection can be made by the detection of immunoglobulin M (IgM) antibodies, which appear
during the first week of infection and peak during the second to fourth weeks.
80 Among other diagnostic methods are the methylene blue dye test, indirect hemagglutination, indirect immunofluorescence,
and immunoelectrophoresis. With the indirect hemagglutination test, antibody titers above 1:256 are
generally indicative of active infection.
Although toxoplasma infection induces protective immunity, it is, in part, cell mediated. In many
bacterial infections where phagocytes ingest the cells, their internal granules release enzymes that
destroy the bacteria. During this process, aerobic respiration gives way to anaerobic glycolysis, which
results in the formation of lactic acid and the consequent lowering of pH. The latter contributes to
the destruction of the ingested bacteria along with the production of superoxide, which, at the acid
pH, yields singlet oxygen (
1 O 2 ). The latter is quite toxic. T. gondii tachyzoites are unusual in that
once they are phagocytosed, the production of H 2 O 2 is not triggered, and neither do the acid pH
nor the singlet oxygen events occur. Also, they reside in vacuoles of phagocytes that do not fuse
with preexisting secondary lysosomes. Thus, it appears that their mode of pathogenicity involves
an alteration of phagocyte membranes in such a way that they fail to fuse with other endocytic
or biosynthetic organelles, in addition to the other events noted.
55 T cells play a role in immunity
to T. gondii, and this has been demonstrated by use of nude rats, where T cells from T. gondiiinfected normal rats conferred to nude rats the ability to resist infection by a highly virulent strain of
T. gondii.
29
Antimicrobial therapy for toxoplasmosis consists of sulfonamides, pyrimethamine, pyrimethamine
plus clindamycin, or fluconazole. Pyrimethamine is a folic acid antagonist that inhibits dihydrofolate
reductase.
Distribution of T. gondii
Toxoplasmosis is regarded as a universal infection, with the incidence being higher in the tropics
and lower in colder climes. It is estimated that 50% of Americans have circulating antibodies to T.
gondii by the time of adulthood.
80 In a study of U.S. Army recruits, 13% were positive for toxoplasma
antibodies.
36 In the United States, it is estimated that over 3000 babies are infected each year with T.
gondii because their mothers acquire the infection during pregnancy.
33 Fetal infections occur in 17%
of first-trimester and 65% of third-trimester cases, with the first-trimester cases being more severe.
80
Among 3000 pregnant women tested for T. gondii antibodies, 32.8% were positive.
58