Foodborne Animal Parasites 683
of stools from patients. Later symptoms consist of pronounced abdominal pain, fever, severe diarrhea,
vomiting, and lumbago, and somewhat resemble those of shigellosis. Weight loss is common, and all
patients have heme-positive stools. According to Jackson,
48 fulminating amebiasis with ulceration of
the colon and toxicity occur in 6–11% of cases, especially in women stressed by pregnancy or nursing.
Masses of amebae and mucus may form in the colon, leading to intestinal obstruction. Amebiasis
may last in some individuals for many years, in contrast to giardiasis, where disease symptoms rarely
exceed 3 months.
3 Under some conditions, amebiasis may result from a synergistic relationship with
certain intestinal bacteria.
Amebiasis is diagnosed by demonstrating trophozoites and cysts in stools or mucosal scrapings.
Immunological methods such as indirect hemagglutination, indirect immunofluorescence, latex agglutination, and ELISA are useful. The sensitivity of these tests is high with extraintestinal amebiasis,
and a titer of 1:64 by indirect hemagglutination is considered significant.
This syndrome can be treated with the amebicidal drugs metronidazole and chloroquine. Resistance
is mediated by cell immunity. Lymphocytes from patients in the presence of E. histolytica antigens have
been shown to produce γ -interferon, which activates macrophages that display amebicidal properties.
90
Toxoplasmosis
This disease is caused by Toxoplasma gondii, a coccidian protozoan that is an obligate intracellular
parasite. The generic name is based on the characteristic shape of the ameba stage of the protozoan
(Gr. toxo, “arc”). It was first isolated in 1908 from an African rodent, the gondi—hence, its species
name. In most instances, the ingestion of T. gondii oocysts causes no symptoms in humans, or the
infection is self-limiting. In these cases, the organism encysts and becomes latent. However, when
the immunocompetent state is abated, life-threatening toxoplasmosis results from the breaking out
(recrudescence) of the latent infection.
Domestic and wild cats are the only definitive hosts for the intestinal or sexual phase of this organism,
making them the primary sources of human toxoplasmosis. Normally, the disease is transmitted from
cat to cat, but virtually all vertebrate animals are susceptible to the oocysts shed by cats. As few as
100 oocysts can produce clinical toxoplasmosis in humans, and the oocysts can survive over a year in
warm, moist environments.
33 Pigs are the major animal food source to humans.
Symptoms, Diagnosis, and Treatment
In most individuals, toxoplasmosis is symptomless, but when symptoms occur, they consist of fever
with rash, headache, muscle aches and pain, and swelling of the lymph nodes. The muscle pain, which
is rather severe, may last up to a month or more. At times, some of the symptoms mimic infectious
mononucleosis. The incubation period in adults is 6–10 days while in infants it is congenital.
The disease is initiated upon the ingestion of oocysts (if from cat feces), which pass to the intestine
where digestive enzymes affect the release of the eight motile sporozoites. Oocysts are ovoid shaped,
measure 10–12 µm in diameter, and possess a thick wall. Sporozoites are crescent shaped and measure
about 3 × 7 µm. They cannot survive for long outside animal host tissues, nor can they survive the
activities of the stomach. When freed in the intestines, these forms pass through intestinal walls
and multiply rapidly in many other parts of the body, giving rise to clinical symptoms. The most
rapidly multiplying forms are designated tachyzoites (Gr. tachy, “rapid”), and in immunocompetent
individuals, they eventually give rise to clusters that are surrounded by a protective wall. This is a
tissue cyst, and the protozoa inside are designated bradyzoites (Gr. bradus, “slow”). These cysts are
of stools from patients. Later symptoms consist of pronounced abdominal pain, fever, severe diarrhea,
vomiting, and lumbago, and somewhat resemble those of shigellosis. Weight loss is common, and all
patients have heme-positive stools. According to Jackson,
48 fulminating amebiasis with ulceration of
the colon and toxicity occur in 6–11% of cases, especially in women stressed by pregnancy or nursing.
Masses of amebae and mucus may form in the colon, leading to intestinal obstruction. Amebiasis
may last in some individuals for many years, in contrast to giardiasis, where disease symptoms rarely
exceed 3 months.
3 Under some conditions, amebiasis may result from a synergistic relationship with
certain intestinal bacteria.
Amebiasis is diagnosed by demonstrating trophozoites and cysts in stools or mucosal scrapings.
Immunological methods such as indirect hemagglutination, indirect immunofluorescence, latex agglutination, and ELISA are useful. The sensitivity of these tests is high with extraintestinal amebiasis,
and a titer of 1:64 by indirect hemagglutination is considered significant.
This syndrome can be treated with the amebicidal drugs metronidazole and chloroquine. Resistance
is mediated by cell immunity. Lymphocytes from patients in the presence of E. histolytica antigens have
been shown to produce γ -interferon, which activates macrophages that display amebicidal properties.
90
Toxoplasmosis
This disease is caused by Toxoplasma gondii, a coccidian protozoan that is an obligate intracellular
parasite. The generic name is based on the characteristic shape of the ameba stage of the protozoan
(Gr. toxo, “arc”). It was first isolated in 1908 from an African rodent, the gondi—hence, its species
name. In most instances, the ingestion of T. gondii oocysts causes no symptoms in humans, or the
infection is self-limiting. In these cases, the organism encysts and becomes latent. However, when
the immunocompetent state is abated, life-threatening toxoplasmosis results from the breaking out
(recrudescence) of the latent infection.
Domestic and wild cats are the only definitive hosts for the intestinal or sexual phase of this organism,
making them the primary sources of human toxoplasmosis. Normally, the disease is transmitted from
cat to cat, but virtually all vertebrate animals are susceptible to the oocysts shed by cats. As few as
100 oocysts can produce clinical toxoplasmosis in humans, and the oocysts can survive over a year in
warm, moist environments.
33 Pigs are the major animal food source to humans.
Symptoms, Diagnosis, and Treatment
In most individuals, toxoplasmosis is symptomless, but when symptoms occur, they consist of fever
with rash, headache, muscle aches and pain, and swelling of the lymph nodes. The muscle pain, which
is rather severe, may last up to a month or more. At times, some of the symptoms mimic infectious
mononucleosis. The incubation period in adults is 6–10 days while in infants it is congenital.
The disease is initiated upon the ingestion of oocysts (if from cat feces), which pass to the intestine
where digestive enzymes affect the release of the eight motile sporozoites. Oocysts are ovoid shaped,
measure 10–12 µm in diameter, and possess a thick wall. Sporozoites are crescent shaped and measure
about 3 × 7 µm. They cannot survive for long outside animal host tissues, nor can they survive the
activities of the stomach. When freed in the intestines, these forms pass through intestinal walls
and multiply rapidly in many other parts of the body, giving rise to clinical symptoms. The most
rapidly multiplying forms are designated tachyzoites (Gr. tachy, “rapid”), and in immunocompetent
individuals, they eventually give rise to clusters that are surrounded by a protective wall. This is a
tissue cyst, and the protozoa inside are designated bradyzoites (Gr. bradus, “slow”). These cysts are