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Blood (Intracellular) and Other Tissue Protozoa 89

a mild flulike illness or in many cases causes no outward that infection is always followed by lifelong persistence
manifestations of illness occur at all. After the first few of cysts and by a positive serology test for antibodies
weeks of infection have passed, the parasite rarely causes against the toxoplasmosis organism.
any harm or symptoms in healthy adults. However, those
with a weakened immune system, and those infected with Symptoms
HIV or that are pregnant may become seriously ill, with
sometimes fatal results. This parasite may also cause en- For healthy individuals an infection may only be evidenced
cephalitis (inflammation of the lining of the brain), which by lymphadenopathy. Many immunocompromised pa-
includes a number of sensory organs, including the eyes tients such as victims of AIDS may show neurological in-
and ears along with the heart and liver. volvement with confusion, neurological deficits, weakness,
seizures, and decreased levels of consciousness. In addi-
Morphology tion, elevated temperatures may be experienced.

Toxoplasma gondii varies in its morphology during the Life Cycle
developmental cycle. Forms of the parasites that may be
ingested with food contaminated by the organism often While these developments were taking place, there were
appears as a curved banana shape or a crescent shape. The increasing numbers of records of toxoplasma infections
parasite enters the body through the mucus membranes of in virtually all species of mammals and includes many
the intestinal and pharyngeal structures. In humans and in- species of birds. But the nature of the parasite remained
termediate hosts these parasites multiply during the acute obscure until the life cycle had been fully defined. The life
phase of infection by cell division and during this rapidly cycle of T. gondii is a very complex one and it was not un-
dividing stage of development the protozoa are known til 1970 when scientists from the United States and sev-
variously as tachyzoites, trophozoites, or endozoites. Early in eral European countries managed to independently show
the infection, the tachyzoites are actively multiplying and that this parasite was a stage in the life cycle that occurred
may be seen as intracellular inclusions within many tissues as a common intestinal coccidian of cats (Figure 4-10). In
of the body. These forms, 4 to 7 μm long and 2 to 3 μm the simplest form of the life cycle, cats become infected
wide, of the pathogen contain a nucleus toward the bot- when they swallowed oocysts, a resistant infective stage
tom half of the cells that are distributed by the lymph sys- containing sporozoites. These forms invade and multiply
tem and the circulatory system to the entire body. There in intestinal cells, where sexual stages are produced, fertil-
the infected cells may lyse (be destroyed) and move to ization occurs, and more infective oocysts are produced.
nearby cells that become infected. This process eventually However, there is an alternate life cycle. If the
results in damage to the tissue as necrosis with surround- oocysts are swallowed by a nonfeline host, such as a mouse,
ing inflammation. It is possible that permanent damage multiplication occurs in the intestinal cells. But instead of
may occur in vital organs that contain skeletal muscle. sexual stages being produced, a disseminated infection
If intracellular cysts are formed in skeletal muscle, they follows during which resistant stages form in the brain and
may occur in the diaphragm, heart muscle, and the brain, the muscle. The life cycle in the mouse halts at the asexual
affecting the tissue functions of these organs. stage, but if a mouse is eaten by a cat or another mammal
In human infections, most frequently if not solely, that preys on mice, the life cycle reverts to its basic sexual
nonintestinal forms will be found. If the infected organ- pattern. Humans are infected in the same way as are mice if
ism forms antibodies to the pathogen, the free and intra- they consume oocysts. But they can also become infected
cellular forms of the parasite disappear and, as a means by eating any kind of meat containing the resistant forms
of protection, are replaced by tissue cysts with a diameter of the organism. It is therefore not surprising that the life
of 100 to 300 μm. These cysts are walled off and each cycle remained a secret until William McPhee Hutchison,
can contain several thousand bradyzoites that are also working in Glasgow in 1965, showed that the infectious
known as cystozoites. This condition causes clinically agent was passed in the feces of cats (Cox, 2002).
inconspicuous infection and can persist in the host for At the time Hutchison thought that it was transmit-
years because the cyst formation protects the parasites ted along with a nematode worm, as are some other flag-
from attack by the immune system. It is highly probable ellates and nematodes in fowl. Hutchison then identified