The Ecology and Evolution of Toxoplasma gondii

Grace Mahaffey

Toxoplasma gondii in an intracellular obligate protozoan that can parasitize in an

unusually wide host range, which includes almost all warm-blooded animals, causing a

disease called toxoplasmosis. Toxoplasma has several different routes of transmission

within and between different host species.4 It is estimated that in the worldwide around
30-50% of the human population is infected with Toxoplasma gondii, although infection
rates differ greatly from region to region, this is greatly due to different customs and
practices within the separate cultures; in the United States around 60 million people,
about 22.5% of the population are infected, whereas in other areas that number is
estimated to be as high as 95%.1,2 However, few of these cases present with symptoms
indicative of T. gondii infection; typical immune systems are capable of fighting of the
pathogen well enough so that the host is asymptomatic, albit if one is
immunocompromised or even pregnant infection can result in serious consequences.3
In humans, symptoms can range from flu-like symptoms to ocular issues. While
treatment is not usually needed for healthy individuals several different medications can
be prescribed depending on the severity and means of infection.

While the only known definitive host of Toxoplasma gondii is felidae family (cats),

the range of intermediate hosts it incompaces is extraordinary, including most likely all
the warm
blooded animals (mammals and bird) and humans.4 T. gondii is only able to
sexually reproduce within cats and then when transmitted to another host, it will
reproduce solely asexually.5 This process of transmission can occur in several different
ways, typically depending on which intermediate host it is infecting. As aforementioned
the host range is incredibly large however, for the purpose of this paper I will focus on

the two main intermediate hosts that Toxoplasma infects: rodents, particularly mice and
humans and the interaction among the three.
Toxoplasma gondii begins its life when a member of the cat family is infected,
this occurs when one consumes an infected mouse laden with the parasites tissue
cysts. Once Toxoplasma completes its passage through the stomach, it infects the
epithelial cells of the small intestines; note that T. gondii is an intracellular obligate
parasite.6 Thereupon invasion of the intestinal cells, the parasite undergoes sexual
development and reproduction, producing millions of infective oocysts. After the rupture
of the cells the infective particles will be released into the intestinal lumen and then
excreted in the feces.6 The oocysts can then spread to anything contaminated with the
feces. Extremely resilient forms of the parasite have been seen to remain alive and
infective in cold and dry climates for months.7
Once transmitted to an intermediate host T. gondii is considered to have three
stages of infection. The first stage is know as tachyzoite stage of rapid infection in
which sporozoites freed from the oocysts via the dissolution of the cyst wall by the
proteolytic enzymes of the stomach, infect the epithelial cells of the intestine. Inside the
cells the sporozoites differentiate into tachyzoites, which proliferate quickly. They will
replicate until the host cell dies and ruptures, releasing and spreading the tachyzoites
through the bloodstream to all the organs and tissues in the body, including the brain.
By this point, the immune system begins to mount a serious response to the infection,
and under this pressure the tachyzoites will convert to bradyzoites, which marks the
beginning of the second stage of infection. Here the bradyzoites will be semi-dormant

and divide slowly. A cyst wall is formed around cluster of these bradyzoites, this is
known as a tissue cyst; tissue cysts, commonly occur in the brain, eyes and striated
muscle tissues will develop 7-10 days after initial infection.8 The final stage, often known
as the oocyst environmental stage, is that which produces chronic infection. The cysts
can be maintained for the lifetime of the host, however continued presence seems to be
due to the cyclical process of the cysts bursting and re-encysting.8
In mice, infection typically occurs when the rodent comes into direct contact with
infected feces. The aforementioned asexual process will occur within the mouse. 9
Additionally, there seems to be a strong selective pressure for T. gondii to increase the
rate of transmission between the intermediate reservoir and the definitive host, so that
sexual reproduction can occur and the life cycle can be completed.9 This occurs in such
a way that permanent behavioral changes often occur in the mouse, such that there is a
notable reduction in their innate dislike of cats, thusly making it easier for the them to be
prayed upon by the cats.10 In one study, infected mice actually showed a preference
towards areas with cat odor versus the area with rabbit sent.10 Behavioral changes in
humans are still greatly unknown and seem to largely sex-dependant, however a similar
reaction to the mice has been seen in adult females, in which they have a reduced
aversion to cat urine.11
Routes of transmission in humans is much more variable than that of the rodents
and has been more extensively studied. Infection of Toxoplasma gondii can occur at
any point during its life cycle. Horizontal transmission can occur by ingesting oocysts
from the environment (cat litter) or by consuming infected meat containing either tissue

cysts or tachyzoites. Transmission may also occur via tachyzoites contaminated in

blood products, tissue transplants, or unpasteurized milk. If T. gondii is first contracted
during pregnancy, then it can be transmitted vertically to the fetus through the placenta.
As previously mentioned the majority of those who come into contact with Toxoplasma
gondii are able to mount an effective immune response, however some people are
particularly susceptible. This includes young children and immunocompromised people,
such as those with HIV/AIDS, those taking certain types of chemotherapy, or those who
have recently received an organ transplant.3 While this does not include women who
are pregnant, they should still be cautious.
The rates of infection differ so vastly from region to region most likely because of
the customs and practices of the individual cultures and not the separate environments.
While it was originally believed that separate Toxoplasma species were infecting
specific reservoirs, all known Toxoplasma strains have been shown to be Toxoplasma
gondii and derive from a single clonal lineage.12 Husbandry practices, and water
sanitation are presumably the main components in rate differences. This is exemplified
in the United States, where are rate of infection falls far below the global average and
our meats are water is all highly regulated. Information and knowledge in affected areas
may be the best way we currently have to combat this.

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