S8 E4: Here Kitty Kitty: The Story of Toxoplasma gondii

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Hello, and welcome to Cause of Death

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one hundred seconds to midnight. I'm
your host, Jackie Morante. When I

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was in college, I had a
microbiology professor who swore that cats were out

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to kill us all. She told
everyone in any class that she taught that

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cats carried every disease known demand and
they were going to pass them all to

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us. Cats were single handedly going
to end humankind. Now she knew this

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wasn't true, and if you listen
to any of my past episodes, you

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know it's not true. But today
I'm going to talk about a parasite that

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cats carry that could have significant impact
on cat owners. We're going to explore

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Toxoplasma GANDHII. Let's begin with ediola
and pathology. Toxoplasma gandhii is an obligate

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parasitic protozoin that causes toxoplasmosis. The
classification of Toxoplasma Gandhii is as follows.

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It's in the class Canoida Cida,
the genus Toxoplasma, the domain Eukaryota,

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the family sarco cystiday, the order
Eucoxidiorida, and the phylum Apicomplexa. Most

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parasites will have a host animal.
This host is necessary to complete the life

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cycle. For Toxoplasma gandhii. That
host is felines. Unsporeulated ucytes are shed

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in the cat's feces. The cats
only shed the oucytes for between one and

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three weeks, but large numbers of
them may be shed. The ucytes take

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between one and five days to spoulate
in the environment. Then intermediate hosts become

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infected after ingesting infected soil, water, or plant material. Shortly after ingestion,

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the usis transform into tachyozytes, which
localize in neural and muscle tissue.

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These develop into cyst bradiozoids. Cats
become infected when they eat the intermediate hosts,

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including birds and mice. They could
also become infected after coming into contact

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with spoilated usis in the environment.
Livestock and wild game can also become infected

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after ingesting spoiulated usis in the environment. In the human host, the parasites

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form tissue cysts in skeletal muscle,
myocardium, brain, and eyes. These

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cysts may remain throughout the life of
the host. People get infected with Toxoplasma

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gondii through several routes. The most
common are eating undercooked meat of animals that

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harbor the parasite, consumption of food
or water contaminated with cat feces. This

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includes changing the litter boxes from your
favorite motor boat or through blood transfusion or

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organ transplantation, and transfer from mother
to fetus in the womb. Testing includes

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biopsy of tissue cysts, zerology,
and in the cases of transplant scental transfer

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DNA detection by PCR through amnionic fluid. Clinical presentation varies. Immunicompetent people will

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present as a symptomatic since the immune
system suppresses the infection. However, ten

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to twenty percent of patients with acute
infection may develop cervical lymphidemopathy. With or

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without flu like symptoms. My loyal
listeners know that just about everything in one

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way or another presents as flu like
symptoms. In immunocompetent people, the clinical

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course is usually not serious and is
self limited, and symptoms will resolve within

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a few weeks to a few months. In rare cases, ocular infection with

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vision loss can occur. Immunodeficient patients
often have central nervous system disease, but

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may also present with retinol choreoiditis ornuminitis. AIDS patients will experience toxoplasmic encephalitis,

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leading to intra cerebral mass lesions.
It's thought that these lesions are caused by

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a reactivation of chronic infection. Congenital
toxoplasmosis is caused by an acute primary infection

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in the mother during pregnancy. The
incidence and severity of congenital toxoplasmosis ferries by

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the trimester in which the disease was
acquired by the mother. Diagnosis of the

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mother is extremely important because treatment may
reduce the incidence of infection and reduce the

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squalae in the infant. Ocular toxoplasma
infection can be the result of congenital infection

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or infection after birth. In congenital
infection, patients often remain asymptomatic until they're

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in their twenties or thirties, before
lesions develop in the eye. Toxoplasmosis is

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one of the most common human infections
in the world. There are places where

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incident rates are higher. In France, higher rates of disease are related to

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a preference for eating raw or undercooked
meats, while in Central America higher rates

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are blamed on the abundance of stray
cats in an area where usis are likely

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to survive. Treatments target the tachyozod
stage of the parasite, but these drugs

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don't eradicate the insistent parasites in the
tissue. Perimethamine is the gold standard drug

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for treatment of toxoplasmosis. Since it
can also suppress the bone marrow of the

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patient, it's often given with folinic
acid. Pholinic acid protects the bone marrow

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from the toxic effects of parimethamine.
Sulfurdiazine or clindamyasin are often given concurrently.

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In severe cases. Treatment may last
two to four weeks. Toxoplasmosis in immunodeficient

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patients is often fatal if not treated. Treatment may last from four to six

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weeks after resolution of all clinical signs, and may be required for six months

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or longer, depending on the severity
of the disease. Relapses are known to

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occur in AIDS patients, and maintenance
therapy is often suggested until immunologic improvement can

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be achieved in response to antiviral therapy. Let's take a moment to hear from

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my sponsors, then I'll be back
to talk about some history. Charles Nicole

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and Lewis Manceau identified the parasite in
a North African rodent, the Gundi in

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nineteen oh eight. At the same
time, Alfonso Splendore found the same parasite

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in a Brazilian rabbit. Their research
was presented just days apart, and these

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three researchers depicted the parasite in very
similar ways. They described it as a

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parasite found both in side and outside
of nucleated cells, but never in red

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blood cells. It had a round
or puriform shape and was about five to

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eight micrometers in length. Splendore went
on to describe the effect it had on

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rabbits. The hypertrophied and discolored spleens, the enlarged liver and lymph noodes,

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and the ulcerated small intestine. He
wrote that the cysts were eight to forty

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micrometers in diameter. Nicole and Manceaux
described the morphology of the parasite and the

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types of tissues that were affected in
Gundhis. Both papers compare Tea Gandii to

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Leishmania. It was so close that
Nicole and Manso first proposed calling the parasite

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Leishmania gondii. They proposed the name
Toxoplasma Gandii in nineteen oh nine, based

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on the shape of the infectious stage
of the parasite. In Latin, toxin

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means arc or bow, and plasma
means life. It's rumored that Gandie came

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from a misspelling of the animal that
the researchers founded in the Gundi. Castellani

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first described a T. Goondii like
parasite in blood and spleen smears from a

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fourteen year old boy from Ceylon who
died from a disease that presented with severe

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anemia, fever, and splenomegaly.
In nineteen sixteen, Federovich observed similar organisms

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in the blood of a ten year
old boy from the Black Sea region who

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presented with the same symptoms seen in
the boy from Ceylon. In nineteen twenty,

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again, a similar organism was reported
by Chalmers and kamar in a soul

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who presented with symptoms that included chronic
headaches, fever, and diarrhea. These

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cases were not studied in depth,
and it's possible that they could be due

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to leaichmania. The first clear case
of toxoplasmosis wasn't recognized until nineteen twenty three,

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when a carriage driver brought his eleven
month old son to the children's clinic

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of Professor Pesina. The child was
suffering from increasing hydrocephalus. The child died,

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and both the clinical description and autopsy
results showed that the child had congenital

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toxoplasmosis. The autopsy read in part
quote in the papila, the center of

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the area just described there was a
rich black pigment which was combined with a

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grayish white, shiny material of azure
tone and finally stranded running horizontally to the

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nasal edge of the abnormal spot in
the macular region. Retinal veins were missing

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in the area of the lesion end
quote. Several sporosis were identified in the

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child's body. In this case,
photo micrographs were taken of the samples from

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the autopsy, but were later destroyed
in the bombings during World War II,

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so confirmation of the findings is no
longer possible. In nineteen twenty seven,

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Torres described a similar case in an
infant from Brazil who died of convulsions two

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days after birth. Djenku had only
referred to the organisms he found as sporozoa,

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and Torres as encephalitizun Chegazi neither Taurus
nor Jangku definitively named the pathogen as

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tigondii, but in a nineteen twenty
eight review of the cases, Leveeddi suggested

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that both deaths were due to Toxoplasma
gandhii. In nineteen twenty nine, Kulan

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observed parasites in the spinal fluid of
a seventeen year old boy from Corsica who

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died of meningitis. Kulan referred to
the parasite as e brumpti. Wolf and

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Cohen described a parasite in the nervous
system and retina of an infant with encephalitis

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corrioritonitis, an internal hydrocephalus in nineteen
thirty seven, they called it ehominus.

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Staban would look at the samples that
Wolf and Cohen took and would say that

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the parasite that they found was indistinguishable
from TIGANDII. He would note that the

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confusion lay in the difference in appearance
between humans and samples taken from laboratory animals

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that had been infected with Ti GANDII. True research in tigandi I didn't begin

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until nineteen thirty nine, when Wolf, Cohen, and Page identified it as

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a cause of human disease. The
research began when a child was born at

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Baby's Hospital on May twenty eighth,
nineteen thirty eight. The little girl was

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full term and delivered by c section. After three days, the child began

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to have seizures and choreoretinitis was present
in both eyes. The baby died shortly

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after birth, and when an autopsy
was performed, free and intracellular lesions of

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encephalomyelitis and retinitis were found. These
are hallmarks of TIGONDII. Sections of the

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child's cerebral cortex and spinal cord were
homogenized in saline and inoculated interest cerebrally into

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rabbits and mice. Tegondii was isolated
from these animals. Upon netcropsy, Tea

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Gandhii from these animals was inoculated into
other mice, and they in turn developed

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the disease. What this proved was
that the human strain was no different from

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the isolates taken from other animals.
The first reports of Tea. Gandhii infection

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without neurological symptoms came in nineteen forty
and nineteen forty one. In nineteen forty,

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Pinkerton and Wineman reported finding Tea.
Gandhii in the tissues of a twenty

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two year old man from Peru who
died of Bartonella infection and fever. In

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nineteen forty one, Pinkerton and Henderson
reported on two adults aged forty and fifty

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from Saint Louis, Missouri, who
died of atypical pneumonia and a spotted fever

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like syndrome. In nineteen forty two, Sabin proposed that there were four clinical

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signs that could be attributed to congenital
talk so plasmosis. These were hydrocephalus or

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microcephalus, intra cerebral calcification and choreo
retinitis. In nineteen fifty one, this

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proposal was shot down when Frankel and
Friedlander published a detailed account of five fatal

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cases of hydrocephalitis in infants. Tigondii
was only isolated from two of the patients.

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It came to the forefront that rubella, cmv, HSV and syphilis could

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cause the same symptoms that Sabin proposed
in nineteen forty two. Often, tuberculosis

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was also a culprit in infant deaths
where hydrocephalus was present. The first test,

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the dye test, was developed in
nineteen forty eight by Sabin and Feldman.

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This test is still a gold standard
for diagnosis today. It's both sensitive

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and specific, with no false results
in humans. This test accomplished two things.

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It allowed epidemiologists to study the scope
of the infection and determine the prevalence

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of the pathogen worldwide. It also
demonstrated that the symptoms of congenital clinical toxoplasmosis

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occurred in other diseases, but this
test could differentiate between Tigondi and other diseases

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that presented with the same symptoms.
Before nineteen fifty almost all cases of ocular

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toxoplasmosis were considered to be caused by
congenital transmission. In nineteen fifty one,

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Rieger found that post natal transmission of
the disease was possible. He also surmised

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that recurrence was possible in immune compromise
people of all ages. The link between

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T. Goondii and choreoretinitis was found
in nineteen fifty two by Helen R.

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Campbell Wilder Forester, a technician of
the Registry of Ophthalmolic Pathology at the Armed

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Forces Institute of Pathology in Washington,
d c. She studied fifty three eyes

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taken from patients with ocular disease.
It was proposed that the ocular disease was

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associated with tuberculosis, but as Wilder
began to perform tests on the eyes,

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she found no evidence of bacteria or
spirakeets by special staining. She went on

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to perform the dye test on the
retinas of the eyes and found Tegondii as

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the source of choreoretinitis. All the
eyes presented with lesions that were granulomitus and

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had central necrosis. Te Goondie was
consistently found in the nec prodic areas.

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Treatment of ocular toxoplasmosis with antimicrobial drugs
began in the nineteen fifties. Isles and

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Coleman demonstrated the use of pyrimethamine and
sulfonamines in nineteen fifty three. These drugs

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remain the gold standard for treatment of
ocular toxoplasmosis today. Garn and Isles found

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that spermiasin was effective in treating mice
with toxoplasmosis in nineteen fifty eight. Spermiasin

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is non toxic and does not cross
the placenta. This makes it a wonderful

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prophylactic treatment for pregnant women who are
infected with Tigondii to ensure that they don't

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transmit the parasite to their unborn children. George Desmonts began looking at serro conversion

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in pregnant women in the nineteen sixties. These studies were performed in Paris,

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France, and last did fifteen years. This study yielded some of the most

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important findings on Tigondii infection during pregnancy. First, the study found that infection

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acquired during the first two trimesters of
pregnancy was the most damaging to the fetus.

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Secondly, transmission was dependent on when
the women acquired the infection during the

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pregnancy. Thirdly, women who were
seropositive before they became pregnant did not transmit

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the infection to the fetus, and
finally, treatment with spermiasin reduced the chances

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of congenital transmission. A similar experiment
was done in Austria in nineteen seventy three

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and the results were very similar to
Desmond's findings. A screening program was developed

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in Massachusetts during the eighties that encouraged
neonatal serological screening and early treatment for ti

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GANDII infection. While there is no
bulletproof treatment for congenital infection even now,

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research is still ongoing. T GANDII
infection resulting in encephalitis in immunal compromised patients

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was first reported in patients with Hodgkin's
disease during treatment in the late nineteen sixties.

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However, this was rarely seen until
the nineteen eighties when the AIDS pandemic

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occurred. Left In Remington reported a
series of patients with encephalitis during that period.

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It was found that the infection occurred
as a result of reactivation of chronic

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infection related to the defect in T
cell immunity caused by infection with HIV.

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Before antiretroviral therapies were developed, t
gandii infection was one of the most common

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neurological complications patients with AIDS had to
face. Today, this infection is rarely

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seen in patients with HIV thanks to
anti viral treatments. Currently, in the

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US, it is estimated that eleven
percent of the population six years and older

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have been infected with Tea goondii.
In some places around the world, more

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than sixty percent of the population is
infected. The rate of infection is highest

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in lower altitudes, where the weather
tends to be hot and humid. There

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is no human to human transmission of
toxoplasmosis other than congenital transmission. Pregnant women

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who are infected with Tea gondii during
or just before pregnancy are at risk of

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congenital transmission. The women may not
be symptomatic, but the consequences are dire

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for the child. This is why
obstetricians will tell expectant mothers to have someone

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else clean the litter box if they
own a cat. Brady Zoites can be

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transmitted through food, so always could
meet to the proper temperature, and clean

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00:25:10.759 --> 00:25:15.880
utensils and cutting boards thoroughly before cutting
any foods that will be eaten raw.

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To avoid cross contamination, avoid unpasteurized
goat milk. Tachyozites take up residents in

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goats and they can be passed along
in the milk. Actually, just avoid

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unpasteurized milk altogether. Trust me,
you're not losing anything with pasteurization, except

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a lot of diseases you don't want. Cats play a huge role in the

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transmission of toxoplasmosis. They can shed
millions of usis in their feces. People

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00:25:51.599 --> 00:25:59.039
are often infected by accidental ingestion of
cat feces by cleaning litter boxes. The

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00:25:59.119 --> 00:26:03.960
takeaway of that statement is if you
have a cat, wash your hands after

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00:26:03.000 --> 00:26:08.039
you clean the litter box. Soap
and hot water go a long way to

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00:26:08.160 --> 00:26:17.319
preventing disease. There is also the
possibility of accidental ingestion from eating unwashed fruits

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00:26:17.400 --> 00:26:25.799
and vegetables, or accidentally ingesting infected
soil from the environment. You know how

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00:26:25.839 --> 00:26:30.039
I tell you to wash bananas.
No, I'm not crazy. Just wash

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00:26:30.079 --> 00:26:37.000
everything lastly. On rare occasions,
blood transfusions and organ transplants can be the

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00:26:37.039 --> 00:26:42.880
cause of transmission. This doesn't mean
you should turn down treatment, but there

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00:26:42.920 --> 00:26:52.359
is a very small risk associated with
these treatments. Okay, so that's toxoplasmosis.

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00:26:53.599 --> 00:26:57.440
If you'd like to send a nasty
ground because I ruined your love of

245
00:26:57.480 --> 00:27:03.559
your favorite furry feeling, you can
reach me at Jackie at cause of Death

246
00:27:03.680 --> 00:27:07.319
one hundred sex dot net. You
can also head to the website and leave

247
00:27:07.359 --> 00:27:14.000
a message for me at www.
Cause of death one hundred sex dot net.

248
00:27:15.279 --> 00:27:18.680
While you're there, take a look
around read the blog, check out

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00:27:18.720 --> 00:27:22.440
the show notes, and find out
what's happening with the show. Speaking of

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00:27:22.599 --> 00:27:27.759
show notes, they're really worth the
read. They contain all the research that

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00:27:27.839 --> 00:27:33.160
I did for this episode, and
they also give vital information about my sponsors,

252
00:27:33.680 --> 00:27:40.200
my social media accounts, and of
course, my Patreon page. Don't

253
00:27:40.200 --> 00:27:45.000
forget to head to Patreon if you
want to support the show. There you'll

254
00:27:45.000 --> 00:27:48.839
find several tiers that you can sign
up for, and they all have different

255
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pers Finally, share these episodes with
everyone you know. Go leave a rating

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00:27:55.480 --> 00:28:02.880
and review on your favorite podcatcher.
Let your geek flag fly. My podversary

257
00:28:03.039 --> 00:28:07.640
is coming up and I have a
really special episode brewing. I know you'll

258
00:28:07.680 --> 00:28:14.640
all enjoy it. Until then,
don't forget that dogs rule and cats carry

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00:28:14.680 --> 00:29:04.079
every disease known to mankind, at
least according to my microbiology professor, Step

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00:29:06.799 --> 00:29:34.079
School School Stock spoke steps, step
st st st st st st stand still, Stan