1) Peripheral Blood :

- Normochromic normocytic RBCs.

- Normal leukocytes and platelets.

2) Bone Marrow aspirate & biopsy:

- Normocellular bone marrow with normal trilineage hematopoiesis.

Diagnosis:
CSF, cytology:

Negative for malignant cells.

 Serum labartories :
• Toxo IG M 0.12

• Anti Toxoplasma Ab-IgG 27.1 +ve

• Clinical Symptoms
• The clinical manifestations of toxoplasmosis vary greatly, producing a range of
nonspecific symptoms. In immunocompetent patients, infection is usually
asymptomatic or very mild. Common symptoms include cervical
lymphadenopathy and other symptoms of generalized infection. These include
fever, malaise, night sweats, myalgia, sore throat and maculopapular rash.
• The clinical course in immunocompromised patients can be much more severe.
These infections usually stem from reactivated latent infection, rather than
newly acquired infection. Important symptoms include encephalitis,
myocarditis and pneumonitis, with death being almost certain if the disease is
left untreated. In AIDS patients, toxoplasma encephalitis is especially frequent,
occurring in 10-50% of seropositive patients with CD4 T-cell counts less than
100/μL.
• Toxoplasmosis in congenitally infected newborns can present in a nonspecific
manner with a wide range of symptoms, some of which can also be quite
severe. These include chorioretinitis, blindness, epilepsy, mental retardation,
anemia, jaundice, encephalitis, pneumonitis and others. Complete recovery is
very rare.
• https://web.stanford.edu/group/parasites/ParaSites2006/Toxoplasmosis/symp
toms.html
• Diagnosis
• The diagnosis of toxoplasmosis can be done using a variety of methods. The
difficulty lies in determining whether the infection is acute or chronic. Acute
infection can best be verified by isolating T. gondii or T. gondii DNA from the
patient's blood or finding tachyzoites in tissue or bodily fluids. Congenital
infection of fetuses can be identified by the presence of cysts in the placenta or
fetus.
• The isolation of T. gondii tissue cysts is not sufficient to determine whether the
infection is still active or has entered the latent phase. To differentiate the two,
patients are subjected to several serological exams, the specific combination of
which depends on clinical category of the patient. These exams include the
Sabin-Feldman dye test, which tests for IgG antibodies; ELISAs targeted at IgM,
IgA and IgE; differential agglutination tests and IgG avidity tests.
• Of particular interest is determining acute infection in pregnant women, due to
the risk of congenital toxoplasmosis. This is complicated by the fact that many
women have existing IgG and IgM antibodies to T. gondii from infection in the
past. There are effective diagnostic techniques that monitor changes in the
mother's antibody expression over time, but quick diagnosis is greatly preferred
because fetuses often rapidly become infected.
• Treatment
• Treatment of toxoplasmosis in immunocompetent patients is
usually unnecessary. In immunocompromised patients, the
recommended treatment is a combination of pyrimethamine
given at 25-100 mg daily and trisulfapyrimidines given at 2-6
g daily, both for a month. This drug combination inhibits
dihydrofolate reductase in T. gondii, preventing synthesis of
DNA and protein. Folinic acid can also be administered to
reduce bone marrow depression caused by the
pyrimethamine. Clindamycin has been found to be effective
at treating toxoplasma encephalitis in AIDS patients.
• Prevention
• Prevention of primary infection is currently best achieved through
health education. Recommendations include adequately cooking meat
before consumption at temperatures of at least 150 degrees F and
avoiding handling raw meat with ungloved hands. Cat owners are
warned to avoid directly handling litter trays or soil that may be
contaminated with cat feces. Cats that are fed commercial cat food are
less likely to get infected than cats that hunt. Pregnant women
especially should avoid contact with cats or handling litter trays.
• There are no vaccines currently available for T. gondii, although several
are in early in development. Prevention of congenital transmission is
possible through early diagnosis of acute infection in mothers and
administration of a prophylactic regimen of spiramycin.
 Informational Links
DPDx website. Description of T. gondii biology, epidemiology and
clinical aspects.
http://www.dpd.cdc.gov/dpdx/HTML/Toxoplasmosis.htm
CDC fact sheet. Public health information and recommendations.
http://www.cdc.gov/ncidod/dpd/parasites/toxoplasmosis/factsht_to
xoplasmosis.htm
ToxoDB website. Contains unfinished genomic sequence of T.
gondii.
http://www.toxodb.org/ToxoDB.shtml
The New Mexico AIDS InfoNet. Information about toxoplasmosis
directed at AIDS patients.
http://www.aidsinfonet.org/factsheet_detail.php?fsnumber=517
Toxoplasmosis: An Important Message for Women. Fact sheet put
out by the CDC.
http://www.cdc.gov/ncidod/dpd/parasites/toxoplasmosis/ToxoWom
en.pdf
Last Update: 24 May 2006
 
A Toxoplasma-positive reaction, stained by
immunofluroescence (IFA).
• life Cycle:
•  
•  
• The only known definitive hosts for Toxoplasma gondii are members of family Felidae (domestic cats and their
relatives). Unsporulated oocysts are shed in the cat’s feces . Although oocysts are usually only shed for 1-3 weeks,
large numbers may be shed. Oocysts take 1-5 days to sporulate in the environment and become infective.
Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water or plant
material contaminated with oocysts  . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites
localize in neural and muscle tissue and develop into tissue cyst bradyzoites  . Cats become infected after consuming
intermediate hosts harboring tissue cysts  . Cats may also become infected directly by ingestion of sporulated
oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after
ingestion of sporulated oocysts in the environment  . Humans can become infected by any of several routes:Eating
undercooked meat of animals harboring tissue cysts  .
• Consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-
contaminated soil or changing the litter box of a pet cat)  .
• Blood transfusion or organ transplantation  .
• Transplacentally from mother to fetus  .
• In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes;
these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue
cysts may be observed in stained biopsy specimens  . Diagnosis of congenital infections can be achieved by
detecting T. gondii DNA in amniotic fluid using molecular methods such as PCR 
• Healthy people (nonpregnant)
• Healthy people who become infected with Toxoplasma
gondii often do not have symptoms because their
immune system usually keeps the parasite from causing
illness. When illness occurs, it is usually mild with “flu-
like” symptoms (e.g., tender lymph nodes, muscle aches,
etc.) that last for weeks to months and then go away.
However, the parasite remains in the person’s body in an
inactive state. It can become reactivated if the person
becomes immunosuppressed.
• Diagnosis
•  
• A Toxoplasma-positive reaction, stained by immunofluroescence (IFA). (CDC Photo)
• The diagnosis of toxoplasmosis is typically made by serologic testing. A test that measures
immunoglobulin G (IgG) is used to determine if a person has been infected. If it is necessary to
try to estimate the time of infection, which is of particular importance for pregnant women, a
test which measures immunoglobulin M (IgM) is also used along with other tests such as an
avidity test.
• Diagnosis can also be made by direct observation of the parasite in stained tissue sections,
cerebrospinal fluid (CSF), or other biopsy material. These techniques are used less frequently
because of the difficulty of obtaining these specimens.
• Parasites can also be isolated from blood or other body fluids (for example, CSF) but this
process can be difficult and requires considerable time.
• Molecular techniques that can detect the parasite’s DNA in the amniotic fluid can be useful in
cases of possible mother-to-child (congenital) transmission.
• Ocular disease is diagnosed based on the appearance of the lesions in the eye, symptoms,
course of disease, and often serologic testing.
• The common presenting symptom of cerebral
toxoplasmosis is headache, often accompanied by
fever and altered mental status (9). Individuals may
also present with visual disturbances, seizures,
cranial nerve abnormalities, and sensory
disturbances. The common neurological signs include
motor weakness and speech disturbances (7).
• The most common affected areas in CNS include the
basal ganglia, corticomedullary junction, white
matter, and periventricular regions.
• This showed radiating enhancement in
cortical/subcortical regions having very few
nodular or ring-enhancing lesions—quite
different from those in the
immunocompromised patients
• ike toxoplasmosis, CNS lymphoma also has a predilection
for the basal ganglia. Unifocal and multifocal
involvements are observed in both conditions. Both have
varied patterns of enhancement, edema, and mass effect
on CT images, and increased signal intensity on T2-
weighted MR images. Lesions in lymphoma are usually
more locally infiltrative; hence, a butterfly-like pattern of
spread and enhancement favors lymphoma more than
toxoplasmosis. In addition to this, lymphomatous lesions
are usually larger than those of toxoplasmosis (15) and
tend to have a periventricular distribution
• The other differential diagnoses for multiple
intraparenchymal brain lesions include
tuberculoma, aspergillosis, progressive
multifocal leukoencephalopathy, bacterial
abscess, and cryptococcosis 
• In our case, with the multiplicity of lesions and
onset of newer lesions within a span of one
week, showing a mixed, nodular enhancement
pattern and raised lipid lactate peak on MR
spectroscopy, a diagnosis of CNS toxopl
• https://www.ncbi.nlm.nih.gov/pmc/articles/P
MC4838758/
asmosis was made
• CNS Toxoplasmosis
• One of the most common opportunistic infections in the AIDS population caused by the
obligate intracellular protozoan Toxoplasma gondii.
• Almost always caused by reactivation of a chronic infection, and usually becomes symptomatic
when the CD4 count becomes < 100 μL.
• Clinical features: Subacute onset with focal neurologic abnormalities accompanied by
headache, change in mental status and fever.
• Key Diagnostic Features: Favored locations: Basal ganglia and corticomedullary junction. CT:
Iso- to hypodense lesions demonstrating peripheral enhancement. MR: Heterogenous mass
lesion. Typically, central necrosis does not demonstrate restricted diffusion. Hemorrhage may
be seen. MR spectroscopy demonstrates reduction in NAA/Cr with presence of lipid and lactate.
Occasionally, an elevated Cho peak may be seen.
• DDx: Lymphoma, TB, primary brain tumor, metastatic brain tumor, tumefactive demyelinating
lesion.
• Rx: Antitoxoplasmosis treatment
 Similar case
• https://www.ncbi.nlm.nih.gov/pmc/articles/P
MC6290221/
• The incidence of primary toxoplasmosis in
immunocompetent individuals in French
Guiana, according to a study done by Carme et
al, is very minimal, about 0.018% (4).
However, at present, no data is available for
the Indian population.