14 CME REVIEWARTICLE

Volume 56, Number 5

OBSTETRICAL AND GYNECOLOGICAL SURVEY
Copyright 2001
by Lippincott Williams & Wilkins, Inc.

CHIEF EDITORS NOTE: This article is the 14th of 36 that will be published in 2001 for which a total of up to 36 Category 1
CME credits can be earned. Instructions for how credits can be earned appear on the last page of the Table of Contents.

Congenital Toxoplasmosis: A Review

Jeffrey L. Jones, MD, MPH,* Adriana Lopez, MHS,
Marianna Wilson, MS, Jay Schulkin, PhD and Ronald Gibbs, MD
*Medical Epidemiologist, Epidemiologist, and Chief, Reference Immunodiagnostic Laboratory, Division of
Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention,
Atlanta, Georgia; and Director of Research, American College of Obsetricians and Gynecologists,
Washington, DC, and Professor and Chairman of Obstetrics and Gynecology, University of Colorado Health
Sciences Center, Denver, Colorado
Toxoplasmosis is caused by infection with the protozoan parasite Toxoplasma gondii. In the United
States, approximately 85% of women of childbearing age are susceptible to acute infection with T.
gondii. Acute infections in pregnant women may cause serious health problems when the organism is
transmitted to the fetus (congenital toxoplasmosis), including mental retardation, seizures, blindness,
and death. An estimated 400 to 4000 cases of congenital toxoplasmosis occur in the U.S. each year.
Manifestations of congenital toxoplasmosis may not become apparent until the second or third decade
of life. Serologic tests are used to diagnose acute infection in pregnant women, but false-positive tests
occur frequently, therefore, serologic diagnosis must be confirmed at a reference laboratory before
treatment with potentially toxic drugs should be considered. Much of congenital toxoplasmosis can be
prevented by educating women of childbearing age and pregnant women to avoid eating raw or
undercooked meat, to avoid cross-contamination of other foods with raw or undercooked meat, and to
use proper cat-litter and soil-related hygiene.
Target Audience: Obstetricians & Gynecologists, Family Physicians
Learning Objectives: After completion of this article, the reader will be able to outline the biology of
toxoplasmosis, to explain the methods of transmission of toxoplasmosis, and to identify the methods
used to diagnose toxoplasmosis in pregnancy.

Toxoplasmosis is caused by infection with the protozoan parasite Toxoplasma gondii. In the United
States, a serological survey from the Third National
Health and Nutrition Examination Survey found that
an estimated 23% of adolescents and adults have
laboratory evidence of infection with T. gondii (15%
among women of childbearing age) (1; Centers for
Disease Control, unpublished data, 1994). Although
these infections are usually either asymptomatic or associated with self-limited symptoms in adults (e.g.,
fever, malaise, and lymphadenopathy), infections in
pregnant women can cause serious health problems in
the fetus if the parasites are transmitted (i.e., congenital

toxoplasmosis) and cause severe sequelae in the infant

including mental retardation, blindness, and epilepsy.
Practicing obstetricians may be confronted with a number of issues regarding toxoplasmosis, including diagnosis, laboratory testing, screening practices, clinical
presentation, and prevention.
Although congenital toxoplasmosis is not a nationally
reportable disease, extrapolation from regional studies
indicates that an estimated 400 to 4,000 cases occur in
the U.S. each year (24). The most recent data from
New England indicate that congenital toxoplasmosis
occurs in approximately 1 in 10,000 live births (4).

Reprint requests to: Jeffrey L. Jones, MD, MPH, Mailstop F-22,

Centers for Disease Control and Prevention, 4770 Buford Highway
NE, Atlanta, GE 30341-3724. Email: JLJ1@cdc.gov
The authors have disclosed no significant financial or other
relationship with any commercial entity.

BIOLOGY, TRANSMISSION, CLINICAL

SYMPTOMS, AND EPIDEMIOLOGY
T. gondii has a complex life cycle (Fig. 1) consisting of three stages: 1) tachyzoiteduring the acute

296

Congenital Toxoplasmosis Y CME Review Article

stage of infection, this form of the parasite invades

and replicates within cells; 2) bradyzoiteduring
latent infections, this form of the parasite is present
in tissue cysts; and 3) sporozoitethis form of the
parasite is found in oocysts, which are environmentally resistant. T. gondii tachyzoites can invade and
multiply in most cell types and are found in all
organs in acute infection, especially in muscle (including heart), liver, spleen, lymph nodes, and the
central nervous system. The tachyzoite is the form of
the organism responsible for congenital infection.
Cell invasion results in death of parasitized cells and
an acute inflammatory reaction. Placental lesions are
usually microscopic in humans, but macroscopic necrosis has been reported in animals (5).
Members of the family Felidae (including domestic
and feral cats) are the definitive hosts of T. gondii.
During acute infections, cats excrete unsporulated
(i.e., noninfectious) oocysts in their feces; after several days to several weeks, depending on environmental conditions, the oocysts sporulate and become
infectious. Under favorable conditions (i.e., in warm,
moist soil), oocysts can remain infectious for approximately 1 year. They do not survive well in arid, cold
climates and can be destroyed by heating (610).
Toxoplasmosis can be transmitted to humans by
three principal routes. First, humans can eat raw or

Fig. 1.

Life cycle of Toxoplasma gondii.

297

inadequately cooked infected meat (especially pork,

mutton, and wild game meat (11)) or eat uncooked
foods that have come in contact with infected meat.
Second, humans can inadvertently ingest oocysts that
cats have passed in their feces, either in a cat litter
box or in soil (e.g., soil from gardening or unwashed
fruits or vegetables). Third, a woman can transmit the
infection to her unborn fetus transplacentally. In
adults, the incubation period ranges from 10 to 23
days from ingestion of undercooked meat, and from
5 to 20 days from ingestion of oocysts from cat feces.
A report conducted by the Economic Research
Service of the United States Department of Agriculture concluded that one half of the toxoplasmosis
cases in the U.S. are caused by eating contaminated
meat. The estimated economic burden of these infections is $7.7 billion each year, primarily from congenital toxoplasmosis (12). Other data are available
to assist in estimating the portion of the disease
burden of toxoplasmosis attributable to consumption
of infected meat (i.e., raw or undercooked meat or
cross-contamination from raw or undercooked meat).
A recent study compared results from a cross-sectional seroprevalence study of Seventh Day Adventists, a religious group that follows a diet containing no meat, with serologic results from a control
group of volunteers who were not Seventh Day Ad-

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Obstetrical and Gynecological Survey

ventists (13). Results from this study documented a

significantly lower rate of Toxoplasma infection in
Seventh Day Adventists than the control group (24%
vs. 50%, respectively; P .01). Thus, these data
support the estimates that approximately one half of
T. gondii exposure is caused by eating infected meat.
Of the 750 deaths attributed to toxoplasmosis each
year, 375 (50%) are believed to be food-borne, making toxoplasmosis the third leading microbial cause
of food-borne deaths in this country (salmonellosis
and listeriosis are the first and second leading causes,
respectively) (14).
Women infected with T. gondii before conception,
with rare exception (15), do not transmit the infection
to their fetuses. Women infected with T. gondii during pregnancy can transmit the infection across the
placenta to their fetuses. The risk of congenital disease is lowest (1025%) when acute maternal infection occurs during the first trimester and highest
(6090%) when acute maternal infection occurs during the third trimester (10, 16, 17). However, the
severity of disease is worse if infection is acquired in
the first trimester (10, 18). The overall risk of congenital infection from acute T. gondii infection during pregnancy is 20% to 50%.
The classic triad of signs suggestive of congenital
toxoplasmosis includes chorioretinitis, intracranial
calcifications, and hydrocephalus. Most infants infected in utero are born with no obvious signs of
toxoplasmosis on routine examination, but up to 80%
develop learning and visual disabilities later in life if
they are followed into adulthood (19, 20). If untreated, congenital toxoplasmosis can be associated
with severe and even fatal disease (21).
In adults, the severity of T. gondii infection is
correlated with the immune status of the infected
person. Toxoplasmosis in immunocompetent adolescents or adults is generally mild or inapparent. Mild
infections can result in lymphadenopathy, fever, fatigue, and malaise, all of which usually resolve
within weeks to months without specific treatment.
However, infection in immunocompromised persons
can be severe. Immunosuppression caused by AIDS
or therapies for malignancies, transplants, or lymphoproliferative disorders can result in reactivation of
preexisting latent T. gondii infections. Reactivation
most often involves the central nervous system, and
symptoms may include those of meningoencephalitis or
a mass lesion. Women with reactivated T. gondii infection can transmit the organism congenitally (22, 23).
Recent epidemiologic studies have identified the
following risk factors for T. gondii infection: owning
cats (24), seropositive cats in farming areas (25),

cleaning the cat litter box (26), eating raw or undercooked pork, mutton, lamb, beef, or mince meat
products (24, 26, 27), gardening (25), eating raw or
unwashed vegetables or fruits, eating raw vegetables
outside the home (24), contact with soil (27), washing kitchen knifes infrequently (26), having poor
hand hygiene (24), and travel outside of Europe,
U.S., or Canada (27). Protective factors for T. gondii
infection include a meat-free diet (13), living at high
altitudes and in arid climates (28, 29), and living in
climates with frequent freezing and thawing (30).
Owning a cat has not been a consistent risk factor
for T. gondii infection. Owning a cat was not shown
to be a risk factor for T. gondii infection in two
studies of pregnant women (27, 31) and in a study of
HIV-infected persons (32). Risk for T. gondii infection does not occur from merely owning a cat, but
rather from being exposed to cat feces from a cat
shedding oocysts. Cats generally only shed oocysts
for several weeks during their lives if they become
infected with T. gondii. Cats kept indoors that do not
hunt prey or are not fed raw meat are not likely to
acquire T. gondii infection and, therefore, pose little
risk. Unless cats are sick with diarrhea, little or no
feces will stick to their perianal area (11). Usually,
adult cats are not diarrheal during the period in which
they are shedding oocysts (11). Because of their
grooming habits, fecal matter has not been found on
the fur of clinically normal cats (11). In addition, in
a study of cats induced to shed oocysts, no oocysts
could be found on the cats fur after they shed oocysts (33). Therefore, the possibility of transmission
to human beings via touching cats is thought to be
minimal or nonexistent (11). Neighborhood or feral
cats that defecate in gardens or sandboxes may pose
the greatest risk for toxoplasmosis for some persons,
whether or not they own a cat.
It should also be noted that because cats may not
develop antibodies to T. gondii during the oocystshedding period, serologic examination of cats does
not provide useful information regarding the ability
of a particular cat to transmit toxoplasmosis (11). A
cat that has a positive serologic test for T. gondii
probably has shed oocysts previously and, therefore,
may pose less of a risk than a serologically negative
cat, but cats can shed oocysts more that once, thus,
serologic testing of cats is not really helpful in this
instance either.
Outbreaks of toxoplasmosis in humans have been
attributed to ingestion of raw or undercooked ground
beef, lamb, pork, venison (3439), unpasteurized
goats milk (40), contaminated, unfiltered drinking

Congenital Toxoplasmosis Y CME Review Article

299

water (41, 42), soil exposure (43), and aerosolized

soil exposure (44).
High T. gondii seroprevalence is found in countries
such as France where undercooked meat is commonly eaten (45, 46), and in tropical areas of Latin
America or sub-Saharan Africa where cats are abundant and the climate favors survival of oocysts (47
54). Studies in Scandinavian countries (5557) and
England (58) show lower seroprevalence, more similar to that in the U.S.
DIAGNOSIS OF TOXOPLASMOSIS IN
PREGNANCY
Acute toxoplasmosis is diagnosed rarely by detecting the parasite in body fluids, tissue, or secretions;
the most common method of diagnosis is based on
antibody detection. The presence of elevated levels
of Toxoplasma-specific IgG antibodies indicates infection has occurred at some point, but does not
distinguish between an infection acquired recently
and one acquired in the distant past. In acute infection, IgG and IgM antibodies generally rise within 1
to 2 weeks of infection (59). Determining when T.
gondii infection occurred in a pregnant woman is
important because infection before conception poses
little risk for transmission of infection to the fetus;
however, infection after conception does pose such
risk. Detection of Toxoplasma-specific IgM antibodies has been used as an aid in determining the time of
infection, but IgM antibodies have been reported to
persist for up to 18 months postinfection (6). A
negative IgM with a positive IgG result indicates
infection at least 1 year previously. A positive IgM
result may indicate more recent infection or may be
a false-positive reaction. A flow diagram for T. gondii testing and guide to interpretation of T. gondii
tests are presented in Figure 2 and Table 1.
In the United States, commercial test kits for Toxoplasma-specific IgG and IgM antibodies are readily
available. Some commercial IgM tests have had
problems with specificity, resulting in unacceptably
high rates of false-positive test results. In 1996, the
Food and Drug Administration (FDA) and Centers
for Disease Control (CDC) conducted extensive evaluations of the six most commonly used commercial
IgM kits in the U.S. to determine the extent of the
problem with the specificity of these kits. Sensitivity
and specificity rates for these six kits ranged from
93.3% to 100.0% and from 77.5% to 99.1%, respectively (60).
As a result of these findings, in 1997 FDA distributed an advisory to physicians in the U.S. highlight-

Fig. 2. Algorithm for the serodiagnosis of toxoplasmosis in

people older than 1 year of age. Adapted from Wilson M, McAuley
JM. Toxoplsama. In: Murray PR, Baron EJ, Pfaller MA et al., eds.
Manual of Clinical Microbiology, 7th Ed. Washington DC: ASM
Press, 1999, pp 13471382.

ing these test limitations. The agency provided a

guide for interpreting test results (Table 1) and issued
a recommendation to laboratory personnel and physicians advising them to be aware of the specificity
problems associated with some commercial test kits
before making decisions about the clinical management of their patients.
IgM-positive results should be confirmed by a Toxoplasma reference laboratory (60). A toxoplasmosis
reference laboratory may be able to help narrow
down the time of infection with tests such as the IgG
avidity test (61, 62). IgG avidity, or the strength with
which IgG binds to T. gondii, usually shifts from low
avidity to high avidity at about 5 months after infection and can be used to rule out primary T. gondii
infection in early pregnancy in approximately three
quarters of women with positive IgM serum tests
(61). Although commonly used in Europe, the IgG
avidity test is available currently in only two labora-

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Obstetrical and Gynecological Survey

TABLE 1
Guide to general interpretation of Toxoplasma
gondii serology results obtained with commercial assays
Results
IgG

IgM

Negative

Negative

Negative

Equivocal

Negative

Positive

Equivocal

Negative

Equivocal

Equivocal

Equivocal

Positive

Positive
Positive

Negative
Equivocal

Positive

Positive

Report/Interpretation for humans (except

infants)
No serological evidence of infection with
Toxoplasma.
Possible early acute infection or falsepositive IgM reaction. Obtain a new
specimen for IgG and IgM testing. If
results for the second specimen remain the same, the patient is probably
not infected with Toxoplasma.
Possible acute infection or false-positive
IgM result. Obtain a new specimen for
IgG and IgM testing. If results for the
second specimen remain the same,
the IgM reaction is probably a falsepositive.
Indeterminate: obtain a new specimen
for testing or retest this specimen for
IgG in a different assay.
Indeterminate: obtain a new specimen
for both IgG and IgM testing.
Possible acute infection with Toxoplasma. Obtain a new specimen for
IgG and IgM testing. If results for the
second specimen remain the same or
if the IgG becomes positive, both
specimens should be sent to a reference laboratory with experience in the
diagnosis of toxoplasmosis for further
testing.
Infected with Toxoplasma for 1 year.
Infected with Toxoplasma for probably
1 year, or false-positive IgM reaction. Obtain a new specimen for IgM
testing. If results with the second
specimen remain the same, both
specimens should be sent to a reference laboratory with experience in the
diagnosis of toxoplasmosis for further
testing.
Possible recent infection within the last
12 months, or false-positive IgM reaction. Send the specimen to a reference laboratory with experience in the
diagnosis of toxoplasmosis for further
testing.

tories in the U.S.1 Confirmatory testing with a serologic profile including the Sabin-Feldman dye test,
IgM enzyme-linked immunosorbent assay (ELISA),
IgA ELISA, IgE ELISA, and differential agglutina1
Editors Note: Toxoplasma Serology Laboratory, Research Institute, Palo Alto Medical Foundation, Ames Building, 795 El
Camino Real, Palo Alto, CA 94301; phone: 650-853-4848, and
MRL Reference Laboratories, 5785 Corporate Ave., Cypress, CA
90630; phone: 800-445-0185.

tion (AC/HS) test has also been useful in distinguishing recently acquired infections (63).
For identification of T. gondii intrauterine infection, polymerase chain reaction (PCR) testing of amniotic fluid has allowed earlier testing than fetal
blood sampling (6468). In addition, PCR of amniotic fluid is more sensitive than fetal blood sampling
(69) and is safer. However, false-positive and falsenegative tests do occur with PCR (70). Because of
advances in PCR testing of amniotic fluid, cordocentesis is indicated rarely today.
SCREENING AND TREATMENT
In France, a screening program was implemented
in 1976 to detect and treat T. gondii infection during
pregnancy. The goal of this program is to institute
preventive measures for seronegative women and to
ensure early diagnosis and treatment of infection
acquired during pregnancy. Since the beginning of
the program, premarital and prenatal medical examinations for T. gondii antibodies have been performed. Premarital examinations are conducted to
distinguish previously infected women from women
who have not been previously infected. When an
uninfected woman becomes pregnant, testing is conducted at her first prenatal examination during her
first trimester and at six additional examinations conducted monthly during her second and third trimesters. In addition, women are educated about prevention methods during pregnancy (71). If these
screening tests detect evidence of acute infection
during pregnancy, treatment for the woman is initiated with spiramycin in an effort to prevent transmission to the fetus. If infection in the fetus is confirmed
through fetal blood sampling and amniocentesis, pyrimethamine and sulfadiazine or sulfadoxine is added
to the regimen (72, 73) because spiramycin does not
generally cross the placenta.
Although the proportion of the population included
in the French program has been incomplete, it has
been associated with a decline in the incidence of
congenital infection, as well as a decline in severe
disease detected at birth. The proportion of the decline specifically attributable to the program or to the
general decline in Europe in rates of seropositivity is
difficult to determine because no unscreened group
of women exists for comparison.
Austria implemented a toxoplasmosis-screening
program in 1975. Nearly all women who become
pregnant are serologically screened early in pregnancy and, if the results are found to be negative
initially, are tested again during the second and third

Congenital Toxoplasmosis Y CME Review Article

trimesters. Women with T. gondii infections are treated

as soon as infection is detected. Although seropositivity
rates among pregnant Austrian women have declined
from approximately 50.0% during the late 1970s to
36.7% during the early 1990s, the incidence of congenital T. gondii infection has declined even more, from 50
to 70 cases per 10,000 births before the program to 1
per 10,000 births during the early 1990s (74). As with
the French program, the lack of an unscreened comparison group precludes determining the proportion of the
decline attributable to the screening program, and the
lack of cost figures precludes cost-effectiveness
analyses.
The European Research Network on Congenital
Toxoplasmosis was established in 1993 and has
sponsored several studies regarding public health interventions for congenital toxoplasmosis. Most recently, a multicenter study was conducted to evaluate
the effectiveness of toxoplasmosis treatment administered during pregnancy in preventing transmission
of maternal infection to the fetus. Pregnant women
who visited one of five European university medical
centers for prenatal care were screened for T. gondii
antibodies at their first prenatal visit. Women who
were seronegative were retested at least once every
trimester in two centers and monthly in the other
centers, until the birth of the infant. For women who
seroconverted during pregnancy, prenatal antibiotic
treatment was started, and their infants were followed for 1 year after birth. Treatment regimens
consisted of spiramycin or a combination of pyrimethamine and sulfadiazine. If prenatal infection
was confirmed with amniocentesis or cordocentesis,
women were treated with pyrimethamine and sulfadiazine or sulfadoxine. Of the women who screened
positive and did not receive prenatal therapy, transmission from mother to infant occurred in 72% of the
mother-infant pairs; of women who received prenatal
therapy, transmission occurred in 39% of the motherinfant pairs. However, this difference was not statistically significant when the time of gestation that T.
gondii infection occurred was accounted for in the
treated and untreated groups. Nevertheless, 20% of
the untreated mothers gave birth to infants with severe sequelae, whereas only 3.5% of the treated
mothers gave birth to infants with severe sequelae.
Furthermore, the earlier antibiotics were administered after infection, the less likely sequelae were
detected in the infant (75).
From January 1988 through June 1989, a costbenefit analysis of T. gondii screening during pregnancy was conducted in a prospective study in Finland. The study compared costs of screening

301

alternatives for primary infections during pregnancy

with the costs of no screening. With screening, the
annual costs of congenital toxoplasmosis were
U.S.$95 per pregnancy; without screening, annual
costs were U.S.$128 per pregnancy. Furthermore,
screening along with health education was more beneficial than health education alone (76). The study
findings suggest screening is cost beneficial in countries with a low incidence of congenital toxoplasmosis, such as Finland. The findings of other studies
suggest screening programs can also be beneficial in
areas with high incidences of congenital toxoplasmosis (72, 77, 78).
Although the findings of some European studies
suggest T. gondii screening programs of women of
childbearing age can prevent cases of congenital
toxoplasmosis, several concerns limit support for
such programs in the U.S. Some researchers have
argued that because the prevalence of congenital
toxoplasmosis is so rare in the United States, acute
early pregnancy toxoplasmosis is far too uncommon
to warrant routine screening (79). The American
College of Obstetricians and Gynecologists (ACOG)
(80) does not recommend routine screening. Screening may lead to equivocal or false-positive test results (60, 77), which could lead to inappropriate
treatment. There have been no randomized trials using spiramycin or other medications to assess the
effect of treatment on congenital transmission. Authors conducting a review of studies performed from
1966 through 1997 concluded that it is unclear
whether antenatal treatment in women with toxoplasmosis reduces congenital transmission (81). In a multicenter evaluation of 144 pregnant women with
acute toxoplasmosis in Europe, prenatal antibiotic
therapy had no impact on the maternal-fetal transmission rate. However, prenatal treatment reduced
the rate of severe sequelae among infected infants
from 20% to 3.5% (75). In their review of the literature, authors from Norway, a country with a low
incidence of toxoplasmosis similar to the U.S., concluded that sufficient scientific evidence is not yet
available to propose screening for toxoplasmosis in
pregnant women (82). In addition, the Royal College
of Obstetricians and Gynecologists in the United
Kingdom has recommended that prenatal screening
for toxoplasmosis should not be introduced in the
U.K. (83). Finally, researchers from the U.S. used
decision analysis to evaluate clinical outcomes with
three alternatives: 1) no testing for congenital toxoplasmosis, 2) targeted screening in cases of incidental abnormalities noted on ultrasound, and 3) universal serologic screening of pregnant women followed

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Obstetrical and Gynecological Survey

by amniocentesis to diagnose fetal infection in cases

of maternal seroconversion. Universal screening reduced the total number of cases of congenital toxoplasmosis compared with no testing or targeted
screening. However, compared with no testing, universal screening with medical treatment resulted in
18.5 additional pregnancy losses for each case of
toxoplasmosis avoided (84). Risks associated with
amniocentesis were an important factor (0.36% fetal
death rate). No cost assessment was done in this
analysis. There is still a need for cost-effectiveness
studies to enable comparison of the benefits of expanded testing in the U.S., the costs of such testing,
and the unintended adverse consequences that might
accompany such testing.
Side effects of treatments must be considered when
treating pregnant women. Spiramycin is a macrolide
antibiotic that can cause gastrointestinal and dermatologic reactions in the mother. The Medical Letter lists
spiramycin as the drug that should be used for toxoplasmosis for prophylactic use during pregnancy, however, it is an investigational drug in the U.S. and can
only be obtained through the manufacturer (85). Although sulfonamides have been associated with kernicterus in the newborn when given in late pregnancy,
this complication was not noted to occur in a review of
screening programs by French authors (86). Pyrimethamine is not generally recommended for pregnant women because it is a folic acid antagonist (pregnancy category C). Folate serves as a coenzyme in the
synthesis of DNA, RNA, myelin, and lipids. A lack of
folic acid in pregnancy has been associated with neural
tube defects early in pregnancy before the neural tube
has closed. Screening programs do not generally recommend pyrimethamine and sulfadiazine treatment before 18 weeks gestation (10). Pyrimethamine has also
been associated with heart and kidney malformations in
infants and may increase the risk of central nervous
system cancer in childhood (87, 88). Pyrimethamine
and sulfadiazine also carry a risk of bone marrow suppression in both the mother and the infant (10). A
supplement of folinic acid should be given with pyrimethamine to compensate for the reduction of folic
acid caused by pyrimethamine. Unfortunately, because
there are few cases available for study, it has not been
possible to fully assess the risks of side effects due to
treatment for toxoplasmosis during pregnancy.
Much of the above discussion raises the issue of
when targeted screening should be done for toxoplasmosis in the U.S. In their decision analysis, Bader et al.
(84) determined that screening high risk women (defined as a five-fold increase in risk or a rate of maternal
toxoplasmosis as high as 1 in 100 pregnancies) would

still lead to at least 2.9 fetal losses per case of toxoplasmosis avoided. Therefore, they concluded that screening of cat owners would probably not be appropriate. In
a large well-designed study of acute T. gondii infection
in pregnant women from the European Research Network on congenital toxoplasmosis, none of the risk
factors for T. gondii infection increased the risk by as
much as five-fold (27). Nevertheless, in this study, the
highest risks were associated with eating undercooked
lamb or other less conventional meats that included
wild game meats and with travel outside Europe, U.S.,
or Canada.
It would seem prudent to screen pregnant women
for acute toxoplasmosis if there were suspicious ultrasound findings. Such findings include hydrocephalus, intracranial calcifications, microcephaly, fetal
growth restriction, ascites, and hepatosplenomegaly.
In addition, HIV-infected women should be screened
for toxoplasmosis (80).
PREVENTION OF TOXOPLASMOSIS IN
PREGNANT WOMEN
Recommendations for prevention of toxoplasmosis in
pregnant women were discussed at a conference at the
Centers for Disease Control and Prevention and published (71). These recommendations were as follows:
To prevent toxoplasmosis and other food-borne
illnesses, food should be cooked to safe temperatures. A food thermometer should be used to
measure the internal temperature of cooked meat
to ensure that meat is cooked all the way
through. Beef, lamb, and veal roasts and steaks
should be cooked to at least 145F; and pork,
ground meat, and wild game should be cooked
to 160F before eating. Whole poultry should be
cooked to 180F in the thigh to ensure that the
meat is cooked thoroughly.
Fruits and vegetables should be peeled or
washed thoroughly before eating.
Cutting boards, dishes, counters, utensils, and
hands should always be washed with hot soapy
water after they have contacted raw meat, poultry, seafood, or unwashed fruits or vegetables.
Pregnant women should wear gloves when gardening and during any contact with soil or sand
because cat waste might be in soil or sand. After
gardening or contact with soil or sand, hands
should be washed thoroughly.
Pregnant women should avoid changing cat litter if possible. If no one else is available to
change the cat litter, pregnant women should use

Congenital Toxoplasmosis Y CME Review Article

gloves, then wash hands thoroughly. The litter

box should be changed daily because T. gondii
oocysts require several days to become infectious. Pregnant women should be encouraged to
keep their cats inside and not adopt or handle
stray cats. Cats should be fed only canned or
dried commercial food or well-cooked table
food, not raw or undercooked meats.
Health education for women of childbearing age
should include information about meat-related
and soil-borne toxoplasmosis prevention.
Healthcare providers should educate pregnant
women at their first prenatal visit about food
hygiene and prevention of exposure to cat feces.
Healthcare providers who care for pregnant
women should be educated about two potential
problems associated with the T. gondii serology
tests. First, no assay exists that can determine
precisely when the initial T. gondii infection
occurred. Second, in populations with a low
incidence of T. gondii infection, such as in the
U.S., a substantial proportion of the positive
IgM test results will probably be false-positive.
The government and the meat industry should
continue their efforts to reduce T. gondii in
meat.
One approach to preventing toxoplasmosis focuses
on educating women of childbearing age about minimizing their risk for infection with T. gondii. Educational interventions assume that increased knowledge results in awareness, which consequently
results in changes in risky behavior and declines in
infection rates. Messages emphasize the importance
of avoiding eating raw or undercooked meat, handling raw meat safely, and washing hands after gardening or changing the cat litter box.
A study conducted as part of prenatal classes at
Canadian public health agencies evaluated the effect
of a 10-minute teaching session on three behaviors:
practices associated with cleaning the cat litter box
and limiting the cats diet to cooked food; safe foodhandling practices; and hand washing after exposure
to cat feces, garden soil, or raw meats. Among
women in the classes, behavior improved regarding
practices associated with cats; however, behavior
regarding food-handling practices remained unchanged. In addition, only professional women
showed improvement in their hand washing practices
(89).
During 1979 to 1990, a Belgian study assessed the
effectiveness of educational sessions held in hospital
settings. Baseline data were collected during 1979

303

to1982, when no education measures were in effect.

During 1983 to 1990, education sessions were provided to pregnant women. The intervention was associated with a 63% decrease in seroconversion rates
(90). Although it is possible that other factors such as
a reduction of T. gondii infection in meat could be
responsible for the reduction in seroconversion rates,
this study suggests that educational intervention is
beneficial in preventing acute toxoplasmosis among
pregnant women.
Educational programs are a potentially powerful
intervention because of their low cost, and because
pregnant women are motivated to protect the health
of their babies. However, the impact of educational
programs is difficult to evaluate because of the limited number of comparative studies conducted with
rigorous scientific methodology and of sufficient size
to enable calculation of the effectiveness of the intervention compared with its cost.
AREAS FOR FUTURE RESEARCH
There is a need for more complete and accurate
population-based data regarding the incidence of toxoplasmosis and the number of cases by mode of
transmission. Development of techniques that would
enable tracing the source of individual infections to
food-borne, cat-borne, or soil-borne transmission
would help in defining the best approaches for preventive education. Efforts are needed to develop
more accurate screening diagnostic tests and improved confirmatory tests. Research is needed also to
further determine the therapeutic value, costs, and
benefits of prenatal toxoplasmosis screening. Genetic
research is underway to determine if specific strains
are more infectious or pathogenic to humans. It is
already known that at least three clonal lineages of T.
gondii exist (91). It also may be possible with genetic
research to determine the source and spread of T.
gondii infections in animals and humans. Finally,
more research needs to be done on the most effective
means of primary prevention of toxoplasmosis
through education.
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