-
ARTICLE
Toxoplasmosis: DTreatment, and Pin Congenitally E
ABSTRACT
KEY WORDSCongenital toxoplasmosis, toxoplasmosis, ocular
toxoplas-mosis, retinochoroiditis, hydrocephalus, pPediatrics,
nurse
andunderstandhow it is diagnosedand treated. This ar-ticle will
review the epidemiology, pathophysiology,transmission, risk
factors, clinical presentation, diag-
mosis andtitioner in
clinical education and research.
tly around-Lewis, &to dependces, waterure to
soilregardingStates, se-000 volun-Nutrition04 (Jonestrated that
among women of childbearing age (15-44 years),
thedoi:10.1016/j.pedhc.2010.04.008www.jpedhc.org November/December
2011 355The TORCH complex refers to five major congenitalinfections
that, when contracted by a fetus in utero,lead to serious and often
life-threatening clinical EPIDEMIOLOGY
The prevalence of toxoplasmosis varies greathe world (Jones,
Kruszon-Moran, SandersWilson, 2007). Prevalence rates are thoughton
food production and harvesting practitreatment, environment,
climate, and exposor sand (Jones et al., 2007). To gather datathe
prevalence of this parasite in the Unitedrum samples were taken
from more than 15,teers as part of the National Health
andExamination Survey between 1999 and 20et al., 2007). Results of
this study demons
AlysonKaye, recentgraduateofColumbiaUniversity,NewYork,NY.
Conflicts of interest: None to report.
Correspondence: Alyson Kaye, CPNP, MS, BS, 600 ColumbusAve, Apt
10M, New York, NY 10024; e-mail: ark2135@columbia.
edu.
0891-5245/$36.00
Copyright Q 2011 by the National Association of Pediatric
Nurse Practitioners. Published by Elsevier Inc. All rights
reserved.practitioner, congenital infections, TORCH nostic
methods, and treatment of toxoplaswill emphasize the role of the
nurse pracToxoplasmosis is a rare disease caused by the obligate
intra-cellular protozoan parasite, Toxoplasma gondii. Mostpersons
with toxoplasmosis in the United States are asymp-tomatic, but if a
woman is infected during pregnancy, the par-asite can cross the
placenta and cause congenitaltoxoplasmosis in the fetus. The
severity of congenital toxo-plasmosis depends on when in the
pregnancy the mother isexposed, but it can cause ocular and central
nervous systemdisease as well as lead to growth failure and hearing
and vi-sion abnormalities. Congenital toxoplasmosis is treated
witha combination of pyrimethamine, sulfadiazine, and leuco-vorin.
It is important for pediatric nurse practitioners to beaware of the
clinical presentation and treatment of congenitaltoxoplasmosis. J
Pediatr Health Care. (2011) 25, 355-364.Alyson Kaye, CPNP, MS,
BSInfantssequelae. The T in TORCH stands for toxoplasmosis,an
infection by the intracellular parasite Toxoplasmagondii
(Gerber&Hohlfeld, 2003).T. gondii is amemberof the phylum
Apicomplexa and parasitic subclass coc-cidian. The primary host of
this parasite is the cat (felinefamily), and it is passed through
the feces of felines(Pradhan, Yadav, & Mishra, 2007). Humans
can act asan intermediate host in the parasites life cycle. Ifa
woman is infected while pregnant, this parasite cancross the
placenta frommother to fetus and cause dam-aging effects to the
fetal eye, brain, and other tissuesleading to congenital
toxoplasmosis (Gerber &Hohlfeld, 2003). It is important that
pediatric nursepractitioners (PNPs) be aware of this disease,
recognizewhen it should be considered as adifferential
diagnosis,iagnosis,reventionxposed
-
prevalence of women with IgG antibodies to T. gondiiborn within
the United States is 11%. For women bornoutside of the United
States, the prevalencewas higher,at 28.1% (Jones et al., 2007). The
prevalence rates of IgGantibodies to T. gondii in women of
childbearing ageare important to monitor because they provide
insightinto the prevalence of congenital toxoplasmosis.
Nolarge-scale studies have examined the prevalence ratesof IgG
antibodies to T. gondii in pregnant women, andtoxoplasmosis is not
a nationally reported disease(Lopez,Dietz,Wilson,Navin,& Jones,
2000). Accordingto theDivision of Parasitic Diseases of theNational
Cen-ter for Infectious Diseases, it was estimated in theUnited
States in the year 2000, 1 in 10,000 live birthsresults in
congenital toxoplasmosis (Brown, Chau,Atashband, Westerberg, &
Kozak, 2009; Lopez et al.,2000). The incidence of congenital
toxoplasmosis isthen estimated to be around 400 to 4000 new
casesevery year (Lopez et al., 2000; Pinard, Leslie, &
Irvine,2003).
PATHOPHYSIOLOGYT. gondii is an obligate intra-cellular
protozoanparasite that is responsible for the disease
toxoplasmo-sis (Tamma & Serwint, 2007). This parasite has a
com-plex life cycle that is relatively host specific and isdivided
into three infectious stages (Dubey, 2004;Kravetz & Federman,
2005). The preferred primaryhost for T. gondii is felines (cats),
but humans canbecome infected when they act as an intermediatehost.
When an intermediate host ingests T. gondii,the first stage,
tachyzoites, enter a cell and createa vacuole to protect themselves
from the hostsimmune system (Dubey, 2004). Tachyzoites are
resil-ient and are capable of entering and reproducing inalmost any
mammalian or avian cell (Rorman, Zamir,Rilkis, & Ben-David,
2006). Tachyzoites containedwithin certain immune cells can be
disseminatedthroughout the body until an adequate immuneresponse is
mounted between 7 and 10 days after infec-tion (Kravetz &
Federman, 2005). In response to thehosts immune system, tachyzoites
multiply asexuallyand produce cysts, each of which contains the
nextstage, bradyzoites (Dubey, 2004). Each individual cystcan
contain hundreds of bradyzoites and can be foundwithin many
different types of tissue (Dubey, 2004).The most common tissues
include tissue in the eye,heart, brain, lungs, liver, and lymph
nodes. The intactcysts canpersist for life in adormant stage in an
interme-diate host (Kravetz & Federman, 2005). If the
immunesystem becomes compromised, these bradyzoites canbegin
replicating asexually again and will exit the cystas tachyzoites
and be spread through the body in bloodand lymph systems (Kravetz
& Federman, 2005).When a cat ingests a tissue cyst in meat it
consumed,
enzymes in the stomach and intestine degrade the cystand
bradyzoites are released. Through asexual repro-356 Volume 25
Number 6duction these bradyzoites will become tachyzoitesagain, the
first aforementioned stage (Dubey, 2004.)Some bradyzoites will
invade the epithelial tissue ofthe feline intestine and will begin
to multiply throughsexual reproduction to form a fertilized
oocyst(Kravetz & Federman, 2005). These oocysts can onlybe
formed in the intestine of awild or domesticmemberof the feline
family and cannot be formed in an interme-diate host such as humans
(Dubey, 2004).Oocysts pass out of the feline host through feces
and
become sporulated in the environment, forming thethird stage,
sporozoites (Jones, Lopez, & Wilson,2003). Any host that
ingests sporozoites from the envi-ronment or acquires tissue cysts
from eating infectedmeat will become infected with T. gondii
(Jones,Lopez et al., 2003). In humans, contaminated fruit,
veg-etables, or water that has been in contact with cat fecesis the
source of ingestion of sporozoites from the envi-ronment. Tissue
cysts are usually acquired through theingestion of undercooked
infected meat (Jones, Lopezet al., 2003; Pradhan et al., 2007).
Bradyzoites releasedfrom an ingested tissue cyst or sporozoites
releasedfrom an ingested oocyst penetrate the humanintestine and
become tachyzoites again. Thesetachyzoites then follow the cycle
described previously(Dubey, 2004).T. gondii has been shown to be a
highly mobile par-
asite and actively travels through blood and lymph fluidand
across biological barriers such as the intestinalwall,blood-brain
barrier, and the placenta (Rorman et al.,2006). In humans, the
transplacental passage of tachy-zoites from mother to fetus leads
to congenital toxo-plasmosis (Dubey, 2004). In healthy adults,
aninfection of T. gondii is asymptomatic in most cases.The immune
system will prevent replication of the par-asite and destroy any
bradyzoites that are released fromdormant tissue cysts (Dubey,
2004). However, ifa woman is infected during pregnancy,
tachyzoitescan cross the placenta and infect the fetus
(Dubey,2004). The symptoms and course of infection dependon many
factors including inoculation factors, viru-lence of the particular
organism, gestational age attime of infection, sex, genetic
factors, and immunestatus of the mother and fetus (Pradhan et al.,
2007).The cycle of exposure that leads to congenital toxoplas-mosis
is illustrated in Figure 1.
VERTICAL TRANSMISSIONTransplacental transmission of T. gondii
occurs in ap-proximately 40% of pregnancies in which the motheris
exposed for the first time during the course of thepregnancy
(Bonfioli & Orefice, 2005). In 90% of cases,themotherwill be
asymptomatic at the time of infection(Kravetz & Federman,
2005). It is estimated that 50% ofexpectant mothers who give birth
to infants congeni-tally infected with T. gondii have no
recollection ofsymptoms or any obvious exposure to the
parasiteJournal of Pediatric Health Care
-
ongenital toxoplasmosis. This figure is available in(Montoya
& Remington, 2008). In symptomatic cases,the mother may
experience a range of flu-like symp-toms including fever, malaise,
and cervical lymphade-nopathy (Kravetz & Federman, 2005).
Mothers
FIGURE 1. The cycle of exposure that leads to ccolor online at
www.jpedhc.org.infected prior to conception rarely transmit the
parasiteto the fetus except in cases where the parasite
becomesreactivated because of the immune suppression of themother
(Jones, Lopez et al., 2003).In the majority of cases of congenital
toxoplasmosis,
the fetus is exposed during the last trimester and symp-toms in
the infant range from mild to asymptomatic(Bonfioli &Orefice,
2005). If the fetus is infected duringthe first trimester, clinical
manifestations are signifi-cantlymore severe andmay result in
spontaneous abor-tion of the fetus. Infection during the second
trimesteralso may result in a symptomatic infection, but the
clin-icalmanifestations vary frommild to severe anddependon
individual factors (Bonfioli & Orefice, 2005; Jones,Lopez et
al., 2003).
RISK FACTORSThe risk factors for T. gondii exposure are
directlyrelated to exposure to cats and more specifically tocat
feces (Box 1). Because cats are the primary hostfor T. gondii, cats
in the house or stray cats in andaround the house or property are
considered a primaryrisk factor for acquiring this parasite during
pregnancy.Any job or activity that puts a pregnant woman in
directcontact with soil, sand, or other material that could
con-tain cat feces puts her at risk for being infected
www.jpedhc.org(Rabinowitz, Gordon, & Odofin, 2007). Drinking
waterthat has been contaminatedby cat feces also can exposea
pregnant woman to T. gondii (Holland, 2003). In theUnited States,
the majority of cases of congenital toxo-
plasmosis can be traced back to an exposure tomaterialcontaining
cat feces or the ingestion of raw food grownin soil containing cat
feces (Safadi, Berezin, Farhat, &Carvalho, 2003). The ingestion
of undercooked orrawmeat during pregnancy is also a risk factor
becausethe tissue may contain T. gondii cysts that, unless
de-stroyed by cooking heat or food preparation practices,could
infect a pregnant woman (Safadi et al., 2003).
CLINICAL PRESENTATIONCongenitally acquired toxoplasmosis causes
a widevariety of signs and symptoms and typically presentsin one of
three ways. In the majority of cases, an infant
BOX 1. Risk factors for contractingtoxoplasmosis
d Cats in the home or stray cats in or around the homed Any job
or activity that requires contact with dirt, soil, orother material
that could contain cat feces
d Ingestion of raw meat, raw eggs, or unpasteurized milkd
Drinking untreated waterd Touching the eyes or face during or
immediately afterfood preparation
d Ingestion of unwashed fruit or vegetables
November/December 2011 357
-
for any of the aforementionedms. Differential diagnoses foris
also include other congenitalegalovirus (CMV), rubella, orones,
Lopez et al., 2003).cells in the eye of the fetusy of the eye and
cause congen-is. Ocular toxoplasmosis is re-of cases of uveitis and
25% ofveitis in the United Statescular effects of toxoplasmosis
ndingonwhether the signs andthe neonatal period or if theylife
(Bonfioli &Orefice, 2005).nfected with T. gondii who docular
lesions will develop bythe time they reach childhood or early
adolescence(Wallon et al., 2004). The risk of ocular
lesionsdecreases over time if no lesions are noted in the
infantperiod (Freemanet al., 2008). Symptoms of ocular
toxo-plasmosis can vary depending on the age of the patient.Reduced
visual acuity, strabismus, leukocoria, photo-phobia, pain, and
nystagmus are common signs thatshould alert a medical provider to
the possibility oftoxoplasmosis (Bonfioli & Orefice, 2005;
Jedari,Maliky, & Daneshjou, 2008).remember to place conof
differential diagnosesconstellation of symptocongenital
toxoplasmosinfections such as cytomherpes viral infections (JT.
gondii can enter
through the blood supplital ocular toxoplasmossponsible for up
to 17%cases of posterior u(Soheilian et al., 2005). Ocanbe
categorizeddepesymptoms are present indo not occur until later inIn
up to 80% of infants inot receive treatment, owill be asymptomatic
or have subclinical symptoms atbirth, making the condition
difficult to diagnose(Brown et al., 2009; Safadi et al., 2003). A
smallerminority of infants will present with overt symptomsin the
neonatal period, while the third class of infantswill present with
symptoms within the first few weeksto months of life (Brown et al.,
2009).A PNP should be aware of any red flags in the history
that would allude to the possibility of congenital
toxo-plasmosis. A history of hydrocephalus, retinochoroidi-tis, and
calcifications inthe central nervoussystem in the newbornperiod
should immedi-ately alert a care pro-vider to the possibilityof
toxoplasmosis. Thesigns and symptomsmay be less specific,however,
and may notbe present until laterin infancy and child-hood (Jones,
Lopezet al., 2003). Thesesymptoms includeconvulsions,
palsies,growth or mental retar-dation, visual or hearing
impairment, learning disabil-ities, organomegaly, lymphadenopathy,
fever, andrash (Jones, Lopez et al., 2003). It is important to
genital toxoplasmosis on a list
A history ofhydrocephalus,retinochoroiditis,and calcifications
inthe central nervoussystem in thenewborn periodshould
immediatelyalert a care providerto the possibility
oftoxoplasmosis.358 Volume 25 Number 6T. gondii also can invade
tissues in the centralnervous system of the developing fetus and
can causeareas of focal and diffuse necrosis in the
cerebellum,cerebrum, spinal cord, and brain stem
(Lago,Baldisserotto, Hoefel Filho, Santiago, & Jungblut,2007).
These areas of necrosis eventually become thecentral nervous system
calcifications that are character-istic of this disease. It is
believed that these areas of cal-cified tissue are formed from an
inadequate amount ofdendritic cells removing necrotic tissue at the
affectedsites (Lago et al., 2007). The site of these
calcifiedlesions varies to some degree by the gestational age
atwhich a developing fetus is exposed to T. gondii. A fe-tus
exposed before the 20thweek of gestation oftenwillhave large dense
lesions seen in the basal ganglia (Lagoet al., 2007). A fetus
exposed between the 20th and 30thweeks of gestation typically will
present with smalllesions seen in the lateral ventricles. A fetus
exposedafter 30 weeks gestation may have diffuse lesions inthe
cerebral parenchyma (Lago et al., 2007).It is important that any
infant with suspected or con-
firmed congenital toxoplasmosis receive imaging of thecentral
nervous system. A computed tomography (CT)scan and ultrasound are
the preferred diagnosticmethods. It is important to use a
diagnostic methodthat can adequately pick up areas of calcification
inthe infant brain (Lago et al., 2007). CT scanning is
thefirst-line diagnostic method used in North America todetect
central nervous system abnormalities causedby toxoplasmosis. If
concerns exist about the effectsof radiation in the neonatal
period, an ultrasound canbe used as an alternative diagnostic
method. However,a negative ultrasound in a patient with
confirmedcongenital toxoplasmosis may need to be followed bya CT
scan for confirmation because ultrasound resultscan vary depending
on the examiner and technologyused (Lago et al., 2007). Therefore,
in an infant withconfirmed congenital toxoplasmosis or in an
infantwho has symptoms, it may be advisable to order a CTscan to
limit the amount of diagnostic imaging needed.
PHYSICAL ASSESSMENTOcular ToxoplasmosisToxoplasmosis affects the
retina and the underlyingchoroid, causing retinochoroiditis, the
most commonmanifestation of ocular toxoplasmosis (Smith
&Cunningham, 2002). Retinochoroiditis is described
asmacular-pigmented lesions with a central necroticarea primarily
found on the retina and can be observedby funduscopic examination.
Retinochoroiditis is illus-trated in Figure 2. In more than 50% of
cases of ocularcongenital toxoplasmosis, the lesions are found
onthe posterior pole of the retina and are unilateral(Bonfioli
& Orefice, 2005). Upon examination of theeye, amedical provider
will see a gray-white area of ret-inal necrosis with or without
exudates with adjacentswelling of the optic disc, vitreitis,
vasculitis, andJournal of Pediatric Health Care
-
hemorrhage (Bonfioli & Orefice, 2005; Smith &Cunningham,
2002). A headlight in the fog isa common description of ocular
toxoplasmosis, and itrefers to the retinal inflammation seen
through aninfected and opaque vitreous (Bonfioli &
Orefice,2005). Active inflammation and infection in the eye
typ-ically lasts about 6 weeks, at which time the lesion willbegin
to regress, leaving behind a characteristic pig-mented scar on the
retina (Smith &Cunningham, 2002).Ocular toxoplasmosis that is
allowed to proceed un-
checked without treatment can lead to devastatinglong-term
effects. It has been associated with glau-coma, cataracts, vitreous
opacification, retinal hemor-rhage or detachment, and optic
atrophy. All of theseconditions can lead to permanent blindness
(Bonfioli& Orefice, 2005). Ocular lesions can recur in
adoles-cence and adulthood, even after treatment in
infancy.Follow-up of these patients is extremely important
toprevent further damage to the eyes (Phan et al., 2008).
FIGURE 2. Fundoscopic view ofretinochoroiditis. This figure is
available incolor online at www.jpedhc.org.Central Nervous System
ToxoplasmosisA congenitally exposed infant with central nervous
sys-temcalcificationsmayormaynot haveovert neurologicsymptoms.
Symptoms that have been documented ininfants with congenital
toxoplasmosis include convul-sions, abnormal tearing of the eye,
nystagmus, strabis-mus, hearing and visual impairments, and growth
anddevelopmental delays (Jones, Lopez et al., 2003).Many of these
symptoms overlap with symptoms ofocular toxoplasmosis and could be
attributed to eithermanifestation of this parasitic infection
(Jedari et al.,2008). Toxoplasmosis can also cause hydrocephalusand
microcephaly in the developing fetus (Dimarioet al., 2009).
Sensorineural Hearing Loss and ToxoplasmosisToxoplasmosis also
has been associated with sensori-neural hearing loss. A literature
review looking at the
www.jpedhc.orgassociation between this parasitic infection and
hearingloss found a scarcity of reliable data (Brown et al.,2009).
Only five studies met the inclusion criteria forthe literature
review, and they reported such differentresults that it is
impossible to discern the associationbetween hearing loss and
toxoplasmosis (Brownet al., 2005). Although the association and
cause arenot fully understood at this time, a nurse
practitionershould be aware that the hearing of any childwith a
his-tory of toxoplasmosis should be evaluated on a regularbasis and
that the child should be referred to an audiol-ogist and ear, nose
and throat specialist for follow-up(Brown et al., 2005).
DIAGNOSTIC TESTSThe prevention and treatment of congenital
toxoplas-mosis begins with identifying infection in pregnantwomen.
Antibody testing that measures the amount ofIgG and IgM is used to
confirm exposure to T. gondii.IgG and IgM levels rise within 2
weeks of being ex-posed to the parasite (Jones, Lopez et al.,
2003). Ele-vated IgG levels confirm a patient has been exposedto
the parasite but do not differentiate between a recentexposure and
an exposure that occurred in the past be-cause IgG will persist at
a low level throughout the lifeof the patient (Jones, Lopez et al.,
2003). IgM antibodylevels can be used to confirm an acute exposure,
andthe degree of elevation can be used to discern whenthe exposure
occurred (Lopez et al., 2000). AlthoughIgM antibodies are almost
always present followingan acute exposure, they can persist in some
patientsat high levels for up to 18 months, leading to an
inaccu-rate assessment of when the exposure occurred. Thissituation
can be problematic because congenital toxo-plasmosis occurs when
the mother is infected duringher pregnancy, and the severity of the
disease is deter-mined by ascertainingwhen in the pregnancy the
infec-tion occurred (Nascimento, Suzuki, & Rossi, 2008).
Asignificant increase in specific antibody titers or
sero-conversion during pregnancy is usually considered di-agnostic
of a recent exposure (Nascimento et al., 2008).Despite serologic
evidence demonstrating the likeli-
hood of recent exposure, a T. gondii reference labora-tory must
confirm the diagnosis, in part because ofquestions about the
sensitivity and specificity of IgGand IgM antibody testing (Tamma
& Serwint, 2007).The Sabin FeldmanDye test is performedby a
referencelaboratory and is considered the gold-standard diag-nostic
test for toxoplasmosis. This test detects a changeinT.
gondiispecific antibody titers (IgG) over a 3-weekperiod or detects
a single elevated (IgG) antibody titer(Rorman et al., 2006). A
four-fold increase in titer levelsover a three-week period or a
single titer above 250 IU/ml is considered highly suggestive of
infection (Rormanet al., 2006). Polymerase chain reaction testing
of amni-otic fluid is the preferred method for providing
confir-mation of fetal exposure (Jones, Lopez et al.,
2003).November/December 2011 359
-
enital Toxoplasmosis Studyound that treatment with
themedications significantly de-nd symptoms associated withs,
including ocular and centralms and sensorineural hearing). This
combination of medica-ed by the American Academyatients with
sensitivity to sulfa-be used in combination with
ernative (AAP, 2009). Informa-dications and other
alternative
TABLE.Medicationsusedto
treattoxoplasmosis
Medication
Mechanismofaction
Dose
Length
oftherapy
Adverseeffects
Sulfadiazine*
Inhibits
folic
acid
synthesis
100mg/kg/daydividedevery12hours
1year
Bonemarrowsuppression,fever,
vasculitis,rash,nausea,vomiting,
nephropathy
Pyrimethamine*
Inhibits
tetrahydrofolic
acid
synthesis
1mg/kg/day
1mg/kg/daythreetim
esperweek
First6months
Second6months
Bonemarrowsuppression,rash,
seizures,
fever,vomiting,diarrhea,
hematuria
Folinicacid
(leucovorin
)*Areducedform
offolic
acid
5-10mgevery
3days
10mgthreetim
esperweek
First6months
Second6months
Rash,erythema,urticaria,wheezing,
thrombocytosis,
hypersensitivity
Trim
ethoprim
sulfamethoxazole
Inhibits
dihydrofolic
acid
synthesis
Consultinfectiousdisease
specialist
Consultinfectiousdisease
specialist
Bonemarrowsuppression,
hypotension,rash,seizures,
fever
Clindamycin
Inhibits
proteinsynthesis
Nostandard
dose;dose
isbasedon
weightandpostnatalage;consult
infectiousdisease
specialist
fordosing
Consultinfectiousdisease
specialist
Pseudomembranouscolitis,
hypotension,cardiacarrhythmia,
rash,bonemarrowsuppression
Azithromycin
Inhibits
proteinsynthesis
Consultinfectiousdisease
specialist
Consultinfectiousdisease
specialist
Palpitations,
chest
pain,QT
prolongation,d
iarrhea,nausea,rash,
ototoxicity,hypersensitivity
*Standard
ofcare.medications that could be used to treat toxoplasmosiscan
be found in the Table (Soheilian et al, 2005;Taketomo, Hodding,
& Kraus, 2008). A provider alsomay add a corticosteroid to
decrease the inflammationcaused by the replication of the parasite
and tomanage the associated ocular complications (AAP,2009;
Soheilian et al., 2005).Both pyrimethamine and sulfadiazine act by
inhibit-
ing folic acid synthesis in T. gondii. By using
differentmechanisms of action, they complement one anotherto create
a combined effect (Schmidt et al., 2006).Although they have been
proven effective, they do notcome without serious adverse effects
and should neverbe prescribed without diagnostic confirmation of
toxo-plasmosis (Schmidt et al., 2006). As previously
stated,spective study calledChicago Based Cong(NCCBTS). This study
fthree aforementionedcreased adverse signs acongenital
toxoplasmosinervous system symptoloss (McLeod et al., 2006tions
also is recommendof Pediatrics (AAP). For pdiazine, clindamycin
canpyrimethamine as an alttion regarding these meThis test should
be performed at or after 18 weeks ges-tation and only in women with
preliminary positiveserologic results indicative of acute
exposure(Montoya & Remington, 2008). Polymerase chain reac-tion
testing of cerebrospinal fluid also can be used toconfirm the
presence of infection in the central nervoussystem after birth
(Tamma & Serwint, 2007).
TREATMENTStandard of CareThe goal of initiating treatment is to
arrest the replicationof the parasite and prevent further damage to
the organsinvolved. It is especially important to stop replication
inthe eye to prevent irreversible damage to the retina andoptic
nerve that can lead to permanent blindness(Soheilian et al.,
2005).Currently, The WorldHealth Organizationand the Centers for
Dis-ease Control and Pre-vention recommendpyrimethamine,
sulfa-diazine, and leucovorinas the standard ofcare for persons
withcongenital toxoplas-mosis (Rorman et al.,2006). These
medica-tions were proven to be effective in a randomized pro-
the National Collaborative
Thegoal of initiatingtreatment is toarrest thereplication of
theparasite andprevent furtherdamage to theorgans involved.360
Volume 25 Number 6 Journal of Pediatric Health Care
-
pyrimethamine decreases the synthesis of folic acid bothin T.
gondii and in its human host. Thus a major adverseeffect of this
treatment regimen is bonemarrowsuppres-sion (Schmidt et al., 2006).
Bone marrow suppressionleads to neutropenia, anemia, and
thrombocytopenia.This adverse effect may be avoided with the
simulta-neous administration of folic acid during treatment(Schmidt
et al., 2006; Soheilian et al., 2005).Leucovorin, a folic acid
derivative, also can be used tocombat myelosuppression and is given
concurrentlywith pyrimethamine and sulfadiazine (Jones, Lopezet
al., 2003). Despite these preventative measures,weekly monitoring
of cell counts and platelet countsshould be done to assess the
level of marrow suppres-sion and adjust these medications as
necessary(Soheilian et al., 2005).At this time, debate exists about
the appropriate length
of therapy. Some studies that argue in some patients, 3months of
therapy may be sufficient to eradicate theparasite andprevent
long-termeffects aswell as decreasethe burden of long-term
medication usage on theaffected infant and family (Freeman et al.,
2008). How-ever,most treatment recommendations suggest that
deci-sions concerning whether therapy should be continuedor
discontinued be based on patient response to therapyaswell as the
severity of symptoms and the age of the pa-tient at the
timeofdiagnosis (Schmidt et al., 2006). Resultsfrom the NCCBTS
study and the AAP recommend treat-ment of pyrimethamine,
sulfadiazine, and folic acid(leucovorin) for a prolonged period,
often up to 1 year(AAP, 2009; McLeod et al., 2006). At this time
thereis still debate regarding dosages and length of therapy,and
thus a specialist in infectious disease andtoxoplasmosis should be
consulted prior to treatmentinitiation or treatment discontinuation
(AAP, 2009).
Treatment for Expectant MothersTreatment of a woman during
pregnancy also has beenstudied to prevent congenital toxoplasmosis.
Duringthe first trimester of pregnancy, pyrimethamine is
con-traindicated because of the teratogenic effects of
thismedication. Sulfadiazine may be used alone duringthe first
trimester and pyrimethamine may be addedto the regimen after this
crucial period of fetal develop-ment if the benefit of this drug
outweighs the risk to thefetus (Freeman et al., 2008). Although not
yet approvedby the Food and Drug Administration in the
UnitedStates, another medication called spiramycin is usedto
prevent transplacental infection in many other coun-tries.
Spiramycin is available in the United States underspecial
circumstances as an investigational medication(Rorman et al.,
2006).Overall, the research pertaining to anti-toxoplasmic
treatment is lacking. The majority of studies are
retro-spective, and few randomized control trials exist thatlook at
medication efficacy. More research must bedone in this area to
develop the best treatment forwww.jpedhc.orgpregnant women and
neonates congenitally exposedto T. gondii.
NEONATAL SCREENINGScreening for toxoplasmosis is a controversial
topic. Inpopulations with a low prevalence, screening of preg-nant
mothers is not believed to be cost-effective, noris treatment
during pregnancy guaranteed to preventcongenital toxoplasmosis
(Dimario et al., 2009).Screening in the neonatal periodmaybe amore
feasibleoption for primary care providers (Jara, Hsu, Eaton,
&Demaria, 2001). In 1986, Massachusetts added toxo-plasmosis to
its newborn screening and createdfollow-up recommendations for
infants with positiveserologic findings (Jara et al., 2001).
Currently in theUnited States, Massachusetts and New Hampshire
arethe only two states that routinely screen for toxoplas-mosis at
birth. IgM and IgG antibody testing is used toscreen all infants in
these two states at the same timethat all other newborn screening
is conducted (Jaraet al., 2001). It is important to note that
positive sero-logic results demonstrate that the mother has
beenexposed and do not definitively indicate
congenitaltoxoplasmosis in the infant (Jara et al., 2001).
Theresults simply allow the primary care provider to beaware of the
possibility and provide further follow-upas indicated.Preliminary
data from these two states suggest that
the prevalence of congenital toxoplasmosis is 1 in12,000 live
births and that providing treatment tothese infants early in life
significantly decreases theneurologic and ophthalmologic effects of
this disease(Jara et al., 2001). Between 1986 and 1992, 52
infantsin Massachusetts and New Hampshire were identifiedas having
been congenitally infected. Fifty of these in-fants were identified
through neonatal screening alone,and after 1 year of treatment,
only one infant demon-strated a neurologic deficit and four infants
demon-strated lesions in the eye (Lopez et al., 2000). Thusthese
preliminary data demonstrate that early screeningand treatment can
significantly decrease the long-termsequelae of congenital
toxoplasmosis. Neonatalscreening has limitations, however, and
should neverbe used as diagnostic confirmation of congenital
toxo-plasmosis because the sensitivity and specificity of
suchtesting, especially using filtered blood samples, is lowand
could provide false results (Dimario et al., 2009).
ROLE OF THE NURSE PRACTITIONERImplications for Clinical
PracticePNPs play an important role in recognizing and
treatingcongenital toxoplasmosis. Because screening for
toxo-plasmosis does not always occur during the prenatalperiod,
many prenatal infections go unnoticed and un-documented. A mother
may be unaware that she hasbeen exposed to the parasite and unaware
of the risksthat T. gondii can pose to her infant. The first step
forNovember/December 2011 361
-
for example, also can limit theoman may have with thesePinard et
al., 2003). The skinstables should be washed andse oocysts may be
attached toand could be ingested. Again,strongly emphasized after
han-luding fruits, vegetables, andal., 2000).T. gondii cysts can
re-different types of mammals ors, it is estimated that 8% of
beefkmeat contains T. gondii tissueall PNPs in primary care is to
be aware of this infectionand to ask each new mother about her
possible expo-sure to the organism. Important screening
questionspresented in Box 2 should be asked at newborn visitsand
any prenatal visits. These questions can providean idea of the
level of risk andwhether congenital toxo-plasmosis is a
possibility, especially if any abnormalitiesare noted in the
newborn.An infant that has been congenitally exposed to
T. gondii will require medical care, monitoring, andfollow-up
throughout infancy, childhood, and adoles-cence. A PNP can provide
a medical home and cancoordinate primary care with specialty care
includingophthalmology, neurology, audiology, and infectiousdisease
specialists, depending on the clinical needs ofthe patient.
Although treatment during infancy can
BOX 2. Important screening questions forToxoplasma gondii
seronegative expectantmothers to assess the risk of T.
gondiiexposure
Questions
d Do you own a cat?d If you own a cat, does your cat go outdoors
or hunt andeat raw meat?
d Do you garden?d Do you work or participate in any activity
where you aredirectly exposed to sand, dirt, or soil?
d Do you eat meat? If yes, how is it prepared?d Do you eat raw
fruit and vegetables? If yes, how are theyprepared?
d Have you traveled to any foreign countries? If yes,whereand
what did you eat, and did you drink the water?
Based on the answers to these questions, a
practitionercanprovide thenecessary education toprevent
exposure.decease the long-term effects of congenital
toxoplas-mosis, children and adolescents whowere treated in
in-fancy are still at risk for ocular complications later in
life.Because of this risk, it is important to ensure thatpatients
receive routine ophthalmologic monitoring toidentify ocular
complications before they lead topermanent damage of the eye (Phan
et al., 2008).
Patient EducationIn the United States it is estimated that 85%
of pregnantwomen have never been exposed to T. gondii and thusare
at risk for contracting the parasite during pregnancy(Jones,
Ogunmodede et al., 2003). Prevention of con-genital toxoplasmosis
begins with preventing primaryinfection. Despite the fact that T.
gondii can be avoidedby implementing relatively simple strategies
in dailylife, the majority of pregnant women are unaware ofhow to
prevent exposure (Jones, Ogunmodede et al.,2003). A survey of 400
pregnant women in the UnitedStates demonstrated that only half were
aware of
362 Volume 25 Number 6cysts (Kravetz & Federman, 2005). All
pregnant womenshould be taught to never ingest raw meat and to
cookall meat to an internal temperature of at least 152F todestroy
the tissue cysts (Kravetz & Federman, 2005).Because cats are
theprimaryhost forT. gondii, it is im-
portant that pregnant women be aware of the risks theymay pose.
Contact with cat litter should be avoided ifpossible, and if
contactis unavoidable, glovesshould be worn whilechanging the
litter boxand hands should bewashed thoroughly af-terward (Lopez et
al.,2000; Pinard et al.,2003). Frequent litterchanges should bedone
because it takesseveral days foroocysts to becomeinfectious, and
the box should be thorou-ghly cleaned with disinfecting agents
(Lopez et al.,2000; Pinard et al., 2003). Preventing a cat
fromhunting outdoors or eating raw meat also can preventthe feline
from being infected with T. gondii.Practitioners should encourage
pregnant women tokeep indoor-only cats and to feed them only
cannedor dry food that has been bought in a store (Lopezet al.,
2000).Providing education to expectant mothers is an im-
portant part of the provision of primary care for PNPs.A
practitioner should providematerials and information
Because cats arethe primary host forT. gondii, it isimportant
thatpregnant womenbe aware of therisks they maypose.(Dimario et
al., 2009;gloves while gardening,contact a pregnant wenvironmental
hazards (of all raw fruit and vegethen peeled away becauthese parts
of the foodhandwashing should bedling any raw food incmeat products
(Lopez etside in the meat of manybirds. In the United Stateand
20%of lamb andportoxoplasmosis. Most of these women knew
toxoplas-mosis was associated with cat litter but were unsureas to
why and did not know about exposure in theenvironment through food,
water, dirt, sand, or soil(Jones, Ogunmodede et al.,
2003).Sporulated oocysts can be found in dirt, sand, or soil
and on the skins of raw fruits and vegetables grown inthese
substrates (Lopez et al., 2000). Limiting contactwith dirt, sand,
or soil can help prevent the ingestionof oocysts from the
environment, and if contact occurs,an expectant mother should be
taught to thoroughlywash her hands to avoid ingesting the
parasite
Lopez et al., 2000). WearingJournal of Pediatric Health Care
-
givFIGURE 3. An example of a handout that could bein color
online at www.jpedhc.org.in a variety of languages and use common
language in-stead of medical jargon to teach important points to
pa-tients. Handouts that are culturally sensitive andappropriate
for mothers with low literacy skills or whocannot read should be
used (Montoya & Remington,2008). Using pictures and color
demonstrations ofhand washing, cooking, and wearing gloves may
behelpful when teaching about toxoplasmosis if transla-tion into
another language is difficult (Montoya &Remington, 2008). In
addition, creating handouts thata patient can simply hang in the
home as a quick re-minder may be useful. Figure 3 is an example of
a hand-out for expectantmothers. Although research that looksat the
role of prenatal education in preventing congen-ital toxoplasmosis
is limited, current recommendationssuggest that all pregnant women
be given informationthrough written materials and discussions with
medicalproviders (Dimario et al., 2009). PNPs play an importantrole
in providing this information to their patients and toexpectant
mothers.
www.jpedhc.orgen to expectantmothers. This figure is
availableCONCLUSIONPNPs play an active role in the primary care of
infants. APNP may be the first medical provider who sees a new-born
after he or she is released from the hospital andcan provide
primary care throughout infancy and child-hood. It is important
that PNPs be able to recognize anddiagnose congenital toxoplasmosis
as well as provideand coordinate treatment and long-term
follow-upcare for these patients.
The author wishes to thank Dr. Rita Marie John,CPNP, DNP, EdD,
Columbia University School ofNursing, for her guidance and review
of this article.
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Toxoplasmosis: Diagnosis, Treatment, and Prevention in
Congenitally Exposed InfantsEpidemiologyPathophysiologyVertical
transmissionRisk factorsClinical presentationPhysical
assessmentOcular ToxoplasmosisCentral Nervous System
ToxoplasmosisSensorineural Hearing Loss and Toxoplasmosis
Diagnostic testsTreatmentStandard of CareTreatment for Expectant
Mothers
Neonatal screeningRole of the nurse practitionerImplications for
Clinical PracticePatient Education
ConclusionReferences