TOXOPLASMOSIS

Toxoplasma gondii:

parasito protozoo
intracelular
obligado.
Formas
infecciosas:
Ooquistes, Quistes
tisulares y
Taquizoitos.

A case-control study for risk factors for the acquisition of toxoplasmosis was
conducted in pregnant women positive or negative for IgM antibodies to T.
gondii in six European centers. Risk factors by multivariate analysis included
consumption of undercooked or raw lamb, beef, or game; contact with soil;
and travel outside

Sources of toxoplasma infection in pregnant women:

European multicentre case-control study. European
Research Network on Congenital Toxoplasmosis. Cook
AJ, BMJ.2000;321(7254):142.

Acute toxoplasmosis usually is asymptomatic; the occasional pregnant woman may

have lymphadenopathy. Primary infection during pregnancy is associated with
approximately a one-third chance of fetal infection. Although the rate of fetal
infection is noted to be higher when maternal infection occurs in the third compared
to the first trimester, fetal death or severe congenital infection are more likely to
result from infection during the first trimester

McAuley, JB, Boyer, KM, Remington, JS, McLeod, RL. Toxoplasmosis. In:
Textbook of Pediatric Infectious Diseases, 6th ed, Feigin, RD, Cherry, JD,
Demmler-Harrison, GJ, Kaplan, SL (Eds), Saunders, Philadelphia 2009.
p.2954.

Numerous studies have shown that apparently normal infants at birth who have
congenital toxoplasmosis and do not receive treatment have a high probability of
subsequently developing abnormalities. The most common late finding is
chorioretinitis, which can result in unilateral vision loss [20]. In one histopathologic
study of affected fetuses, retinitis, retinal necrosis, disruption of retinal pigment
epithelium, choroidal inflammation, and congestion all were detected in a
proportion of the eyes, suggesting early involvement, which may manifest later with
a subsequent host inflammatory response
Most infants with congenital toxoplasmosis (70 to 90 percent) are asymptomatic or
without apparent abnormalities at birth. Even though subclinical disease is the
rule, signs present at birth may include fever, a maculopapular rash,
hepatosplenomegaly, microcephaly, seizures, jaundice, thrombocytopenia, and,
rarely, generalized lymphadenopathy. The so-called classic triad of congenital
toxoplasmosis consists of chorioretinitis, hydrocephalus, and intracranial
calcifications.
Histopathological features of ocular toxoplasmosis in the fetus
and infant. Roberts F, Arch Ophthalmol. 2001;119(1):51

Many diagnostic tests are available, but results

must be interpreted carefully. T. gondii can be
isolated from the placenta, umbilical cord, or
infant blood by inoculation into mice or cell
culture. Polymerase chain reaction (PCR) for T.
gondii on peripheral blood white blood cells,
cerebrospinal fluid (CSF), and placenta also
are available

Boyer KM. Diagnostic testing for congenital

toxoplasmosis. Pediatr Infect Dis J 2001;

Spiramycin (2 to 3 g/day) has been used in many parts of the world in pregnant
women with acute toxoplasmosis during pregnancy for the prevention of congenital
toxoplasmosis. This treatment appears to reduce the likelihood of congenital
transmission by as much as 50 percent
McAuley, JB, Boyer, KM, Remington, JS, McLeod, RL. Toxoplasmosis. In:
Textbook of Pediatric Infectious Diseases, 6th ed, Feigin, RD, Cherry, JD,
Demmler-Harrison, GJ, Kaplan, SL (Eds), Saunders, Philadelphia 2009.
p.2954.
If a prenatal diagnosis of toxoplasmosis is made in the fetus, most experts
recommend the addition of pyrimethamine (100 mg/day in 2 divided doses for 2
days followed by 50 mg/day) and sulfadiazine (75 mg/kg per day in 2 divided doses
for 2 days followed by 100 mg/kg per day in 2 divided doses [maximum dose for
each of 4 g/day]) to spiramycin in the mother. Leucovorin, which is folinic acid, (5 to
20 mg/d) must be taken with pyrimethamine to rescue human cells; T. gondii cannot
use exogenous folinic acid. Spiramycin does not appear to treat established
disease in the fetus
Fetal toxoplasmosis: outcome of pregnancy and infant follow-up
after in utero treatment. Hohlfeld P, J Pediatr. 1989;115(5 Pt 1):765.

CONGENITAL SYPHILIS

Congenital syphilis occurs when the spirochete Treponema pallidum is transmitted

from a pregnant woman to her fetus. Infection can result in stillbirth, hydrops
fetalis, or prematurity and associated long-term morbidity. Because of this
morbidity, great emphasis has been placed on routine syphilis screening of all
pregnant women
Most neonates with congenital syphilis are
asymptomatic at birth. Overt infection can
manifest in the fetus, the newborn, or later
in childhood. Clinical manifestations after
birth are divided arbitrarily into early (2
years of age (table 1)) and late (>2 years of
age (table 2)).

CONGENITAL RUBELLA
Clinical manifestations of CRS include sensorineural deafness, cataracts ,
cardiac malformations (eg, patent ductus arteriosus, pulmonary artery
hypoplasia), and neurologic and endocrinologic sequelae. Neonatal
manifestations may include growth retardation, radiolucent bone disease
(not pathognomonic of congenital rubella), hepatosplenomegaly,
thrombocytopenia, purpuric skin lesions (classically described as "blueberry
muffin" lesions that represent extramedullary hematopoiesis), and
hyperbilirubinemia.

The manifestations of CRI vary depending upon the timing of maternal

infection. (See "Rubella in pregnancy", section on 'Congenital rubella
syndrome'.) The incidence of defects may be as high as 80 to 85 percent if
maternal rubella is acquired during the first trimester [19,34,56]. Little, if any,
risk of congenital defects is associated with infection after 18 to 20 weeks'
gestation [19,57]; intrauterine growth retardation may be the only sequela of
third-trimester infection

CONGENITAL CYTOMEGALOVIRUS Cytomegalovirus (CMV) is a

ubiquitous virus worldwide. Despite its listing as the fourth infection in the
TORCH designation, CMV has emerged as the most common congenital
viral infection.

Asymptomatic infection Approximately 90 percent of infants with congenital

CMV infection are asymptomatic at birth. However, 0.5 to 15 percent of these
children are at risk for development of psychomotor, hearing, neurologic,
ocular, or dental abnormalities within the first few years of life [49,50]. Some
otherwise asymptomatic infants with congenital CMV infection are identified
through newborn hearing screening [51]. In particular, sensorineural hearing
loss will appear in 5 to 10 percent of cases and may interfere with learning
abilities (table 3) [52-58]. Hearing loss appears to be associated with increased
concentrations of CMV in peripheral blood and urine

percent of infants with congenital CMV

infection are symptomatic [60]. One study
suggested that symptomatic congenital
infection correlated with the amount of
virus present in the amniotic fluid; infants
born to mothers with 10(3) genome
equivalents in amniotic fluid by polymerase
chain reaction (PCR) had a 100 percent
probability of acquiring CMV, and for those
with 10(5) genome equivalents, this
infection was symptomatic [61].
Fifty percent of symptomatic infants
present with an attenuated form of
congenital infection, usually consisting of
isolated splenomegaly, jaundice, and/or
petechiae [60,62]. The other 50 percent of
symptomatic infants present with the
syndrome of cytomegalic inclusion disease,
consisting of (picture 1) [63]:
Jaundice 67
percentHepatosplenomegaly 60
percentPetechial rash 76
percentMultiorgan involvement (eg,

TOXOPLASMOSIS
CONGENITA
20

70 % de embarazadas son
seropositivas.
Solo en infeccin materna
primaria.
Transmisin de 50%, mayor
transimisin en el 3er. Trimestre.
Afecta a 1 de cada 1000 nv.
80% asintomticos.

TOXOPLASMOSIS
CONGENITA
Triada

clsica: Hidrocefalia,
coriorretinitis y calcificaciones
intracraneanas.
Presentaciones:
Aparentemente asitomtico.
Enfermedad generalizada.
Afeccin neurolgica.

PREVENCIN
Evitar

comer carne cruda o poco

cocida.
Lavar cuchillos y tablas de picar.
Lavar vegetales y frutas.
Cuidado al hacer trabajos de
jardinera.
Manejo cuidadoso de heces de
gato.

TRATAMIENTO
Evitar

enf. congnita:
Espiramicina, claritromicina o
azitromicina.
Tratamiento prenatal:
Pirimetamina y sulfadiazina
Tratamiento Postnatal:
Pirimetamina y sulfadiazina por
1 ao.

DIAGNOSTICO DE
TORCH
No

pedir prueba de
TORCH
Dirigir la investigacin
hacia la sospecha ms alta.
Pruebas serolgicas,
cultivos, PCR

Sfilis: VDRL FTA

La
transmisin en humanos es con el consumo de sangre contaminada y de
madre a hijo. El feto es afectado va transplacentaria, dependiendo la
edad
gestacional; en la primera mitad hay un 10% de contagio, pero la
enfermedad es mucho ms severa; en el ltimo trimestre la transmisin
es
de 60-80%.