See

discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/11231571

TORCH Infections. Toxoplasmosis, Other

(syphilis, varicella-zoster, parvovirus B19),
Rubella, Cytomegalovirus (CMV), ....

Article in Current women's health reports · September 2002

Source: PubMed

CITATIONS READS

51 1,017

2 authors, including:

Barbara Stegmann
Aspire Fertility
92 PUBLICATIONS 697 CITATIONS

SEE PROFILE

All content following this page was uploaded by Barbara Stegmann on 15 April 2016.

The user has requested enhancement of the downloaded file.

r
TORCH Infections
Barbara]. Stegmann, MD and]. Christopher Carey, MD
Address
Department of OBiGYN, Phoenix Integrated Residency in OB/GYN,
Maricopa Medical Center. 260 I E. Roosevelt, Phoenix.
AZ 85008. USA.
Email: BJStegmann@aol.com
Current Women's Health Reports 2002, 2:253-258
Current Science Inc. ISSN 1534-5874
Copyright © 2002 by Current Science Inc.
Perinatal infections account for 2% to 3% of all congenital
anomalies. TORCH. which includes Toxoplasmosis.
Other (syphilis. varicella-zoster. parvovirus B 19). Rubella.
Cytomegalovirus (CMV). and Herpes infections. are some
of the most common infections associated with congenital
anomalies. Most of the TORCH infections cause mild
maternal morbidity, but have serious fetal consequences.
and treatment of maternal infection frequently has no
impact on fetal outcome. Therefore, recognition of
maternal disease and fetal monitoring once disease is
recognized are important for all clinicians. Knowledge of
these diseases will help the clinician appropriately counsel
mothers on preventive measures to avoid these infections.
and will aid in counseling parents on the potential for
adverse fetal outcomes when these infections are present.
Introduction
As mentioned above, perinatal infections are responsible
for 2% to 3% of all congenital anomalies [lee]. Infections
with the TORCH organisms frequently cause only mild
maternal infection, but can result in serious consequences
to the fetus . Recognizing these infections in both the
mother and fetus is an important part of prenatal care.
Toxoplasmosis
fnfection with the protozoan parasite Toxoplasma gondii
was the first to be linked to a fetal syndrome [2ee]. This is
the only species of Toxoplasma known to infect humans,
and overall, about ooe half of maternal infections are
transmitted to the fetus with approximately 10 per 10,000
live births affected [3]. Maternal infections early in gesta­
tion have the most severe fetal consequences, but are less
likely to be transmitted to the fetus [3] . Conversely, the
fetal infection rate is higher in late gestation, but has
virtually no risk of severe congenital infection [2 ee ,4..,5J.
Most maternal infections are acquired through
ingestion of uncooked meat or contaminated fruits and
vegetables, with the rest resulting from contact with the
oocytes in cat feces or contaminated soil. Only 10% of
maternal infections are symptomatic, presenting with pos­
terior cervical lymphadenopathy and mononucleosis-type
symptoms [4"]. Maternal diagnosis is made by isolating
T gondii from blood and body fluids , or by detecting a
fourfold increase in antibody titers in serial blood samples
[2",5]. High Toxoplasma-specific IgM titers ;n conjunc­
tion with high IgG titers also indicates infection \-vithin the
last 3 months [3] . The presence of Toxoplasma IgM or 19A
antibodies in amniotic fluid or fetal blood, after 20 weeks,
or the detection of parasite particles by polymerase chain
reaction (PCR) after 20 weeks is highly suggestive of fetal
infection [2",4ee,6]. Testing of the fetus prior to 20 weeks
should be avoided since the/etal immune system cannot
produce sufficient immunoglbbin for laboratOlY detection
until this point [2" ,4",6]. At birth, cultures of the
placenta and cord tissue provide evidence of prenatal
infection, and IgM, 19A, or IgG antibodies that persist in
the infant's blood beyond 12 months are diagnostic of
prenatal infections [6,7].
The classic triad ofToxoplasma infection is chorioretin­
itis, intracranial calcifications, and hydrocephalus. How­
ever, rash, lymphadenopathy, hepatosplenomegaly,
jaundice, thrombocytopenia, and microcephaly are also
seen [6,8] . Ninety percent of infected infants are asymp­
tomatic at bil1h, and may not demonstrate symptoms,
such as mental retardation, blindness, learning disabilities,
and epilepsy, until later in life [3].
Twenty five percent of first- and early second-uimester
infections that are untreated result in severe and/or fatal
disease [3,4",6,7]. Because of the high rate of unfavorable
outcomes, termination of the pregnancy should be
discussed when unu-eated early infection is recognized [4"],
Maternal treatment is an effective means of impacting fetal
disease, and can reduce the incidence of fetal infeaion by
50% to 60% [2",3,6J. Treatment includes the use of spira­
mycin, sulfadizine, or the combination of pyrimethamine
and sulfadiazine in both mothers and infants, and infected
infants should receive pyrimethamine and sulfadiazine for
up to one year regardless ofsymptoms [2..].
All women who are pregnant or attempting pregnancy
should be educated in preventive measures to avoid infec­
tion . Exposure to oocytes can be reduced by thoroughly
cooking all meats, and by washing or peeling fruits and
vegetables. Washing all cooking utensils and food prepara­
tion surfaces with hot, soapy water also prevents the spread
of infeaion. Pregnant women should avoid changing litter
...,
p
254 Pelvic Infections
boxes, and if unavoidable, the box should be changed daily
to prevent time for oocytes to become infectious. Gloves
should be worn while changing litter boxes or working
with soil [3].
Other (Syphilis, Varicella, Parvovirus B19)
Syphilis
Syphilis infections, caused by the spirochete Treponema
pallidum, have decreased in prevalence since the early 1990s
[9-]. Overall, one per 10,000 adults is infected, with the
highest incidence seen in non-Hispanic blacks [9-,10].
Spread is by hematogenous infection of the fetus during
pregnancy, and is more likely when the pregnancy occurs
close to or during the initial infection. Congenital infection
occurs in 0.4% of children born to infected mothers [8, lOJ.
Primary syphilis infections manifest within 3 weeks of
exposure as a painless chancre, most commonly on the
genitalia , which may go unnoticed [1O} . The chancre
undergoes fibrosis within 2 to 8 weeks, and the infection
·remains quiescent until secondary lesions develop . Sec­
ondary lesions affect tissues of ectodermal origin (skin,
mucous m embranes, and the central nervous system
[CNS]), which become inflamed, and develop the charac­
teristic rash of disseminated infection [10]. The pink to red,
discrete, macular lesions measuring 3 to 10 mm in diame­
ter are present when the patient is most infectious [lOJ.
These lesions resolve within 1 to 3 months, but the.disease
can relapse, and secondary symptoms can recur for up to 4
years [10].
Once the secondary symptoms resolve, the patient
enters the latent stage where there is positive serology but
no symptoms. The early la'~nt phase spans the first year,
and is the time when most relapses are seen [10J . The late
latent phase starts 1 year from initial resolution of second­
ary symptoms, and during this phase, the patient is resis­
tant to both reinfection and relapse~ 10]. Tertiary syphilis,
the final stage of the disease process, is heralded by the
appearance of gummas in the skin , liver, bones, and
spleen, the presence of obliterative endarteri tis of the aorta
and the CNS [10]. Tertiary symptoms develop in up to one
third of untreated patients. Maternal screening consists of
serology testing at the first prenatal visit and again at 28
weeks [9-]. If positive, specific testing for antitreponemal
antibodies is needed to confirm infection.
Since inflammatory changes occur after the first trimes­
ter, organ development in the fetus is not affected
[6,9-,10,11] . Common findings include preterm labor,
intrauterine growth restriction (IUGR), hydrops fetal is,
hepatosplenomegaly, lymphadenopathy, osteochondritis,
hemolytic anemia, mucocutaneous lesions, and thromb­
ocytopenia. Perinatal deaths occur in more than 40% of
untreated pregnancies, of which 75% are stillbil1hs and
25% are neonatal deaths . Affected survivors are classified
with either early or late congenital symptoms. Early symp­
toms appear in the first 2 years of life, and include poor
~.
feeding, repeated sniffing, hepatosplenomegaly, pneumo­
nia alba enteritis, pancreatitis, nephrosis or neprhitis,
edema, ascites, uveitis, chorioretinitis, glaucoma, and
aseptic meningitis [10]. The symptoms of late congenital
syphilis result from scarring, and include interstitial
dermatitis, uveitis, glaucoma, frontal bossing, short max­
ilia, high palatal arch, saddle nose, saber shins, scaphoid
scapula, clutton joints (painless hydrathrosis), mulberry
molars, Hutchinson teeth (notched incisors) , enamel
dystrophy, 8th nerve deafness, mental delay, convulsive
disorders, paresis, paralysis, rhagades (linear scars) ,
gummas, and palatal perforations [8,10] .
Infants with rising titers, or titers that are four times
greater than maternal titers, are considered infected. How­
ever, this may actually reflect maternal IgG levels, since the
assays do not distinguish fetal antibodies from passively
transferred maternal antibodies [10]. Therefore, infants
should be examined closely for symptoms of active disease
regardless of titers.
Penicillin is the only drug proven effective against
syphilis. Patients with a known penicillin sensitivity
should be hospitalized and undergo desensitization [10J.
Preventive measures should be emphasized to all at-risk
women, and include the use of condoms, and avoidance of
sexual contact with infected individuals.
Varicella
Chickenpox and varicella zoster are caused by a DNA her­
pesvirus. Chickenpox is the initial systemic infection, after
which the virus remains dormant in the dorsal nerve
ganglia. \A/hen reactivated, the disease is referred to as vari­
cella zoster. Both forms of the infection are contagious
[2.. J. Over 90% of people contract chickenpox before the
age of 14, so relatively few women of childbearing age are
susceptible to the disease, and only 3000 cases per year are
reported in pregnant women [2--,4--,12]. Spread is by
respiratory droplets and personal contact, and the incuba­
tion period lasts 10 to 21 days. Infected individuals are con­
sidered contagious 24 to 48 hours before the rash appears,
and remain infectious until crusting of the exam them
occurs [1 .. J. Congenital infection is uncommon , and
development of the congenital syndrome is limited to
exposure in the first 20 weeks of gestation. After a first­
trimester infection the risk for defects is 2.2%, which
decreases to 2.0% in weeks 13 to 20. The overall risk of
defects following infection is 0.7% [4--, 12J.
Maternal symptoms of headache, malaise, and fever are
followed by puritic vesiculopapular lesions on the face and
trunk that spread to the eA.'lremities [12]. Definitive diagno­
sis by culture is often difficult, and serology results may
take up to 4 weeks. Therefore, diagnosis is usually based on
observation of the classic rash of this disease [12J.
Ultrasound remains the preferred method for fetal
diagnosis. Infection is suggested by hydrops, hypere­
chogenic foci in the bowel and liver, cardiac malforma­
tions, limb deformities, IUGR (in up to 40% of fetuses),
 TORCH Infections - Steg,mann -and Carey 255

and microencephaly [1 .. ,13]. Skin scrapings and serum . 2% to 9% [2--,G, 17] . If hydrops is present and the fetus is
immunoassay can be used to confirm suspected congenital past 20 weeks' gestation, cordocentesis and intrauterine
infection in the postnatal period [G]. Sequelae of congeni­ transfusion should be considered, since aggressive
tal infection include limb atrophy, hypoplasia, scarring, management of fetal anemia in utero improves fetal sur­
microcephaly, psychomotor retardation, various eye abnor­ vival as much as GO% [lG-J. Long-term development in
malities, rash, cutaneous scars, and muscle atrophy [G, 12] . survivors tends to be normal [2 --I. Other rare symptoms
Treatment with acyclovir, and prophylaxis with varicella­ of parvovirus infection include hydrocephalus, craniofacial
zoster immune globulin (VZIG) is benefidal to the mother, anomalies, encephalopathy, and vasculitis [2"1 .
but does not prevent fetal disease [2",4",G,12]. If a mater­ Routine screening is not recommended , since most
nal outbreak develops near term, attempt to delay delively adults have been immune t9 parvovirus since childhood.
for 5 days after the viral exanthem appears to minimize trans­ However, screening of women in high-risk situations,
mission to the fetus [1 .. J. If the delivery cannot be delayed (eg, nursery-school teachers and health-care providers)
or if the mother develops symptoms within 2 days of may be considered along with counseling on good
delivery, VZIG should be given to the infant [12J. hygiene practices [2.. J.
A varicella vaccine has been available since 1995, and
should be given to all nonimmune women. Avoidance of
pregnancy is advised for 3 months after vaccination Rubella
because of the theoretical risk of congenital infection [14]. Rubella, or German measles, is caused by an RNA virus
Despite an adequate response to the vaccine, 20% to 30% with an incubatio,p period from 12 to 23 days [18,19-].
of people do not mount a detectable antibody response. The virus is spread by close contact or airborne droplets,
However, revaccination is not recommended [14]. and the patient is most contagious when the rash is erupt­
ing [19-,20J . Most outbreaks are now seen in Hispanics
Parvovirus B 19 and foreign-born persons, or , in persons in closed environ­
Erythema infectiosum, or fifth disease, is caused by ments such as the workplace, religious communities,
Parvovirus B19, which is the only strain of parvovirus that schools, and jails [19-J.
causes disease in humans [I--].lt is a smalL nondeveloped, Rubella is often difficult to diagnose because of its mild .
single-stranded DNA virus that infects rapidly dividing cells presentation and nonspecific symptoms. Virus isolated
such as bone marrow erythroid progenitor cells, and is from the nasal secretions or a fourfold or greater rise in
spread by respiratory droplets and contaminated blood antibody titers confirms the diagnosis [18J. Fetal testing is
products [2--,4--,15]. The transmission rate can be as high not recommended, but neonatal infection is confirmed by
as 33%, with most cases occurring in late winter and early the presence of rubella-specific IgMI antibodies, stable or
spring [G, 15J. The annual seroconversion rate in women of increasing IgG levels from the first several months of life,
childbearing age is 1.5%, and one in 400 pregnancies is or positive cultures from the throat, blood, urine, and cere­
complicated by this infection [15,lG-]. brospinal fluid (CSF) [G,18J.
Maternal infections are generally asymptomatic, but The classic triad of congenital rubella syndrome (CRS)
occasionally present with arthropathies, fever, and mild is heart disease, vision problems, and hearing loss, but CRS
constitutional symptoms [15]. The characteristic "slapped can include spontaneous abortion, stillbirth, meningoen­
cheek" rash is usually seen only in children. At the onset of cephalitis, mental retardation, IUGR (in up to GO% of
the rash and arthralgias, patients are no longer infectious fetuses), hepatosplenomegaly, thrombocytopenia, and a
[2-- J. The presence of IgM antibodies confirms an acute purple rash ("blueberry muffin" appearance) [G ,18J .
infection, while IgG antibodies appear later and may Infection in the first 2 months of pregnancy holds a higher
persist for years [G, 1G-]. Serial titers using enzyme-linked risk for CRS (85%), which decreases to 20% to 25% at 20
immunosorbent assay (ELISA) or western blot analysis are weeks. Infections after 20 weeks rarely result in CRS
the most reliable methods of detection [1 .. ,2.. J. Since [9-,18,19-]. Sixty percent of infected infants will have
most maternal infections are asymptomatic, ultrasound subclinical infections in the neonatal period, but 71 %
findings may be the only clue to the exposure [4",9-J . If manifest symptoms within the first 5 years. Hearing loss is
an infection is suspected, serial (weekly or biweekly) ultra­ the most common of the permanent sequelae, affecting
sounds are indicated for up to 12 weeks. If no evidence of G8% to 93 % of children [8, 19-J. The virus has recently
fetal disease is seen by that time, fetal infection is unlikely, been isolated from the pancreas, and is associated with
and further ultrasounds are unnecessary [4",9-]. diabetes in later life [18J.
Parvovirus is rarely assodated v-rith fetal malformation The disease is largely self-limited in the mother, and
because the virus usually attacl{s red blood cells, leading to requires only supportive care. However, once fetal infection
hemolytic and aplastic anemia, hydrops, high output fail­ is suspected, mothers should be given the option of tenni­
ure, myocarditis, and fetal death [4" J. The most severe nating the pregnancy because of the high rate of fetal infec­
symptoms are seen after first- or second-trimester infec­ tion and congenital syndrome [9-J. Neonates who are
tion, with fetal loss from hydrops fetalis running as high as infected can shed the virus for up to 1 year, and should be
256 Pelvic Infections
isolated from other infants [6,18]. CRS babies can be con­
sidered noninfectious at 3 months of age if nasopharynx
and urine cultures are negative [19-]. The use of immuno­
globin for postexposure prophylaxis is not recommended,
and should only be considered if termination is not an
option. However its use does not reduce the incidence of
CRS [18,19-].
Herd immunity, or vaccination of all nonimmune
women and all children at 12 to 15 months and again at
school entry, is recommended to help prevent congenital
disease. Vaccine efficacy is about 90%. However there is no
good evidence that herd immunity has any impact on the
incidence of CRS [6,18]. The theoretical risk to the fetus if
the vaccine is administered during pregnancy is estimated
to be about 1.6% [18].
Cytomegalovirus (CMV)
[6] . Isolation of infected infants is advised as neonates may
CMV is a double-stranded DNA herpesvirus that is one of
shed virus for many years [2..,12].
the most common perinataJ infections [2",9-,21,22]. It is
There are currently no maternal or fetal treatments for
transmitted by infected blood, saliva, urine, or sexual
CMV [2.. ,9-]. Ganciclovir is currently being studied for
contact, and has a 28- to 60-day incubation period [2"] ,
this use, but is not yet recommended [1 .. ,6, 12]. A live
The virus infects lymphocytes, monocytes, and neutro­
attenuated CMV vaccine (Towne 125 strain) has been
phils, and once contracted, persists for life [14]. At concep­
developed and holds some promise, but thcre are concerns
tion, one third of all pregnant women are seronegative,
about viral reactivation with its use (l..]. Women in high­
2.5% to 6.8% ")'ill become infected during pregnancy, and
risk environments (eg , day care centers, nurseries ,
24% will transmit the virus to the fetus [8]. The infection
elementary schools, or health-care facilities) do not require
can cross the placenta, and the infant can be. infected
screening, but should be counseled about risks and appro­
during delivery by exposure to genital tract secretions, and
priate hygiene procedures [9-)
during breastfeeding [2--,9-].
Maternal infections are largely asymptomatic, but
about 10% will have a mononucleosis-like syndrome
including fever, fatigue" myalgias, pharyngitis, cough,
nausea, and headache [i.. ,2..,9-]. Multiple primary
infections are possible, since prior infection does not con­
fer immunity to infection by a different CMV strain [1 .. ].
CMV infections in the third trimester can be just as
devastating as first-trimester inftfctions [4--] . Approxi­
mately 30% of severely infected infants die, and of the
infants that survive, 80% will have severe neurologic mor­
bidity, including mental retardation and sensorineural
hearing loss [2 ..,8]. Antenatal infections resulting from
reactivation of maternal disease are generally less severe,
and these infants are usually asymptomatic at birth. Most,
however, go on to develop hearing loss later in life
[1",2..,22]. CMV inclusion disease, the more severe form
of infection, consists of hepatomegaly, jaundice, throm­
bocytopenia, purpura, chorioretinitis, microphthalmia,
interstitial pneumonitis, hearing loss, CNS anomalies, and
mental retardation [4..,6,9-,12,23] .
Maternal diagnosis is based on a fourfold rise in IgM
antibodies in serial titers, or by culture [l",2--, 12,23].
Once an infection has been documented, amniocentesis
should be offered 4 to 6 weeks after the primary infection
[2.. ,9-]. Viral detection by amniotic fluid culture has a
sensitivity of 50% to 69%, and PCR on amniotic fluid has
a sensitivity of 77% to 100% (2 .. ]. Fetal IgM is not be
detectable for the first 20 weeks of gestation due to an
immature fetal immune system. Therefore testing prior to
20 weeks should be avoided [1 .. J.
Because most maternal infections are silent, fetal diag­
nosis is usually based on ultrasound findings, whi ch
include symmetric IUGR, microcephaly, ventriculomegaly,
periventricular calcifications, intrahepatic calcifications,
and fetal ascites [2",9-,23]. Changes related to CMV
infection may appear very late in pregnancy, so serialultJa­
sounds are walTanted [4"] , At birth, the clinician should
check the neonate's blood for CMV IgM, and culture the
urine. Early evidence of antigens (between 2 days and 1
week of age) are helpful in determining congenital infec­
tions from those acquired post-partum, and proof of
congenital infection requires specimens positive for
disease that have been obtained within 3 weeks of bilth
Herpes Simplex
Herpesvirus is an enveloped, double-stranded DNA virus
with two distinct types. HSV-l generally occurs in child­
hood, and is not usually sexually transmitted. HSV-2 is
related to sexual activity [24-]. Approximately 45
million Americans are infected with HSV-l or 2, and 1500
to 2000 newborns contract neonatal herpes each year from
contact with maternal secretions. These neonates suffer
significant morbidity and mortaJity [8,9-,24-1.
In HSV-2, multiple painful vesicles appear in clusters
between 2 to 14 days after exposure, and can be recurrent
[9-] . Systemic symptoms, such as malaise, myalgias, and
fever, usually occur with primary infections, while local
symptoms of pai n, dysuria, and soreness of the vulva and
vagina occur with both primary and recurrent infections.
Primary lesions usually resolve within 3 weeks, but the
patient continues to shed the virus for up to 3 months after
the infection [24-]. The absence of episodes of symptom­
atic genital HSV infections during pregnancy does not
eliminate the chance of asymptomatic shedding, but in
these cases, the risk of fetal infection is low (14%) (24-] .
The greatest risk to the fetus occurs when the mother has a
first episode in the later stages of pregnancy [9-].
Primary HSV-2 outbreaJ<s may be blunted if the woman
has had a previous HSV-l infection. Nonprimary first

episodes occur when the primary infection (usually with
HSV-1) was asymptomatic, and the recurrence (usually
HSV-2) is the first recognized episode [24-J. Recurrent
HSV-2 infections are usually confined to the genital area,
can be symptomatic or asymptomatic, and can shed virus
sporadically [24- J.
True congenital herpes is associated with miscarriage,
premature delivery, and neonatal herpes. Vertical transmis­
sion is related to gestational age at the time of infection,
and whether the disease is primary (50% transmission
rate), nonprimary first episode (33% transmission rate), or
recurrent (0% to 3% transmission rate). There are isolated
reports of infection in the first 12 to 14 weeks of
pregnancy, resulting in microcephaly, microphthalmia,
intracranial calcification, and chorioretinitis [24-J.
Neonatal herpes can present as late as 4 to 6 weeks of age
as a generalized systerrlic infection, respiratory clistress, sepsis,
hearing loss, encephalitis, or disease of the skin, eyes, and
mouth [6,8,9-,l1J. Most neonates with HSV encephalitis sur­
vive, but suffer substantial neurologic sequelae, and 50% of
neonates with disserrlinated disease die [25] .
The gold standard in diagnosing this disease is culture
of vesicular fluid from an active lesion, but the culture still
has a maximum sensitivity of 60% to 70%, even with overt
clinical disease. The best cultures are obtained from
primalyand nonprimary first infections that can yield a
positive culture rate of up to 80% . Positive cultures
obtained from recurrent lesions can be as low as 40%
124-]. Cultures taken from the neonate at the time of birth
should include blood, urine, stool/rectum, CSE conjuncti­
vae, skin vesicles, nasopharynx, and mouth . All surface
cultures should be taken within 48 hours of delivery [6] .
Cesarean section is generally recommended \.vithin 6
hours of rupture of membranes when any active genital
lesion is present. Use of scalp electrodes during labor
should be limited when there is a known history of HSV.
Prophylactic acyclovir (400 mg orally twice daily) from 36
weeks to delivery has been suggested as a way of decreasing
disease recurrence and preventing cesarean sections
[9-,24-]. Cesarean section is not recommended for non­
genital lesions, although the lesions should be covered
during delivery to avoid accidental contamination. Tf
premature rupture of membranes occurs in a woman with
active lesions, the use of steroids and delay of delivery
should be considered if clinically applicable [24-]. Weekly
maternal cultures are no longer recommended due to the
low sensitivity of culture with recurrent lesions [25] .
Currently, acyclovir is the only drug recommended for
treatment of pregnant women since it is the only drug that
has been studied. Valcyclovi r, faciclovir, and penciclovir
(class B) are effective as well as acyclovir, and have easier
dosing schedules.
TORCH Infections - Stegmann and Carey 257
Conclusions
Perinatal infections are a major source of serious congenital
anomalies, and can lead to significant fetal morbidity and
mortality. By recognizing these infections, the clinician is
better able to monitor and treat both the mother and fetus,
and advise parents on possible fetal consequences.
References and Recommended Reading
Paper of palticular interest, published recently,
have been highlighted as:
• Of importance
•• Of major importance
1. •• Kuhlmann RS. Autry AM: An approach to nonbacterial
infections in pregnancy. Ciin Fam Pract 2001 , 3 :267-286.
This article provides a logical approach to the diagnosis. treatment
and outcomes of cytomegalovirus (CMV), varicella-zoster. parvovirus.
and toxopla smosi s infections in both maternal and fetal patients.
2.·· Perinatal viral ani! parasitic infections. ACOC Pract Btlll
2000, 20:425-432.
This is a co ncise review of the etiology. diagnosis. implications.
and availabl e treatments for toxoplasma. CMV, parvovi rus B1 9.
and varicella infections.
3. Lopez A, Wilson M. Navin~. lones IL: Preventing congenital
toxoplasmosis. MMWR 2000, 49.
4 .•• Chescheir NC, Hansen WF: What's new in perinatology.
Pediatr Rev 1999. 20:57-63.
This article is a review of the current methods for the diagnosis of
CMV. toxoplasmosis. parvovirus. and varicella-zoster.
5 . Montoya IG, Remington IS: Toxoplasma gondii. In Mandell.
Douglas, and Bennett's Principles and Practice of Infectious Diseases.
edn 5 . Ed ited by Mandell GL. Bennett IE, Dolin R. Philadelphia:
Churchill Livingstone; 2000:2861-2881.
6. Getachew A. Kaufman BD: Infectious diteases. In The Ha rriet
Lan e Handbook: A Mantlal for Pediatric House-Officers. Edited by
Siberry GK. Iannone R. Childs B. SI. Louis: Mosby. Year-Book;
2000:379 -380 .
7. 2000 Red Book: Report of the Committee on Infectious Diseases.
edn 5. Edited by Pickering LI<. Elk Grove Village. IL:
American Academy of Pediatrics; 2000.
8. Roizen Nl: Etiology of hearing loss in children.
Nongenetic causes. PediaLT Clin NOl1h Am 1999 , 46:49-64 .
9.· Cline MK, Bailey-Dorton C, Cayelli M: Maternal infections:
diagnosis and management. Prim Care 2000, 27:13 -33.
The authors provide an excellent overview of the etiology, diagnosis,
and management of matemal infections with syphilis. rubella. CMV.
and herpes.
10. DarvilleT: Syphilis. PedialT Rev 1999, 20:160-164.
1I . Arce DA: Hepatobiliary disease in children.
Ciin Fam Pract 2000.2:189.
12. Summary of infectious diseases. In 2000 Red Book: Repmt of the
Committee on Infectiolls Diseases, edn 25 . Edited by Pickering LI<.
Elk Grove Village. IL: American Academy of Pediatrics;
2000:583-586.
13. Intrauterine gmwth restriction. ACOC Pract Bilil 2000.
12 :34 4-346.
14 . Krause PRo Straus S: Herpesvirus vaccines. Development, contro­
versies, and applications. Infect Dis c/ill NOl1h Am 1999. 13:61-81.
15 . Sabella C, Goldfarb J: Parvovirus B19 infections.
Am Fam Physician 1999. 60:1455-1460.
16.· MuqJhy!. lones 0: Managing the gravida with parvo.
OBC Management 2000. 12:55-64.
This article provides a well defined management algorithm for the
treatment of parvovirus-infected gravida.
17. Skjoldebrand-Sparre L, Nyman M. Broliden K. Wahre n B:
All cases of intrauterine fetal death should be evaluated
for parvovirus B19 viral deoxyribonucleic acid [letter] .
Am]ObsrerCynecoiI999,180:1595-1596.
258 Pelvic Infections
18. Summary of infectious diseases . In 2000 Red Bool1: Repan
of the Committee on Infectious Diseases, edn 25. Edited by
Pickering LK. Elk Grove Village, IL: American Academy of
Pediatrics; 2000:495 - 500.
19 .• Conuol and prevention of rubella: evaluation and
management of suspected outbreaks, rubella in pregnant
women, and surveillance for congenital rubella syndrome.
MMWR 2001,50:1-23.
This is a comprehensive review on the current knowledge base
for the controL evaluation, management, and prevention of rubella.
20. Gershon AA: Rubella virus (German measles). In Mandel/,
Douglas, and Bennett's Principles and Pranice of Infectious Diseases,
edn 5. Edited by MancJell GL, Benneu)E, Dolin R. Philadelphia:
Churchill Livingstone; 2000: 1709.
21. Lazzarotlo T, Varani S, Guerra B, et al.: Prenatal indicators
of congenital cytomegalovirus infection. J Pedial), 2000,
137:90-95.
22. Guerra B, LazzarotLo 1; Quana S, er. al.: Prenatal diagnosis
of symptomatic congenital cytomegalovirus infection.
Am J Obstef Gyneco/ 2000, 183:476-82 .
23. Crumpacker CS: Cytomegalovirus. In Mandell, Douglas, and
Benneu's Principles and Pracrice of Infecrio us Diseases, edn 5.
Edited by Mandell GL, Bennett JE, Dolin R. Philadelphia:
Churchill Livingstone; 20001595-1596.
24 .. Management of herpes in pregnancy. Clinical management
guidelines for obstetrician-gynecologists. ACOG Prace
Bull 8, 1999 .
This is an excellent review of the current data on herpes in pregnancy
that includes expert opinion on the topic.
25. Summary of infectious diseases. In 2000 Red Booll: Report of (he
Comm i tree on I nfectious Diseases, ed n 25. Ed i ted by Pickeri ng LK.
Elk Grove Village, IL: American Academy of Pediatrics;
2000:309-318.
View publication stats