Tuberculosis in pregnancy

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TC:TOPIC_PAGE
Tuberculosis in pregnancy
Authors
Lloyd N Friedman, MD
Lynn T Tanoue, MD
Section Editors
C Fordham von Reyn, MD
Charles J Lockwood, MD
Deputy Editor
Elinor L Baron, MD, DTMH
Disclosures
All topics are updated as new evidence becomes available and our
peer review process is complete.
Literature review current through: Oct 2013. | This topic last
updated: Jan 8, 2013.
INTRODUCTION Prenatal care presents a unique opportunity
for evaluation and management of latent and active tuberculosis
(TB) in pregnant women [ 1 ]. Routine tuberculin skin test (TST)
screening is not indicated for all pregnant women. However,
individuals with an increased risk of tuberculosis may seek medical
care only during pregnancy (such as foreign born individuals within
five years of immigration from TB endemic countries or individuals
with HIV infection) [ 2 ]. (See "Epidemiology of tuberculosis" .)
The pathogenesis of tuberculosis infection and disease in pregnant
women is similar to that in nonpregnant women [ 3,4 ]. There is no
firm evidence that the risk of new infection or reactivation of
tuberculosis in pregnant women is significantly different from
matched controls. However, tuberculosis in pregnant women can
present insidiously, since symptoms of malaise and fatigue may be
attributed to pregnancy rather than disease [ 5 ]. In addition, during
pregnancy it can be difficult to recognize weight loss. (See
"Microbiology and pathogenesis of tuberculosis" .)
Since pregnancy has not been shown to increase the risk of TB, the
epidemiology of TB in pregnancy is a reflection of the general
incidence of disease [ 6 ]. This also is true in HIV-infected women,
as shown in a group of predominantly HIV-infected pregnant women
in New York City during 1991 to 1992, where the rate of TB was
94.8 per 100,000 deliveries [ 7 ].
Issues related to diagnosis and treatment of latent TB infection and
active TB disease in pregnant women will be reviewed here. Issues
related to the management of latent and active TB in nonpregnant
patients are discussed in detail separately. (See "Diagnosis of latent
tuberculosis infection in HIV-negative adults" and "Diagnosis of
pulmonary tuberculosis in HIV-negative patients" and "Treatment of
pulmonary tuberculosis in HIV-negative patients" .)
LATENT TB Pregnancy has not been shown to influence the
pathogenesis of TB or the likelihood of progression from latent to
active disease, nor has it been shown to affect the response to
treatment [ 8,9 ].
Diagnosis Routine testing for latent tuberculosis in pregnant
women is not indicated. Testing should be performed during
pregnancy only if there is an indication for prompt treatment of
latent tuberculosis infection (LTBI); a decision to test presupposes a
decision to treat promptly if the test is positive. However, contact
with the health system during pregnancy is an opportunity to
identify patients at risk for LTBI who should be evaluated further
following pregnancy. Appropriate groups for testing include those at
high risk for progression of LTBI to active disease, especially those
who are significantly immunocompromised (eg, HIV infection,
immunosuppressive therapy) or those who have been infected with
TB recently [ 10 ]. (See "Diagnosis of latent tuberculosis infection in
HIV-negative adults" .)
If indicated, testing for LTBI prior to pregnancy is preferred (if
feasible); this allows opportunity for counseling about the risk of
becoming pregnant while on therapy [ 11 ]. If treatment for LTBI is
initiated and the patient becomes pregnant subsequently, therapy
should be continued [ 12 ]. In the absence of major risk factors for
progression to active infection during pregnancy, testing and
treatment for LTBI in those for whom targeted testing is indicated
should be delayed until three months after delivery to minimize risk
of adverse drug effects. (See 'Toxicity and monitoring' below.)
Diagnostic tools for latent tuberculosis include tuberculin skin
testing (TST) and interferon gamma release assays (IGRAs).
Tuberculin skin testing can be performed safely in pregnant women,
and pregnancy does not alter the response to the TST [ 10,13 ].
Definitions of positive skin tests are outlined in the Table ( table 1 ).
Interferon gamma release assays are also safe in pregnancy and
likely as effective for diagnosis of LTBI in pregnancy as in other
circumstances; data are limited [ 14-17 ]. (See "Interferon-gamma
release assays for diagnosis of latent tuberculosis infection" .)
Patients with positive LTBI screening results ( table 1 ) must
undergo clinical evaluation to rule out active tuberculosis. This
includes evaluation for symptoms (eg, fever, cough, weight loss)
and radiographic examination of the chest (with appropriate
shielding). (See "Interferon-gamma release assays for diagnosis of
latent tuberculosis infection" .)
Treatment Testing and treatment for latent tuberculosis
infection should be pursued during pregnancy only if there is an
indication for prompt management of LTBI (usually in recent
infection or immunocompromised hosts); a decision to test
presupposes a decision to treat promptly if the test is positive (even
during the first trimester). Therefore, patients appropriately
targeted for LTBI screening with positive TST results should initiate
treatment during pregnancy [ 10 ]. If treatment for LTBI is initiated
prior to pregnancy for the usual indications noted in the CDC
statement [ 10 ], and the patient becomes pregnant subsequently,
therapy should be continued [ 12 ]. (See 'Diagnosis' above and
"Diagnosis of latent tuberculosis infection in HIV-negative adults" .)
However, if a skin test has been performed in the absence of an
indication for prompt LTBI management and is positive, a chest
radiograph should be performed. Delaying therapy is appropriate for
patients with positive TST in the absence of a major risk factor for
progression to active disease, ie, recent infection or
immunosuppression. Therapy may be initiated three months after
delivery to minimize concern for hepatitis in the postpartum period.
If treatment for LTBI is deferred until after delivery, repeat
evaluation for active disease, including chest x-ray, should be
performed to confirm that active tuberculosis did not develop in the
intervening time between diagnosis and treatment. (See 'Toxicity
and monitoring' below.)
Adherence may suffer when patients identified with LTBI during
pregnancy delay treatment. In a study evaluating 393 women with
LTBI during pregnancy who delayed treatment until the postpartum
period, only 42 percent attended a follow up visit in the TB clinic,
and only 18 percent completed treatment [ 18 ]. Therefore, close
follow-up is required.
The regimen of choice for treatment of LTBI is isoniazid (5 mg/kg up
to 300 mg daily) for nine months ( table 2 ). This should be
combined with pyridoxine supplementation (25 mg daily) [ 10 ].
Minor interruptions in therapy are acceptable, so long as 270 doses
are completed within 12 months. A six month regimen of daily
isoniazid also provides protection but is less desirable, although in
the setting of difficulty with adherence, providers may prefer to
concentrate efforts in ensuring six months of therapy [ 10 ].
Another choice for treatment of LTBI is rifampin (daily for four
months) ( table 2 ) [ 10 ]. Rifampin should be used for patients who
are intolerant of INH or who are presumed to have infection with
INH-resistant, rifampin-sensitive strains of TB. It may also be useful
in the setting of difficulty with adherence. (See "Diagnosis of latent
tuberculosis infection in HIV-negative adults" .)
Toxicity and monitoring Pregnancy and the early postpartum
period may confer increased risk for isoniazid hepatotoxicity [ 19-22
]. Among 3681 pregnant and postpartum women with LTBI,
isoniazid was associated with a 2.5-fold increase in fulminant
hepatitis and a fourfold increase in mortality compared with
nonpregnant women, although these data did not reach statistical
significance [ 19 ].
Pregnant and postpartum women should have pre-treatment liver
transaminases and bilirubin function tests and, if normal, isoniazid
can be started with follow up symptom evaluations, and exams
every month. Initially LFTs should be obtained every month for at
least two months until shown to remain within normal limits. The
evaluation of pregnant and postpartum women receiving LTBI
treatment (either isoniazid or rifampin ) also should include testing
for HIV, hepatitis B and C, and a general evaluation for chronic liver
disease, alcohol use, and exposure to other hepatotoxins. If there is
a mild elevation of transaminases, more frequent monitoring may
be necessary until stability is established.
Patients should receive explicit instructions to stop therapy
immediately and contact their healthcare provider upon the
development of any symptoms that are consistent with hepatitis.
Isoniazid should be discontinued if the patient is symptomatic and
the ALT is more than three times the upper limit of normal [ 23 ]. It
should be discontinued in asymptomatic patients when the ALT is
more than five times the upper limit of normal [ 23 ].
Other side effects of isoniazid include rashes, neuropsychiatric
disturbances including depression, mania, and memory loss,
pellagra, peripheral neuritis, and seizures [ 24 ].
Adverse effects due to rifampin include hepatitis, thrombocytopenia,
hemolytic anemia, and fever and rash. (See "Rifampin and other
rifamycins" and 'First line drugs' below.)
ACTIVE TB Pregnancy has not been shown to influence the
pathogenesis of TB or the likelihood of progression from latent
infection to active disease, nor has it been shown to affect the
response to treatment [ 8,9 ]. Active maternal infection can lead to
congenital infection by hematogenous dissemination via the
placenta, although congenital infection is very rare. (See 'Congenital
and neonatal TB' below.)
Clinical manifestations Pregnant patients with pulmonary
tuberculosis typically have the same clinical manifestations as
nonpregnant patients. However, tuberculosis in pregnant women can
present insidiously, since malaise and fatigue may be attributed to
pregnancy rather than disease [ 22 ]. In addition, during pregnancy
it can be difficult to recognize weight loss. In the setting of
extrapulmonary disease symptoms may be especially vague and the
diagnosis can be significantly delayed [ 25-27 ]. (See "Clinical
manifestations and evaluation of pulmonary tuberculosis" .)
Diagnosis The evaluation for active tuberculosis in pregnant
women should proceed as in nonpregnant individuals, including
chest X-ray, with appropriate protection of the fetus [ 28 ].
Evaluation for extrapulmonary disease should be guided by clinical
symptoms and/or radiographic findings. Diagnosis of TB also should
prompt evaluation for HIV infection. (See "Diagnosis of pulmonary
tuberculosis in HIV-negative patients" and "Acute and early HIV
infection: Treatment" .)
TREATMENT OF ACTIVE TB Treatment of tuberculosis in the
setting of pregnancy should be initiated if the suspicion of active
disease is moderate to high (such as a persistent upper lobe
infiltrate and cough in a high-risk individual and/or a positive AFB
smear or nucleic acid amplification test), since untreated disease
represents a greater hazard to the mother and fetus than
antituberculous therapy. The principles of treatment of active
tuberculosis in HIV-seronegative pregnant patients are the same as
for nonpregnant patients, except for the exclusion of certain
medications [ 29 ]. HIV-positive patients are discussed in detail
separately, and decisions about therapy in these individuals should
be made in consultation with an expert. (See "Treatment of
pulmonary tuberculosis in HIV-negative patients" and "Treatment of
pulmonary tuberculosis in the HIV-infected patient" .)
The approach to treatment also includes consideration of issues
related to transmission, including separation of mother from
newborn in certain circumstances. (See 'Controlling transmission'
below.)
First line drugs The initial treatment regimen (for presumed
drug sensitive disease) for active TB during pregnancy in the United
 States typically consists of isoniazid , rifampin and ethambutol
administered for two months followed by isoniazid and rifampin for
seven months, for a total of nine months [ 4,8,15,29,30 ]. If the
results of drug sensitivity studies are available and the organism is
known to be susceptible to isoniazid and rifampin, then ethambutol
may be discontinued after one month.
Pyrazinamide is not absolutely necessary as part of a first line
regimen, and because of limited safety data, it is not used routinely
for pregnant women in the United States. However, pyrazinamide is
recommended by the World Health Organizations as part of a
standard regimen for treatment of TB in pregnant women [ 31,32 ].
In circumstances such as HIV coinfection, tuberculous meningitis,
very extensive disease, and any form of drug resistance, it would be
prudent to consider the use of pyrazinamide [ 15,33 ]. The absence
of pyrazinamide from the treatment regimen results in a treatment
duration of nine months instead of six months.
Steroids for manifestations such as meningitis and pericarditis
should be used as discussed separately [ 29 ]. (See "Central
nervous system tuberculosis" and "Tuberculous pericarditis" .)

Isoniazid is considered acceptable for use in pregnancy and is not

considered to be a human teratogen, although the risk of hepatitis
and peripheral neurotoxicity may be increased in the peripartum
period [ 29,30,34,35 ]. In general, the benefit of isoniazid (given its
importance for treatment of active TB) justifies the potential risk to
the fetus. Pyridoxine (25 mg/day) should be administered to
pregnant women receiving isoniazid (and to their breastfeeding
infants, even if the infant is not receiving isoniazid therapy) [ 10,29
].
Rifampin is considered acceptable for use in pregnancy; rare cases
of fetal abnormalities and hemorrhagic disease have been reported [
10,12,29,35,36 ]. Rifabutin often is used as an alternative to
rifampin in patients with HIV infection on antiretroviral medications.
There is insufficient safety information relating to the use of
rifapentine in pregnancy (category C). (See "Treatment of
pulmonary tuberculosis in the HIV-infected patient" .)
Ethambutol is considered acceptable for use in pregnancy [
29,34,35 ].
Pyrazinamide is not universally considered acceptable for use in
pregnancy; the adverse effects of pyrazinamide in pregnancy are
not certain. Because detailed teratogenicity data are not available
for this agent, it is not used routinely for pregnant women in the
United States since it is not absolutely necessary as part of a first
line regimen [ 9,29 ].
 Dosing regimens for treatment of tuberculosis are outlined
separately. (See "Treatment of pulmonary tuberculosis in HIV-
negative patients" .)
Second line drugs Pregnant women with drug resistant
tuberculosis or who have difficulty taking first line drugs should be
managed in consultation with an expert in treating tuberculosis. In
the setting of monoresistance it may be acceptable to treat with first
line drugs during pregnancy, especially if a determination is made
that it is acceptable to use pyrazinamide .
In the setting of resistance to multiple agents, there may be no
choice but to use a regimen with some potential toxicity to the
fetus; women should be counseled accordingly. There have been
multiple cases in which mothers with MDR-TB have been treated
with second line agents and delivered at term; most of these babies
were delivered without evidence of adverse effects [ 37-40 ].
Agents to avoid Streptomycin (category D) is a known
teratogen; it interferes with inner ear development and may cause
congenital deafness [ 35 ]. Among 40 pregnant women treated with
streptomycin, 17 percent of the babies had eighth nerve damage
with deficits ranging from mild hearing loss to bilateral deafness [
41 ]. Given this risk and the availability of effective and less toxic
alternatives, streptomycin should NOT be used for treatment of TB
in pregnancy.
Kanamycin (category D) and amikacin (category D) presumably
share this potential for toxicity and should NOT be administered in
pregnancy, although there is little specific information on the fetal
effects of these drugs. Capreomycin (category C), which is assumed
to have eighth nerve and renal toxicity in fetuses, also should be
avoided.
Agents to consider These agents should be used in pregnancy
only when there are no suitable alternatives for treatment (eg, due
to drug resistance or adverse effects of safer agents) and only in
consultation with an expert in the treatment of tuberculosis.

The adverse effects of cycloserine (category C) in pregnancy are

unproven. This agent crosses the placenta and should be used for
pregnant women only where there are no suitable alternatives [ 35
].
The adverse effects of PAS ( para-aminosalicylic acid ) (category C)
in pregnancy are not certain. There appears to be no evidence for
teratogenicity among babies whose mothers received isoniazid with
PAS [ 30,35 ]. PAS should be used in pregnancy only where there
are no suitable alternatives.
 Ethionamide (category C) crosses the placenta and is teratogenic in
laboratory animals [ 35 ]. It should be used in pregnancy only when
there are no suitable alternatives.
The fluoroquinolones (category C) have been associated with
arthropathies and should be used in pregnancy only where there are
no suitable alternatives [ 35 ].

Follow up Treatment should be administered by directly

observed therapy (DOT). To improve adherence and to evaluate for
drug toxicity, patients should be seen and examined every month.
An expert in tuberculosis should be consulted for interruptions
longer than two weeks or for sporadic adherence, especially within
the first two months of treatment [ 29 ]. (See "Adherence to
tuberculosis treatment" .)
As noted above, careful clinical monitoring for hepatitis is especially
important for pregnant and postpartum women; pre-treatment liver
transaminases and bilirubin function tests followed by monthly liver
enzyme testing should be obtained, and patients should be
instructed to call immediately if any symptoms or signs of hepatitis
occur. In general, isoniazid should be discontinued for the same
indications as for treatment of LTBI. (See 'Toxicity and monitoring'
above.)
BREAST FEEDING Breast feeding is not contraindicated if the
mother is being treated for active TB or LTBI with usual first line
agents, since the small concentrations of these drugs in breast milk
do not produce toxic effects in the nursing infant (ie, approximately
20 percent or less of a normal newborn infant dose) [ 10,29,35,42
].
All infants receiving isoniazid (either via breast milk or as directed
therapy) should receive supplemental pyridoxine. If the infant
already is receiving isoniazid therapy, then breast feeding will
increase the infant's total daily exposure to INH. There are no
specific recommendations concerning this or other antituberculous
drugs, and it would be difficult to make accurate adjustments of the
daily dose to compensate for the amount received in the breast
milk.
Breast feeding in the setting of rifabutin or fluoroquinolones is not
recommended [ 29,35 ]. Decisions about breast feeding with other
second-line agents should be made in consultation with an expert.
Decisions regarding choice of these agents should be individualized
in consultation with an expert [ 35 ].
CONGENITAL AND NEONATAL TB Congenital TB is very rare;
a 1980 review noted that only 24 cases had been described in the
literature since the introduction of isoniazid in 1952 [ 43 ].
Congenital TB is associated with maternal HIV infection, tuberculous
endometritis and miliary tuberculosis [ 29 ]. The index of suspicion
should be increased in regions with high prevalence of both
maternal HIV and tuberculosis [ 44 ]. It can occur hematogenously
via the placenta and umbilical vein or by fetal aspiration (or
ingestion) of infected amniotic fluid [ 8 ]. Clinical manifestations of
congenital TB include respiratory distress, fever, hepatomegaly,
splenomegaly, poor feeding, lethargy, irritability, low birth weight,
and low APGAR scores [ 43,45 ]. Clinical evaluation of the infant in
the setting of suspected congenital TB should include routine
evaluation in addition to lumbar puncture and evaluation of the
placenta with histologic examination (including acid fast bacillus
[AFB] staining) and AFB culture [ 34 ]. The tuberculin skin test in
the infant most often is negative.
Neonatal TB develops following exposure of an infant to his or her
mother's aerosolized respiratory secretions. This is more common
than congenital TB, and diagnosis of neonatal TB can lead to
identification of previously unrecognized diagnosis of TB in the
mother [ 46 ]. Clinical evaluation of the infant and the mother
should be pursued as outlined in detail separately. (See "Diagnosis
of pulmonary tuberculosis in HIV-negative patients" .)
The mortality in the setting of congenital and neonatal TB is about
50 percent [ 8,43 ].
CONTROLLING TRANSMISSION If a mother has established
or suspected active pulmonary TB at the time of delivery, she and
the infant should be separated until both have been fully evaluated [
34 ]. The same is true for household contacts of the infant.
If both the mother (or household contact) and infant are found to
have active TB and both are started on treatment, separation is not
necessary as long as both adhere to treatment. The mother (or
household contact) should wear a mask until no longer infectious.
If the mother (or household contact) has active TB disease, and the
infant has a positive skin test (in the absence of evidence for active
disease), the mother should be treated for active disease and the
infant should be treated for latent TB infection. Separation is not
necessary as long as both adhere to treatment. The mother (or
household contact) should wear a mask until no longer infectious.
If the mother (or household contact) has TB but the infant does not
have active TB or a positive skin test, the mother should be treated
for active disease and the infant should be treated for LTBI for three
to four months, at which time a skin test should be repeated. If the
repeat skin test is positive, the infant should be reevaluated for
active TB, and a full course of treatment for either latent or active
TB should ensue, based on the result of the reevaluation. If the
 repeat skin test is negative, and the mother is no longer contagious,
the infant's LTBI treatment may be discontinued. Separation is not
necessary as long as both adhere to treatment; the mother (or
household contact) should wear a mask until she is no longer
infectious.
If the mother has known or suspected pulmonary drug resistant TB
and the newborn does not have evidence of active or latent
infection, they should remain separated until the mother is not
infectious. Routine BCG vaccination at birth is warranted in countries
where tuberculosis is endemic [special considerations apply for
children born to HIV infected mothers as discussed separately; (see
"BCG vaccination" )]. In countries where BCG administration is not
routine, BCG immunization should be considered for the infant of a
mother with tuberculosis in consultation with an expert in TB. (See
"BCG vaccination" .)
BCG vaccination should not be administered during pregnancy for
prevention of tuberculosis since it is a live vaccine. (See "BCG
vaccination" .)
SUMMARY AND RECOMMENDATIONS

Pregnancy is not a risk factor for TB and has not been shown to
influence the pathogenesis of TB or the likelihood of progression
from latent infection to active disease. However, maternal infection
can lead to congenital infection or neonatal infection. In addition, TB
in pregnant women can present insidiously since symptoms of
malaise and fatigue may be attributed to pregnancy rather than
infection. (See 'Introduction' above.)
Screening for latent TB infection (LTBI) should be performed during
pregnancy only for those women at high risk for progression from
latent to active disease (eg, women who have been infected recently
and those who have HIV or are otherwise significantly
immunocompromised) ( table 1 ). (See 'Latent TB' above and
"Diagnosis of latent tuberculosis infection in HIV-negative adults" .)
Treatment of LTBI is reserved for pregnant women at high risk for
progression of LTBI to active disease, such as recent infection, HIV
infection, or immunosuppression. In these circumstances, we
recommend isoniazid for treatment of LTBI ( table 2 ) ( Grade 1B ).
We use daily therapy for nine months; for patients with difficulties
related to adherence, six months duration and/or twice weekly
directly observed therapy are alternatives. (See 'Latent TB' above.)
We recommend that the initial treatment regimen for active TB in
pregnancy (for presumed drug susceptible disease) consist of
isoniazid , rifampin and ethambutol administered for two months,
followed by isoniazid and rifampin for seven months for a total of
 nine months ( table 2 ) ( Grade 1B ). Pyrazinamide is not absolutely
necessary as part of a first line regimen, and because of limited
safety data, it is not used routinely for pregnant women in the
United States. However, pyrazinamide is recommended by the World
Health Organizations as part of a standard regimen for treatment of
TB in pregnant women. It may be important to consider in the
setting of HIV coinfection, tuberculous meningitis, extensive
disease, and drug resistance. (See 'Treatment of active TB' above.)
We recommend NOT using streptomycin , kanamycin , amikacin or
capreomycin for treatment of TB in pregnancy ( Grade 1A ).
Streptomycin is a known teratogen that interferes with eighth nerve
development and may cause congenital deafness. Kanamycin and
amikacin presumably share this potential for toxicity, and although
they are also aminoglycosides, there is little specific information on
the fetal effects of these drugs. Capreomycin is assumed to have
eighth nerve and renal toxicity. (See 'Agents to avoid' above.)
The following agents may be useful when there are no suitable
alternatives, but should be considered in consultation with an expert
in treating TB: rifabutin , cycloserine , PAS ( para-aminosalicylic acid
), ethionamide and fluoroquinolones. (See 'Agents to consider'
above.)
Breast feeding is not contraindicated in mothers being treated for
active TB or LTBI with standard first line agents, since the small
concentrations of these drugs in breast milk do not produce toxic
effects in the nursing infant. Supplemental pyridoxine should be
administered to breastfeeding mothers receiving isoniazid as well as
to their infants, even if the infant is not taking isoniazid therapy.
Patients receiving treatment for drug resistant TB with second line
agents should not breast feed. (See 'Breast feeding' above.)
Congenital TB is very rare and most often associated with maternal
HIV infection or maternal miliary or uterine TB. Neonatal TB is more
common than congenital tuberculosis, and diagnosis can lead to
identification of a previously unrecognized diagnosis of TB in the
mother. The mortality of untreated congenital and neonatal TB is
about 50 percent. (See 'Congenital and neonatal TB' above.)
Issues related to separation of mother and infant for controlling
transmission are as outlined above. (See 'Controlling transmission'
above.)

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