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the antiviral immune response, cough, coryza, conjunctivitis, neously. Maternal symptoms do not correlate with the presence
and temperature greater than 1018F during three or more days. or severity of fetal infection. The fetus can be normal or suffer
Antibody status can be determined by ELISA. A retrospective from aplastic anemia, myocarditis, nonimmunologic hydrops,
study of 58 women with measles during pregnancy revealed that and increased perinatal mortality. Ultrasonographic signs of
pregnant women were nearly twice as likely to be admitted to a fetal infection include ascites, pleural or pericardial effusions,
hospital, nearly three times as likely to be diagnosed with pneu- skin edema, polyhydramnios, cardiomegaly, placentomegaly,
and decreased fetal movement.114 Maternal serum a-fetoprotein
monia, and more than six times as likely to die from measles™
complications.106 In a study of eight infected pregnant women,107 elevation may be the result of hepatic or placental damage and
predicts poor fetal outcome.115 Treatments have included fetal
three of the four cases that presented before 24 weeks™ gestation
transfusion,116 digitalization,117 serial thoracocentesis, or para-
ended in abrupt spontaneous abortion or stillbirth. In contrast,
the four pregnancies that presented after 25 weeks™ gestation centesis. There is no parvovirus vaccine for humans currently.
ended in live term deliveries, but two of the four neonates had
congenital measles.107
Rubella (German measles)
Susceptible pregnant women exposed to measles should
Rubella is a self-limiting low-risk maternal viral infection119 that
receive immunoglobulin within six days of exposure. Infants
born to infected mothers should also receive immunoglobulin. has the potential to cause serious fetal disease including the
Maternal HIV infection may reduce levels of measles antibodies congenital rubella syndrome (CRS). It is caused by a togavirus of
in newborns, and low levels of measles antibodies at birth render the genus Rubivirus. Some recommend a review of the rubella
children susceptible to measles infection at an early age. A com- vaccination recommendations because most healthcare provi-
ders are seronegative.120 Rubella is unlikely to be acquired as a
bination measles, mumps, rubella, and varicella vaccine that
produces nearly 100% seropositive conversion is now available. result of casual or brief contact. Seronegative patients are at
Vaccination is contraindicated during pregnancy and nonpreg- greater risk of acquiring infection when they have been exposed
nant women receiving rubeola vaccination should use effective more closely over a long period. Maternal postauricular adeno-
contraception for three months after inoculation.108 pathy may be detectable a week prior to development of a char-
acteristic maculopapular rash and may persist for one to two
weeks after disappearance of the rash. A high incidence of arthri-
Influenza virus
tis among young women has been described.121
Influenza is highly contagious and a major cause of respiratory Congenital rubella syndrome will occur in infants born to
disease in adults. Pregnant women do not get influenza pneumonia mothers infected during the first half of pregnancy and may result
more often than nonpregnant women, but it can result in greater in miscarriage, stillbirth, mental retardation, sensorineural deaf-
morbidity and mortality. Yearly immunization is recommended, ness, cataracts, and heart disease. The risk of congenital rubella
and during the ˜˜flu season™™ influenza vaccine is recommended for infection in seropositive pregnant women appears to be relatively
all pregnant women in their second or third trimester. Fetal expo- low. In one study the intrauterine infection rates were 10%, 11.8%,
sure to influenza infection two to four months prior to birth may be 2.9%, and 6.5% after maternal infection at 1“10, 11“14, 15“19,
a risk factor for developing schizophrenia in adult life.109 and 20“29 weeks™ gestation, respectively. Six of 95 fetuses from
China is an epicenter for the emergence of pandemic influenza rubella-infected mothers had serologic evidence of congenital
viruses. However, the intensification of the poultry industry infection. Among the six fetuses, one had CRS with sensorineural
worldwide, coupled with the spread of viruses such as the deafness, two were terminated at midtrimester, two were normal,
Eurasian lineage of H9N2, suggests that a pandemic could take and one was lost to follow-up. No evidence of rubella defects was
place elsewhere in the world. Although the highly pathogenic found in the other 81 children during a two- to four-year follow-
up period.119
avian influenza virus H5N1 has produced little human disease
to date, its evolution over time is concerning.110

Hantavirus pulmonary syndrome
Parvovirus B19 (Fifth disease)
Hantaviruses are rodent-borne bunyaviruses that lead to two clin-
Parvovirus B19, the causative agent of Fifth disease, is associated ical disease states in humans: hemorrhagic fever with renal syn-
with hydrops fetalis. Approximately 35“50% of the general drome, and hantavirus pulmonary syndrome. A North American

5 Other disorders

hantavirus was first identified in 1993 as a cause of acute pulmon- dogs but no human-to-human transmission was known to occur,
ary edema, respiratory failure, and shock with a mortality rate although such transmission has been reported during an out-
>50%.122 Fortunately, hantavirus infection in pregnancy is rare, break in the Republic of the Congo.132 No mother-to-fetal trans-
with few reported cases of hantavirus pulmonary syndrome. One mission of the disease has been reported.
case describes a 29-year-old woman with persistent, high fever for Severe acute respiratory syndrome, a highly contagious infec-
six days, no fetal movement for two days, frequent vomiting, head- tion caused by a strain of coronavirus (SARS-CoV) produced
ache, lumbodynia, and orbital pain. On examination, she had a numerous deaths during an epidemic in Hong Kong and
normal body temperature, facial flushing, conjunctival congestion, Toronto in 2003. Severe acute respiratory syndrome has been
pharyngeal congestion, bulbar and conjunctival edema, severe reported in pregnancy, with subsequent delivery of an unin-
fected, healthy baby.133 Overall, however, adverse outcomes in
jaundice, petechiae and ecchymoses at sites of venipuncture,
abnormal liver and renal function tests, heavy proteinuria and mothers with SARS are usual, with 57% of patients presenting in
hematuria, and coagulation disturbance. A diagnosis of hemorrha- the first trimester with spontaneous miscarriage. The remaining
gic fever with renal syndrome was confirmed with an antihanta- pregnancies are often complicated by preterm delivery and
IUGR.134 Pregnant women do worse than nonpregnant women
virus IgM titer of 1:20. Her condition rapidly deteriorated, with
with SARS, having more renal failure and DIC.135 Stepwise proto-
frank hematuria, oliguria progressing to anuria, and shock.
cols for handling outbreaks have been developed.136
Hemodialysis was started and a stillborn male infant, of 3200 g,
was delivered vaginally following induction of labor 12 hours later.
The fetus showed no obvious abnormalities, but the parents
Other viruses
declined an autopsy. Following delivery the patient recovered
and was discharged three weeks later. The repeat titer for antihan- A classification of viruses including other viruses causing human
tavirus IgM was 1:80 ten days after presentation.123 infection is shown in the Appendix to Chapter 18.
An outbreak of hantavirus pulmonary syndrome occurred in
the western United States in the 1990s. Five pregnant women
Tropical diseases
were affected at gestational ages from 13 to 20 weeks. Although
no placental transmission of hantavirus was evident, two fetal
Dengue virus
losses and one maternal death occurred. Fetal losses were related
to severe hypoxemia and lactic acidemia. The disease was similar Dengue fever is caused by a flavivirus and is likely the most
in pregnancy as in nonpregnant patients, although fevers were important arthropod-borne viral disease in the world with an
noted to be lower in the pregnant women.124,125 estimated 50“100 million cases annually. In most cases, it is a
No specific treatment for hantavirus exists, so anesthetic care benign acute febrile illness with few consequences. However,
is supportive. The hemorrhagic nature of the disease usually in less than 1% of cases, particularly after a secondary infection
precludes regional anesthesia and pulmonary involvement by a different dengue virus serotype, the virus may cause severe
may complicate GA. Human-to-human transmission has been disease manifested primarily as a bleeding diathesis known as
reported for hantavirus (incubation period 15“24 days)126 so stan- dengue hemorrhagic fever (DHF).137 About 20“30% of those with
dard barrier precautions should be used. DHF develop dengue shock syndrome (DSS) that, if untreated,
has a mortality of 50%. The severity of secondary infections may
present problems in vaccine development, particularly if immu-
Emerging infections
nity is achieved against only some of the serotypes.138 Some viral
infections (including dengue, Ebola,139 and HIV, among others)
Emerging infections include West Nile virus (WNV), monkeypox,
and severe acute respiratory syndrome (SARS). West Nile virus, may exhibit antibody-dependent enhancement (ADE) of infec-
like avian influenza, is primarily a disease of birds, but is spread tion where, in the presence of virus, reactive antibody increases
by mosquitoes. National blood donor screening for West Nile viral entry into target cells. The development of DSS has been
attributed to ADE.140
virus RNA suggests asymptomatic infections are widespread
with approximately 735 000 cases occurring in the United States Dengue is transmitted by mosquitoes (Aedes aegypti) that
in 2003.127 West Nile virus causes significant neurologic disease in carry dengue virus types 1, 2, 3, or 4. Most cases involve type
a small portion of infections (1 per 256 cases). A severe case of 1. Dengue hemorrhagic fever is characterized by intense, sustai-
neurointensive illness in a parturient was reported by Skupski ned abdominal pain; persistent vomiting; sudden change from
and colleagues.128 After elective termination, fetal tissues showed fever to hypothermia; and marked restlessness or lethargy.
no evidence of WNV transmission. However, intrauterine WNV Hemoconcentration may occur. Confirmatory diagnostic tests
infection can occur. In one WNV epidemic in Colorado, 4% of include capture ELISA, rapid immunochromographic tests, and
cord blood samples were positive for WNV-specific immunoglo- polymerase chain reaction (PCR). The number of female mos-
bulin G antibodies.129 Currently it appears that the risk to the quitoes, Aedes aegypti, in a household is a significant risk factor
in outbreaks of the disease.141 Notably, the characteristic feed-
fetus from maternal WNV infection is low although a congenital
WNV syndrome has been described.130 ing and breeding patterns of these mosquitoes in southwestern
An outbreak of monkeypox occurred in the United States in United States (Tuscon, Arizona) suggest dengue fever outbreaks
2003.131 The infection was related to exposure to infected prairie could occur in the US.142 Clinical manifestations, laboratory

Chapter 18

Table 18.3 Dengue disease

Clinical manifestations Hematology Treatment

Dengue fever (a) 4“5 day incubation period; sudden fever (39.5“41.48C); intense Leukopenia, relative Symptomatic treatment.
(self-limited headache, generalized muscular pain, periorbicular and joint pain, lymphocytosis, and Avoid nonsteroidal
viruses) lymphadenophathy, and anorexia (5“7 days). mild to severe anti-inflamatory
(b) In two thirds of cases, a maculopapular blanching rash may thrombocytopenia. drugs, which may
appear on the third day, with petechiae in the axilla and on hands impair coagulation.
or feet. There is a pulse/temperature dissociation (i.e. high fever
and low pulse rate). May have bone pain lasting several weeks
although such pain is absent in DHF/DSS. Depression and fati-
gue generally persist after resolution of acute symptoms.143
Dengue Most cases occur during a second DV infection; severity varies from Leukopenia, As above; there is no way
hemorrhagic insignificant to life-threatening bleeding with death within 12“24 lymphocytosis, and to prevent
fever “ dengue hours in the absence of adequate symptomatic treatment. thrombocytopenia. hemorrhagic
shock Abdominal pain mimics an acute abdomen. Hypotension with sequelae.
syndrome narrowed pulse pressure from intravascular volume depletion.
(DHF-DSS) Antibody-dependent enhancement of DV growth in mononuclear
phagocytes is thought to be the mechanism whereby preexisting
dengue antibodies confer excess risk for DHF-DSS.145
Interleukin-1146 and plasminogen cross-reactive antibodies147
may play an important role in the etiology of DHF-DSS.

signs, and treatment are described in Table 18.3. After resolut- be avoided during the active viral phase due to neurological
ion of the disease, mental depression and fatigue generally manifestations of dengue, the frequency of which is unknown.
persist.143 In a review of 41 cases with neurologic symptoms,154 it was found
It is unknown whether dengue virus infection during preg- that dengue involved regions of the brain (61%), spinal cord (6%),
nancy causes teratogenicity, abortion, or IUGR. Chong and Lin and peripheral nerves (34%). Intravenous or inhalational analge-
reported nine cases of women infected with dengue fever in early sia may be alternatives to regional anesthesia during labor.
pregnancy who received amniocentesis or chorionic villus sam- Dengue hemorrhagic fever/dengue shock syndrome requires
pling. The chromosome analysis was normal, and the level of aggressive fluid resuscitation, effective utilization of blood bank
alpha-fetoprotein in amniotic fluid and maternal sera was within technology, and preventive measures during delivery to minimize
the normal range. Anti-dengue activity was found in the lipid blood loss. Emergency C/S usually requires GA, with ketamine a
component of human milk and colostrum. This suggests that recommended induction agent.
breast feeding will protect the infant from the dengue virus in
the endemic area of dengue infection.148 In contrast to this report,
Yellow fever virus
however, some have reported a high incidence of prematurity,
fetal distress, and occasional fetal death.149,150 Mother and fetus Yellow fever (YF) virus was first recorded in Barbados in 1647.
are at risk from hemorrhagic events when dengue infections This virus is transmitted between individuals by infected mosqui-
occur near the time of delivery.149 A live attenuated vaccine toes including the Aedes species, Haemagogus species, and
others. The fatality rate of severe YF is approximately 20%,155
should soon be available for dengue virus. In addition, a DNA
but can be as high as 57% in individual epidemics.156 Clinical
vaccine against the nonstructural 1 protein of dengue 2 virus is
under development in Brazil.151 However, as antibodies to all four management, laboratory signs, and treatment are described in
serotypes of dengue can cross the placenta to the fetus and persist Table 18.4. Diagnostic serology involves IgM antibody capture
in the fetus for nearly a year, vaccination of the infant in endemic enzyme linked immunosorbent assay (MAC-ELISA), ELISA inhi-
areas is not recommended until one year of age.152 bition, or neutralizing antibodies.155
Vertical transmission of dengue fever is sporadic and most The 2002 Yellow Fever Vaccine Recommendations of the
often the neonate recovers uneventfully. However, neonatal Advisory Committee on Immunizations Practices reported
death from uncontrolled intracerebral hemorrhage and multior- that YF vaccine is considered to be one of the safest and most
gan failure has been reported.153 effective live virus vaccines ever developed. Nonetheless, the
A self-limited dengue fever should be treated symptomatically. report also details vaccine-related complications including
It is better to avoid NSAIDs for fever because of the possibility of vaccine-associated neurotropic disease (encephalitis), and
worsening any coagulopathy. Cyclooxygenase-2 inhibitors may vaccine-associated viscerotropic disease (febrile multiple organ
be a good alternative. Neuraxial anesthetic techniques should system failure). The incidence of these severe life-threatening

5 Other disorders

Table 18.4 Yellow fever Table 18.5 Leptospirosis

Clinical Yellow fever is characterized by a biphasic illness: Clinical Vary greatly with most infections being subclinical.
5“10% result in severe infection.164 (Following 1“2
(a) First stage: after 3“6 day incubation period )
findings findings
fever, rigors, headache, backache, myalgia, and week incubation period, after penetrating the skin
prostration, which improves in 2“3 days. or mucosa, the leptospiretes invade the
(b) After one day of apparent cure, a flushed face, bloodstream and spread throughout the body
swollen lips, bright red tongue, nausea, causing hepatomegaly, meningitis, pancreatitis,
bradycardia, vomiting, tendency to bleed (black diarrhea, hemorrhage, hypotension, and ARDS.)
vomit, melena, bleeding gums, ecchymoses); Severe fatal form usually presents as hepatorenal
may result in hepatorenal failure and death. The failure although any organ may be involved.
disease can progress from prodrome to death in Abdominal pain and vomiting (71.4%) are major
7“10 days. presenting symptoms in the severe form.
Laboratory (a) First stage: lymphocytosis. Coagulation abnormalities may contraindicate
neuraxial block.165 Mortality rate is 1“5%.161
findings (b) Albuminuria, oliguria, anuria, electrolyte
i.v. penicillin; doxycycline is an alternative therapy.161
imbalance, thrombocytopenia (signs of hepatic Treatment
and renal failure).
Treatment Symptomatic, best in a hospital setting
people who work outdoors in contaminated areas or with ani-
(antiemetics, acetaminophen, avoid nonsteroidal
mals, for example, farmers, sewer workers, veterinarians, fish
anti-inflammatories that can impair
workers, dairy farmers, or military personnel.161 The pathogenic
coagulation). Serum electrolytes and acid-base
spirochetes are classified into a variety of serogroups and sero-
balance should be estimated daily. Few cases
types including fortbragg, hardjo, interrogans (icterohaemorrha-
may require hemodialysis, cardiotonic drugs, or
giae), autumnalis, bataviae, canicola, pomona, grippotyphosa,
monitoring of respiratory function.
javanica, mankarso, djasmani, cynopteri, and others. Each sero-
Prevention Highly effective vaccine is available.
type tends to be associated with a particular vertebrate that acts
as a natural reservoir. Human infection is acquired through
disorders among those vaccinated in the United States is esti- mucosal or skin contact with a contaminated substance, such as
mated to be 1:400 000.155 urine or feces. The organism is not spread from person to person.
The safety of YF vaccination during pregnancy has not been The Spirolept human vaccine induces a protective response
established and it is recommended only if travel to endemic areas against Leptospira interrogans ss icterohemorrhagiae, a serogroup
is unavoidable. Vertical transmission from the vaccine is very low that can be transmitted to the animal model and is linked to a
(1 in 81) and is not associated with congenital anomalies.155,157 humoral response.162 Leptospirosis has a well-known abortive
Yellow fever vaccination may be associated with an increased risk effect in animals and is thought to lead to perinatal deaths in
of spontaneous abortion.158 The developing nervous system is endemic areas.
particularly sensitive to the effects of YF virus and some believe The clinical manifestations and treatment are described in
that vaccination should be avoided during pregnancy since the Table 18.5. The diagnosis can be established by serological inves-
live virus is transmissible to the fetus.159 However, the high risk of tigation and isolating the leptospire. The most important ingre-
natural infection plus maternal death during YF epidemics may dient for the control of preventable infectious diseases is
˜˜political will™™.163
outweigh the theoretical contraindications to vaccination. The
relative safety of vaccinating pregnant women is supported in a
review of 480 pregnant women who received YF immunization
Plasmodium species (malaria)
before pregnancy was diagnosed.160 Maternal seroconversion
was very high when immunization was carried out in early preg- Malaria is a tropical parasitemia transmitted by mosquitoes
nancy. Overall, first trimester vaccination did not cause malfor- (Anopheles spp.) infected with Plasmodium spp. (vivax, falci-
mations, CNS complications, or adverse perinatal outcomes.160 parum, malariae, or ovale). It is responsible for 11% of deaths
Despite numerous reports of YF during pregnancy and the in children within developing countries despite the fact that
puerperium, obstetric anesthesia concerns during YF have not treatment of malaria is quite inexpensive (US$0.13 for chloro-
quine; US$2.68 for a seven-day course of quinine in 2004).166
been described. However, as neurologic disease may result and
coagulopathies may occur, the risks of regional techniques may The disease predominates in the rainy season or near water
outweigh the benefits in many cases. sources. A complete diagram of the life cycle of malaria is avail-
able at Infectivity
can be measured by the numbers of parasites in peripheral blood
Leptospira species
using the conventional Giemsa-stained blood smear, which
Leptospirosis occurs worldwide but is most common in temper- remains the gold standard for laboratory confirmation of the
ate or tropical climates. It presents an occupational hazard for disease. The sequestration of erythrocytes containing mature

Chapter 18

are generally not recommended in pregnancy. An increase in
Table 18.6 Manifestations and treatment of malaria stillbirths has been reported with mefloquine.176 McGready and
colleagues reported the relatively safe use of artemisinin deriva-
Clinical (a) 85“90% of parasitemic episodes are
tives in women with multidrug resistance, recrudescent infection,
manifestations asymptomatic. An estimated three to four
or hyperparasitemia.177
48-hour cycles of schizogony may occur
Severe malaria in the pregnant woman is treated with parent-
without eliciting either fever or macrophage
eral quinidine gluconate in a dose sufficient to maintain a quini-
activation. Fever develops, followed a day
dine level of 3“8 mg/l for at least 24 hours (loading dose followed
later by a spike in urinary neopterin, a
by infusion). At these doses, quinidine may have significant car-
product of monocytes/macrophages.168
diac effects including ventricular dysrhythmia, hypotension, and
(b) If symptomatic: recurrent episodes of fever
prolongation of the QTc interval.178 It may also cause hypoglyce-
and shivering are related to the cycles of
mia. However, as most deaths from severe malaria occur within
intra-erythrocytic schizogony; vomiting,
the first one to two days, the use of a loading dose is recom-
anemia; splenomegaly and muscle pains
mended. Finally, should parasite density exceed 10%, or if cere-
occur. Headache, convulsions, and mental
bral malaria, nonvolume overload pulmonary edema or renal
slowness, in cerebral malaria, icterus or
failure occur, exchange transfusion may be used to reduce para-
acute renal failure may occur. Hemoglobin
site derived toxins and cytokines.179,180
<8 g/dl is associated with IUGR. The mother
There are no reports detailing obstetric anesthesia in women
may develop pulmonary edema and
with malaria. Anesthetic concerns would include the theoretical
hypoglycemia169 in the third trimester.
risk of CNS infection from transfer of infected erythrocytes during
Hypoglycemia is possibly due to inhibition
dural puncture, exacerbation of hepatic dysfunction by anesthe-
of gluconeogenesis caused by failure of
sia-induced hypotension, and accentuation of maternal anemia
hepatic lactate uptake. There is a 50%
by excessive preanesthetic hydration. As malaria may affect vir-
reduction in serum vitamin A, due in part to
tually any organ system, the precise interactions of malaria with
impaired hepatic function.170
an anesthetic technique would depend on the organ systems
Treatment Traditional seven-day course of quinine therapy
is associated with a 50% failure rate in
pregnant women.171 Pregnant patients may
require multidrug therapy or larger dose of
Mycobacterium tuberculosis
mefloquine, in order to achieve comparable
Tuberculosis (TB) is estimated to infect one-third of the world™s
blood levels, due to increased volume of
population, with most of those affected living in developing coun-
distribution.172 The combination of
tries. About 10% of infected patients will develop symptoms of
pyrimethamine/chloroquine appears to be
disease, but this number is rising as a result of HIV coinfection.181
highly effective.173
Individuals in certain occupations have an increased risk of TB
Chemoprophylaxis or avoidance of exposure are
(see Table 18.7).182
the only measures likely to protect both
Each year approximately 2 million deaths occur worldwide
mother and baby.
from TB, 98% of them in developing countries.181,182 After a
steady decline in TB rates from 1953 to 1985, the United States
had a resurgence of TB in the late 1980s and early 1990s due to
forms of P. falciparum in the microvasculature of vital organs
increased immigration from countries with high prevalence, HIV
may cause large discrepancies between the peripheral blood
parasite count and the total body parasite burden.167 Clinical infection, emergence of resistant strains, poverty, homelessness,
drug abuse, and a decline in TB-related health services.182,183
manifestations and treatment are described in Table 18.6.
Cases began to decrease again in 1993 after the institution of
Malaria in pregnancy increases maternal and perinatal mor-
control measures. In 1998, 18 361 cases of TB (6.8 per 100 000
bidity and mortality. Pregnancy is associated with increased sus-
ceptibility to falciparum malaria, especially in primigravidae,174 population) were reported to the CDC, a 31% decrease from
1992.182 This downward trend in case numbers has continued
and pregnant women are three times as likely to develop severe
although at a slower rate with 14 093 TB cases (4.8 per 100 000)
disease than nonpregnant women in the same area. The placenta
reported in 2005. This represents the fewest cases recorded since
appears to be a preferential site for parasite sequestration and
national reporting began in 1953. Although the numbers of cases
replication. Indeed, the placenta may be black with malarial pig-
ment, even when the mother is asymptomatic.175 Malarial infec- are decreasing, not all data are reassuring. For example, the inci-
dence of TB in minorities is significantly higher than that in
tion may lead to miscarriage, premature delivery, low
birthweight, congenital infection, and/or perinatal death.166 whites. Also, the number of multidrug-resistant cases increased
13% from 2004 to 2005.184 Nevertheless, based on the decrease in
Most malarial infections may be treated with chloroquine or
the number of work-related TB cases among healthcare workers
quinine and clindamycin. Optimal therapy depends on know-
in San Francisco, it appears better control measures work and
ledge of the area where the disease was acquired and likely drug
lower the risk of TB in this high-risk group.185 Control measures
resistances. Alternative drugs, e.g. mefloquine and primaquine,

5 Other disorders

with coinfection with HIV as its potential for fetal toxicity is
Table 18.7 Personnel with increased risk of tuberculosis182 uncertain, thereby contraindicating routine use.187 Many agents
used to treat TB have the potential for significant maternal side
Hospital employees in wards with TB patients
effects. For example, adverse effects of rifampicin include renal

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