Congenital Flashcards

1
Q

During pregnancy a set of tissue potentially susceptible to infection which are (3)

A

Fetus, placenta, lactating

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2
Q

How does the placenta shield microbes in the genital tract

A

it acts as a barrier and fetal membrane

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3
Q

The mother not rejecting the fetus is accomplished by

A

absence or low density of histocompatibility complex (MHC) antigens on placental cells

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4
Q

once a fetus is infected it is exquisitely susceptible because

A

IgM adn IgA antibodies are not produced

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5
Q

When are IgM and Iga start producing during pregnancy

A

second half of pregnancy

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6
Q

What antibody does the fetus not get as well as inadequate

A

IgG and inadequate cytokines

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7
Q

After Primary infection, certain microbes can enter via

A

Blood placenta or fetus

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8
Q

I am a toga and rubivirus

A

Rubella

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9
Q

I am a restricted host range and only infect humans

A

Rubella

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10
Q

My core consists of single RNA and protein C

A

Rubella

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11
Q

My lipid envelope is two viral glycoproteins E1 and E2

A

Rubella

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12
Q

I have 9 genotypes, and immunity to 1 protect against all

A

Rubella

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13
Q

I use to be called German measles or 3-day measles?

A

Rubella

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14
Q

I was considered an independent disease in 1881, isolated in 1962, and vaccine in 1996

A

Rubella

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15
Q

100,000-200,000 this syndrome occurs annually

A

Rubella

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16
Q

Postnatal characteristics acute onset generalized maculopapular rash, mild fever, arthritis, arthralgia, lymphadenopathy, conjunctivitis

A

acute onset generalized maculopapular rash, mild fever, arthritis, arthralgia, lymphadenopathy, conjunctivitis

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17
Q

I am mild and 50% of my postnatal cases are not diagnosed

A

Rubella

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18
Q

Major concern for Rubella

A

Nonimmune pregnant women

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19
Q

I am the most potent infectious tertogenic agent identified

A

Rubella

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20
Q

When is Rubella most susceptible

A

first 3 months of pregnancy, interferes with development

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21
Q

Rubella clinically (3)

A

Low BW, fail to thrive, eye adn heart lesions, brain and heart defect may become detectable until later in the form of retarded adn deaf

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22
Q

Rubella can be isolated from infants adn how long does it shed

A

throat or urine adn sheds for several months

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23
Q

Infected fetus of rubella produces and is detecible where

A

IgM, cord adn blood

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24
Q

a live virus is given during pregnancy and pregnancy is a condridiction to vaccination

A

Rubella

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25
Q

my belong to Cytomegalovirus fam

A

CMV

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26
Q

I am a DS DNA icosahedral capsid amorphous tegument or matrix

A

CMV

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27
Q

i infect WW all ages and not seasonal nor do i have a pattern of transmission

A

CMV

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28
Q

Seroprevalence increases with age in all populations

A

CMV

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29
Q

I am acquired early in life, and i am prevelance in lower SES

A

CMV

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30
Q

Vertically or Horizontally

A

CMV

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31
Q

mostly transmitted by direct contact

A

CMV

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32
Q

i am detecatable in all bodily fluids

A

CMV

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33
Q

i can shed for weeks to years

A

CMV

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34
Q

Transplacental infection risk of transmission is lower then primary maternal infection

A

CMV

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35
Q

Fetal damage is highest b/w 12-16w

A

CMV

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36
Q

Most common congenital infection

A

CMV

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37
Q

10-15% of congenitally infected infants develop symptoms during the newborn period. who am i ? and what do these symptoms include

A

CMV;

retardation, jaundice, myocarditis, pneumonitis, CNS abnormalities, deafness, and chorioretinitis.

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38
Q

symptomatic infants may die from me from complications during first month

A

CMV

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39
Q

If infant has symptoms and survives it is neurologically damaged who am i

A

CMV

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40
Q

Some(10%) women shed near or during time of delivery

A

CMV

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41
Q

50% chance of transmission during delivery. Such infants begin to excrete virus at 3 – 12 weeks of age but usually remain asymptomatic and do not develop neurologic sequelae.

A

CMV

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42
Q

CMV infections are greatest among what kind of infants

A

low BW

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43
Q

common to get from milk

A

CMV

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44
Q

Day care has high risk, adn can experience infection for over 1-2 yrs which is usually asymptomatic, but can transmit to parents/unborn child

A

CMV

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45
Q

I am latent in endothelial cells and leukocytes

A

CMV

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46
Q

CMV diagnosis

A

Diagnosis IgM infant blood within 3w of delivery adn in DNA in blood or urine, throat swab

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47
Q

I am now rare and in resource-poor countries

A

Syphilis

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48
Q

Clinically rhinitis skin/musical lesions/, abnormalities in bone teeth and cartilage ( saddle-shaped nose)

A

Syphilis

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49
Q

Pregnancy masks early signs, mother will have serological evidence of treponemal infection

A

Syphilis

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50
Q

how to diagnosis syphilis

A

Treponemal IgM detected in fetal blood

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51
Q

i am transmitted only vertical and only infectious after 4month of pregnancy AKA treatment before 4m should prevent transmission

A

Syphili

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52
Q

I am a red-copper maculopapular lesion

A

Syphilis

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53
Q

Clinical: Convlusion, micerocephaly, chorioretinitis, hepasplen, jauindice, later hydroc. retarded, defective vision

A

Toxoplasmosis

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54
Q

No detectable abnormalities at birth but may appear after a few yrs

A

Toxoplasmosis

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55
Q

contracting me during embryo is rare, adn more serious

A

T.Gondii

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56
Q

Infection and Damage (abortion) increase in 3rd semester

A

Toxoplasmosis

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57
Q

Damage is more severe the earlier, what is opposite of this

A

Toxoplasmosis;

T.Gondii

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58
Q

Infection during 3rd trimester results asymptomatic, if not treated develop retinochoroiditis and neurologic deficits in childhood

A

T.Gondii

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59
Q

IgM in cord or Blood

A

Toxoplasmosis

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60
Q

no vaccine

A

Toxoplasmosis

Listeria Monocytogenes

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61
Q

How to avoid getting Toxoplasmis

A

Avoid ingesting cysts from cats or lightly cooked meat

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62
Q

Serological prevalence indicates most common infections of humans WW

A

Toxoplasmosis

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63
Q

In Canada no specific info available

A

Toxoplasmosis

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64
Q

Common in warm lower altitude favoring sporulation of oocyst

A

Toxoplasmosis

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65
Q

how to aquire Toxoplasmosis (9)

A

Meat- T.Gondii

Soils, food, water, feces, organ transplant, blood fusion, transplacentral transmission, inoculation of tachyzoites

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66
Q

Major routes are congenital or oral

A

Toxoplasmosis

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67
Q

Toxoplasmosis life cycles

A

ingestion of cysts- epitheliam, dissmentiate- multiply host cells release tachzoites and invade

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68
Q

Tachyzoites are pressure by host immune to transform into bradyzoites and

A

form tissue cyst- in skeletal myocardium and brain, cyst may remain thought life.

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69
Q

T.gondii treated under 4 circumstances-

A

pregnant with acute infection or prevent fetal infection

Congenitally infected infants

CMI person with reactivated disease

acute recurrent ocular disease

70
Q

How long doe it take T.Gondii to become infectious in liter box

A

1 day

71
Q

How to prevent Toxoplasmosis

A

wear gloves in garden, wash veggies, cutting board etc

72
Q

Clinically: poor weight, sepsis, delays lymphocytic, pneumonitis, oral thrush, enlarged lymph nodes

A

HIV

73
Q

HIV in some infants can develop

A

encephalophy and aids by 1yr

74
Q

Transmission reduced by aniretro drugs, and C-section no breastfeeding

A

HIV

75
Q

Diagnosis RNA by PCR in conjunction with antibody and antigen detection

A

HIV

76
Q

Facultative intracellular bacterial target the macrophage cellular lineage

A

Listeria Monocytogenes

77
Q

Gram + Rod, global nature found in a variety of animals, and fresh produce

A

Listeria Monocytogenes

78
Q

Ability to servive cold temp = biological advantage

A

Listeria

79
Q

Transmission: animals feces, unpasteurized milk, soft cheese contaminated veggies

A

Listeria Monocytogenes

80
Q

Mild influenza, frank sysetmic illness, fever, chills

A

Listeria Monocytogenes

81
Q

mostly asymptomatic

A

Listeria Monocytogenes

82
Q

ALWAYS bacteremia which leads to infection of placenta and then fetus

A

Listeria Monocytogenes

83
Q

Fetal infection= fetal loss, premature, septiemia, meningitis, pnemonis, abscess or granulomas

A

Listeria Monocytogenes

84
Q

Child can be infected during or after birth

A

Listeria Monocytogenes

85
Q

Swallowing amniotic fluid infection of lung and gut tissue

A

Listeria Monocytogenes

86
Q

Listeria Monocytogenes

A

Listeria Monocytogenes

87
Q

Listeria Monocytogenes Diagnoiss

A

Isolated from blood, culture, CSF, or newborn skin lesions

88
Q

Facultative gram + coccus

A

Grp B Streptococcus

89
Q

V factors = polysaccharide cap, lipoteichoic acid

A

Grp B Streptococcus

90
Q

Ten type=specific polysaccharide cap serotypes have been described

A

Grp B Streptococcus

91
Q

Asymp in mucous membranes, including genital rectal pharyngeal mucosa

A

Grp B Streptococcus

92
Q

Global colonization rate , significant regional variations in colonization prevalence

A

Grp B Streptococcus

93
Q

Maternal GBS colonization results in infant colonization in approximately 50% of cases, and infants become colonized either intrapartum (childbirth) or through bacterial translocation despite intact membranes.

A

Grp B Streptococcus

94
Q

Early- sepsis & pneumonia within first 7 days of life

Later- meningitis and sepsis b/w 7 and 3m age

A

Grp B Streptococcus

95
Q

Diagnosis: 35-37w gestation by vaginal rectal swab- cultured, enrich media subculture to BA and CAN plates, examining plated for..?

A

Grp B Streptococcus

96
Q

Administer antibiotic 4 hrs before delivery

A

Grp B Streptococcus

97
Q

Gram – rod

A

E.Coli

98
Q

Second leading cause of EOS in neonates

A

E.Coli

99
Q

I am an anitgen that is specific to neonatal sepsis. Closely linked to neonatal meningitis and best described v factor. Impairs phagocytic killing by PMNS and macrophages

A

K1 cap antigen (e.coli)

100
Q

E.coli severity is due to

A

Severity related to amount/persistence of K1 antigen in CSF

101
Q

Gram - organisms importance

A

less ferequent causes of EOS, remain important cause of LOS and are increasing importance to growing antimicrobial resistance concerns,

102
Q

Gram - organims are

A

Enterbacter, Kelb, Serratia, Citro, Crono Sakasakii

103
Q

GRAM + ORGANISMS common in

A

Both Staph A and coagulase- staphly are more frequent causes of LOS and nosocomial sepsis in neonatal, esp in very low BW

104
Q

Fungal EOS sepsis and risk factors

A

EOS fungal sepsis is infrequent cause of sepsis, risk factors include maternal fungal colonization and vaginal route delivery

105
Q

Fungal in NICU setting

A

most common is Candida, more ass with LOS with inversely proportional to the gestational age and BW

106
Q

RNA representing 2 genera in Picornaviridae

A

Enterovirus and Parechovirus

107
Q

neontal infection Is not rare and reported in infant <29D

A

Enterovirus

108
Q

symptomatic enternoviral illness

A

Neonates <29day; 20% will present severe sepsis-like syndrome

109
Q

which disease is most likely required differentiation from bacterial EOS

A

Enterovirus

110
Q

transmitted via fecal-oral and possible oral-oral (respitory)

A

Enterovirus and Parechovirus

111
Q

evidance support transmission to neonates before, during or after delivery.

A

Enterovirus and Parechovirus

112
Q

May occur antenatally through maternal viremia and transplacental spread to fetus

A

Enterovirus and Parechovirus

113
Q

Intrapartum by exposure to maternal blood, secretion and or stool or postnatally from close contact with infected caregivers

A

Enterovirus and Parechovirus

114
Q

EOS are more likely acquired vertically via presenting on the first day of life

A

Enterovirus and Parechovirus

115
Q

Culture positive for Enterovirus identified from?

And what is detected first day of life

A

amniotic fluid, umbilical cord blood, neonate organs; detection of neutralizing IgM in serum by first day of life

116
Q

Clinical presentation of Enterovirus and Parechovirus EOS, LOS

A

EOS- sepsis, fever, irritability, poor feeing rash (indistinguishable from bacterial EOS)
LOS- aspetic meningitis, abrupt onset of fever, poor feeding, vomiting, diarrhea, rash resp symptoms, Neurological symptoms (lethargy/irritability to nuchal rigidity)

117
Q

iron structure- linear, DS DNA, icosahedral capsid, tegument layer surrounded by spike enveloped containing viral glycoprotein that aid in attachment penetration and immune evasion

A

HSV

118
Q

Trilaminar, lipid-rich layer derives largely from nuclear membrane of infected cells

A

hsv

119
Q

B/c of membrane virus is inactivated by lipid solvents such as ethanol

A

HSV

120
Q

One of the most serious consequences of genital HSV infection

A

neonatal herpes

121
Q

mother experiencing unrecognized primary infection during time of labor are more contagious then

A

those shedding HSV as a result of recurrent or reactivation

122
Q

Which HSV transmission is higher 1 or 2?

A

1

123
Q

50-80% of all cases of neonatal herpes occur in children of women who acquire HSV infection during what part of the term

A

near term

124
Q

HSV is acquired mostly in

A

peripartum (period shortly before during and after birth

125
Q

What ways can HSV in neonates be presented

A

1 in 3 ways
Skin, eye and mouth (45%)

Meningoencephalitis (CNS 30%)

Disseminated (25%)

126
Q

1/300,000 of HSV can have

A

cutaneous scarring or rash; hyper/phytopigment’s CNS abnormities, calcification or encephalomalacia and ocular anomalies optic atrophy ETC.

127
Q

Infants with HSV skin, eye, mouth diagnosed

A

based on characteristics vesicular skin lesions that demonstrate HSV culture, fluorescent antibody staining or PCR

128
Q

Other HSV diagnosis

A

MRI EEG

129
Q

Disseminated HSV infection most liekly to have

A

EOS and multiple organs with pneumonia and hepatitis occurring most freq.

130
Q

Herpes fam, Icosahedral nucleocapsid surrounded by tegument structure

A

VZV

131
Q

lipid envelope and linear DS DNA

A

VZV

132
Q

fusion or endocytosis

A

VZV

133
Q

Low genomic diversity among isolates in comparison to others in its fam

A

VZV

134
Q

No evidence that naturally circulating ? strains differ in virulence

A

VZV

135
Q

Ubiquitous and highly contagious PI occurs in early childhood

A

VZV

136
Q

Mostly ages of 10-15 are seropositive

A

VZV

137
Q

Aerosol transmission

A

VZV

138
Q

After PI (mucocutaneous kin lesion – vesicles) the virus remains latency in ganglia

A

VZV

139
Q

VZV reactivation what can developed

A

Zoster

140
Q

VZV PI of first 21d may lead to

A

Congenital varicella syndrom

141
Q

varciella syndrome is characterized by

A

Cutaneous scarification’s

Atrophy extremities

Seizures, microcephaly and other sequelae

142
Q

confirmed detection of Varciella is

A

in fetal tissue

143
Q

Severe disseminated infection in babies born inwithin 4 days to 2 days proppr to

A

maternal varicella rash appears.

144
Q

Erythrovirus one of 5 genera in parvoviridae

A

HPV B19

145
Q

icosahedral, lacks envelope hence resistant to solvents, ss DNA

A

HPV B19

146
Q

smallest known DNA virus that infect mammalian cells

A

HPV B19

147
Q

Extremely limited cell tropism, replicating only in the nuclei of erythroid progenitor cells

A

HPV B19

148
Q

Common WW In temp climate winter. Summer

A

HPV B19

149
Q

Epidemic peaks occur in cycles every 3-5yrs

A

HPV B19

150
Q

HPV most common in

A

Most coming in young children

151
Q

manifest itself as erythema infectious (EI), (fifth disease or slapped cheek syndrome)

A

HPV B19

152
Q

in HPV; individual who have disorders that shorter red cell half-life, results in

A

(TAC)transient aplastic crisis= life threating anemia

153
Q

Both TAC and EI manifest are usually

A

self-limiting

154
Q

HPV transmission

A

most often by respiratory secretions saliva, esp. sneeze or cough

155
Q

HPV veritcal or horizontal transmission

A

both, horizontal more common

156
Q

transmission to infants is not synonymous with poor pregnancy outcomes or adverse consequences to the infant

A

Vertical transmission of HPV

157
Q

50-60% women reproductive years have circulating

A

B-19

158
Q

HPV Can be transmitted parenterally from

A

blood or blood products

159
Q

HPV symptoms severity

A

asymp to life threating

160
Q

1st and 2nd phase of HPV

A

1- fever, headache, myalgia, chills, itching

2-absence of reticulocytes, drop in hemoglobin, transient decrease in neutrophils, lymph or platelets

161
Q

HPV IgM became detectable how long after vaccination

A

2 weeks post inoculation (vaccination)

162
Q

EI/Fifth disease

A

Prodromal symptoms, low grade fever, headache, and one or more : conjunctivitis upper resp, cough, myalgia, masueas, diarrhea. Specific rash on face as confluent maculopapular erythema on check ( slapped check app)

Rash may appear bilateral , rarely on palms or feet

Rash may at least 3w

163
Q

TAC

A

Acute, self-limiting cessation of the regenerative process within the erythropoietic cell lineage

Catheterized by abrupt onset of sever anemia ass with dramatic decline in circulating reticulocytes. This is an issue in all indiv. with underlying chronic hemo anemia

164
Q

most important complications of infection is ass with pregnancy loss

A

TAC

165
Q

HPV rate of transmission across placenta

A

High

166
Q

HPV risk of death

A

low

167
Q

HPV is greates risk during what age of gestation

A

infection occuring on/before 20w gestation

168
Q

HPV is responsible for the most cases of

A

idiopathic nonimmune hydrops fetalis - resolve spontaneously

169
Q

Fetus is vulnerable and developing hydrops during (whihc term) and is correlated to

A

second trimester. HPV

rapid expansion fo RBC, including erythrocytes precursor cells, the target cell for B19

170
Q

HPV Diagnosis:

A

Rash difficult to diagnose outside of outbreak

Serology: IgM

171
Q

Prenatal screening in Manitoba always

A

Hep B

Rubell

Syph

HIV

172
Q

Prenatal screening in Manitoba on request

A

Toxo

Varicella

HCV

HTLC

Parvovirus