Congenital Flashcards
(172 cards)
1
Q
During pregnancy a set of tissue potentially susceptible to infection which are (3)
A
Fetus, placenta, lactating
2
Q
How does the placenta shield microbes in the genital tract
A
it acts as a barrier and fetal membrane
3
Q
The mother not rejecting the fetus is accomplished by
A
absence or low density of histocompatibility complex (MHC) antigens on placental cells
4
Q
once a fetus is infected it is exquisitely susceptible because
A
IgM adn IgA antibodies are not produced
5
Q
When are IgM and Iga start producing during pregnancy
A
second half of pregnancy
6
Q
What antibody does the fetus not get as well as inadequate
A
IgG and inadequate cytokines
7
Q
After Primary infection, certain microbes can enter via
A
Blood placenta or fetus
8
Q
I am a toga and rubivirus
A
Rubella
9
Q
I am a restricted host range and only infect humans
A
Rubella
10
Q
My core consists of single RNA and protein C
A
Rubella
11
Q
My lipid envelope is two viral glycoproteins E1 and E2
A
Rubella
12
Q
I have 9 genotypes, and immunity to 1 protect against all
A
Rubella
13
Q
I use to be called German measles or 3-day measles?
A
Rubella
14
Q
I was considered an independent disease in 1881, isolated in 1962, and vaccine in 1996
A
Rubella
15
Q
100,000-200,000 this syndrome occurs annually
A
Rubella
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
17
Q
I am mild and 50% of my postnatal cases are not diagnosed
A
Rubella
18
Q
Major concern for Rubella
A
Nonimmune pregnant women
19
Q
I am the most potent infectious tertogenic agent identified
A
Rubella
20
Q
When is Rubella most susceptible
A
first 3 months of pregnancy, interferes with development
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
22
Q
Rubella can be isolated from infants adn how long does it shed
A
throat or urine adn sheds for several months
23
Q
Infected fetus of rubella produces and is detecible where
A
IgM, cord adn blood
24
Q
a live virus is given during pregnancy and pregnancy is a condridiction to vaccination
A
Rubella
25
my belong to Cytomegalovirus fam
CMV
26
I am a DS DNA icosahedral capsid amorphous tegument or matrix
CMV
27
i infect WW all ages and not seasonal nor do i have a pattern of transmission
CMV
28
Seroprevalence increases with age in all populations
CMV
29
I am acquired early in life, and i am prevelance in lower SES
CMV
30
Vertically or Horizontally
CMV
31
mostly transmitted by direct contact
CMV
32
i am detecatable in all bodily fluids
CMV
33
i can shed for weeks to years
CMV
34
Transplacental infection risk of transmission is lower then primary maternal infection
CMV
35
Fetal damage is highest b/w 12-16w
CMV
36
Most common congenital infection
CMV
37
10-15% of congenitally infected infants develop symptoms during the newborn period. who am i ? and what do these symptoms include
CMV;
| retardation, jaundice, myocarditis, pneumonitis, CNS abnormalities, deafness, and chorioretinitis.
38
symptomatic infants may die from me from complications during first month
CMV
39
If infant has symptoms and survives it is neurologically damaged who am i
CMV
40
Some(10%) women shed near or during time of delivery
CMV
41
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.
CMV
42
CMV infections are greatest among what kind of infants
low BW
43
common to get from milk
CMV
44
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
CMV
45
I am latent in endothelial cells and leukocytes
CMV
46
CMV diagnosis
Diagnosis IgM infant blood within 3w of delivery adn in DNA in blood or urine, throat swab
47
I am now rare and in resource-poor countries
Syphilis
48
Clinically rhinitis skin/musical lesions/, abnormalities in bone teeth and cartilage ( saddle-shaped nose)
Syphilis
49
Pregnancy masks early signs, mother will have serological evidence of treponemal infection
Syphilis
50
how to diagnosis syphilis
Treponemal IgM detected in fetal blood
51
i am transmitted only vertical and only infectious after 4month of pregnancy AKA treatment before 4m should prevent transmission
Syphili
52
I am a red-copper maculopapular lesion
Syphilis
53
Clinical: Convlusion, micerocephaly, chorioretinitis, hepasplen, jauindice, later hydroc. retarded, defective vision
Toxoplasmosis
54
No detectable abnormalities at birth but may appear after a few yrs
Toxoplasmosis
55
contracting me during embryo is rare, adn more serious
T.Gondii
56
Infection and Damage (abortion) increase in 3rd semester
Toxoplasmosis
57
Damage is more severe the earlier, what is opposite of this
Toxoplasmosis;
| T.Gondii
58
Infection during 3rd trimester results asymptomatic, if not treated develop retinochoroiditis and neurologic deficits in childhood
T.Gondii
59
IgM in cord or Blood
Toxoplasmosis
60
no vaccine
Toxoplasmosis
| Listeria Monocytogenes
61
How to avoid getting Toxoplasmis
Avoid ingesting cysts from cats or lightly cooked meat
62
Serological prevalence indicates most common infections of humans WW
Toxoplasmosis
63
In Canada no specific info available
Toxoplasmosis
64
Common in warm lower altitude favoring sporulation of oocyst
Toxoplasmosis
65
how to aquire Toxoplasmosis (9)
Meat- T.Gondii
| Soils, food, water, feces, organ transplant, blood fusion, transplacentral transmission, inoculation of tachyzoites
66
Major routes are congenital or oral
Toxoplasmosis
67
Toxoplasmosis life cycles
ingestion of cysts- epitheliam, dissmentiate- multiply host cells release tachzoites and invade
68
Tachyzoites are pressure by host immune to transform into bradyzoites and
form tissue cyst- in skeletal myocardium and brain, cyst may remain thought life.
69
T.gondii treated under 4 circumstances-
pregnant with acute infection or prevent fetal infection
Congenitally infected infants
CMI person with reactivated disease
acute recurrent ocular disease
70
How long doe it take T.Gondii to become infectious in liter box
1 day
71
How to prevent Toxoplasmosis
wear gloves in garden, wash veggies, cutting board etc
72
Clinically: poor weight, sepsis, delays lymphocytic, pneumonitis, oral thrush, enlarged lymph nodes
HIV
73
HIV in some infants can develop
encephalophy and aids by 1yr
74
Transmission reduced by aniretro drugs, and C-section no breastfeeding
HIV
75
Diagnosis RNA by PCR in conjunction with antibody and antigen detection
HIV
76
Facultative intracellular bacterial target the macrophage cellular lineage
Listeria Monocytogenes
77
Gram + Rod, global nature found in a variety of animals, and fresh produce
Listeria Monocytogenes
78
Ability to servive cold temp = biological advantage
Listeria
79
Transmission: animals feces, unpasteurized milk, soft cheese contaminated veggies
Listeria Monocytogenes
80
Mild influenza, frank sysetmic illness, fever, chills
Listeria Monocytogenes
81
mostly asymptomatic
Listeria Monocytogenes
82
ALWAYS bacteremia which leads to infection of placenta and then fetus
Listeria Monocytogenes
83
Fetal infection= fetal loss, premature, septiemia, meningitis, pnemonis, abscess or granulomas
Listeria Monocytogenes
84
Child can be infected during or after birth
Listeria Monocytogenes
85
Swallowing amniotic fluid infection of lung and gut tissue
Listeria Monocytogenes
86
Listeria Monocytogenes
Listeria Monocytogenes
87
Listeria Monocytogenes Diagnoiss
Isolated from blood, culture, CSF, or newborn skin lesions
88
Facultative gram + coccus
Grp B Streptococcus
89
V factors = polysaccharide cap, lipoteichoic acid
Grp B Streptococcus
90
Ten type=specific polysaccharide cap serotypes have been described
Grp B Streptococcus
91
Asymp in mucous membranes, including genital rectal pharyngeal mucosa
Grp B Streptococcus
92
Global colonization rate , significant regional variations in colonization prevalence
Grp B Streptococcus
93
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.
Grp B Streptococcus
94
Early- sepsis & pneumonia within first 7 days of life
Later- meningitis and sepsis b/w 7 and 3m age
Grp B Streptococcus
95
Diagnosis: 35-37w gestation by vaginal rectal swab- cultured, enrich media subculture to BA and CAN plates, examining plated for..?
Grp B Streptococcus
96
Administer antibiotic 4 hrs before delivery
Grp B Streptococcus
97
Gram – rod
E.Coli
98
Second leading cause of EOS in neonates
E.Coli
99
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
K1 cap antigen (e.coli)
100
E.coli severity is due to
Severity related to amount/persistence of K1 antigen in CSF
101
Gram - organisms importance
less ferequent causes of EOS, remain important cause of LOS and are increasing importance to growing antimicrobial resistance concerns,
102
Gram - organims are
Enterbacter, Kelb, Serratia, Citro, Crono Sakasakii
103
GRAM + ORGANISMS common in
Both Staph A and coagulase- staphly are more frequent causes of LOS and nosocomial sepsis in neonatal, esp in very low BW
104
Fungal EOS sepsis and risk factors
EOS fungal sepsis is infrequent cause of sepsis, risk factors include maternal fungal colonization and vaginal route delivery
105
Fungal in NICU setting
most common is Candida, more ass with LOS with inversely proportional to the gestational age and BW
106
RNA representing 2 genera in Picornaviridae
Enterovirus and Parechovirus
107
neontal infection Is not rare and reported in infant <29D
Enterovirus
108
symptomatic enternoviral illness
Neonates <29day; 20% will present severe sepsis-like syndrome
109
which disease is most likely required differentiation from bacterial EOS
Enterovirus
110
transmitted via fecal-oral and possible oral-oral (respitory)
Enterovirus and Parechovirus
111
evidance support transmission to neonates before, during or after delivery.
Enterovirus and Parechovirus
112
May occur antenatally through maternal viremia and transplacental spread to fetus
Enterovirus and Parechovirus
113
Intrapartum by exposure to maternal blood, secretion and or stool or postnatally from close contact with infected caregivers
Enterovirus and Parechovirus
114
EOS are more likely acquired vertically via presenting on the first day of life
Enterovirus and Parechovirus
115
Culture positive for Enterovirus identified from?
And what is detected first day of life
amniotic fluid, umbilical cord blood, neonate organs; detection of neutralizing IgM in serum by first day of life
116
Clinical presentation of Enterovirus and Parechovirus EOS, LOS
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
iron structure- linear, DS DNA, icosahedral capsid, tegument layer surrounded by spike enveloped containing viral glycoprotein that aid in attachment penetration and immune evasion
HSV
118
Trilaminar, lipid-rich layer derives largely from nuclear membrane of infected cells
hsv
119
B/c of membrane virus is inactivated by lipid solvents such as ethanol
HSV
120
One of the most serious consequences of genital HSV infection
neonatal herpes
121
mother experiencing unrecognized primary infection during time of labor are more contagious then
those shedding HSV as a result of recurrent or reactivation
122
Which HSV transmission is higher 1 or 2?
1
123
50-80% of all cases of neonatal herpes occur in children of women who acquire HSV infection during what part of the term
near term
124
HSV is acquired mostly in
peripartum (period shortly before during and after birth
125
What ways can HSV in neonates be presented
1 in 3 ways
Skin, eye and mouth (45%)
Meningoencephalitis (CNS 30%)
Disseminated (25%)
126
1/300,000 of HSV can have
cutaneous scarring or rash; hyper/phytopigment's CNS abnormities, calcification or encephalomalacia and ocular anomalies optic atrophy ETC.
127
Infants with HSV skin, eye, mouth diagnosed
based on characteristics vesicular skin lesions that demonstrate HSV culture, fluorescent antibody staining or PCR
128
Other HSV diagnosis
MRI EEG
129
Disseminated HSV infection most liekly to have
EOS and multiple organs with pneumonia and hepatitis occurring most freq.
130
Herpes fam, Icosahedral nucleocapsid surrounded by tegument structure
VZV
131
lipid envelope and linear DS DNA
VZV
132
fusion or endocytosis
VZV
133
Low genomic diversity among isolates in comparison to others in its fam
VZV
134
No evidence that naturally circulating ? strains differ in virulence
VZV
135
Ubiquitous and highly contagious PI occurs in early childhood
VZV
136
Mostly ages of 10-15 are seropositive
VZV
137
Aerosol transmission
VZV
138
After PI (mucocutaneous kin lesion – vesicles) the virus remains latency in ganglia
VZV
139
VZV reactivation what can developed
Zoster
140
VZV PI of first 21d may lead to
Congenital varicella syndrom
141
varciella syndrome is characterized by
Cutaneous scarification's
Atrophy extremities
Seizures, microcephaly and other sequelae
142
confirmed detection of Varciella is
in fetal tissue
143
Severe disseminated infection in babies born inwithin 4 days to 2 days proppr to
maternal varicella rash appears.
144
Erythrovirus one of 5 genera in parvoviridae
HPV B19
145
icosahedral, lacks envelope hence resistant to solvents, ss DNA
HPV B19
146
smallest known DNA virus that infect mammalian cells
HPV B19
147
Extremely limited cell tropism, replicating only in the nuclei of erythroid progenitor cells
HPV B19
148
Common WW In temp climate winter. Summer
HPV B19
149
Epidemic peaks occur in cycles every 3-5yrs
HPV B19
150
HPV most common in
Most coming in young children
151
manifest itself as erythema infectious (EI), (fifth disease or slapped cheek syndrome)
HPV B19
152
in HPV; individual who have disorders that shorter red cell half-life, results in
(TAC)transient aplastic crisis= life threating anemia
153
Both TAC and EI manifest are usually
self-limiting
154
HPV transmission
most often by respiratory secretions saliva, esp. sneeze or cough
155
HPV veritcal or horizontal transmission
both, horizontal more common
156
transmission to infants is not synonymous with poor pregnancy outcomes or adverse consequences to the infant
Vertical transmission of HPV
157
50-60% women reproductive years have circulating
B-19
158
HPV Can be transmitted parenterally from
blood or blood products
159
HPV symptoms severity
asymp to life threating
160
1st and 2nd phase of HPV
1- fever, headache, myalgia, chills, itching
| 2-absence of reticulocytes, drop in hemoglobin, transient decrease in neutrophils, lymph or platelets
161
HPV IgM became detectable how long after vaccination
2 weeks post inoculation (vaccination)
162
EI/Fifth disease
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
TAC
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
most important complications of infection is ass with pregnancy loss
TAC
165
HPV rate of transmission across placenta
High
166
HPV risk of death
low
167
HPV is greates risk during what age of gestation
infection occuring on/before 20w gestation
168
HPV is responsible for the most cases of
idiopathic nonimmune hydrops fetalis - resolve spontaneously
169
Fetus is vulnerable and developing hydrops during (whihc term) and is correlated to
second trimester. HPV
rapid expansion fo RBC, including erythrocytes precursor cells, the target cell for B19
170
HPV Diagnosis:
Rash difficult to diagnose outside of outbreak
| Serology: IgM
171
Prenatal screening in Manitoba always
Hep B
Rubell
Syph
HIV
172
Prenatal screening in Manitoba on request
Toxo
Varicella
HCV
HTLC
Parvovirus
