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Micro Exam 2 > Neely: Obstetric and Perinatal Infections > Flashcards

Neely: Obstetric and Perinatal Infections Flashcards

1
Q

Obstetric and Perinatal Infections

DEFINITION:

A

Infections acquired in utero, during delivery, or shortly after delivery.

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2
Q

PERIOD OF HIGH SUSCEPTIBILITY

Time period:
Why?

A

Birth through 1st 4 weeks of life

Fetus had previously been living in a germ free environment; Now exposed to a whole zoo of pathogens that can infect them

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3
Q

PERIOD OF HIGH SUSCEPTIBILITY

Risk of infection and the types of pathogens encountered depends on several factors: (5)

A

o State of maternal health
o Maternal susceptibility to certain agents
o Nutrition (both before and during pregnancy)
o Integrity of fetal membranes
o Degree of maturity at birth

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4
Q

PERIOD OF HIGH SUSCEPTIBILITY

Special Defenses: (4)

A

Fetal membranes: physical barrier to infection

Placenta/Maternal Immunity: protect against bloodborne pathogens

Transplacental IgG: present weeks to months after birth

Breast-fed infants: IgA provides some protection against pathogens invading GI tract

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5
Q

Special Susceptibility

When is the competent state of immunity reached?
What is decreased in fetal immunity? (2)

A

Fetal immune system is immature:
o Competent state not reached until age 2
o Decreased phagocytic activity
o Decreased levels of complement

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6
Q

Special Susceptibility

What happens to mother’s immunity?
What rates are highest at this time?

A

Mother’s immune system also suppressed: protects mother and fetus from activation of immune response, preventing immunological rejection of the fetus

Cell growth and organ differentiation rates are highest at this time: especially susceptible to permanent damage.

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7
Q

Congenital (In Utero)
Definition:

What agents? (2)

A

Congenital (In Utero): across placenta

L.monocytogenes
T.gondii

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8
Q

Perinatal
Definition:

What agents? (3)

A

Perinatal: from maternal bloodstream or during passage down the birth canal

o E. coli
o L.monocytogenes
o S.agalactiae

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9
Q

Post-natal
Definition:

What agents? (3)

A

Post-natal: milk, blood, saliva, contact

o E. coli
o L.monocytogenes
o S.agalactiae

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10
Q

Streptococcus agalactiae (Group B Strep)

G +/-?
Shape:
Cat +/-?
Type of hemolysis:

A

Basic ID: Gram positive, diplococci or short chain in liquid media

Lab Test ID: catalase negative, beta-hemolytic

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11
Q

Streptococcus agalactiae (Group B Strep)

Normal flora of where?

A

Normal flora: of GI tact and female genitourinary tract (~40% of females colonized in vagina); opportunistic pathogens.

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12
Q

What is the leading cause of bacterial meningitis in newborns?

A

Streptococcus agalactiae (Group B Strep)

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13
Q 
Streptococcus agalactiae (Group B Strep)
Infection occurs by exposure to organism

Ascending route in utero via:
Contamination during:

A

Ascending route in utero through ruptured membranes

Contamination during passage through birth canal

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14
Q

Streptococcus agalactiae (Group B Strep)

Where does the infant become infected? How?
How does the colonization of the maternal vaginal tract relate?

A

Infant becomes infected in mucus membranes (oropharynx, GI tract): via inhalation of amniotic fluid or maternal vaginal secretions; organism then penetrates into the bloodstream.

The heavier the colonization of the maternal vaginal tract, the higher the risk to the newborn.

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15
Q 
Streptococcus agalactiae (Group B Strep)
Early Onset Disease (EOD)

Age:

A

<7 days

Usually withing 24 hours of birth

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16
Q 
Streptococcus agalactiae (Group B Strep)
Early Onset Disease (EOD)

Risk Factors: (4)

A
  1. Heavily colonized mother without specific Ab
  2. Premature rupture of membranes
  3. Pre-term delivery and low birth weight
  4. Prolonged labor, obstetric complications such as intrapartum fever
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17
Q 
Streptococcus agalactiae (Group B Strep)
Early Onset Disease (EOD)

Type of Disease:

A

Bacteremia, pneumonia, meningitis

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18
Q 
Streptococcus agalactiae (Group B Strep)
Early Onset Disease (EOD)

Serotype:
Meningitis mainly due to:

A

All serotypes

Meningitis mainly due to type III

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19
Q 
Streptococcus agalactiae (Group B Strep)
Early Onset Disease (EOD)

Outcome:

A

~60% fatal; serious sequelae in survivors

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20
Q 
Streptococcus agalactiae (Group B Strep)
Early Onset Disease (EOD)

Prevention:

A

Antibiotic treatment does not reliably abolish carriage in mother

“Blind” treatment of sick baby who has risk factors (treat on suspicion)

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21
Q 
Streptococcus agalactiae (Group B Strep)
Late Onset Disease (LOD)

Age:

A

1 week to 3 months

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22
Q 
Streptococcus agalactiae (Group B Strep)
Late Onset Disease (LOD)

Risk Factors: (3)

A
  1. Lack of maternal Ab
  2. Exposure to cross infection from heavily colonized babies
  3. Poor hygiene in the nursery
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23
Q 
Streptococcus agalactiae (Group B Strep)
Late Onset Disease (LOD)

Type of Disease:

A

Predominantly meningitis

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24
Q 
Streptococcus agalactiae (Group B Strep)
Late Onset Disease (LOD)

Serotype:

A

90% due to type III

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25
Q 
Streptococcus agalactiae (Group B Strep)
Late Onset Disease (LOD)

Outcome:

A

~20% fatal

26
Q 
Streptococcus agalactiae (Group B Strep)
Late Onset Disease (LOD)

Prevention:

A

Good hygiene practices in the nursery

Do not allow mothers to handle other babies

27
Q

Streptococcus agalactiae (Group B Strep)
Virulence Factors
Adherence:

A

Initial event in colonization and invasion

28
Q 
Streptococcus agalactiae (Group B Strep)
Virulence Factors
Polysaccharide capsule

How many serotypes?
What is on the terminal sugar?
What does it limit the deposition of on the surface? What does this lead to?
What happens during invasion?

A

9 different serotypes

Sialic acid moiety on terminal sugar

Limits C3b deposition on surface (decreased phagocytosis)

Note: will turn off capsule during invasion

29
Q

Streptococcus agalactiae (Group B Strep)
Virulence Factors
Invasion

A

Ability to invade respiratory epithelium and BBB (lack of capsule promotes invasion)

30
Q

Streptococcus agalactiae (Group B Strep)
Virulence Factors
Beta-hemolysis is cytolytic for what? What is promoted?

A

Cytolytic for lung epithelial cells and human brain endothelial cells (promotes BBB invasion)

31
Q

What is the most important virulence factor for Streptococcus agalactiae (Group B Strep)?

A

Polysaccharide capsule

32
Q

Streptococcus agalactiae (Group B Strep)

Diagnosis
EOD presents as:
LOD:
Lab diagnosis:

A

EOD – first 5 days after birth – presents as septicemia, pneumonia or meningitis

LOD – 3 to 8 weeks after birth

Lab diagnosis of cerebrospinal fluid or blood. Commercial kits can detect the group B antigen

33
Q 
Streptococcus agalactiae (Group B Strep)
Treatment

What is intrapartum prophylaxis?
When do you treat?

A

Intrapartum prophylaxis: administer antibiotic course during delivery (most important prevention)

TREAT ON SUSPICION: do NOT wait for lab results to get back

34
Q

E.Coli K1

G +/-?
Shape:
Normal flora of what?
Another common cause of what?

A

Basic ID: Gram negative bacillus

Normal Flora: major inhabitant of large intestine

Another common cause of neonatal meningitis

35
Q

E.Coli K1

How does vaginal E.Coli colonize the infant?
Mortality Rate:

A

Ruptured amniotic membranes, OR

During delivery

High mortality rate (40-80%): survivors have neurological or developmental abnormalities

36
Q

E.Coli K1

Risk Factors:

A

Prematurity
Low birth weight
Prolong rupture of membranes

37
Q

E.Coli K1

When does septicemia present?
When does meningitis present?

A

Septicemia: at birth or within 2 days after birth

Meningitis: infection in infants more than 2 days old

38
Q 
E.Coli K1
Virulence Factors (4):
A

K1 Polysialic Capsule
Invasins (IbeA and IbeB)
Type O Antigen on LPS
S.fimbriae

39
Q

K1 Polysialic Capsule

What percent of E.coli isolates from neonates have this capsule?

Resists killing by what?

How does it affect BBB crossing?

A

80% of E.coli isolates from neonates have this capsule

Resistance to killing by neutrophils and normal serum (aids in survival in the blood and CSF)

However, not necessary for invasion across BBB

40
Q

E.Coli K1

What do invasins do?
What is Type O Antigen important for?
What is S.fimbriae important for?

A

Invasins (IbeA and IbeB): contribute to crossing the BBB

Type O Antigen on LPS: important for establishing infection

S.fimbriae: important for establishing infection

41
Q

E.Coli K1
Diagnosis

Symptoms: (3)
Cultures (2):
When do you treat?

A

Symptoms Variable: respiratory distress, fever, poor feeding, abdominal distention (can all be subtle)

Cultures: CSF and blood

TREAT ON SUSPICION: do NOT wait for lab results to return

42
Q

Listeria Monocytogenes

G +/-?
Shape:
Growth temperature:
Found where?

A

Basic ID: Gram positive rod

Growth: grows at temperatures between 4-41 degrees C (can grow in the refrigerator)

Ubiquitous in the environment: ~5% of people asymptomatic fecal carriers

43
Q

Listeria Monocytogenes
Can cause all of the following (4):

Where is listeriosis contracted during delivery localized to?

A

Congenital (transplacental) infections

Perinatal (ascending) infections

Listeriosis contracted during delivery is localized to the CNS (usually meningitis)

Post-natal infections

44
Q

Listeria Monocytogenes

Transmission:
At Risk Populations:

A

Transmission: primarily food-borne (contaminated foods eaten by the mother transferred to the fetus)

At Risk Populations: immnocompromised (AIDS, chemotherapy, transplant patients, pregnant women, neonates)

45
Q

Listeria Monocytogenes

Primarily what type of immunity?
What are first line defense?
What does later defense depend on?

A

Primarily cell-mediated

Macrophages are first line (non-specific defense)

Later immunity dependent upon CD8+ T cells

46
Q

Listeria Monocytogenes

Tropism for:
What can infections in utero lead to?
In live-birth, when does septecemia begin?

A

Tropism: for the fetus and placenta

Infections in utero can lead to spontaneous abortion, premature birth, stillbirth, or death within a short time after birth

If infant is born alive, septicemia begins within hours

47
Q

Listeria Monocytogenes

Virulence Factors (4):

How does it evade the immune system?
How does it invade cells?
What helps it escape from host vacuoles?
What helps it recruit host cell-derived actin filament? What does this allow?

A

Intracellular lifestyle: infects many types of cells; evades immune system

Internalins: cell invasion

Listeriolysin O: escape from host vacuoles (Hemolysin)

ActA: recruits host cell-derived actin filaments for cell-to-cell spread (allows it to evade Ab mediated host responses)

48
Q

Listeria Monocytogenes
Diagnosis

Samples:
Commercial Kits:
PCR:

A

Samples: blood, CSF, amniotic fluid and genital tract secretions

Commercial kits: detection using specific Abs

PCR: for specific genes

49
Q

Toxoplasma gondii

What type of parasite?
What are the 2 phases of the life cycle? Where does each one take place?

A

Obligate intracellular parasites

Life cycle has 2 phases:

  • Sexual phase (takes place only in cats)
  • Asexual phase (takes place in any warm-blooded animal)
50
Q

Toxoplasma gondii

What are the 3 morphological forms?

A

Oocyst
Tachyzoites (Trophozoites)
Tissue Cysts/Bradyzoites

51
Q

Toxoplasma gondii
Oocyst

Shape:
Produced where? Spreads via what route?
What happens within 1-5 days in the environment?
How long can it survive in the environment?

A

Ovoid with thick protective wall

Produced in cats and responsible for spread to other animals via fecal oral route

Sporulates into sporocysts within 1-5 days in the environment (infective) (Natalja’s notes)

Can survive in the environment for long periods of time

52
Q

Toxoplasma gondii
Tachyzoites (Trophozoites)

When does it form from the oocyst?
What form invades host cells and replicates?
Where is it localized?

A

Form from the oocyst AFTER ingestion

Asexual proliferation form (invade host cells, rapidly replicate- burst cells released)

Localize in neural and muscle tissue

53
Q

Toxoplasma gondii
Tissue Cysts/Bradyzoites

When is the more slowly growing form elicited?
How can it persist? Present where?
What happens during immunosuppression?

A

More slowly growing form elicited once an immune response is generated

Can persist for the life of the host in cyst-like structures present in the brain and other tissues

During immunosuppression, the parasite can resume rapid replication as a tachyzoite

54
Q

Toxoplasma gondii

Transmission (4):

A

Transmission: humans can become infected several ways

  1. Eating undercooked meat of animals with tissue cysts
  2. Consuming food or water contaminated with cat feces or by contaminated environmental samples
  3. Blood transfusion or organ transplantation
  4. Transplacentally from mother to fetus
55
Q

Toxoplasma gondii

Formation of tissue cysts:
Where in the host? (4)

Once ingested, what happens?

A

Occurs in the human host in the following tissues and can remain throughout life of the host

  • Skeletal muscle
  • Myocardium
  • Brain
  • Eyes

Once ingested: sporozites enter macrophages and parasite is then transported to all organ systems n the macrophages

56
Q

Toxoplasma gondii

Congenital Infection

What affects the seriousness of the infection?
What can it result in?
What may live-born children demonstrate?
What can happen to healthy children?

A

Congenital Infection: the earlier the infection is acquired, the more severe the consequences

Can result in spontaneous abortion and stillbirth

Live-born children may demonstrate microcephaly, hydrocephaly, psychomotor disturbances, and convulsion

Children may also appear healthy at birth, but can develop epilepsy or retardation months to years later

57
Q

Toxoplasma gondii

When does it occur?
What happens in subsequent pregnancies?

A

Only occurs when the mother was infected for the first time during the pregnancy. If it was not her first time being infected, she would have immunity to it

Therefore, no subsequent pregnancies will result in transplacental infection

58
Q

Toxoplasma gondii

Most common manifestation:

A

Chorioretinitis (bouts of eye pain and loss of visual acuity)

59
Q

Toxoplasma gondii

Virulence Factors
Where does the parasite acquire its actin?
What does T.gondii do to the host cell vacuole? What is prevented?

A

Actin-based motor: parasite has its own actin; used for invasion

Modification of host cell vacuole: secretes proteins into the vacuole membrane that prevents fusion with lysosomes

60
Q

Toxoplasma gondii
Diagnosis

Symptoms similar to:
What does acute infection result in? In which specimens? When must acute specimen be collected?
IgG titers:

A

Symptoms similar to the flu: swollen LNs, fever, headache, anemia

Acute infection: a four-fold rise in IgG antibody titer between acute and convalescent serum specimens. Acute specimen must be collected early in the course of the illness

Very high IgG titers (greater than 1:1000)

61
Q

Toxoplasma gondii

Prevention:

A

Have someone else change the litter box during pregnancy

Avoid uncooked or lightly cooked meat during pregnancy

Wash hands well after handling raw meat during pregnancy

Micro Exam 2 (18 decks)

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