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Human Development 2 > Effects of Infection in Early Pregnancy > Flashcards

Effects of Infection in Early Pregnancy Flashcards

1
Q

Why are pregnant women more at risk of infection

A
  • pregnancy is an immunosuppressive state

- physiological changes to the mothers body

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2
Q

describe why pregnant women are more at risk of infection

A
  • Relative immune-suppression – pregnancy is relatively immunosuppressed state, certain conditions are for some reason a lot worse in pregnancy than others for example Hep E this carries a 25-30% mortality risk, this is significant in the regions of the word where this happens
  • Physiological changes in mother - pregnant women who get influenza have a worse outcome than non-pregnant women, this is not an immunological reason but is because of anatomy reasons this puts pressure of the diagram and reduces the overall expansion of the lungs therefore this reduces the spread
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3
Q

What infections are

  • harmful to the mother
  • harmful to the foetus
  • harmful to both
A

Harmful to the mother
- Influenzas

harmful to the foetus

  • Toxoplasmosis
  • HSV
  • Syphilis
  • Parvovirus B19
  • CMV
  • Rubella

Harmful to both

  • VZV
  • HIV
  • Hepatitis A/E/B/C
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4
Q

What does TORCHES stand for

A 
Toxoplasmosis 
Other 
Rubella
Cytomegalovirus (CMV)
Hepres Simple virus
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5
Q

What is toxoplasmosis

A

a disease that results from infection with the Toxoplasma gondii parasite,

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6
Q

How do we diagnose infection in pregnancy

A

Serology and PCR

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7
Q

what do you look at in serology

A
  • Look at IgM and IgG
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8
Q

what is the difference between IgM and IgG

A
  • IgM is the antibody that goes up in an acute infection and then goes down
  • IgG is a memory antibody so evidence of IgG signifies a past infection and is protective in many cases
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9
Q

what happens at 10 weeks

A
  • all serologies get tested
  • therefore you have a baseline at that moment in time as to what infections you have previously had
  • have blood tests to compare it to if you become infected later
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10
Q

how do you use PCR

A
  • DNA and RNA is present in viruses

- Can find a bit of DNA or RNA you can amplify it and match it against the database and diagnose it

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11
Q

how common is CMV

A
  • VERY COMMON

- 50% OF UK adults

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12
Q

What type of virus is CMV

A

Herpes virdae virus

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13
Q

What does CMV stand for

A

Cytomegalovirus

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14
Q

describe how CMV can cause flairs

A

A flair is a reactivation of CMV can happen at points of stress or at any time in your life
- if it happens during pregnancy it will spread to the baby and cause problems

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15
Q

what vaccine is used to prevent chicken pox

A

VZV vaccine

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16
Q

How does the transmission of CMV happen

A

via saliva, blood or blood products, sexual intercourse, organ transplantation or via mother

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17
Q

what is a primary infection of CMV likely to cause

A

congenial CMV - this is because the viral load is higher therefore the chance of transferring the virus to the foetus
- more likely to happen in the 1st trimester of pregnancy

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18
Q

What is the prevalence of congenital CMV

A

~ 7 per 1000 live births (0.7%)

• only 13% of babies with congenital CMV are symptomatic

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19
Q

How do you diagnose CMV

A
  • maternal serology CMV IgG and IgM
  • neonatal urine/saliva for CMV DNA PCR test and look directly for the virus
  • blood, saliva and urine
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20
Q

What are the symptoms of CMV

A
  • severe: Intra Uterine Growth Retardation (IUGR), hepatosplenomegaly, microcephaly
  • sensorineural deafness
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21
Q

What is the main symptom affect of CMV

A

sensorineural deafness

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22
Q

why do you not do a serology test on babies in the first 6 months of life and while they are breastfeeding

A

because they do not have their own antibodies

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23
Q

what is the commonest cause of congenital sensorineural hearing loss

A

CMV

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24
Q

What is the heel prick test

A
  • Can be stored for life
  • used to mark specific disease

disease

  • sickle cell disease
  • cystic fibrosis
  • congenital hypothyroidism
  • PKU
  • MCADD
  • MSUD
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25
Q

what does the VZV virus cause

A

Chicken pox

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26
Q

how many people are now immune to VZV

A

• 80-90% UK adults are immune to VZV i.e. VZV IgG positive

27
Q

how infectious is VZV

A
  • extremely infectious – droplet/airborne

* 1 person can infect 10-12 susceptible individuals

28
Q

what is RO

A
  • the number of people that one sick person will infect on average is called Ro
29
Q

How do you diagnose VZV

A
  • clinical syndrome
  • swab of vesicle fluids (viral PCR)
  • maternal serology
30
Q

how do you manage VZV

A
  • prevention
  • varicella zoster immunoglobulin (post exposure)
  • vaccination (pre exposure)
    Treatment (val) acyclovir – safe during pregnancy
31
Q

What are the risks of VZV in the 1st and 2nd trimester

A

1st: 0.5%, 2nd: 1.4%

32
Q

what are the effects of congenital varicella syndrome

A 
Skin lesions (73%)
•	leading to limb hypoplasia

CNS (62%)
• microcephaly, hydrocephaly, neurodevelopmental delay

• cataracts/other eye problems

  • also GI, genitourinary & cardiac abnormalities
  • miscarriage
33
Q

what happens in neonatal varicella

A
  • mother has VZV around the time of delivery
  • most severe if 5 days before to 2 days after delivery
  • can be extremely severe/even fatal
  • neonate should receive VZIG and acyclovir
34
Q

What is the treatment for neonatal varicella

A

• neonate should receive VZIG and acyclovir

35
Q

when do you transmit neonatal VZV to the neonate

A
  • 7 days before delivery and 7 days after
36
Q

what are the two types of HSV viruses

A

oral - HSV1

Genital herpes - HSV2

37
Q

When do you get neonatal HSV infection

A
  • most likely to get it through vertical transmission at the time of delivery, this is a direct infection at the time of delivery
  • be caused by primary HSV2 infection at delivery
38
Q

How do you diagnose neonatal HSV infection

A

clinical, HSV DNA PCR neonate blood/vesicle swab/maternal vesicle swab

39
Q

how do you treat neonatal HSV infection

A

• mortality (untreated) 65% mortality reduced to 25% with aciclovir treatment

40
Q

What are the symptoms of rubella

A

rash, lymphadenopathy, arthralgia

41
Q

How do you diagnose rubella

A

serology/oral fluid PCR

42
Q

what is the treatment for rubella

A

No available treatment

43
Q

describe the congenial risk of rubella

A

• also 20% risk of foetal loss if < 20 weeks

44
Q

what does MMR affect against

A
  • 2 doses considered to provide lifelong protection against 3 viruses:
  • Measles Mumps Rubella
45
Q

what is parvovirus B19

A

Primate erythroparvovirus

- IT AFFECTS THE RED BLOOD CELLS

46
Q

how do you diagnose paravirus B19

A

maternal serology/PCR, fetal ultrasound

47
Q

what complications can Paravirus B19 cause

A

miscarriages, intrauterine growth restriction

48
Q

What is the risk of pregnancy in parvovirus B19

A
  • 0-20 weeks: 9% risk of fetal loss
  • 9-20 weeks: 3% risk of hydrops fetalis
  • > 20 weeks: negligible risk
49
Q

What is amniocentesis and how does it work

A
  • Take ammonitic fluid from the room, gold standard for diagnosing congenital pregnancy
  • Then do PCR on the fluid
  • Risk of 1% miscarriage specialist investigation only be done when all the risks are fully disclosed
50
Q

what is toxoplasmosis

A

• infection due to parasite Toxoplasma gondii

51
Q

What is the natural host of toxoplasmosis and how does it spread

A
  • humans are an intermediate host through ingestion of oocysts
  • either via contact with cat faeces
  • or eating infected meat
52
Q

what does toxoplasmosis cause

A

• IUGR

  • hydrocephalus,
  • cerebral calcification
  • microcephaly
  • hepatosplenomegaly
53
Q

What are the risk factors for acquiring toxoplasma gondii

A
  • cat ownership
  • gardening
  • eating raw meat
  • eating cured meat
54
Q

What is the treatment of toxoplasmosis

A
  • spyramicin, pyrimethamine/sulfadiazine/folinic acid

* depends on trimester

55
Q

How do you prevent toxoplasmosis

A
  • no vaccine
  • avoidance behaviour only:
  • no gardening
  • don’t handle cat litter
  • avoid uncooked meats or cured meats
  • hand hygiene
56
Q

What is syphilis

A

• sexually transmitted infection due to spirochete Treponema pallidum

57
Q

How do you diagnose syphilis

A

clinical syndrome and serology

58
Q

when are you at high risk of transmission of syphilis

A

• highest risk of transmission during 1st trimester or peripartum

59
Q

What is the affect of syphilis on birth

A

• miscarriage/still birth/prematurity

60
Q

How do you treat syphilis

A
  • Penicillin
61
Q

What are the symptoms of congenial syphilis

A
  • Early i.e. 0 to 2 years
  • rash
  • rhinorrhoea
  • osteochondritis
  • perioral fissures
  • lymphadenopathy
  • GN
  • Late i.e. > 2 years
  • Hutchinson’s teeth
  • Clutton’s joints
  • high arched palate
  • deafness
  • saddle nose deformity
  • frontal bossing
62
Q

What is permpartum sepsis

A

infection of retained products of conception, chorioamnionitis

63
Q

what does Group B strep increase risk of

A

neonatal sepsis

64
Q

What are the ethical issues surrounding infection and screening

A
  • antenatal screening allows early detection of high risk pregnancies
  • serology can be difficult to interpret
  • retrospective testing for TORCH infections may lead to:
  • further diagnostic procedures e.g. amniocentesis
  • decisions regarding continuation of pregnancy
  • often no treatment is available

Human Development 2 (34 decks)

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