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Neonate > Congenital infections > Flashcards

Congenital infections Flashcards

1
Q

Infections causing teratogenesis (6)

A
  1. Rubella
  2. CMV
  3. Varicella
  4. Parvovirus B19
  5. Toxoplasmosis
  6. Syphilis
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2
Q

Infections causing maternal illness, miscarriage or serious damage to the neonate

A
  1. Listeria
  2. Group B streptococcus
  3. HSV
  4. HBV, HCV
  5. HIV
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3
Q

Rubella - epi

A
  1. RNA togavirus
  2. Spread by respiratory droplets - person to person (highly infectious)
  3. Incubation 14-21d
  4. Infectious for 7d before and after appearance of rash
  5. Re-infection can occur (mostly with vaccine-induced immunity - ?)
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4
Q

Rubella - symptoms

A
  1. Mild, febrile illness
  2. Maculopapular rash
  3. Arthralgial
  4. Lymphadenopathy
  5. Symptoms only present in 50-75% of cases
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5
Q

Rubella - dx (3)

A
  1. Requires serological confirmation with paired samples - acute and convalescent phase (10-14 d later)
  2. Appearance of IgM antibodies
  3. 4-fold increase in IgG antibody titres or increasing IgG avidity
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6
Q

Rubella - associated congenital defects

A

Note - the virus disrupts mitosis, retarding cellular division and causing vascular damage. Defects include:

  1. Sensorineural deafness
  2. Cardiac abnormalities - including VSD and PDA
  3. Eye lesions (congenital cataracts, microphthalmia, glaucoma)
  4. Microcephaly and mental retardation
  5. Endocrine manifestations (late-developing sequelae) - diabetes, thyroid disorders
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7
Q

Rubella - prevention

A
  1. Vaccine = live attenuated virus; contraindicated in pregnancy. Part of MMR vaccine.
  2. Ideally - women should be tested before pregnancy to ensure immunity
  3. Women counselled to avoid pregnancy for 1mo after vaccination
  4. If maternal rubella infection confirmed in first 12 weeks of pregnancy, termination of pregnancy should be offered due to the high likelihood of fetal infection and the severe consequences of CRS (almost all fetus infected are at risk of congenital abnormality). Confirmed infection at 13-25 weeks has a 15-20% chance of an affected fetus (mainly deafness). If infection at >16 weeks, surveillance of fetal growth should occur
  5. Women non-immune to rubella on antenatal screening should be offered postpartum immunisation (breastfeeding not a contraindication)
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8
Q

CMV - epi

A
  1. Herpes virus
  2. Transmitted in bodily fluids - low infectivity
  3. Can remain dormant in host for life - reactivation common
  4. Seroprevalence - 50% of women (UK - ?)
  5. Incidence of primary infection in pregnancy = 1 in 100
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9
Q

CMV - symptoms (3)

A

Asymptomatic in 95% of cases

  1. Fever
  2. Malaise
  3. Lymphadenopathy, atypical lymphocytosis, mononucleosis
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10
Q

CMV - dx

A

Maternal infection (3)
1. Serological confirmation with paired samples - acute and convalescent phase (14d later)
Recent infection confirmed by:
2. Significant increase in IgM antibodies (may persist up to 8mo)
3. Increase in IgG antibody titres

Fetal infection (1)
1. Culture/PCR of amniotic fluid after 20 weeks
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11
Q

CMV - congenital defects

A
  1. IUGR
  2. Microcephaly
  3. Hepatosplenomegaly, thrombocytopenia and jaundice
  4. Chorioretinitis
  5. Later-developing sequelae = psychomotor retardation (accounts for up to 10% of mental retardation in children
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12
Q

CMV - outcome

A
  1. With primary maternal infection, 40% of fetuses will be infected, irrespective of gestation
  2. Of these, 90% are normal at birth
  3. Of those normal at birth, 20% will develop late, usually minor sequelae at birth (hearing and neurodevelopmental problems)
  4. 10% of infected fetuses are symptomatic at birth
  5. Of these, 10% will die and 80% will have long-term problems (hearing loss, vision impairment, intellectual disability)
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13
Q

CMV - mx

A
  1. As most fetuses are unaffected, counselling about mx (including TOP) is very difficult, even in the face of confirmed fetal infection
  2. Close monitoring of fetal wellbeing
  3. Paediatric follow-up
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14
Q

Varicella (chickenpox) - epi

A
  1. Varicella zoster virus (VZV) - DNA virus
  2. Spread by respiratory droplets and contact with vesicle fluid
  3. Incubation 10-21d
  4. Infectious from 2d before rash until all vesicles are crusted
  5. Seroprevalence - 90% of women in UK immune; incidence of primary infection in pregnancy = 3:1000
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15
Q

Varicella - symptoms (3)

A
  1. Fever
  2. Malaise
  3. Myalgia
    Prodrome (symptoms above) lasts for 1-4d, then rash appears
  4. Maculopapular rash which becomes vesicular then crusts over
  5. Complicated varicella in pregnancy = most often varicella pneumonia (appearing several days afte rthe rash)
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16
Q

Varicella - dx/mx

A
  1. Dx usually made on history of contact and appearance of typical rash
  2. If there has been exposure without good hx of previous infection, test serum for VZV IgG antibodies
  3. If antibodies detected within 10d of contact, immunity can be assumed and reassurance given
  4. If not, varicella-zoster immunoglobulin (VZIG) should be given ASAP (within 96 hours of exposure). Babies born to women with VZV infections should be given VZIG, and breastfeeding should be encouraged
  5. Oral aciclovir - given if window for VZIG missed, and also if complications of VZV develop. Aciclovir reduces the duration of symptoms if given within 24h of rash appearing
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17
Q

Varicella - maternal risks (3)

A

Varicella in pregnancy is often more severe and may be life-threatening as a consequence of:

  1. Varicella pneumonia
  2. Hepatitis
  3. Encephalitis
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18
Q

Varicella - fetal risks

A

Fetal risks - congenital defects

  1. Skin scarring
  2. Limb hypoplasia
  3. Eye lesions (congenital cataracts, microphthalmia, chorioretinitis)
  4. CNS abnormalities - mental retardation, microcephaly, cortical atrophy
  5. Dysfunction of bladder and bowel sphincters
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19
Q

Varicella - neonatal risks

A
  1. Neonatal varicella seen in babies whose mothers contracted it in the last 4 weeks of pregnancy
  2. Severe infection, which may be fatal, is most likely to occur if the rash appears 5d before delivery or 2d after
  3. These babies should all receive VZIG as soon as possible
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20
Q

Parvovirus B19 (fifth disease/erythema infectiosum/slapped cheek syndrome) - epidemiology

A
  1. DNA virus
  2. Spread by respiratory droplets - person to person
  3. Incubation 4-20d
  4. Seroprevalence- 35-50% of Australian women have pre-existing immunity
  5. Incidence of primary infection in pregnancy
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21
Q

Parvovirus B19 - symptoms

A
  1. Often asymptomatic
  2. Typical ‘slapped cheek’ rash (erythema infectiosum)
  3. Maculopapular rash
  4. Fever
  5. Arthralgia
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22
Q

Parvovirus B19 - dx

A
  1. Requires serological confirmation with paired samples - acute and convalescent phase (>10d later). Recent infection confirmed by:
  2. Appearance of IgM antibodies
  3. Increase in IgG antibodies
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23
Q

Parvovirus B19 - maternal risks

A
  • Minimal in fit and healthy women

- Immunocompromised individuals at risk of sudden haemolysis potentially severe enough to require blood transfusion

24
Q

Parvovirus B19 - fetal risks

A
  1. Fetal infection rate 30%
  2. Approximately 10% of fetuses infected at cardiac failure and hydrops fetalis
  3. Risk of fetal anaemia developing after maternal parvovirus infection = 3-5% for infection dx before 32 weeks, and
25
Q

Parovirus B19 - management

A
  1. Serial U/S (weekly, for 8-12 weeks after infection), measuring the peak systolic velocity of the fetal MCA - monitoring for anaemia (as this may develop many weeks after the initial infection)
  2. In utero RBC transfusion - consider to prevent fetal demise in severely anaemic, hydropic fetuses
  3. These patients should be cared for in a specialist fetal medicine unit
  4. Many of these fetuses will also be severely thrombocytopenic -> platelet transfusion must be considered to reduce the risk of fetal bleeding at the time of the in utero transfusion
  5. No maternal treatment or vaccine is available
26
Q

Toxoplasmosis - epi

A
  1. Protozoan parasite Toxoplasma gondii
  2. Spread by contact with cat faeces and eating undercooked meat
  3. Incubation
27
Q

Toxoplasmosis - symptoms (3)

A

Asymptomatic in 80% of cases

May have:

  1. Low-grade fever
  2. Malaise
  3. Lymphadenopathy
28
Q

Toxoplasmosis - dx (3)

A
  1. Test serology for specific IgG and IgM
  2. Interpretation is complex bc positive IgM does not necessarily indicate acute infection; expert advice should be sought
  3. Testing of amniotic fluid for toxoplasma PCR may be performed
29
Q

Toxoplasmosis - outcomes

A

In 10% of cases, intrauterine infection leads to a fetal syndrome with (3):
1. Chorioretinitis
2. Intracranial calcification
3. Hydrocephaly
Some initially asymptomatic patients may later have:
4. Visual sequelae
5. Neurodevelopmental sequelae

30
Q

Toxoplasmosis - mx

A
  1. Antibiotic regimens to decrease risk of vertical transmission +/- ameliorate severity of congenital disease - benefit uncertain, use after appropriate specialist consultation
    Advise pregnant women to:
  2. Eat only well-cooked meat
  3. Wash hands and kitchen surfaces/utensils after contact with raw meat
  4. Wash fruit and vegetables prior to consumption
  5. Avoid handling of cat litter or gardening if possible
31
Q

Syphilis - general

A

Caused by the spirochaete Treponema pallidum, a corkscrew shaped bacterium

General

  1. Very uncommon in general population, but rates increasing; prevalence in Indigenous pregnant women = 2.5%
  2. Routine antenatal screening = pregnancy-associated syphilis most commonly diagnosed in latent phase

Perinatal transmission occurs in:

  1. 50% with primary or secondary syphilis
  2. 40% with early latent syphilis (within 4y of infection)
  3. 10% with late latent syphilis or tertiary disease
32
Q

Syphilis - consequences

A
  1. Fetal = preterm delivery, stillbirth, IUGR, perinatal death
  2. Maternal (secondary syphilis) = see symptoms

Congenital defects:

  1. 8th nerve deafness
  2. Hutchinson’s teeth
  3. Skeletal abnormalities = saddle nose, sabre shins
33
Q

Syphilis - dx

A
  1. Serology for IgG (Treponema-specific enzyme immune assays, such as Treponemal IgG EIA)
  2. Primary lesion smear may show spirochaetes on dark field microscopy
  3. Other serological tests required to correctly stage and tx the infection (bc all treponemal-specific tests remain positive after successful tx, rendering them useless as a test-of-cure). Rapid plasmin reagin test (RPR) = most commonly used test in Australia
34
Q

Syphilis - symptoms

A

Early syphilis = 2y or unknown duration

  1. Late latent syphilis (asymptomatic)
  2. Tertiary syphilis (cardiovascular, CNS or skin/bone involvement)

Primary syphilis (3)

  1. 10-90d post-infection
  2. Painless, genital ulcer with indurated edges (chancre) - may pass unnoticed on cervix
  3. Inguinal lymphadenopathy

Secondary syphilis (5)

  1. Occurs within first 2y of infection
  2. Generalised polymorphic rash affecting palms and soles
  3. Generalised lymphadenopathy
  4. Genital condyloma lata (clusters of soft, moist lumps in skin folds of anogenital area)
  5. Mucosal lesions, hepatitis, meningitis, anterior uveitis

Tertiary syphilis (3)

  1. Neurosyphilis = tabes dorsalis (slow degeneration of nerves in dorsal column), dementia
  2. Cardiovascular syphilis = commonly affecting the aortic root
  3. Gummata = inflammatory plaques or nodules
35
Q

Listeria - general

A
  1. Anaerobic gram-positive bacillus, rare (
36
Q

Group B streptococcus - epi

A
  1. Streptococcus agalactiae
  2. Common bowel commensal
  3. Up to 20% of women carry it vaginally
  4. Between 15 and 40% of women are asymptomatically colonised with GBS. Approximately 50% of colonised pregnant women (i.e. around 20%) will transmit it to their baby at birth. Only 1-2% of babies of colonised mothers develop GBS disease -> 1-2 in 1000 untreated neonates develop GBS sepsis
  5. Risk higher in mothers with hx of infected infant or GBS bacteriuria, premature infants, and where there has been premature/prolonged rupture or membranes or hx maternal fever
    (GBS is also a cause of maternal UTI, chorioamnionitis and endometritis)
37
Q

GBS - symptoms

A
  1. Usually asymptomatic
  2. Can present with UTI symptoms
  3. Can present with maternal endometritis (fever, abdominal pain, offensive vaginal discharge) or rarely with sepsis
  4. Neonate = invasive GBS usually manifests as sepsis, pneumonia or meningitis in the first 24h of life
  5. Minority of cases = late-onset invasive GBS, up to 6wks after birth
38
Q

GBS - dx (2)

A
  1. Maternal colonisation status best dx by taking rectovaginal swab (i.e. culture from lower vaginal swab + perianal swab) at 35-37 weeks’ gestation
  2. Women with GBS bacteriuria at any time during pregnancy are also considered colonised
39
Q

GBS - mx and outcomes

A
  1. Fetal = PPROM, preterm delivery
  2. Neonatal risks from early-onset GBS infection (7d) is not associated with maternal GBS carriage
  3. If GBS positive, give intrapartum antibiotics (benzylpenicillin 3g IV for first dose, then 1.8g IV, 4-hourly until delivery), with the first dose >4hrs before delivery. Continue until neonate delivered
  4. Neonatal observations should occur for >24h post-delivery (+/- neonatal antibiotics if there is clinical suspicion of GBS or significant risk factors)
    Note: GBS is the most frequent cause of early-onset, severe neonatal infection
40
Q

HSV - epi

A
  1. Herpes simplex virus (HSV) - type 2 causes >70% genital infections
  2. Spread by sexual contact
  3. Incubation 2-7d
  4. Individual may be infectious even when apparently asymptomatic
  5. 75% and 15% of Australian adults have prior exposure to HSV-1 and HSV-2 respectively. Both HSV subtypes can cause genital herpes
41
Q

HSV - symptoms

A
  1. Primary HSV infection is the most severe. Usually results in:
  2. Mild flu-like illness
  3. Inguinal lymphadenopathy
  4. Vulvitis; pain sometimes severe enough to cause urinary retention
  5. Small, characteristic vesicles on the vulva`
42
Q

HSV - maternal risks

A
  1. In pregnancy, a primary attack may be severe. Complications include:
  2. Meningitis
  3. Sacral radiculopathy -> causing urinary retention and constipation
  4. Transverse myelitis
  5. Disseminated infection
43
Q

HSV - fetal risks (3)

A
  1. Miscarriage
  2. Preterm labour
  3. But no related congenital defects have been identified
44
Q

HSV - neonatal risks

A
  1. Transmission rate from vaginal delivery during primary maternal infection may be as high as 50%, but is relatively uncommon during a recurrent attack (
45
Q

HSV - dx

A

Swab for HSV type-specific nucleic acid amplification testing (NAAT) - e.g. PCR

Note - culture not recommended bc less sensitive than NAAT

46
Q

HSV - mx (2)

A
  1. For primary infection late in pregnancy, antiviral treatment (valaciclovir or acyclovir) is recommended to reduce maternal symptom duration, and CS delivery to reduce neonatal risk of HSV
  2. For primary infections in early pregnancy and women with recurrent HSV, suppressive therapy from 36 weeks is recommended, with vaginal birth unless there are active lesions present at labour onset or known viral shedding
47
Q

HBV - epi

A
  1. Hepatitis B virus (HBV) - DNA virus
  2. Spread by infected blood, blood products or sexual contact
  3. Incubation period 2-6mo
  4. 0.5-0.8% of Australian population chronically affected with HBV
  5. Most pregnant chronic carriers of HBV were born overseas, in high HBV prevalence areas such as the Asia-Pacific. However, Indigenous Australians, partners of HBV carriers and injecting drug users also have an increased HBV prevalence
48
Q

HBV - symptoms

A
  1. Non-specific prodromal illness (5) = headache, myalgia, arthralgia, nausea, anorexia
  2. Prodrome precedes development of jaundice by a few days to 2 weeks
  3. Vomiting/diarrhoea may follow
  4. Abdominal discomfort common
  5. Dark urine and pale stools may precede jaundice
49
Q

Hepatitis B - signs (3)

A
  1. Liver often tender but only minimally enlarged
  2. Occasionally, mild splenomegaly and cervical lymphadenopathy seen
  3. Jaundice may be mild
50
Q

Hepatitis B - dx

A
  1. Based on clinical picture + serological markers for hepatitis B
  2. HB surface antibody = present in immune and immunised individuals (bc immunisation contains viral particles that replicate the virus’ outer capsule)
  3. HB core antibody = only seen following natural infection
  4. HB surface antigen = indicates the presence of the virus/current infection. When it persists in the serum for >6mo, the person is said to be a carrier. This occurs in 5% of those infected as adults but in 90% of those infected as infants
  5. HBe antigen = highly infectious carrier/active viral replication
51
Q

Hepatitis B - risks

A

Maternal
1. 65% subclinical disease with full recovery
2. 25% develop acute hepatitis
3. 10% become chronic carriers - at risk of progressive liver damage
4.

52
Q

Hepatitis B - mx

A
  1. Neonates at risk of vertical transmission of hepatitis B should be given hepatitis B immune globulin (HBIG) within 12h of birth
    - Note: vertical transmission occurs in up to 80% of high risk carriers whose infants do not receive immunoprophylaxis
  2. Subsequent course of active HBV vaccination should be commenced within 12h of birth
  3. Women with high viral load - utility of antenatal viral therapy is under study
  4. Breastfeeding not contraindicated
  5. Mother and baby should have specialist review for appropriate follow-up and consideration of antiviral therapy
53
Q

HCV - epi (3)

A
  1. 1.5% of Australian population chronically infected with HCV
  2. Major risk factors = injecting drug use (past or present), hx blood transfusion (pre-1990 Australia, any time overseas), immigration from high-prevalence regions (Asia, Africa, Middle East)
  3. Acute HCV results in chronic infection in >70% of cases. Can result in end-stage liver disease (including cirrhosis, liver cancer and death)
54
Q

HCV - dx, mx

A
  1. Initially, test for anti-HCV
  2. If anti-HCV detected, viral load (HCV RNA) performed, as this reflects chronic infection
  3. Risk of perinatal transmission is 5%, but no specific measures have been shown to decrease this. Avoid measures that breach fetal skin intrapartum (e.g. scalp pH)
  4. Breastfeeding not contraindicated, although if nipples are bleeding, expressing milk should be considered
  5. Mother and baby need post-partum follow-up to determine infant antibody status and consideration of maternal antiviral tx (these are not safe in pregnancy)
55
Q

HIV - general

A
  1. Prevalence of HIV in pregnancy in Australia is low (0.04%)
  2. Universal antenatal screening recommended to allow appropriate maternal tx and to minimise risk of perinatal transmission
  3. Perinatal transmission = 30% if no tx instituted
  4. Unless maternal progression to AIDS has already occurred, women with HIV generally have uncomplicated pregnancies
  5. Management of these women should be shared with an ID physician, with regular checking of CD4 count and viral load
56
Q

HIV - mx strategies to decrease perinatal transmission

A
  1. Combination antiretroviral therapy (cART)
    — Most women with known HIV will already
    be on a cART regimen; if not it should be
    commenced to attain an undetectable viral
    load during pregnancy19
  2. Neonatal antiretroviral therapy
  3. Avoidance of breastfeeding (in resource-rich
    countries where safe artificial formula is
    available)
  4. Elective caesarean delivery — this remains of
    benefit in women with high viral load.
  5. Where maternal viral load is less than 1000
    copies/mL, the added benefit of elective
    caesarean delivery is unclear, with
    transmission rates less than 2%.
57
Q

Syphilis - mx

A
  1. Early syphilis = benzathine penicillin 1.8g IM, single dose or procaine penicillin 1.5g IM, daily for 10d
  2. Late latent syphilis = benzathine penicillin 1.8g IM, once weekly for 3 wks, or procaine penicillin 1.5g IM, daily for 15d
  3. Tertiary syphilis = benzylpenicillin 1.8g IV, 4-hourly for 15d

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