Congenital and Perinatal Infections Flashcards
At what time are babies infected with congenital or perinatal infections?
Timing
Prenatal / Intrauterine
- Infection acquired/carried by the mother and transmitted to the developing fetus
Perinatal
- Infection transmitted around the time of delivery
Postnatal / Postpartum
- Infection acquired after delivery
- Family, health care workers, community
By what modes of transmission are babies infected with congenital or perinatal infections
**Vertical transmission **
- From mother to fetus (eg. transplacental)
- From mother to baby (eg. breast milk)
Horizontal transmission
- From one person/baby to another
Ascending infection
- Vaginal organisms producing fetal infections
Generally, what are the differences in the effects of infections that affect a pregnant mother compared to directly affecting the foetus?
There are non-specific effects of maternal infections that have foetal consequences; specifically:
- Fetal death
- Premature delivery
**Specific effects of direct foetal infection **can lead to:
- Benign / self-limiting effects
- End-organ damage
- Chronic infections (e.g Hep B, HIV)
Discuss the pathology/pathophysiology of chicken pox
Chicken pox arises from infections of Varicella Zoster Virus
Infections occur as a result of respiratory or direct contact -> replication in lymph nodes -> primary viraemia -> replication in liver -> secondary viraemia -> infection of skin + rash formation “chicken pox” -> chronic latent period in dorsal root ganglions -> reactivation to DRG dermatome causing shingles
Characterised by fever, lethargy and pruritic vesicular rash
Complications of chicken pox include:
-
Secondary bacterial infection
- commonly Strep pyogens + Staph aureus
-
Pneumonitis
- 25x more common in adults
- tachypnoea, cough and haemoptysis
-
Acute Cerellar ataxia
-
Immunological response with a cross antigen effect on the cerebellum
*
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Immunological response with a cross antigen effect on the cerebellum
Discuss Maternal Varicella infections in pregnancy
Chicken pox during pregnancy is a severe form of VZV infection
Is particularly severe in the 3rd trimester of pregnancy with 2% mortality rate
Productive cough with haemoptosis, fever and lathargy sccompany this condition
Characterise Congenital Varicella Syndrome
Mother has chicken pox -> crosses to baby -> baby fights chicken pox infection -> re activation several weeks later with severe shingles - > leads to death
The incidence of Congenital Varicella Syndrome increases with maternal infection present further in gestation
First trimester infections are most severe as it impacts on organogenesis; leading to limb hypoplasia, cicatrical scarring > microcephaly > mental retardation
Characterise Perinatal Varicella
Perinatal varicella infections tend to occur when the mother aquires a primary infection -7 to +2 days from delivery
17-30% transmission rate to neonate via birth exposure and maternal contact
May lead to haemorrhagic varicella
Mortality rate = 25-30%
What treatments and management options are available to combat VZV infections during and following pregnancy?
Prophylactic Varicella Zoster Immunoglobulin (VZIG)
Indicated in:
- susceptible pregnant women who have no history of VZV infection (thus no immunity to it)
- Infants whose mothers develop varicella <7 days prior to delivery or in 1st month of life
- immunocompromised mothers/neonates
-
premature babies
- Haven’t acquired full complement of maternal antibodies across placenta - this mainly happen in last trimester. Give Ig irrespective of the mothers immune status and history of chicken pox infections
Acyclovir
- Treatment of acute VZV
- Oral if <24 hours of rash and no systemic symptoms **VS **Intravenous if pneumonitis, neurological symptoms, organ involvement or haemorrhagic rash
Varicella Vaccine
- Live attenuated virus
- Given at 18 months of age
- 2 doses for > 12-year-olds if they werent vaccinated as an infant
- Shingles vaccine for adults greater than 65 years of age - based on chicken pox virus but 14x as potent
Characterise Cytomegalovirus
Cytomegalovirus is a beta herpes virus with icosahedral capsid, dsDNA and is capable of inducing latent infections
Primary infections and secondary infections ( re-activation or re-infection) can occur. Reactivation is normally asymptomatic unless the patient is immunocompromised.
It is transmitted via shedding through:
- Saliva
- Urine
- Blood
- Semen
- Breastmilk
- Cervical secretions
- Transplacental
- Transplant tissue
CMV is a ubiquitous infection that 60% of the developed populations have been exposed to over their life time; with a prevalence of more than 90% in high-risk groups.
Increased rate during progression from childhood to adolescence to child-bearing years in developed nations; developing nations have sigificantly higher rates of child CMV infections
Characterise Congenital CMV
Congenital CMV is the most important congenital infection
Occurs in 0.3-2% of all live births
Congenital CMV infection occurs when the mother suffers a primary infection or reactivation during pregnancy. Primary infections are worse for the foetus
- Primary infection = 1% of women ; 20-50% chance of fetal infection ; 10% symptomatic; 10-30% mortality
- Reactivation infection = 10-30% women; 1-3% fetal infection; 10-30% mortality
Symptoms include rashes + hepatosplenomegaly + inclusion bodies
Symptomatic neonates have an 80-100% risk of long term sequale including: **deafness, learning difficulties, liver disease and epilepsy **
What testing is required to determine a diagnosis of CMV?
In the general population:
- IgG (seroconversion)
- IgM positive
- IgG avidity
- Nucleic acid detection (in body fluids)
In symptomatic babies of congenital CMV:
-
Confirm diagnosis with CMV detection in first 2 weeks/52 - urine
- Urine presence up to 2 week post birth for congenital infection. Positive after two weeks indicative of an acquired infection in the community
Characterise the Rubella Virus
The Rubella virus is a **Togavirus **that is spread via nasopharyngeal secretions.
Individuals are infectious -7 to +14 days following symptoms.
Clinical presentation in adults:
- Fever - low grade
- Lymphadenopathy
- Exanthem (maculopapular rash over face, trunk and eventually limbs
- Polyarthalgia /arthritis
Discuss Congenital Rubella Syndrome
With the widespread use of vaccination, congenital rubella is rare in developed countries.
The occurrence of congenital defects approaches:
- 85% if infection is acquired during the first 4 weeks of gestation
- 20% if infection acquired weeks 4-8
- 5% if infection acquired weeks 9-12
- Infection after 4 months’ gestation does not seem to cause disease
Most common abnormalities :
- ophthalmologic (cataracts, retinopathy, and glaucoma)
- cardiac (patent ductus arteriosus and peripheral pulmonary artery stenosis)
- auditory (sensorineural hearing loss)
- neurologic (behavioral disorders, meningoencephalitis, and mental retardation) conditions
- purpuric skin lesions (“blueberry muffin” appearance from dermal erythropoiesis)
Morbidity of congenital rubella syndrome:
- 1/3 lead normal life
- 1/3 live with parents
- 1/3 institutionalised
Outline how to test for rubella
What is the effectiveness of the Rubella vaccine?
Serological confirmation:
IgG seroconversion/rising titre
IgM
Fetal diagnostic testing:
Amniotic fluid sample
Fetal IgM concentration
Infants with congenital rubella are chronically and persistently infected and tend to shed live virus in urine, stools, and respiratory secretions for up to 1 year
The Rubella vaccine is stimulates an immunogenic response in 95% of poeple while providing life-long protection in 90% of patients
Characterise congenital Parovirus infections
Parovirus B19 is an erythrovirus virus that infects RBC’s in the foetus
It causes **hydrops foetalis (anaemia) **as a result of reducing th life span of RBC progenitors
Treatment is **intrauterine blood transfusions **to replace blood and ensure developing organ tissues have sufficient oxygen for development
If not treated, foetal misscariage can occur (<10 weeks = 10% ; 9-20 = 3%)
