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%)
How is congenital parvovirus diagnosed?
Serology:
–IgG past infection; immunity
–IgM present at time of rash; positive for 2-4 months
Nucleic acid detection
–Detects persistent infections in immunocompromised hosts
Fetal blood sampling
Intrauterine transfusion
Characterise congenital Herpes Simplex Virus infections
Most commonly, neonatal infections are acquired from the mother shortly before (ascending infection) or during passage through the birth canal at delivery
The severity of the congenital disease depends on the time at which the child is infected:
- Primary infection during pregnancy
- Abortion, IUGR and preterm labour in <1%
- Treatment is acyclovir, suppression until delivery and caesarian section
- Primary infection near delivery
- Skin, eye and mouth vesicles and encephalitis
- Acyclovir and suppression
What are the pathological outcome of congenital syphilis
Still birth
Hepatosplenomegaly
Lymphadenopathy
Snuffles (secretion from nose loaded with spirochetes)
Rash
Osteochondritis syphilitica
Hereditary gumma
What type of maternal syphilis infection is the most common cause of congenital syphilis
Transmission to fetus:
- Primary 90%
- Secondary 60-90%
- Early latent 40%
- Late latent <10%
- Tertiary rare
Characterise Neonatal Chlamydia
Chlamydia trachomatis is the most common reportable sexually transmitted infection, with a high rate of infection among sexually active adolescents and young adults.
Chlamydia can be transmitted from the genital tract of an infected mother to her newborn during birth
There is a 50% chance of the neonate being infected if the mother is affected in birth
In neonatal chylamidia; patients demonstrate **conjuctivitis +/- haemorrhagic conjuctivitis (25%) **and pneumonia (10%)
Chartacterise Toxoplasma Gondii infections
Toxoplasmosis has a primary infection incidence rate = 1/10000 and is quite rare in the developed world. Infections can be avoided by hygienic practices surroudning raw meat and cat litter
70-90% of neonates are assymptomatic at birth
Can cause Rash, LN, chorioretinitis, hydrocephalus
Discuss Hepatitis B virus as a congenital infection
Hepatitis B is a blood borne virus that is aquired by a neonate by blood contact during labour
90% of congenitally infected babies go on to develop chronic carriage
**Higher rate of developing cirrhosis and hepatocellular carcinoma **
0.2% of women are chronic carriers capable of infecting their children
What treatments should be considered for HBV
Universal infant vaccination
Hepatitis B immunoglobulin within first 12 hours (no later than 48)
Characterise Group B Streptococcus infections of new borns
Group B Streptococcus infections result from the baby becoming* infected via ascending infection or colonised at delivery*
GBS is carried in the bowel/vagina of 20-30% of females
40-70% babies colonised
Pathology includes pneumonia, sepsis and meningitis
