Micro - Specific Groups Affected Flashcards
Congential Rubella
- Blueberry muffin rash
- Sensorineural deafness, cataracts
- PDA/ASD/VSD
- Microcephaly/psychomotor retardation
- Worse outcomes if infected earlier in pregnancy
- Rare (MMR) - rubella eliminated in the UK in 2015 and removed from routine antenatal screening in 2016
Congenital HSV
Blistering rash –> babies become septic
- SEM disease (45%) - localised to skin/eyes/mouth
- CNS disease +/- SEM (30%). Can present late - 10days-4 weeks postnatally
- Disseminated (25%) - multiple organs (CNS, lungs, liver, adrenals, skin, eyes, mouth). High mortality. >20% won’t have skin lesions.
IV aciclovir ASAP
Congenital Parvovirus B19
Seroprevalence in pregnant women in 50-60%
Baby only affected if mother infected <20wks (transplacental transmission approx 33%)
Virus destroys RBC precursors:
- Slapped Cheek Syndrome = Erythema Infectiosum = Fifth Disease
- Transient aplastic crisis
- Arthralgia
- Foetal anaemia –> cardiac failure –> non-immune hydrops fetalis
Treatment: human immunoglobulin
- Referral to specialist foetal medicine unit
- Intrauterine blood transfusion
- Some cases resolve spontaneously
- If infant survives the hydropic state, long-term prognosis is usually favourable
Congenital CMV
- DNA virus
- Detection of CMV from body fluids or tissues within 21 days of birth
- Commonest congenital infection (can also get vertically and horizontally - salivary contact)
- Primary infection or reactivation of maternal CMV (reactivation = lower risk)
- 12.7 % congenitally infected babies born with sx. 75% of these will have CNS involvement.
- Of those who are asymptomatic, 10% have abnormalities on follow up.
- Sensorineural deafness, microcephaly
- Treatment: IV ganciclovir
Other issues include:
Eyes - Chorioretinitis
Heart - Myocarditis
Neurological - Encephalitis
Lung - Pneumonitis
Liver- Hepatitis, Jaundice, Hepatosplenomegaly
Other- IUGR, Thrombocytopenia +/- anaemia
Neonatal Early Onset Sepsis (<3 days)
Group B strep (mainly), E. coli, listeria
Ix: FBC, CRP Blood cultures --> lumbar puncture if +ve cultures Deep ear swab Surface swabs
Rx - benzylpenicillin and gentamycin (plus supportive - ventilation, circulation, nutrition etc)
Neonatal Late Onset Sepsis (>3 days)
Coagulase-negative staph (epidermis, saprophyticus = from skin)
Ix: FBC, CRP Blood cultures --> lumbar puncture if +ve cultures Deep ear swab Surface swabs
Rx
1st line - Cefotaxime and Vancyomycin
2nd line - meropenem
Community acquired late onset neonatal infections: cefotaxime, amoxicillin +/-gentamicin
Congenital Infection - things we screen for and those we don’t but are able to
Current screening: Hep B HIV Rubella Syphilis
Not screening: CMV Toxoplasmosis Hep C Group B Streptococcus
Congenital Toxoplasmosis
Cat faeces. Undercooked meat.
May be asymptomatic at birth – 60% but may still go on to suffer long term sequelae e.g. deafness, low IQ, microcephaly
40% symptomatic at birth
- Choroidoretinitis
- Microcephaly/hydrocephalus
- Intracranial calcifications
- Seizures
- Hepatosplenomegaly/jaundice
Congenital chlamydia infection
- Causes neonatal conjunctivitis, or rarely pneumonia
- Treated with erythromycin
Neonatal Group B Strep Infection
Gram positive coccus Catalase negative Beta-haemolytic Lancefield Group B In neonates: - Bacteraemia - Meningitis - Disseminated infection e.g. joint infections
Neonatal E.coli Infection
Gram negative rod In neonates: - Bacteraemia - Meningitis - UTI
RFs for Early Onset Neonatal Sepsis
Maternal:
- PROM/prem. Labour
- Fever
- Foetal distress
- Meconium staining
- Previous history
Baby:
- Birth asphyxia
- Resp. distress
- Low BP
- Acidosis
- Hypoglycaemia
- Neutropenia
- Rash
- Hepatosplenomegaly
- Jaundice
Other organisms causing late onset neonatal sepsis
Coagulase negative Staphylococci (CoNS) is the main one. Others include:
Group B streptococci E. coli Listeria monocytogenes S. aureus Enterococcus sp. Gram negatives – Klebsiella spp. /Enterobacter spp. /Pseudomonas aeruginosa/Citrobacter koseri Candida species
Childhood Strep Pneumonia Infection
- Leading cause of morbidity and mortality esp. in < 2y.o.
- Gram positive diplococcus – alpha haemolytic streptococcus
- Meningitis, bacteraemia, pneumonia
- > 90 capsular serotypes
- Increasing penicillin resistance
Pneumococcal Conjugate Vaccines
Conjugated vaccine immunogenic in children from 2 months.
- Prevenar introduced in U.K. in 2006 (7 serotypes, individually conjugated to a carrier, then mixed
- These 7 serotypes are responsible for approx 80% of IPD in the UK in 2006
- Vaccine serotypes were almost eradicated since introduction of PCV7
- BUT still seeing much IPD (invasive pneumococcal disease) in children
- ? Due to replacement phenomenon i.e. serotype replacement
- ?Could this lead to change in disease phenotype e.g. HUS (serotype 19a), empyema (serotype 1)
- Introduction of Prevenar 13 in UK in 2010
Meningitis at Different Ages
<3/12: N. meningitidis; S. pneumoniae; (H. influenzae (Hib) if unvaccinated); GBS; E. coli; Listeria sp.
3/12 - 5 years:N. meningitidis; S. pneumoniae; (Hib if unvaccinated)
> 6 years: N. meningitidis; S. pneumoniae
Bacterial RTI Causes and Rx in children
- S. pneumoniae (pneumococcus) is the most important bacterial cause
- Most UK strains remain sensitive to penicillin or amoxicillin
- Mycoplasma pneumoniae tends to affect older children (>4 years) – Macrolides are treatment of choice e.g. Azithromycin
Mycoplasma Pneumoniae
Acquired by droplet transmission person to person.
Epidemics occur every 3-4 years. Occurs in school age children and young adults.
Incubation period 2-3 weeks.
Many asymptomatic Classically presents: - Fever - Headache - Myalgia - Pharyngitis - Dry cough
DDx if fails to respond to treatment: whooping cough, TB (inc MDRTB, XDRTB)
Mycoplasma Pneumoniae - Extrapulmonary Manifestations
Haemolysis
- IgM antibodies to the I antigen on erythrocyte
- Cold agglutinins in 60% patients
Neurological (1% cases)
- Encephalitis most common
- Aseptic meningitis, peripheral neuropathy, transverse myelitis, cerebellar ataxia
- Aetiology unknown ?antibodies cross react with galactocerebroside
Cardiac
Polyarthralgia, myalgia, arthritis
Otitis media and bullous myringitis
UTIs in children
Common
Up to 3% girls and 1% boys by age 11
Diagnosis:
- Symptoms – if child old enough to give clear history
- Pure growth >105cfu/ml
- Pyuria – pus cells on urine microscopy
N.B. Get sample before starting treatment
Organisms: E.coli, proteus, klebsiella, enterococcus, coagulase -ve staph (Staph saprophyticus)
Recurrent/persistant infections in children
May be a sign of immunodeficiency – either congenital or acquired – e.g. HIV, SCID
Warrants investigation by Paediatric Infectious Diseases doctors
Congenital Rubella Syndrome - Mechanism
Mechanism:
- Mitotic arrest of cells –> Necrotic change in placental cells due to viral replication –>
- Infected placental endothelial cells desquamate into vessels causing transport of virus-infected ‘emboli’ to foetus (antipathy) –>
- Viral infection of foetal cells during organogenesis –> Viral mediated apoptosis –> Interference with development of key organs (growth inhibitor effect)
Diagnosis of Rubella (in the mother) and Rx
Clinical:
- Maculopapular rash
- Lymphadenopathy
- Fever
- Lesions on soft palate
- Headache
Lab: Rubella serology (IgM and IgG), detection of virus (molecular diagnosis - PCR of secretions)
Rx - none available (but vaccinated against in MMR)
Maternal Diagnosis of CMV
Lab: virus and serology
Detection of virus (blood, urine, respiratory secretions)
- Cell culture
- Detection of Early Antigen Fluorescent Foci
- DEAFF – accelerated cell culture system
- CMV DNA (Polymerase Chain Reaction)
CMV Serology - IgM, IgG seroconversion, IgG avidity
Foetal/Neonatal Diagnosis of CMV
Pre-natal:
Detection of CMV DNA in amniotic fluid at 21 weeks gestation
Post-natal:
- CMV detection within 21 days of life. (Positive result beyond that time will NOT make a diagnosis of congenital infection) - Urine/Salivary swab/blood for CMV PCR
- CMV Serology - CMV IgM (low sensitivity)
Prevention and Treatment of CMV
Vaccine
None at present – in development
Prevention
“universal precautions”
Antiviral treatment: - Not used during pregnancy – toxicity Congenital CMV with end organ disease - Valganciclovir / Ganciclovir for 6/12 - Audiology review until age 6 - Ophthalmology review
Classification of maternal HSV infection and associated risk of neonatal infection
First episode, primary infection - 57%
First episode, non-primary infection - 25%
Recurrent infection - 2%
Symptomatic/Asymptomatic
Highest risk = Maternal primary HSV infection in the third trimester.
- particularly within 6 weeks of delivery: continuing viral shedding , birth before development of protective maternal antibodies. C-section recommended.
Factors influencing neonatal transmission in HSV
Type of maternal infection
Maternal antibody status (neutralizing Ab)
Duration of rupture of membranes
Integrity of mucocutaneous barriers (eg use of foetal scalp electrodes)
Mode of delivery (caesarean section versus vaginal)
Highest risk of transmission is in the permpartum(perinatal period) - 85% (as opposed to 5% in utero and 10% postpartum).
Diagnosis and Treatment HSV
- Decrease the time to diagnostic consideration (mum&baby)
- Early initiation of antiviral therapy
- Prompt collection of specimens for diagnosis - HSV cultures/PCR, liver transaminase levels (suggest disseminated HSV infection)
Rx:
- High dose aciclovir at 60 mg/kg/day IV in three divided daily doses
- Continute for 21 days in CNS/disseminated, 14 in SEM
- Continue acyclovir until PCR -ve
- Monitor neutrophil count and renal function
VZV in Pregnancy
- DNA virus - HHV3
- Droplet transmission
- 90% women of childbearing age immune
- Spread through local nerves with latency in the sensory dorsal root ganglia
- Zoster (shingles) - no risk to the foetus
Foetus - risk of transmission:
- Congenital varicella syndrome
- Neonatal varicella
- Herpes zoster in early childhood
Mother: pneumonitis, encephalitis, sepsis
Congenital Varicella Syndrome
Eyes:
- Chorioretinitis
- Cataracts
Neurological:
- Microcephaly
- Cortical atrophy
Musculoskeletal/Skin:
- Limb hypoplasia
- Cutaneous scarring
Other:
- IUGR
Maternal infection during 13-20 weeks’ gestation = highest risk (2%)
Neonatal Varicella Infection
Newborn is vulnerable when maternal infection occurs within 7 days prior to delivery or 7 days post-partum - No time for passive transfer of VZV antibodies
Manifestations of infection may include
- Mild course of infection
- Disseminated skin lesions
- Purpura fulminans
- Visceral infection
- Pneumonitis
20% mortality untreated
Diagnosis: clinical or VZV PCR of lesion
Varicella Prevention in Pregnancy
Vaccine:
Live virus vaccine available (give preconception)
Avoidance of exposure in pregnancy if susceptible
Post-exposure prophylaxis:
- Varicella-zoster immunoglobulin (given with 10 days of exposure) up to 20/40
- Antiviral chemotherapy: Aciclovir 800mg x4/day from day 7-14 post exposure after 20/40
