8. Neonatal and Childhood Infections Flashcards
What infections are currently screened for during pregnancy?
Hep B, HIV, rubella, syphilis
What is currently NOT screened but possible?
CMV (most common cause of congenital deafness in the UK), toxoplasmosis, Hep C, Group B Streptococcus
What is the old mnemonic used to consider infections?
TORCH screen - toxoplasmosis, other (e.g. syphilis, HIV, hepatitis), rubella, CMV, HSV
What are common clinical features of congenital infections?
Mild/no apparent maternal infection; wide range of severity in the baby; similar clinical presentation; serological diagnosis; long-term sequelae if untreated.
What are examples of common clinical features?
Thrombocytopaenia; rash; cerebral abnormalities; hepatosplenomegaly/ hepatitis/ jaundice
How does toxoplasmosis start and end up in humans?
The acute infection will start off in a cat. It produces faeces containing oocysts. Mice and birds eat the faeces. Cats eat birds and mice. This ends up becoming a cycle. Having cats as pets can mean that the oocysts get ingested by humans.
What percentage of those with congenital toxoplasmosis are asymptomatic at birth and what long term effects might they have?
May be asymptomatic (60%) at birth but may still go on to have long-term sequelae such as: deafness, low IQ, microcephaly.
What percentage of those with congenital toxoplasmosis are symptomatic at birth and what long term effects might they have?
40%? Choroidoretinitis, microcephaly/hydrocephalus, intracranial calcificiations, seizures, hepatosplenomegaly/jaundice.
What is the mechanism of congenital rubella syndrome?
Mitotic arrest of cells, angiopathy, growth inhibitor effect
What is the classical triad of congenital rubella syndrome?
Cataracts, congenital heart disease (PDA is not common), deafness
What are other features of congenital rubella syndrome?
Microphthalmia, glaucoma, retinopathy, ASD/VSD, microcephaly, meningoencephalopathy, developmental delay, growth retardation, bone disease, hepatosplenomegaly, thrombocytopaenia, rash
How does HSV present?
Can spread to the neonate through the genital tract, can cause blistering and rash, disseminated infection with liver dysfunction and meningoencephalitis. (Infection control is particularly important)
How is Chlamydia trachomitis transmitted?
During delivery, mother may be asymptomatic.
What does Chlamydia trachomitis cause?
Causes neonatal conjunctivitis or pneumonia (RARE)
How is Chlamydia trachomatis treated?
Erythromycin
What mycoplasma species may cause a congenital disease?
Mycoplasma hominis and Ureaplasma urealyticum
What is the neonatal period?
Generally the first 4-6 weeks of life. If born premature, the neonatal period is longer and is adjusted for the expected birth date
Why are premature neonates at an increased risk of infection?
Less maternal IgG, NICU care, exposure to micro-organisms, colonisation and infection
What organisms cause early-onset infection (within 48 hours of birth)
(*Some definitions say 3-5 days). Organisms: Group B Streptococcus, Escherichia coli, Listeria monocytogenes
What organism is Gram-positive coccus, catalase-negative and beta-haemolytic?
Group B Streptococcus (it is Lancefield Group B)
What proportion of women are colonised by GBS in their vagina?
1/3
What can Group B Streptococcus cause in neonates?
Bacteraemia, meningitis, disseminated infection
What is gram-negative rods? (NOTE: K1 antigen is particularly problematic)
Escherichia coli
What organism is gram-positive rods, can cause sepsis in both mother and baby and is catastrophic?
Listeria monocytogenes
What are maternal risk factors for early-onset sepsis?
PROM/premature labour, fever, foetal distress, meconium staining, previous history
What are signs of early-onset sepsis?
Birth asphyxia, resp. distress, low BP, acidosis, hypoglycaemia, neutropenia, rash, hepatosplenomegaly, jaundice
What are investigations for early-onset sepsis?
FBC, CRP, blood culture, deep ear swab, LP, surface swabs, CXR
What is treatment for early-onset sepsis?
Supportive: ventilation, circulation, nutrition, antibiotics e.g. benzylpenicillin and gentamicin (this choice of antibiotics tends to be used because GBS is treated by benzylpencillin and E.coli is treated by gentamicin)
When does late-onset sepsis occur?
After 48-72 hours
What organisms are causes of late-onset sepsis?
Coagulase-negative Staphylococci (CoNS), Group B Streptococcus, Escherichia coli, Listeria monocytogenes, Staphylococcus aureus, Enterococcus sp., Gram-ngeatives - Klebsiella, Enterobacter, Pseudomonas aeruginosa, Citrobacter koseri, Candida Species
What are clinical features of late-onset sepsis?
Bradycardia, apnoea, poor feeding/biliary aspirates/abdominal distension, irritability, convulsions, jaundice, respiratory distress, increased CRP, sudden changes in WCC and platelets, focal inflammation (e.g. umbilibus, drip sites)
What is treatment for late-onset sepsis?
Treat early - low threshold for starting therapy, review and stop antibiotics if cultures are negative and clinically stable, guidelines for antibiotics differ.
What are examples of antibiotics for late-onset sepsis?
1st line: cefotaxime and vancomycin, 2nd line: meropenem. For community-acquired late-onset neonatal infection: cefotaxime, amoxicillin with or without gentamicin
Bacterial infections are important and may cause secondary infection after viral illness. What is an example of this?
Invasive Group A Streptococcus infection after VZV
Typical investigations for infections in childhood?
FBC, CRP, blood cultures, urine, sputum, throat swabs
What investigations for the diagnosis of meningitis?
Clinical features, blood cultures, throat swab, LP if possible (NOTE: in meningococcal disease the patient may be coagulopathic in which case doing a lumbar puncture is dangerous), rapid antigen screen, EDTA for blood PCR, clotted serum for serology if needed later
When should you not do a LP (to collect CSF) in a patient with meningitis?
In meningococcal disease the patient may coagulopathic in which case doing a lumbar puncture is dangerous. High ICP?
What will be the pressure of CSF in normal, bacterial, viral and fungal/TB?
Normal: 5-20; bacterial: >30; viral: normal or mildly increased; fungal/TB …
What will be the appearance of CSF in normal, bacterial, viral and fungal/TB?
Normal: normal; bacterial: turbid; viral: clear; fungal/TB: fibrin web
What will be protein level in CSF in normal, bacterial, viral and fungal/TB?
Normal: 0.18-0.45 g/L; bacterial: > 1 g/L; viral: <1 g/L; fungal/TB: 0.1-0.5 g/L. Bacterial meningitis has high protein in CSF
What will be the glucose level in CSF in normal, bacterial, viral and fungal/TB?
Normal: 2.5-3.5 mmol/L; bacterial: <2.2 mmol/L; viral: normal; fungal/TB: 1.6-2.5. Bacteria uses up glucose, and fungal/TB meningitis also use up a bit of glucose
What will be the Gram stain of CSF in normal, bacterial, viral and fungal/TB?
Normal: normal; bacterial: 60-90% positive; viral: normal
What will be the glucose - CSF: serum ratio in normal, bacterial, viral and fungal/TB?
Normal: 0.6; bacterial: < 0.4; viral > 0.6; fungal/TB < 0.4
What will be the WCC in CSF in normal, bacterial, viral and fungal/TB?
Normal: < 3; bacterial: > 500; viral: < 1000; fungal/TB: 100-500
What types of cells are seen in CSF in normal, bacterial, viral and fungal/TB?
Bacterial: 90% PMN; viral: monocytes, 10% have > 90% PMN and 30% have > 50% PMN; fungal/TB: monocytes
What to do if there is no growth in a meningitis sample?
If there is no growth, a PCR may be positive. Rapid antigen tests may be useful.
Which vaccination programmes have helped decrease the cases of meningitis?
Hib, Men C, and pneumococcus
What is the main cause of meningitis at the moment?
Men B
The meningococcal disease can be fulminant to the point …
… where limb amputation is necessary
The Men B vaccine because available in 2015 and it showed to reduce the incidence of meningococcal disease in the cohort that they were studying. What is an issue with this vaccine?
This vaccine is very immunogenic and is usually given with paracetamol because it can make the child ill
What organism is the leading cause of morbidity and mortality especially in < 2 years?
Strep pneumoniae
What is a gram-positive diplococcus, alpha-haemolytic, has more than 90 capsular serotypes and is increasing in penicillin resistance?
Streptococcus pneumoniae
Why was the pneumococcal conjugate vaccine found?
- Previously there was a polysaccharide vaccine with 23 capsular types of pneumococcus.
- Children < 2 showed a poor response.
- Antibody response was improved by conjugating the polysaccharide with proteins such as CRM
- The conjugate vaccine is immunogenic in children from 2 months
- This conjugate vaccine was called Prevenar 7 which targeted 7 serotypes
- These serotypes were almost eradicated
- However, we are still seeing a lot of cases of invasive pneumococcal disease
- More serotypes were added to create Prevenar 13
What can Strep Pneumonia lead to?
Meningitis, bacteraemia and pneumonia
What is a Gram-negative rod, grows glossy colonies on blood agar and causes meningitis at all ages?
Haemophilus influenzae
Typical causes of meningitis in under 3 months:
- Neisseria meningitidis
- Streptococcus pneumoniae
- Haemophilus influenzae
- Group B Streptococcus
- Escherichia coli
- Listeria monocytogenes
Typical causes of meningitis in 3 months to 5 years:
- Neisseria meningitis
- Streptococcus pneumoniae
- Haemophilus influenzae
Typical causes of meningitis in over 6 years:
- Neisseria meningitis
* Streptococcus pneumoniae
What constitutes 1/3 of all childhood illnesses?
Respiratory tract infections
What are respiratory tract infections mostly?
Mostly URTI, mostly viral
What is the most important bacterial cause and why?
Streptococcus pneumonia because most UK strains of pneumococcus remain sensitive to amoxicillin or penicillin
Who does mycoplasma pneumoniae tend to affect?
Older children (>4 years)
How is mycoplasma pneumoniae treated?
Macrolides (azithromycin)
How does mycoplasma pneumonia spread?
Person-to-person droplet infection
What is the incubation period of mycoplasma pneumoniae?
2-3 weeks. (Epidemics occur every 3-4 weeks)
What is the clinical presentation of mycoplasma pneumonia?
Mainly asymptomatic. Fever, headache, myalgia, pharyngitis, dry cough
What extrapulmonary manifestations may mycoplasma pneumoniae have?
Haemolysis, neurological, cardiac, musculoskeletal, otitis media, bullous myringitis
What neurological extrapulmonary manifestations does mycoplasma pneumoniae have?
Encephalitis, aseptic meningitis, peripheral neuropathy, transverse myelitis, cerebellar ataxia
What musculoskeletal manifestations may mycoplasma pneumoniae have?
polyarthralgia, myalgia, arthritis
What is bullous myringitis?
Vesicles on the tympanic membrane - pathognomonic of mycoplasma disease
If a respiratory tract infection fails to respond to treatment, what else should we consider?
Whooping cough (Bordatella pertussis) and TB
How is a UTI diagnosed in a child?
Symptoms - if child can give a history; pure growth of > 10^5 CFU/mL; pyuria - pus cells on urine microscopy. Obtain sample before starting treatment. Renal tract imaging may be required to check for congenital anomalies
What organisms can cause UTIs?
Escherichia coli - MAIN ORGANISM, other coliforms (Proteus, Klebsiella, Enterococcus sp.), coagulase-negative Staphylococcus (Staphylococcus saprophyticus)
What may recurrent or persistent infections in a child be a feature of?
Immunodeficiency - either congenital (e.g. SCID) or acquired (e.g. HIV). Warrants investigation by paediatric ID specialist
