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PathY5 > Neonatal and Childhood Diseases > Flashcards

Neonatal and Childhood Diseases Flashcards

1
Q

What is a congenital infection?

A

An infection with which a baby is born with.

The mother may be infected any time during pregnancy.

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2
Q

What is the current screening of the mother during pregnancy?

A

Hep B
HIV
Rubella
Syphilis

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3
Q

What is currently not screened in the mother during pregnancy but may still undergo vertical transmission?

A

CMV
Toxoplasmosis
Hep C
Group B Streptococcus

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4
Q

What is the (outdated) torch screen?

A

Toxoplasmosis
Other – syphiliss; HIV; hepatitis B/C
Rubella
Cytomegalovirus (CMV)
Herpes simplex virus (HSV)

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5
Q

What are the common clinical features of congenital infections?

A

Mild/no apparent maternal infection

Wide range of severity in the baby

Similar clinical presentation
Low platelets, rash
Cerebral abnormalities
Hepatosplenomegaly/hepatitis/jaundice

Serological diagnosis

Long term sequelae if untreated

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6
Q

What is the life cycle of toxoplasmosis?

A
  1. Unsporulated oocysts are shed in cats faeces
  2. Oocysts shed for 1-2 weeks
  3. Intermediate hosts infected
  4. Oocysts transform into tachyzoites and move to neural/ muslce in hosts
  5. Oocysts may infect human meat consumption
  6. Humans infected (definitive host) via undercooked food, contaminated water, blood transfusion, transplacentally
  7. Stay in human skeletal muscle, heart, brain and eyes
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7
Q

How do you diagnose toxoplasmosis?

A

Serology
Stained biopsy

Amniotic fluid PCR - T gondii

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8
Q

How does congenital toxoplasmosis present?

A

May be asymptomatic at birth – 60% but may still go on to suffer long term sequelae
Deafness, low IQ, microcephaly

40% symptomatic at birth
Choroidoretinitis
Microcephaly/hydrocephalus
Intracranial calcifications
Seizures
Hepatosplenomegaly/jaundice

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9
Q

How does congenital rubella present?

A

Effect on foetus – dependent on time of infection
Mechanism – mitotic arrest of cells; angiopathy; growth inhibitor effect

Eyes: cataracts; microphthalmia; glaucoma; reintopathy

Cardiovascular syndrome; PDA; ASD/VSD

Ears; deafness

Brain: microcephaly; meningoencephalitis; developmental delay

Other: growth retardation; bone disease; hepatosplenomegaly; thrombocytopenia; rash

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10
Q

What does a HSV rash look like?

A

Red, blistering and pustulated

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11
Q

Other than toxoplasmosis and HSV what other congenital infections may occur?

A

Hepatitis B and C
HIV
Listeria monocytogenes
Group B Streptococcus
Syphilis
Chlamydia trachomatis
Mycoplasma species (Mycoplasma hominis and Ureaplasma urealyticum)
Parvovirus

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12
Q

What happens in neonatal Chlamydia?

A

Infection transmitted during delivery
Mother may be asymptomatic
Causes neonatal conjunctivitis, or rarely pneumonia
Treated with erythromycin

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13
Q

How do you treat neonatal chlamydia?

A

Erythromycin

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14
Q

What does Neonatal mean?

A

Definition varies
First 4-6 weeks of life

If born early (premature)
Neonatal period longer and is adjusted for expected birth date

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15
Q

Why are neonatal infections bad?

A

Higher incidence of infections
Can become ill rapidly and seriously
Unlike adults or older children – need to treat with antibiotics when first suspicion of infection

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16
Q

Why can’t neonates protect against infection?

A

Immature host defences

Increased risk with increased prematurity
Less maternal IgG
NICU care
Exposure to microorganisms; colonisation and infection

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17
Q

What are early onset infections?

A

Early onset – usually within 48 hours of birth
Some definitions 3-5 days

Organisms:
Group B streptococci
E. coli (Vaginal canal bacteria)
Listeria monocytogenes

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18
Q

What are group B Streptococci?

A

Gram positive coccus
Catalase negative
Beta-haemolytic
Lancefield Group B

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19
Q

What can group B streptococci cause?

A

Bacteraemia
Meningitis
Disseminated infection e.g. joint infections

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20
Q

What does E.coli cause in neonates?

A

Bacteraemia
Meningitis
UTI

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21
Q

What is Listeria Monocytogenes?

A

L. monocytogenes is a Gram-positive, non-spore-forming, motile, facultatively anaerobic, rod-shaped bacterium.

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22
Q

What are the maternal RFs for early onset sepsis?

A

PROM/prem. Labour
Fever
Foetal distress
Meconium staining
Previous history

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23
Q

What are the baby RFs for early onset sepsis?

A

Resp: Birth asphyxia, Resp. distress

Metabolic: Acidosis, Hypoglycaemia

Signs: Neutropenia, Rash, Hepatosplenomegaly, Jaundice, Low BP

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24
Q

What investigations would you do for early onset sepsis?

A

Bloods: FBC, CRP, Blood culture

Samples: Deep ear swab, Lumbar puncture (CSF), Surface swabs

Imaging: Chest X-ray (full body)

25
Q

What is the treatment for early onset sepsis?

A

Supportive management: Ventilation, Circulation, Nutrition

Antibiotics: e.g. benzylpenicillin & gentamicin

26
Q

What causes late onset sepsis?

A

Coagulase negative Staphylococci (CoNS)
Group B streptococci
E. coli
Listeria monocytogenes
S. aureus
Enterococcus sp.
Gram negatives – Klebsiella spp. /Enterobacter spp. /Pseudomonas aeruginosa/Citrobacter koseri
Candida species

27
Q

What does late onset mean?

A

after 48-72 hours

28
Q

What are the clinical features of late onset sepis?

A

Bradycardia
Apnoea
Poor feeding/bilious aspirates/ abdominal distension
Irritability
Convulsions
Jaundice
Respiratory distress
Increased CRP; sudden changes in WCC/platelets
Focal inflammation – e.g. Umbilicus; drip sites etc.

29
Q

What investigations do you do for late onset sepsis?

A

Bloods: FBC, CRP, Blood culture(s)

Source identification: Urine, ET secretions if ventilated, Swabs from any infected sites

30
Q

What is the treatment for late onset sepsis?

A

Treat early – lower threshold for starting therapy

Review and stop antibiotics if cultures negative and clinically stable

NICU-Example of antibiotics for late onset sepsis:
1st line: cefotaxime & vancomycin
2nd line: meropenem
Community acquired late onset neonatal infections: cefotaxime, amoxicillin +/-gentamicin

31
Q

What infections are common in childhood?

A

Viral infections are very common e.g. Chickenpox (VZV); Herpes simplex – cold sores/stomatitis; HHV6; HHV8; EBV; CMV; RSV; enteroviruses etc

Bacterial infections are important and may cause secondary infection after viral illness e.g. iGAS disease post VZV infection

May be difficult to ascertain site of infection from history/examination depending on age of child

32
Q

What are common non specific symptoms?

A

Fever
Abdominal pain

33
Q

What investigations can you do in ill children?

A

FBC
CRP
Blood cultures
Urine
+/- Sputum; throat swabs etc

34
Q

What do you do if you suspect a child has meningitis?

A

Most important bacterial cause of paediatric morbidity and mortality

Clinical features

Lab tests:
Blood cultures
Throat swab
LP for CSF if possible
Rapid antigen screen
EDTA blood for PCR
Clotted serum for serology if needed later

35
Q

What causes bacterial meningitis?

A

N. meningitidis - meningococcal septicaemia causes a non blanching erythmatous rash

36
Q

How has the Men B vaccine helped?

A

50% incidence rate ratio (IRR) reduction in MenB cases

(37 cases Vs average 74 cases; IRR 0.50 [95% CI 0.36-0.71; p=0.0001)

37
Q

What does S. pneumoniae cause?

A

Meningitis, bacteraemia, pneumonia

38
Q

Why is S.pneumoniae bad?

A

Leading cause of morbidity and mortality esp. in < 2y.o.
>90 capsular serotypes
Increasing penicillin resistance

39
Q

What type of bacteria is S. pneumoniae?

A

Gram positive diplococcus – alpha haemolytic streptococcus

40
Q

How do we vaccinate against pneumococcus?

A

Due to large health burden and emergence of antibiotic resistance - vaccination programme introduced in the USA in 2000
Previously available pneumococcal polysaccharide vaccine – 23 capsular types of pneumococcus
Children< 2years poor response – antibody response improved by conjugating the polysaccharide to proteins such as CRM
This conjugated vaccine – immunogenic in children from 2 months

41
Q

What does the pneumococcal vaccine do?

A

Prevenar introduced in U.K. in 2006 (7 serotypes, individually conjugated to a carrier, then mixed
These 7 serotypes in Prevenar 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 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 (serotypes 4, 6B, 9V, 14, 18C, 19F, 23 and additional serotypes 1, 3, 5, 6A, 7F and 19)

42
Q

What ages do the different bacteria cause meningitis?

A

<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

43
Q

What is the background of RTIs?

A

Account for 1/3 of all childhood illnesses
Mostly upper respiratory tract infections
Mostly viral
Age is important
Sputum is often difficult to obtain
Often need to give empiric treatment

44
Q

What bacteria causes pneumonia?

A

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

45
Q

How does mycoplasma pneumoniae cause problems?

A

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

46
Q

What are the symptoms of mycoplasma pneumoniae infection?

A

Many asymptomatic

Classically presents:
Fever
Headache
Myalgia
Pharyngitis
Dry cough

47
Q

What are the extrapulmonary manifestations of mycoplasma pneumoniae?

A

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

48
Q

If meningitis fails to respond to accurate treatment what else could you consider?

A

Whooping cough – Bordetella pertussis especially if unvaccinated
TB including MDRTB and XDRTB

49
Q

How common are UTIs in children?

A

Common
Up to 3% girls and 1% boys by age 11

50
Q

How do you diagnose UTIs?

A

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

51
Q

What organisms cause UTIs?

A

E. coli

Other coliforms e.g. Proteus species, Klebsiella Enterococcus sp.
Coagulase negative Staphylococcus
Staph saprophyticus

52
Q

What is the management of a suspected uti in a child?

A

See notes.

53
Q

What is important to do in UTIs?

A

Early diagnosis and antibiotic treatment important
Renal tract imaging
Antibiotic prophylaxis after treatment of the infection (NICE guidance)

54
Q

How do you manage recurrent or persistent infections?

A

May be a sign of immunodeficiency – either congenital or acquired – e.g. HIV, SCID

Warrants investigation by Paediatric Infectious Diseases doctors

55
Q

What is the current vaccination schedule?

A
56
Q

What is the commonest cause of neonatal sepsis?

A

Gp B strep

57
Q

What is the most common type of meningococcal disease in the UK?

A

Men B

58
Q

What is the commonest cause of death worldwide in children under 5yrs?

A

Pneumonia

PathY5 (98 decks)

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