Neonatal and Childhood Infections Flashcards

1
Q

Define congenital infections.

A

Babies are born with congenital infections i.e. transmitted vertically from mother to baby.

Infection can occur at any time during pregnancy, between first trimester and birth.

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2
Q

What is included in current maternal screening?

A

Hep B

HIV

Syphilis

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3
Q

What is not currently screened but is possible?

A

CMV

Toxoplasmosis

Hep C

Group B Streptococcus

Rubella

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4
Q

What is the presentation of congenital infections?

A

Varied presentations and non-specific signs.

Need to be considered in any sick neonate.

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5
Q

What is TORCH?

A
  • Toxoplasmosis
  • Other – syphilis; HIV; hepatitis B/C
  • Rubella
  • Cytomegalovirus (CMV)
  • Herpes simplex virus (HSV)
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6
Q

What are common signs of congenital infections?

A

Common clinical features:

  • Mild/no apparent maternal infection
  • Wide range of severity in the baby
  • Similar clinical presentation
  • Serological diagnosis
  • Long term sequelae if untreated

Examples:

  • Low platelets, rash
  • Cerebral abnormalities
  • Hepatosplenomegaly/hepatitis/jaundice
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7
Q

What is toxoplasmosis?

A

The only known definitive hosts for Toxoplasma gondii are members of family Felidae (domestic cats and their relatives).

Unsporulated oocysts are shed in the cat’s feces. Although oocysts are usually only shed for 1-2 weeks, large numbers may be shed. Oocysts take 1-5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water or plant material contaminated with oocysts.

Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites. Cats become infected after consuming intermediate hosts harboring tissue cysts. Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment.

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8
Q

How can humans contract toxoplasmosis?

A

Humans can become infected by any of several routes:

  • Eating undercooked meat of animals harboring tissue cysts.
  • Consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat).
  • Blood transfusion or organ transplantation.
  • Transplacentally from mother to fetus.

In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host.

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9
Q

How is toxoplasmosis diagnosed?

A

Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens. Diagnosis of congenital infections can be achieved by detecting T. gondii DNA in amniotic fluid using molecular methods such as PCR.

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10
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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11
Q

How does congenital rubella syndrome affect children?

A

Effect on foetus – dependent on time of infection.

Mechanism: Mitotic arrest of cells; angiopathy; growth inhibitor effect.

  • Eyes: Cataracts; microphthalmia; glaucoma; retinopathy
  • Cardiovascular syndrome: PDA; ASD/VSD
  • Ears: Deafness
  • Brain: Microcephaly; meningoencephalitis; developmental delay
  • Other: Growth retardation; bone disease; hepatosplenomegaly; thrombocytopenia; rash
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12
Q

What are other congenital infections to be aware of?

A
  • Hepatitis B and C
  • HIV
  • Syphilis
  • Listeria monocytogenes
  • Group B Streptococcus
  • Parvovirus
  • Chlamydia trachomatis
    • Infection transmitted during delivery
    • Mother may be asymptomatic
    • Causes neonatal conjunctivitis, or rarely pneumonia
    • Treated with erythromycin
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13
Q

Define neonatal infections.

A

Definition varies: First 4-6 weeks of life.

If born early (premature), neonatal period longer and is adjusted for expected birth date.

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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14
Q

What is the aetiology/risk factors of neonatal infections?

A

Immature host defences.

Increased risk with increased prematurity:

  • Less maternal IgG
  • NICU care
  • Exposure to microorganisms; colonisation and infection
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15
Q

What are features of neonatal infections? What are some causative organisms of neonatal infections?

A

Early and late onset infection.

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

Organisms:

  • Group B streptococci
  • E. coli
  • Listeria monocytogenes
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16
Q

What is Group B Strep.?

A

Gram positive coccus, catalase negative.

Beta-haemolytic.

Lancefield Group B.

In neonates:

  • Bacteraemia
  • Meningitis
  • Disseminated infection e.g. joint infections
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17
Q

What is E. Coli?

A

Gram negative rod

In neonates:

  • Bacteraemia
  • Meningitis
  • UTI
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18
Q

What are maternal risk factors for early onset sepsis?

A
  • PROM/prem. Labour
  • Fever
  • Foetal distress
  • Meconium staining
  • Previous history
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19
Q

What are neonatal risk factors for early onset sepsis?

A
  • Birth asphyxia
  • Resp. distress
  • Low BP
  • Acidosis
  • Hypoglycaemia
  • Neutropenia
  • Rash
  • Hepatosplenomegaly
  • Jaundice
20
Q

What are appropriate investigations for early onset sepsis?

A

Full blood count

C-reactive protein (CRP)

Blood culture

Deep ear swab

Lumbar puncture (CSF)

Surface swabs

Chest X-ray (full body)

21
Q

What is the management for early onset sepsis?

A

Supportive management:

  • Ventilation
  • Circulation
  • Nutrition
  • Antibiotics: e.g. benzylpenicillin & gentamicin
22
Q

What are causative organisms of late onset sepsis (48-72 hours)?

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
23
Q

What are the clinical features of late onset sepsis?

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.
24
Q

What are appropriate investigations for late onset sepsis?

A
  • FBC
  • CRP
  • Blood culture(s)
  • Urine
  • ET secretions if ventilated
  • Swabs from any infected sites
25
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.

26
Q

What is an example of an antibiotic regimen for late onset sepsis?

A

1st line: Cefotaxime & vancomycin

2nd line: Meropenem

Community acquired late onset neonatal infections: cefotaxime, amoxicillin +/-gentamicin

27
Q

What are common causative organisms of childhood infections?

A

Child’s age is important in considering likely pathogens:

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.

28
Q

What are common presenting symptoms of childhood infections?

A

May be difficult to ascertain site of infection from history/examination depending on age of child. Common non-specific symptoms:

  • Fever
  • Abdominal pain
29
Q

What are appropriate investigations of childhood infections?

A
  • FBC
  • CRP
  • Blood cultures
  • Urine
  • +/- Sputum; throat swabs etc
30
Q

What is the most important bacterial cause of paediatric morbidity and mortality?

A

Meningitis

31
Q

How is meningitis diagnosed?

A
  1. Clinical features
  2. 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
32
Q

What is the leading cause of morbidity and mortality especially in children < 2y.o?

A

Streptococcus pneumoniae

33
Q

What is Streptococcus pneumoniae?

A

Gram positive diplococcus – alpha haemolytic streptococcus

Meningitis, bacteraemia, pneumonia

>90 capsular serotypes

Increasing penicillin resistance

34
Q

What are pneumococcal conjugate vaccines?

A

Due to large health burden and emergence of antibiotic resistance - vaccination programme introduced in the USA in 2000.

Previously available pneumococcal polysaccharide vaccine were 23 capsular types of pneumococcus.

Children< 2years had poor response, but antibody response improved by conjugating the polysaccharide to proteins such as CRM. This conjugated vaccine is immunogenic in children from 2 months.

35
Q

What are the most common causes of meningitis in a child <3 months?

A

N. meningitidis

S. pneumoniae

H. influenzae (Hib) if unvaccinated

GBS

E. coli

Listeria sp.

36
Q

What are the most common causes of meningitis in a child aged 3mo-5y?

A

N. meningitidis

S. pneumoniae

Hib if unvaccinated

37
Q

What are the most common causes of meningitis in a child aged >6 years?

A

N. meningitidis

S. pneumoniae

38
Q

What are respiratory tract infections?

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

39
Q

What are the most common causative organisms of respiratory tract infections?

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.

40
Q

How is Mycoplasma pneumoniae transmitted?

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.

41
Q

How does infection with Mycoplasma pneumoniae present?

A

Many asymptomatic.

Classically presents:

  • Fever
  • Headache
  • Myalgia
  • Pharyngitis
  • Dry cough
42
Q

What are 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

43
Q

If a respiratory tract infection fails to recover, what should you consider?

A
  • Whooping cough – Bordetella pertussis especially if unvaccinated
  • TB including MDRTB and XDRTB
44
Q

What are urinary tract infections?

A

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

45
Q

What are common causative organisms of urinary tract infections?

A

E. coli

Other coliforms e.g. Proteus species, Klebsiella Enterococcus sp.

Coagulase negative Staphylococcus e.g. Staph saprophyticus

46
Q

What is the management for urinary tract infections?

A

Early diagnosis and antibiotic treatment important (Nitrofurantoin 7d)

Renal tract imaging

Antibiotic prophylaxis after treatment of the infection (NICE guidance)

47
Q

What may recurrent or persistent infections be indicative of?

A

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

Warrants investigation by Paediatric Infectious Diseases doctors.