Microbiology of neonatal and childhood infections Flashcards

You may prefer our related Brainscape-certified 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

  • if it happens in first trimester - could have more serious consequences.
  • later infection less serious
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does screening target in pregnancy? What else could it look at?

A

•Current screening mother during pregnancy

–Hep B

–HIV

–Syphilis

•Currently NOT screened but possible

–CMV

–Toxoplasmosis

–Hep C

–Group B Streptococcus

–Rubella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How do congenital infections present?

A
  • Varied presentations and non-specific signs
  • Need to be considered in any sick neonate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the ‘TORCH’ screen?

A

•‘TORCH’ screen

–Toxoplasmosis

–Other – syphilis; HIV; hepatitis B/C

–Rubella

–Cytomegalovirus (CMV)

–Herpes simplex virus (HSV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the common clinical features 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the life cycle of 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 (1) . 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 (2) . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites (3) . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts (4). Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment (5) .

Humans can become infected by any of several routes:

•eating undercooked meat of animals harboring tissue cysts (6).•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) (7) .•blood transfusion or organ transplantation (8) .•transplacentally from mother to fetus (9) .

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. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens (10) . Diagnosis of congenital infections can be achieved by detecting T. gondii DNA in amniotic fluid using molecular methods such as PCR (11)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the consequences of congenital toxoplasmosis?

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the mechanism of congenital rubella syndrome infection? What are the consequences?

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the picture

A

Congenital rubella syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the image

A

HSV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the other congenital infections

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the neonatal period

A

•Definition varies

–First 4-6 weeks of life–

•If born early (premature)

–Neonatal period longer and is adjusted for expected birth date

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why is infection relevant in neonatal period?

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
  • Immature host defences
  • Increased risk with increased prematurity

–Less maternal IgG

–NICU care

–Exposure to microorganisms; colonisation and infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do we classify 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe group B streptococci

A
  • Gram positive coccus
  • Catalase negative
  • Beta-haemolytic
  • Lancefield Group B
  • In neonates: Can go to the CNS, into the blood and then the CNS

Bacteraemia

Meningitis

Disseminated infection e.g. joint infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe E.coli

A
  • Gram negative rod
  • In neonates:

Bacteraemia

Meningitis

UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What type of infection might this be?

A

Listeria monocytogenes - food hygiene!

Gram +ve rod

Classical appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are early onset sepsis-risk factors

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do we treat early onset sepsis?

A

•Supportive management:

–Ventilation

–Circulation

–Nutrition

–Antibiotics: e.g. benzylpenicillin & gentamicin

If meningitis, add amoxicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is late onset sepsis? What microorganisms cause it?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
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.
23
Q

What are the investigations for late onset sepsis?

A
  • FBC
  • CRP
  • Blood culture(s)
  • Urine
  • ET secretions if ventilated
  • Swabs from any infected sites
24
Q

How do we treat late onset sepsis?

A
25
Q

What are the infections during childhood

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
26
Q

What are the difficulties with diagnosing infections during childhood?

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

–Fever

–Abdominal pain

27
Q

How do we investigate infections during childhood?

A
  • FBC
  • CRP
  • Blood cultures
  • Urine

+/- Sputum; throat swabs etc

28
Q

What is the clinical significance of meningitis in childhood?

A

It can be difficult to do an LP (low plus) - look for strep and pneumococcus in blood

29
Q

Complete the table

A
  • If no growth PCR may be positive
  • Rapid antigen tests can be useful
30
Q
A

Gram -ve coccus - neisseria meningitides

31
Q

What is this?

A

Non-blanching rash. Bacterial meningitis

32
Q

What is this?

A

Meningococcal rash

33
Q

What is this?

A

Severe meningococcal rash

34
Q

What is this?

A

Streptococcus pneumonias - gram +ve - pneumococcus

35
Q

Describe streptococcus pneumonia.

A
  • 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

36
Q

What type of haemolytic does streptococcus pneumonias exhibit?

A

alpha haemolytic and autolysis (organisms killing themselves within t he centre of the colony)

37
Q

Describe the evolutions of pneumococcal conjugative 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 – 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
  • 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
38
Q
A

Gram -ve rod, haemophilia influenza. Rarely causes meningitis. High morbidity.

Plate - needs to be burned blood (red cell lysed)

39
Q

What are the common organisms causing meningitis in different age groups?

A
40
Q

Describe RTIs in childhood.

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
41
Q

What are the common causative organisms that cause RTIs in childhood?

A
42
Q

Describe mycoplasma pneumonias. How does it present? Who does it affect?

A
43
Q

What are the extra-pulmonary manifestations of mycoplasma pneumonia?

A
44
Q

If persistent cough, what should we consider?

A
45
Q

Describe UTIs in childhood.

A
46
Q

How should UTIs be managed in A&E?

A
47
Q

What is this?

A

E. coli

48
Q

What are the other organisms causing UTIs?

A
49
Q

How should we manage UTIs?

A

Recurrent or persistent infections

  • May be a sign of immunodeficiency – either congenital or acquired – e.g. HIV, SCID•
  • Warrants investigation by Paediatric Infectious Diseases doctors
50
Q

What organisms is not screened for in pregnancy?

  • Hep B
  • HIV
  • Toxoplasmosis
  • Syphilis
A

Toxoplasmosis

51
Q
A

Group B strep

52
Q
A

Men B

53
Q

What is the commonest cause of death under 5 years worldwide?

  • prematurity
  • malaria
  • pneumonia
  • HIV
  • neonatal sepsis
A

Pneumonia