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PATHOLOGY > childhood infectiojs > Flashcards

childhood infectiojs Flashcards

1
Q

when does congenital infection happen

A

can happen at any point in preg

generally - worse consequence if earlier because more development

by 3rd TM usually all important organs developed

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2
Q

what infections do we screen neonates for

A

Hep B
HIV
syphillis

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3
Q

what are the TORCH infections

A

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

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4
Q

general presentation of congenital infections in neonates

A

Low platelets, rash
Cerebral abnormalities
Hepatosplenomegaly/hepatitis/jaundice

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5
Q

life cycle of toxoplasmosis

A

Stays in muscle

Cat faeces have it

Mice and pigs are also involved

Common infection in adult – mild

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6
Q

presentation of congenital toxoplasmosis

A

60% asx at birth 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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7
Q

features of congenital rubella syndrome

A

Effect on foetus - dependent on time of infection

Eyes:
* cataracts;
* microphthalmia;
* glaucoma;
* retinopathy

Cardiovascular syndrome:
* PDA;
* ASD/VSD

Ears: deafness

Brain:
* microcephaly;
* meningoencephalitis;
* developmental delay

growth retardation;

bone disease;

hepatosplenomegaly;

thrombocytopenia;

rash

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8
Q

mech of rubella causing congenital infection

A

mitotic arrest of cells;

angiopathy;

growth inhibitor effect

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9
Q

congenital HSV

A

Problem close to delivery
If present with 1st episode of genital herpes in 3rd trimester – do CS to prevent transmission

Can present in neonate with rash, deranged LFTs

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10
Q

what are the congenital infections

A

Hepatitis B and C
HIV
Syphilis
HSV
Rubella
Toxoplasmosis
Listeria monocytogenes
Group B Streptococcus
Parvovirus
Chlamydia trachomatis

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11
Q

summarise chlamydia trachomatis

A

Infection transmitted during delivery
Mother may be asymptomatic

Causes:
* neonatal conjunctivitis,
* rarely pneumonia

Treated with erythromycin

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12
Q

what is the neonatal period

A

4-6wks of life (longer if preterm)

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13
Q

why do neonates get a lot of 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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14
Q

what time frame is early onset neonatal infection

A

within 48hrs

(some say 3-5 days)

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15
Q

organisms in early onset neonatal infection

A

GBS
E coli
Listeria monocytogenes

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16
Q

summarise GBS

A

Gram positive coccus
Catalase negative
Beta-haemolytic
Lancefield Group B

In neonates:
* Bacteraemia/sepsis
* Meningitis
* Disseminated infection e.g. joint infections

Usually sensitive to penicillin

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17
Q

summarise E coli

A

Gram negative rod
Grow very quickly

In neonates:
* Bacteraemia
* Meningitis – will have long ter sequlae
* UTI

Treat for 3wks with IV Abx

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18
Q

summarise listeria monocytogenes

A

happens in:
* Pregnancy
* Immunocompromsied
* Old people

Food hygiene imoirtant

Gram +ve rod

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19
Q

maternal RFs for early onset sepsis

A

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

20
Q

baby RF for early onset sepsis

A

Birth asphyxia
Resp. distress
Low BP
Acidosis
Hypoglycaemia
Neutropenia
Rash
Hepatosplenomegaly
Jaundice

21
Q

ix 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)

22
Q

Mx for early onset sepsis

A

Supportive management:
Ventilation
Circulation – ionotropes
Nutrition
Antibiotics: e.g. benzylpenicillin & gentamicin
If meningitis – add amoxicillin to cover listeria

23
Q

what are the bugs in late onset neonatal sepsis (48-72hrs)

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

24
Q

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.

25
Q

Ix for late onset sepsis

A

FBC
CRP
Blood culture(s)
Urine
ET secretions if ventilated
Swabs from any infected sites
LP

26
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

1st line: cefotaxime & vancomycin
2nd line: meropenem
Community acquired late onset neonatal infections: cefotaxime, amoxicillin +/-gentamicin

27
Q

ix for childhood infections

A

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

LP less so

28
Q

dx for meningitis

A

Clinical features
Lab tests:
* Blood cultures
* Throat swab
* LP for CSF if possible
* Rapid antigen screen
* EDTA blood for PCR – then do LP when safe to
* Clotted serum for serology if needed later

29
Q

CSF in meningitis

A

Gram stain
+ve in chains = GBS
+ve in pairs = pneumococcus

bacterial - WCC high – polymorphs

Viral can get polymorphs if catch early

30
Q

meningitis

A

neisseria meningitidis - meningococcis

31
Q
A

meningococcal rash
Extremities shut down -> ischemia in arms and legs
Babies lose limbs because of this

32
Q

meningitis

A

streptococcus pneunoniae

gram +ve cocci in pairs

33
Q

summarise streptoccus 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 – consider giving vanc too

34
Q
A

streptococcus pneumoniae

A haemolysis – green around colonies

In colony there is autolysis – colonies look like donuts – it is the organisms killing themselves

35
Q

summarise the vaccine for streptococcus pneumonia

A

Previously available pneumococcal polysaccharide vaccine
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

36
Q
A

haemophilus influenza

Can cause meningitis but causes morbidity inc hearing defects
Can cause Upper and LRT infectios

Gram –ve rods

Need chocolate agar

37
Q
A

Haemophilus influenzae on chocolate agar

38
Q

causes of meningitis at different ages

A

less than 3mo:
* N. meningitidis;
* S. pneumoniae;
* (H. influenzae (Hib) if unvaccinated);
* GBS;
* E. coli;
* Listeria sp.

3mo - 5 years:
* N. meningitidis;
* S. pneumoniae;
* (Hib if unvaccinated)

more than 6 years:
* N. meningitidis;
* S. pneumoniae

39
Q

how do you get sputum off children

A

bronchoscopy

secretion from ET tube

40
Q

what cause resp tract infections in children and Rx

A

S. pneumoniae (pneumococcus) is the most important bacterial cause
* sensitive to penicillin or amoxicillin

Mycoplasma pneumoniae tends to affect older children (>4 years)
* Macrolides are treatment of choice e.g. Azithromycin

41
Q

epidemiology of mycoplasma pneumoniae

A

transmission - droplet transmission

epidemics happen every 3-4 yrs

in school age children and young adults

incubation period 2-3 wks

42
Q

presentation of mycoplasma pneumoniae

A

Many asymptomatic

Fever
Headache
Myalgia
Pharyngitis
Dry cough

43
Q

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

eye
* Otitis media
* bullous myringitis

44
Q

epi of UTI

A

3x more in girls

45
Q

dx of UTI

A

Symptoms – if child old enough to give clear history
Pure growth >105cfu/ml
Pyuria – pus cells on urine microscopy

46
Q

organisms for UTI

A

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

e coli
47
Q

approach to recurrent/persistant UTI

A

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

Warrants investigation by Paediatric Infectious Diseases doctors

PATHOLOGY (94 decks)

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