childhood infectiojs Flashcards by Emily Southall

when does congenital infection happen

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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what infections do we screen neonates for

Hep B
HIV
syphillis

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what are the TORCH infections

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

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general presentation of congenital infections in neonates

Low platelets, rash
Cerebral abnormalities
Hepatosplenomegaly/hepatitis/jaundice

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life cycle of toxoplasmosis

Stays in muscle

Cat faeces have it

Mice and pigs are also involved

Common infection in adult – mild

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presentation of congenital toxoplasmosis

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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features of congenital rubella syndrome

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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mech of rubella causing congenital infection

mitotic arrest of cells;

angiopathy;

growth inhibitor effect

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congenital HSV

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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what are the congenital infections

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

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summarise chlamydia trachomatis

Infection transmitted during delivery
Mother may be asymptomatic

Causes:
* neonatal conjunctivitis,
* rarely pneumonia

Treated with erythromycin

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what is the neonatal period

4-6wks of life (longer if preterm)

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why do neonates get a lot of infections

Immature host defences

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

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what time frame is early onset neonatal infection

within 48hrs

(some say 3-5 days)

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organisms in early onset neonatal infection

GBS
E coli
Listeria monocytogenes

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summarise GBS

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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summarise E coli

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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summarise listeria monocytogenes

happens in:
* Pregnancy
* Immunocompromsied
* Old people

Food hygiene imoirtant

Gram +ve rod

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maternal RFs for early onset sepsis

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

baby RF for early onset sepsis

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

ix for early onset sepsis

Full blood count
C-reactive protein (CRP)
Blood culture
Deep ear swab
Lumbar puncture (CSF)
Surface swabs
Chest X-ray (full body)

Mx for early onset sepsis

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

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

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

clinical features of late onset sepsis

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.

Ix for late onset sepsis

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

what is the treatment for late onset sepsis

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**

ix for childhood infections

FBC CRP Blood cultures Urine +/- Sputum; throat swabs etc *LP less so*

dx for meningitis

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

CSF in meningitis

Gram stain +ve in chains = GBS +ve in pairs = pneumococcus bacterial - WCC high – polymorphs Viral can get polymorphs if catch early

meningitis

neisseria meningitidis - meningococcis

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

meningitis

streptococcus pneunoniae gram +ve cocci in pairs

summarise streptoccus pneumonia

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**

streptococcus pneumoniae A haemolysis – green around colonies In colony there is autolysis – colonies look like donuts – it is the organisms killing themselves

summarise the vaccine for streptococcus pneumonia

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

haemophilus influenza Can cause **meningitis** but causes morbidity inc hearing defects Can cause **Upper and LRT infectios** **Gram –ve rods** Need **chocolate agar**

Haemophilus influenzae on chocolate agar

causes of meningitis at different ages

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

how do you get sputum off children

bronchoscopy secretion from ET tube

what cause resp tract infections in children and Rx

**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**

epidemiology of mycoplasma pneumoniae

transmission - droplet transmission epidemics happen every 3-4 yrs in school age children and young adults incubation period 2-3 wks

presentation of mycoplasma pneumoniae

Many asymptomatic Fever Headache Myalgia Pharyngitis Dry cough

extrapulmonary manifestations of mycoplasma pneumoniae

**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

epi of UTI

3x more in girls

dx of UTI

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

organisms for UTI

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

approach to recurrent/persistant UTI

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