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Andersons pediatric cardiology 1490

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Tiêu đề Andersons Pediatric Cardiology 1490
Trường học Unknown University
Chuyên ngành Pediatric Cardiovascular Medicine
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capitis Oral Streptococcal species Viridans group Streptococcus oralis/mitis Streptococcus sanguinis/mutans group Most common cause in CHD.. Difficult to treat due to relative tolerance

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S hominis

S lugdunensis

S capitis

Oral Streptococcal

species (Viridans

group)

Streptococcus

oralis/mitis

Streptococcus

sanguinis/mutans

group

Most common cause in CHD

Often sensitive to penicillin and third-generation cephalosporin, but resistance to both agents has been observed

Enterococci

E faecalis

E faecium

More common in adults

Difficult to treat due to relative tolerance to β-lactam antimicrobials and increasing

resistance in E faecium.

Nutritionally

variant organism

Abiotrophia spp.

Granulicatella spp.

Difficult to isolate and culture Concerns over relative resistance to β-lactams High relapse rate, need to treat as for enterococcal IE

Other

streptococcal

species

Streptococcus

pneumoniae

Streptococcus

pyogenes

Streptococcus milleri

group

Infrequent but very aggressive cause if IE with severe tissue destruction requiring surgical intervention

HACEK

Haemophilus spp.

Aggregatibacter spp.

Cardiobacterium spp.

Eikenella corodens

Kingella spp.

Affects both prosthetic valves and native valves Generally better prognosis than some causes of IE

Some strains are β-lactamase positive

Hard to grow in laboratory, often require prolonged culture Good pick-up on resected material by molecular methods

Gram negative

Enterobacteriaceae

(Coliforms)

Pseudomonas spp.

More likely in immune-compromised and neonates

Antimicrobial resistance an issue

Specialist advice on combination therapy and length

Fungal Candida spp Cause of both NVE and PVE; very difficult to treat, requiring surgical

resection in most cases, apart from mural IE in neonates

Filamentous fungi Very difficult to manage, almost always requires surgical debridement and aggressive antifungal therapy

Other causes

Bartonella sp.

Coxiella burnetii

Tropheryma whipplei

Mycoplasma spp.

Brucella spp.

Often part of noncultivable or culture-negative endocarditis Serologic testing available for some

Good rate of pick-up on molecular testing of resected material

Combine with epidemiologic exposure for optimal diagnosis

Emerging

pathogens

Mycobacterium

chimaera

M chimaera recently identified as a cause of IE due to contaminated heater cooler units

and bypass circuits used in cardiac surgery

CHD, Congenital heart disease; IE, infective endocarditis; NVE, native valve endocarditis; PVE,

prosthetic valve endocarditis

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Summary of Pediatric-Specific Cohort Studies Evaluating Changes

in Incidence, Risk Factors and Causative Agents of IE

Study

Time

Period,

Study Type

Number of IE Episodes

% of Patients With Preexisting Cardiac Disease/None

Findings/Comments

Day et

al93

2000 and

2003, US

retrospective

cohort

N = 1588 (causative

organisms in 662 cases)

42%/58% IE episodes with coded organisms, n =

622

■ Staphylococcus aureus, 362 (57%)

■ Viridans Streptococcus, 124 (20%)

■ Coagulase-negative Staphylococcus, 91

(14%)

■ Mortality highest in tetralogy of Fallot with PA and TOF

■ In non-CHD cases, highest mortality in infants, especially premature ones and

with S aureus infections

Gupta et

al94

2000–2010,

US CHD

Retrospective

cohort

N = 3840

estimated

53.5%/46.5% ■ 30.2% no organism (culture negative)

■ S aureus, 36.6% (of those, 46.9% had no

underlying cardiac defect, 28.1% with no defect)

■ Other Staphylococcus spp., 6.5% equally

distributed between those with and without preexisting cardiac defect

■ Viridans Streptococcus, 26% (32.7% in

children with underlying cardiac defects, 17.9% in those without)

■ Trend over study period for increase in streptococcal IE

■ Highest mortality in S aureus IE

Sakai

Bizmark

et al95

2001–2012,

interrupted

time series

retrospective

cohort

N = 3748 (weighted

according to whether IE appears in any primary, secondary, or tertiary discharge code)

50.2%/49.8% ■ Staphylococcus IE, 33.6%

■ Streptococcus, 27.4% (VGS 20.4)

■ Culture negative, 30.4%

■ Main finding was that incidence has not changed but decrease in staphylococcal

and increase in streptococcal IE in the 10-to 17-year-old age group post–2007 guideline

CHD, Congenital heart disease; IE, infective endocarditis; PA, pulmonary atresia; TOF, tetralogy

of Fallot; VGS, viridans group streptococci

Laboratory Diagnostic Procedures

BC remains the gold standard investigation for patients with suspected IE;

however, optimal sampling techniques, volumes (based on age of child), and

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following volumes and frequency are recommended:

Volumes:

1 Infants and young children: 1 to 3 mL per bottle

2 Older children: 5 to 7 mL per bottle (up to 30 mL blood/day).

Frequency:

1 Three sets of separate venipunctures over 24 hours, ideally with one set

12 hours apart, but with at least the first and last set 1 hour apart

2 If the patient is unstable and presentation is acute, take two BCs at

separate sites immediately and a third at least 1 hour later and

commence empiric therapy as soon as feasible.

New Laboratory Diagnostic Techniques

Techniques such as broad-range bacterial (16S rDNA) and fungal (18s rDNA) polymerase chain reactions (PCRs), pathogen-specific real-time PCRs, and proteomics (matrix-assisted laser desorption/ionization time-of-flight analysis [MALDI-TOF]) have become widely available and should be used in

conjunction with standard culture techniques Gene-specific primers and

amplification are more sensitive and do not always require a sequence step and

so are more rapid.

1 Molecular methodologies can detect bacterial DNA directly in blood, and, although they have advanced in recent years,

■ They are still somewhat insensitive,96 the likely reason due to the low circulating load of bacteria in IE.

■ Broad-range PCR techniques, bacterial (16S rDNA) and fungal (18S rDNA), are designed to amplify both conserved and variable regions of ribosomal DNA but in general are rather insensitive and in addition require a sequencing step to identify the pathogen.

■ Contamination with environmental DNA can be problematic, particularly for fungal 18S DNA Optimal sampling,

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