Vol. 22, No. 12, Dec.
2003 THE PEDIATRIC INFECTIOUS DISEASE JOURNAL
vancomycin-resistant E. faecium with linezolid in a 7-month-
old preterm infant. This infant received linezolid in a dosage
of 10 mg/kg every 8 h. CSF was sterile at 48 h of treatment.
He completed a 21-day course of therapy with no reported
adverse event.
Several reports have reflected the increased VRE coloniza-
tion or VRE infections in neonatal intensive care unit pa-
tients both in the US and abroad.11–13 Antecedent use of
vancomycin and extended spectrum cephalosporins have
been associated with colonization with VRE and increased
risk of developing invasive disease.14, 15 Nosocomial out-
breaks of VRE infections have been linked to contaminated
objects or person-to-person transmission by health care work-
ers.16
Traditionally mortality from enterococcal infections in ne-
onates had been low1, 2 because of the appropriate use of
effective antibiotics and the focal nature of these infections
such as soft tissue abscesses or central venous catheter-
related infections that were amenable to surgical drainage or
catheter removal that helped in infection resolution.1 As
strains of multidrug-resistant isolates emerged, infections
caused by these organisms have become increasingly more
difficult to treat. Therapy of invasive VRE infections (mostly
E. faecium) is particularly difficult because these organisms
are also resistant to multiple antibiotics such as beta-lactams
and aminoglycosides.17
Linezolid is the first member of a new class of antibiotics
known as the oxazolidinones. It is active against Gram-
positive microorganisms including multidrug-resistant iso-
lates. It inhibits protein synthesis by binding to bacterial 23S
ribosomal RNA.18 Time kill studies have shown that linezolid
is bacteriostatic against enterococci.18 Recent multilabora-
tory assessment of the spectrum of activity of linezolid re-
vealed that it was active against 96% of the 163 VRE
isolates.19 Despite the bacteriostatic activity of linezolid
against enterococci, successful treatment of invasive VRE
infections with linezolid in adult patients has been reported
including VRE meningitis,20 VRE bacteremia,7, 9 VRE perito-
nitis,9 VRE osteomyelitis9 and VRE endocarditis.6, 7
Linezolid given intravenously followed by oral therapy
resulted in bacteriologic cure of VRE endocarditis in our
infant patient. Linezolid appears to be an attractive choice for
the treatment of endocarditis caused by linezolid-susceptible
VRE. However, further studies are needed to confirm lin-
ezolid efficacy and determine treatment duration.
Jocelyn Y. Ang, M.D.
Jorge L. Lua, M.D.
Daniel R. Turner, M.D.
Basim I. Asmar, M.D.
Children’s Hospital of Michigan (JYA, JLL,
DRT, BIA)
Divisions of Infectious Diseases (JYA, BIA),
Neonatology (JLL) and Cardiology (DRT)
Wayne State University School of Medicine
Detroit, MI
Accepted for publication Aug. 29, 2003.
Key words: Vancomycin-resistant enterococcus, endocarditis,
neonate, linezolid.
Reprints not available.
1. Dobson, SRM, Baker CJ. Enterococcal sepsis in neonates:
features by age at onset and occurrence of focal infection.
Pediatrics 1990;85:165–71.
2. Luginbuhl LM, Rotbart HA, Facklam RR, et al. Neonatal
enterococcal sepsis: case-control study and description of an
outbreak. Pediatr Infect Dis J 1987;6:1022–30.
1103
3. Landman D, Quale JM. Management of infections due to
resistant enterococci: a review of therapeutic options. J Anti-
microb Chemother 1997;40:161–70.
4. Nosocomial enterococci resistant to vancomycin: United
States, 1989 –1993. MMWR 42:597–9.
5. Huycke MM, Sahm DF, Gilmore MS. Multiple-drug resistant
enterococci: the nature of the problem and an agenda for the
future. Emerg Infect Dis 1998;4:239 – 49.
6. Babcock HM, Ritchie DJ, Christiansen E, et al. Successful
treatment of vancomycin-resistant Enterococcus endocarditis
with oral linezolid. Clin Infect Dis 2001;32:1373–5.
7. Chien JW, Kucia ML, Salata RA. Use of linezolid, an oxazo-
lidinone, in the treatment of multidrug-resistant Gram-
positive bacterial infections. Clin Infect Dis 2000;30:146 –51.
8. Rao N. Successful treatment of Enterococcus faecalis pros-
thetic valve endocarditis with linezolid. Clin Infect Dis 2002;
35:902– 4.
9. Birmingham MC, Rayner CR, Meagher AK, et al. Linezolid
for the treatment of multidrug-resistant, Gram-positive in-
fections: experience from a compassionate-use program. Clin
Infect Dis 2003;36:159 – 68.
10. Graham LP III, Ampofo K, Saiman L, et al. Linezolid treat-
ment of vancomycin-resistant Enterococcus faecium ventric-
ulitis. Pediatr Infect Dis J 2002;21:798 – 800.
11. Sohn AH, Garrett DO, Sinkowitz-Cochran RL, et al. Preva-
lence of nosocomial infections in neonatal intensive care unit
patients: results from the first national point-prevalence
survey. J Pediatr 2001;139:821–7.
12. Yuce A, Karaman M, Gulay Z, et al. Vancomycin-resistant
enterococci in neonates. Scand J Infect Dis 2001;33:803–5.
13. Singh-Naz N, Rakowsky A, Cantwell E, et al. Nosocomial
enterococcal infections in children. J Infect 2000;40:145–9.
14. Rubin LG, Tucci V, Cercenado E, et al. Vancomycin-resistant
Enterococcus faecium in hospitalized children. Infect Control
Hosp Epidemiol 1992;13:700 –5.
15. Carmeli Y, Eliopoulos GM, Samore MH. Antecedent treat-
ment with different antibiotic agents as a risk factor for
vancomycin-resistant Enterococcus. Emerg Infect Dis 2002;8:
802–7.
16. Coudron PE, Mayhall CG, Facklam RR, et al. Streptococcus
faecium outbreak in a neonatal intensive care unit. J Clin
Microbiol 1984;20:1044 – 8.
17. Gordon S, Swenson JM, Hill BC, et al. Antimicrobial suscep-
tibility patterns of common and unusual species of entero-
cocci causing infections in the United States. J Clin Microbiol
1992;30:2373– 8.
18. Diekema DJ, Jones RN. Oxazolidinone antibiotics. Lancet
2001;358:1975– 82.
19. Jones RN, Ballow CH, Biedenbach DJ, et al. Multi-laboratory
assessment of the linezolid spectrum of activity using the
Kirby-Bauer disk diffusion method: report of the Zyvox An-
timicrobial Potency Study (ZAPS) in the United States. Diagn
Microbiol Infect Dis 2001;40:59 – 66.
20. Zeana C, Kubin CJ, Della-Latta P, et al. Vancomycin-
resistant Enterococcus faecium meningitis successfully man-
aged with linezolid: case report and review of the literature.
Clin Infect Dis 2001;33:477– 82.
ACUTE NEPHRITIS AND RESPIRATORY TRACT
INFECTION CAUSED BY MYCOPLASMA PNEUMONIAE:
CASE REPORT AND REVIEW OF THE LITERATURE
A 6-year-old boy presented with an acute infec-
tion caused by Mycoplasma pneumoniae associated
with respiratory tract and kidney involvement. Re-
nal manifestations included acute nephritis with
decreased C3 fraction of serum complement, occur-
ring concomitantly with the respiratory symptoms.
The child had an excellent outcome, with rapid
normalization of C3 and complete resolution of the
acute nephritis.
1104 THE PEDIATRIC INFECTIOUS DISEASE JOURNAL Vol. 22, No. 12, Dec. 2003
Mycoplasma pneumoniae respiratory infections are occa- hematuria subsided 2 days after admission, followed by
sionally associated with extrarespiratory manifestations.1 microhematuria which persisted for the following 2 months.
This organism can affect children of all ages.2 Renal involve- The proteinuria resolved after 10 days and the C3 returned to
ment is rare, and it usually presents as an acute nephritis normal in 35 days (1,170 mg/l). The anti-M. pneumoniae IgM
that may be manifested simultaneously with the other symp- antibodies were positive 4 months later (ratio 1.3), becoming
toms or 5 to 10 days later.3 negative 6 months later, whereas the IgG remained positive
We present a case of a 6-year-old boy with acute nephritis (ratio 3.9). The child was asymptomatic on follow-up at 6
occurring concomitantly with respiratory tract infection months.
caused by M. pneumoniae and review the pertinent literature. Discussion. Acute postinfectious glomerulonephritis (GN)
Case report. A 6-year-old boy was admitted to the Pedi- in childhood is usually caused by group A beta-hemolytic
atric Nephrology Clinic because of painless macrohematuria. Streptococcus, but it can be caused by other infections.4 It can
Three days earlier he had developed a fever (39°C) that lasted appear simultaneously with bacterial pneumonia (pneumo-
for 24 h and was associated with coryza and nonproductive coccal, staphylococcal) and pneumonia caused by C. pneu-
cough that persisted until admission. moniae, Coxiella burnetii, Nocardia5 and M. pneumoniae.3 In
The clinical and laboratory data are shown in Table 1. our patient the clinical presentation of the child was compat-
Chest roentgenogram revealed peribronchial infiltrates. Ul- ible with M. pneumoniae infection which was subsequently
trasound examination of the kidney was normal. On admis- proved by the detection of borderline positive specific IgM
sion the anti-streptolysin O titer was 200 IU/ml, and it antibodies on admission that increased 15 days later, as well
remained essentially unchanged during the following 2 as the parallel appearance of IgG antibodies. The PCR for M.
weeks. The pharyngeal culture revealed normal bacterial pneumoniae in nasopharyngeal swab is most useful as a rapid
flora. diagnostic test, but it was not available in our laboratory.
An enzyme-linked immunosorbent assay (Alphadia SA/ Radiographically there were peribronchial infiltrates but no
NY) was used for the detection of specific anti-M. pneumoniae evidence of pneumonia. Most (75%) M. pneumoniae infections
IgM and IgG antibodies. The results were expressed as the present with minor respiratory symptoms (pharyngitis, tra-
ratio of the optical density value of the sample to the cutoff cheobronchitis), ⬃20% are asymptomatic and only 3 to 10% of
value and were considered positive when this ratio was ⬎1.1, infected patients develop pneumonia.1, 6
equivocal when it was 0.9 to 1.1 and negative when ⬍0.9. In The diagnosis of acute GN in our case was supported by the
our patient the IgM was equivocal on admission and in- sudden onset of macrohematuria, proteinuria and granular
creased to pathologic values 15 days later (ratios 1.0 and 1.6, casts in the urine. Red blood cell casts are diagnostic of
respectively). The IgG antibody was negative on admission glomerular origin of hematuria.7
and positive 15 days later (ratio 2.6). The direct and indirect Acute poststreptococcal GN typically presents 7 to 14 days
Coombs reaction was negative. The IgM and IgG antibodies after group A beta-hemolytic streptococcal infection and only
for Coxiella burnetii, Rickettsia conorii and Chlamydia pneu- rarely in fewer than 7 days.4 In our patient the illness
moniae were negative. appeared just 3 days before the presentation of nephritis, and
The child was treated with erythromycin orally for 10 days. the fever subsided spontaneously within 24 h without antibi-
He never developed edema or hypertension, and the macro- otics. This clinical course of our patient, in combination with
the laboratory findings that were incompatible with conven-
tional bacterial infection, makes the presence of a poststrep-
TABLE 1. Clinical and laboratory data of the patient at the tococcal GN highly unlikely.
time of admission to the hospital Although M. pneumoniae-associated GN is rare, a few
cases have been reported in children, the clinical character-
Values istics of which are summarized in Table 2.3, 8 –11 Glomerulo-
Clinical data
nephritis can appear either concomitantly with other symp-
Body temperature 36.8°C toms or 5 to 10 days later.3 In cases with renal involvement
Blood pressure 120/80 mm Hg persistence of anti-M. pneumoniae IgM and IgG antibodies
Lymphadenopathy/wheezing Mild cervical/mild has been reported,3 as in our patient. In the study by Saı̈d et
Laboratory data
Blood
al.,3 four of the six reported children were boys. Predomi-
White blood cell count (⫻109/l) 14.2 nance of boys has also been reported by Srivastava et al.5 in
Neutrophils/lymphocytes (%) 63/30 cases with pneumonia-associated acute glomerulonephritis.
Erythrocyte sedimentation rate 42/15 However, the number of reported children is too small to
(mm/h)/C-reactive protein (mg/l)
Urea (mmol/l)/Creatinine (␮mol/l) 13.0/70.7
confirm the male predominance.
Total proteins (g/l)/albumin (g/l) 72/35 The C3 serum complement was initially decreased in 4 of
C3 fraction of serum complement (mg/l) ⬍350 (normal 10 reported children and subsequently normalized in one of
range, 880 –1550) them, whereas in 3 of 4 it remained persistently low.3, 8, 11 In
C4 fraction of serum complement (mg/l) 270 (normal range:
120 –320)
these 3 children renal biopsy revealed membranoproliferative
Antinuclear antibodies Negative glomerulonephritis (MPGN) types I (1 patient) and II (2
Urinalysis patients), and all 3 progressed to chronic renal failure and
Red blood cells Abundant end-stage renal failure.8, 11 Our patient is the second reported
Sediment Neutrophils and
granular casts
case in whom the initially low C3 was only transient, and its
Protein 2⫹ rapid normalization was associated with an excellent clinical
Urine indices outcome. Because of the rapid clinical and laboratory im-
Fractional excretion of sodium (%) 1 provement, a renal biopsy was not performed in our patient.
Renal failure index 1.4
24-h urine collection
Proteinuria resolved within 10 days, and microhematuria
Urine output (ml/kg/h) 3.5 resolved within 2 months, a finding similar to those in other
Creatinine clearance (ml/min/1.73 m2) 67 (normal range, reported cases.3, 9, 10 In a child with acute renal failure
92–142) reported by Saı̈d et al.,3 the glomerular filtration rate re-
Total protein excretion (mg/m2/h) 32
turned to normal in 2 months, whereas the microhematuria
Vol. 22, No. 12, Dec. 2003 THE PEDIATRIC INFECTIOUS DISEASE JOURNAL 1105
resolved after 36 months. MPGN is the most frequent lesion
found in patients with mycoplasmal infection in whom the
acute nephritis is associated with persistently low C3.3

proteinuria (16 mo)

Chronic renal failure

Mild hematuria and

The pathogenesis of GN associated with M. pneumoniae

Recovery* (36 mo)

Recovery* (12 mo)

infection is unclear. In the study by Saı̈d et al.,3 the PCR was

Recovery* (1 mo)
Recovery* (2 mo)

Recovery* (6 mo)

Recovery* (2 mo)

Recovery* (2 mo)
Outcome

negative, and immunofluorescence studies failed to detect M.

ESRF (1 mo)

ESRF (8 yr)
pneumoniae antigen in the renal parenchyma. The authors
(1.5 mo)

argued that this does not necessarily rule out the role of this
microorganism, because the pathogenesis of postinfectious
GN is more likely based on immunologic mechanisms.3 An
immune reaction against the glomeruli could be supported by
the detection of anti-M. pneumoniae antibodies by immuno-
fluorescence in the glomeruli. The antigen involved could be
Minimal change disease mycoplasmal or a cross-reacting renal antigen. Searches for
M. pneumoniae antigen by immunofluorescence in the renal
Renal Biopsy

Endocapillary GN

Endocapillary GN
TABLE 2. Cases in the literature of Mycoplasma pneumoniae-associated nephritis in children

biopsies were negative in the study by Saı̈d et al.3 Circulating

immune complexes, containing either mycoplasmal or autol-
ogous antigen, are likely to participate in the pathogenetic
MPGN II

MPGN II

Not done

Not done

Not done

Not done
MPGN I

MPGN I

mechanism.3 These complexes have been reported in myco-

plasmal extrarespiratory infections, but no specific mycoplas-
mal antigen has been detected12 except for cases with central
nervous system and liver involvement, in which specific
mycoplasmal and autologous antigens were detected.12, 13
Transiently decreased C3 and C4

Ekaterini Siomou, M.D, Ph.D.

Konstantinos D. Kollios, M.D, Ph.D.
Serum Complement

Photini Papadimitriou, M.D.

Persistently decreased C3

Persistently decreased C3

Persistently decreased C3

Transiently decreased C3

Angeliki Kostoula, M.D, Ph.D.

Borderline normal C4

Zoe L. Papadopoulou, M.D, Ph.D.

Normal C3 and C4

Normal C3 and C4

Normal C3 and C4

Normal C3 and C4

Division of Pediatric Nephrology

(ES, KDK, ZLP)
Normal C4

Normal C4

Normal C4

Department of Child Health (PP)

Not done

Not done

Department of Microbiology (AK)

University of Ioannina Medical School
Ioannina, Greece

Accepted for publication Sept. 5, 2003.

Key words: Nephritis, Mycoplasma pneumoniae, child, postin-
Acute renal failure, moderate

fectious glomerulonephritis.
Renal Manifestations in
Addition to Nephritis

Address for reprints: ⌭. Siomou, M.D., Ph.D, Emmanouil

Xanthou 58, GR-454 45 Ioannina, Greece. Fax 302651097032;
Moderate proteinuria

Moderate proteinuria

Moderate proteinuria

Moderate proteinuria
Nephrotic syndrome

Nephrotic syndrome

E-mail xmatsouk@cc.uoi.gr.
Relapse after 6 mo

* Recovery: normal glomerular filtration rate; disappearance of proteinuria and hematuria.

Mild proteinuria
Solitary kidney

1. File TM, Tan JS, Plouffe JF. The role of atypical pathogens:
proteinuria

Mycoplasma pneumoniae, Chlamydia pneumoniae, and Le-

gionella pneumophila in respiratory infection. Infect Dis Clin
North Am 1998;12:569 –92.
2. Principi N, Esposito S, Blasi F, Allegra L, and the Mowgli
Study Group. Role of Mycoplasma pneumoniae and Chla-
mydia pneumoniae in children with community-acquired
lower respiratory tract infections. Clin Infect Dis 2001;32:
1281–9.
Age (yr)

3. Saı̈d MH, Layani MP, Colon S, Faraj G, Glastre C, Cochat P.

7

11

11
17
8

5
10

5
5

Mycoplasma pneumoniae-associated nephritis in children.

Pediatr Nephrol 1999;13:39 – 44.
4. Cole BR, Salinas-Madrigal L. Acute proliferative glomeru-
lonephritis and crescentic glomerulonephritis. In: Barratt
TM, Avner ED, Harmon WE, eds. Pediatric nephrology. 4th
Waskowski and Powers 198310

ed. Baltimore: Lippincott Williams & Wilkins, 1999:669 –

89.
5. Srivastava T, Warady BA, Alon US. Pneumonia-associated
ESRF, end stage renal failure.

acute glomerulonephritis. Clin Nephrol 2002;57:175– 82.

Cochat et al. 198511
Dumas et al. 19768

Vitullo et al. 19789

Source

6. Ferwerda A, Moll HA, de Groot R. Respiratory tract infec-

Saïd et al. 19993

tions by Mycoplasma pneumoniae in children: a review of

diagnostic and therapeutic measures. Eur J Pediatr 2001;
Our patient

160:483–91.
7. ⌴adaio MP, Harrington JT. The diagnosis of glomerular
diseases. Arch Intern Med 2001;161:25–34.
8. Dumas R, Bascoul S, Baldet P, Serre A, Roux J, Jean R.
⌴embranoproliferative glomerulonephritis and Mycoplasma
infection. Arch Fr Pediatr 1976;33:783–94.
1106 THE PEDIATRIC INFECTIOUS DISEASE JOURNAL
9. Vitullo B〉, O’Regan S, de Chadarevian JP, Kaplan BS.
Mycoplasma pneumonia associated with acute glomerulone-
phritis. Nephron 1978;21:284 – 8.
10. Waskowski SD, Powers BJ. Glomerulonephritis and Myco-
plasma infection. Ann Intern Med 1983;98:112–13.
11. Cochat P, Colon S, Bosshard S, Zech P, Traeger J. ⌴embrano-
proliferative glomerulonephritis and Mycoplasma pneu-
moniae infection. Arch Fr Pediatr 1985;42:29 –31.
12. Biberfeld G, ⌵orberg R. Circulating immune complexes in
Mycoplasma pneumoniae infection. J Immunol 1974;112:
413–5.
13. Biberfeld G. Antibodies to brain and other tissues in cases of
Mycoplasma pneumoniae infection. Clin Exp Immunol 1971;
8:319 –33.
MACROPHAGE INFILTRATION OF PANCREATIC ACINI
AND ISLETS IN ACUTE KAWASAKI DISEASE
A report of 2 patients who developed diabetes
after Kawasaki disease (KD) led us to determine
whether macrophages and/or T cells infiltrate acute
KD pancreas. Three of 10 acute fatal KD cases had
diffuse macrophage infiltration of the pancreas; T
cells were not prominent. Affected islets were seen
in close proximity to normal islets. These findings
may explain the rarity of diabetes after KD.
Inflammatory lesions develop in many tissues in acute
Kawasaki disease (KD), most notably the coronary arteries.
Pancreatitis is observed at autopsy in 40% of KD fatalities in
the first month after onset,1 and clinical evidence of pancre-
atitis during acute KD has also been reported.2, 3 We previ-
ously reported IgA plasma cell infiltration in the pancreas in
acute KD.4 Bhowmick et al.5 recently reported two children
with insulin-dependent diabetes mellitus who presented with
ketoacidosis within 4 months of being diagnosed with KD and
suggested that KD may have led to the development of
diabetes mellitus in these patients. In this study we deter-
mined whether T lymphocytes and macrophages infiltrate the
pancreas during the acute phase of KD.
TABLE 1. Clinical data for patients with fatal acute Kawasaki disease and controls in a study of macrophages in the
pancreas
Case Age Sex
Patient with Kawasaki disease
1 3 mo Female
2 8 mo Female
3 4 mo Male
4 21 mo Female
5 7 mo Female
6 4 mo Male
7 10 mo Female
8 4 mo Female
9 4 mo Male
10 22 mo Male
Control
1 4 yr Female
2 2 mo Female
3 3 mo Female
4 6 yr Male
5 2 mo Male
6 12 mo Male
7 2 mo Female
8 2 mo Male
9 3 mo Female
10 7 mo Female
Vol. 22, No. 12, Dec. 2003
Methods. Formalin-fixed, paraffin-embedded pancreas
tissue blocks were evaluated from 10 patients who died in the
acute phase of KD and from 10 control children (Table 1).
Controls were age-matched and from children with infectious
and noninfectious diseases (Table 1). None of the patients or
controls had clinical evidence of pancreatitis or diabetes
mellitus. After xylene deparaffinization the sections were
rehydrated and antigen retrieval enhancement was per-
formed by heating the slides in 10 mM sodium citrate buffer,
pH 6.0, with the use of microwave treatment. Sections were
incubated for 1 h at room temperature with a 1/75 dilution of
mouse anti-human CD68 (Dako, Glostrup, Denmark) or a
1/100 dilution of mouse anti-human CD3 (Novocastra, New-
castle, UK). Biotinylated horse anti-mouse secondary anti-
body was added, and color was developed by use of the
Vectastain Elite ABC Kit (Vector, Burlingame, CA). Diami-
nobenzidine tetrahydrochloride was used as a reaction prod-
uct to generate a brown stain. Sections were lightly counter-
stained with hematoxylin. Normal spleen was used as a
positive control tissue for CD68 and CD3 antibodies; many
positive cells were observed for each antibody. Negative
controls included slides in which the primary antibody was
omitted, and these controls did not demonstrate any staining.
We also performed immunohistochemistry on adjacent, se-
quential sections of pancreas from patient 10 using mouse
anti-human antibodies to CD68 and to insulin (dilution,
1/150; Novocastra) to study the infiltration of CD68⫹ macro-
phages into the islets.
Positive cells were classified as follows: absent; focal (rare
single cells without aggregates); multifocal (discrete foci of
aggregates, 1 to 5 per ⫻20 field); or diffuse (⬎5 foci of
aggregates per ⫻20 field).
Results. Inflammatory infiltrates were present around the
ductular components of the pancreas in all 10 KD patients,
but the severity of infiltration varied, being most severe in
Patients 8, 9 and 10, in whom mild to moderate periductular
fibrosis was also noted. In KD Patients 8, 9 and 10, there was
occasional acinar dropout with resulting fibrosis, but these
changes were present in ⬍20% of the pancreas. In areas of
marked inflammation in the pancreas of these patients, a
contiguous islet was occasionally involved in the process.
Ethnicity Cause of Death
White Myocarditis
Unknown Ruptured coronary artery aneurysm
Hispanic Myocardial infarction
Unknown Ruptured coronary artery aneurysm
White Myocarditis
White Myocarditis
Black Myocardial infarction
White Myocardial infarction
Japanese Ruptured coronary artery aneurysm
White Ruptured coronary artery aneurysm
White Tetralogy of Fallot
Unknown Cardiomyopathy
Black Respiratory syncytial virus pneumonia
White Hypoplastic lung
Hispanic Complex congenital heart disease
Black Rotavirus infection
Unknown Transposition of great arteries
Hispanic Complete atrioventricular canal
Hispanic Influenza B pneumonia
White Influenza A pneumonia