Group C Streptococcal Endocarditis

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ARTHUR N. FEINBERG, MD

CHARLES L. SHABINO, MD

Pediatric Intensive Care Unit

Bronson Methodist Hospital

Kalamazoo, Michigan

mies without postoperative problems.

In case 2, the preoperative evaluation, including

chest roentgenogram, was entirely within normal

limits. The patient suddenly and unexpectedly

de-veloped pulmonary edema. Following recovery, her

cardiac status clinically, and as demonstrated via

noninvasive studies, was normal in spite of her

continued tonsillar hypertrophy. Therefore, we can

conclude that one would have been unable to

pre-dict before surgery this child’s postintubation

de-velopment of pulmonary edema.

In summary, we have presented two cases to

illustrate the problem of postoperative pulmonary

edema following tonsillectomy and adenoidectomy.

Furthermore, we have discussed the difficulty in

predicting those patients who will develop this

corn-plication. Because of the potential seriousness and

unpredictability of acute pulmonary edema

follow-ing tonsillectomy for chronic obstruction, it is

im-portant that medical personnel, including

pediatri-cians caring for patients after tonsillectomy, be able

to readily recognize this phenomenon of acute onset

of congestive heart failure and treat it rapidly with diuretics, continuous positive airway pressure, and respiratory support as needed.

114 PEDIATRICS Vol. 75 No. 1 January 1985

SUMMARY

ACKNOWLEDGMENTS

The authors thank Dr Richard E. Kravath for review-ing the manuscript and Marilyn Carruth for help in preparation of this manuscript.

REFERENCES

1. Lind MG, Lundell BPW: Tonsillar hyperplasia in children: A cause of obstructive sleep apena, CO, retention and re-tarded growth. Arch Otokiryngol 1982;108:650-654

2. Talaat AM, Nahhas MM: Cardiopulmonary changes second-ary to chronic adenotonsillitis. Arch Otolaryngol 1983; 109:30-33

3. Kravath RE, Pollak CP, Borowiecki B: Hypoventilation during sleep in children who have lymphoid airway obstruc-tion treated by nasopharyngeal tube and T&A. Pediatrics

1977;59:865-871

4. Talbot AS, Robertson LW: Cardiac failure with tonsil and adenoid hypertrophy. Arch Otolaryngol 1978;98:277-281 5. Macartney FJ, Panday J, Scott 0: Cor pulmonale as a result

of chronic nasopharyngeal obstruction due to hypertrophied tonsils and adenoids. Arch Di,s Child 1969;44:585-592 6. Nussbaum E, Hirschfeld SS, Wood RE, et al:

Echocardio-graphic changes in children with pulmonary hypertension secondary to upper airway obstruction. J Pediatr 1978; 93:931-936

7. Galves AG, Stool SE, Bluestone CS: Pulmonary edema following relief of acute upper airway obstruction. Arch Otolaryngol 1980;80:112-128

8. Travis DW, Todres ID, Shannon DC: Pulmonary edema associated with croup and epiglottitis. Pediatrics 1977; 59:695-698

9. Utilization and short stay hospital-Annual summary for the United States: Vital Health Stat 1979;B:60

10. Simmons DH, Leonard ML, Shapiro BJ: Effect of blood gases and acid base disturbances on the pulmonary circula-tion. Gun Invest Med 1964;43:1146-1461

11. Luke MJ, Mehriz A, Folger GM, et al: Chronic nasopharyn-geal obstruction as a cause of cardiomegaly, cor pulmonale and pulmonary edema. Pediatrics 1966;37:762-768

Group

C Streptococcal

Endocarditis

Although endocarditis is often caused by

a-he-molytic streptococci, endocarditis due to 13-hemo-lytic streptococci is rare. Most cases of

f3-strepto-coccal endocarditis are due to Lancefield groups B

or G, whereas group C streptococci rarely cause

endocarditis.’ Only 15 cases of endocarditis caused

by group C streptococci, all in adults, have been

reported.2’3 The rarity of this association is

em-phasized by the fact that Mohr et al’3 reported one

patient with group C streptococcal endocarditis

from a series of 150,000 blood cultures. In addition,

Cherubin and Neu’4 found no cases of group C

streptococcal endocarditis while reviewing 656

cases of infective endocarditis.

The purpose of this report is to describe the first

case of group C streptococcal endocarditis in a

pediatric patient.

CASE REPORT

Received for publication Jan 23, 1984; accepted March 23, 1984. Reprint requests to (R.Y.) Department of Pediatrics, North-western University Medical School, The Children’s Memorial Hospital, Chicago, IL 60614.

R.C., an 11-year-old white boy, was admitted to The

Children’s Memorial Hospital complaining of lethargy, chills, fever, and vomiting of 1 week’s duration. Seven years before his admission, the patient underwent repair of a ventricular septal defect. Two years later, cardiac catheterization demonstrated mild subaortic stenosis

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EXPERIENCE AND REASON 115

with mild aortic insufficiency. One month before his admission, the patient underwent a dental procedure. Prophylaxis consisted of four doses (125 mg each) of oral penicillin before the procedure, but none afterwards. Two weeks before his admission, the patient developed fever (40#{176}C),chills, and vomiting. He was treated with oral penicillin for two days and his symptoms resolved. One day before his admission, he developed recurrent high fever with chills and vomiting.

Examination upon admission to The Children’s

Me-morial Hospital revealed a pale and ill-appearing child. Vital signs included: BP, 100/70; pulse, 104 beats per minute and irregular; respirations, 18/mm; and temper-ature, 40.2#{176}Corally. The skin revealed Janeway lesions on the soles of both feet and the palmar surface of the right hand. A subungal splinter hemorrhage was noted on the first digit of the left hand, and a small right conjunctival hemorrhage was found. The neck was supple and lungs were clear. The heart sounds were irregular with a 2/6 systolic murmur at the lower left sternal border, and a 2/6 diastolic blowing murmur heard best at the upper left sternal border and radiating to the apex.

Examination of the abdomen was unremarkable except

for a spleen palpable 2 cm below the left costa! margin. Findings from neurologic examination were within nor-mal limits.

Laboratory tests showed hemoglobin levels of 10.4 g/

dL, leukocyte count 10,800/j.L with 43%

polymorpho-nuclear neutrophils, 40% band cells, 11% lymphocytes, and 6% monocytes; platelet count was 166,000/L. ESR was 55 mm for the first hour. Urinalysis findings were unremarkable. Findings from the chest roentg#{232}nogram revealed mild cardiomegaly with clear lung fields. The

ECG showed a junctional rhythm with frequent

prema-ture atrial contractions, left axis deviation, and right bundle branch block. Echocardiography showed mild sub-aortic stenosis with mild left ventricle hypertrophy. No vegetations were noted.

After five blood cultures were drawn, treatment with

intravenous (IV) nafcillin (200 mg/kg/d every four hours)

and amikacin (7.5 mg/kg/dose every eight hours) was

begun. Within 24 hours, the patient had become afebrile and regained his appetite. Each of the five blood cultures yielded f3-hemolytic streptococci. Serologic grouping

(Phadebact, Pharmacia) demonstrated the organism to

be Lancefield group C. Further characterization of the

organism indicated it to be Streptococcus equisimilia (con-firmed by Dr R. Facklam, Centers for Disease Control, Atlanta). By the tube dilution sensitivity test, this orga-nism was inhibited and killed by 0.015 g/mL of penicillin

G. No synergy between penicillin and amikacin could be demonstrated by tube dilution techniques. Antibiotics

were changed to penicillin (200,000 U/kg/d every six

hours), and the patient made an uneventful recovery with resolution of the enlarged spleen, the Janeway lesions,

and the splinter hemorrhages. There was no change in

the heart murmur. Ten days after the initiation of ther-apy, anti-streptococcal antibodies were found to be ele-vated (antistreptolysin 0 = 1,920 Todd units,

anti-DNAse B 1:960). The patient was discharged after 2 weeks ofIV penicillin to continue 1 week of oral penicillin V (500 mg every six hours). Follow up for 9 months failed to show recurrence of endocarditis.

DISCUSSION

Infections caused by group C streptococci are rare

in humans. In two series, only 0.6% to 0.7% of

streptococci isolated from blood cultures were group

C.’3”5 The only possible reason for this observation

might be misclassification of some group C

orga-nisms as group A if serologic studies are not done.

Both groups C and A are bacitracin-susceptible

f3-hemolytic streptococci.’#{176} Therefore, Lancefield

Se-rologic grouping of bacitracin-sensitive 3-hemolytic

streptococci should be carried out on isolates from

sterile body fluids.

Group C streptococci can colonize humans at a

number of sites including the nasopharynx,’6

um-bilicus,’7 and genital tract.’8 It is probable that the

portal of entry for the bacteria in our patient was

the mouth, following a dental procedure that was

apparently inadequately covered by oral penicillin.

These agents are common causes of infections in

animals and rarely cause human infections.’324

Streptococci belonging to group C are divided into

four species based on hemolytic ability and pattern

of sugar fermentation (Table). S equLsimilis is the

most common cause of infections in humans and is

the only species that elaborates streptokinase and

streptolysin 0. Therefore, some patients can

de-velop elevated antistreptolysin 0 titers.25

Of the 15 previously reported cases of

endocar-ditis due to group C streptococci, seven patients

died, and in three other cases, cardiac surgery was

necessary to avoid a catastrophic outcome. This

experience suggests that group C streptococcal

en-docarditis may pursue a virulent and destructive

course. By contrast, our patient had a mild course

and responded promptly to therapy with penicillin.

Penicillin appears to be the

drug

of choice. Most

TABLE. Hemolysis and Fermentation Patterns of Group C Streptococci

Subgroup Hemolysis Fe rmentation of Streptokinase and

Streptolysin 0 .

Trehalose Sorbitol Lactose

Streptococcus equisimilia f + - ± +

Streptococcus zooepidemicus fi - + ±

-Streptococcus equi fi - - -

-Streptococcus dysgalactiae a or none + ± ±

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I 16 PEDIATRICS Vol. 75 No. 1 January1985 reported group C streptococci strains from patients with endocarditis were highly sensitive to this an-tibiotic, with minimal inhibitory concentrations

(MICs) ranging from 0.16 to 1.0 g/mL. It is

im-portant to note that in one case a penicillin-tolerant

strain was isolated (MIC of 0.007 tg/mL and

mm-imal bactericidal concentration of 1.0 g/mL)6; this

strain demonstrated synergism between penicillin

and gentamicin. In contrast, the strain isolated

from our patient had a low MIC and minimal

bactericidal concentration (0.015 tg/mL), and no

penicillin-aminoglycoside synergism was

demon-strable in vitro. Because of the low minimal

bacte-ricidal concentration of the strain isolated from

this patient and his excellent clinical response, we

elected to treat him with only 2 weeks of IV

peni-cillin and to continue an additional week of oral

penicillin, although a 4-week course of therapy has

previously been recommended.’3 The successful

treatment of our patient with a shorter course of

therapy indicates that when in vitro studies

dem-onstrate exquisite sensitivity to penicillin, a short course of 2 weeks of treatment may be adequate.

PAUL GOLDBERG

STANFORD T. SHULMAN, MD

RAM YOGEV, MD

Department of Pediatrics

Northwestern University Medical School

The Children’s Memorial Hospital

Chicago

REFERENCES

1. Blair DC, Martin DB: Beta hemolytic streptococcal endo-carditis: Predominance of non-group A organisms. Am J Med Sci 1978;276:269-277

2. Ghoneim A, Cooke EM: Serious infection caused by group C streptococci. J Gun Pathol 1980;33:188-190

3. Davies MK, Ireland MA, Clarke DB: Infective endocarditis from group C streptococci causing stenosis of both the aortic and mitral valves. Thorax 1981;36:69-71

4. Lawrence MS, Cobbs CG: Endocarditis due to group C streptococci. South Med J 1972;65:487-489

5. Brown J, Savage D: Group C streptococcal endocarditis.

South Med J 1980;73:86

6. Portnoy D, Wink I, Richards GK, et al: Bacterial endocar-ditis due to a penicillin-tolerant group C streptococcus. CMA

J 1980;122:69-71

7. Finnegan P, Fitzgerald MXM, Cumming G, et al: Lancefield group C streptococcal endocarditis. Thorax 1974;29:245-247 8. Sanders V: Bacterial endocarditis due to group C beta

he-molytic streptococcus. Ann Intern Med 1963;58:858-861 9. Rosenthal AH, Stone FM: Puerperal infection with

vegeta-tive endocarditis: Report of sulfanilamide therapy in two fatal cases due to streptococcus haemolyticus groups B and C. JAMA 1940;114:840-843

10. Feingold DS, Stagg NL, Kunz U: Extrarespiratory strep-tococcal infections. N Engi J Med 1966;275:356-361

11. Bullock JD, Cruz MG, Rabin ER, et al: A fatal case of group C streptococcal endocarditis: A case report. Mo Med

1970;67:595-598

12. Karchmer AW, Moellering RC Jr, Maki DG, et al: Single-antibiotic therapy for streptococcal endocarditis. JAMA

1979;241:1801-1806

13. Mohr DN, Feist DJ, Washington JA II, et al: Infections due to group C streptococci in man. Am J Med 1979;66:450-456 14. Cherubin CE, Neu HC: Infective endocarditis at the

Pres-byterian Hospital in New York City from 1938-1967. Am J Med 1971;51:83-96

15. Duma RI, Weinberg AN, Medrek TF, et al: Streptococcal infections: A bacteriologic and clinical study of streptococcal bacteremia. Medicine 1969;48:87-127

16. Hare R: The classification of haemolytic streptococci from the nose and throat of normal human beings by means of precipitin and biochemical tests. J Pathol 1935;41:499-512 17. Drusin LM, Ribble JC, Topf B: Group C steptococcal

cob-fixation in a newborn nursery. Am J Dis Child 1973; 125:820-821

18. Christensen KK, Christensen P, Flamholc L, et al: Frequen-cies of streptococci of groups A, B, C, D, and G in urethra and cervix swab specimens from patients with suspected gonococcal infection. Acta Pathol Microbiol Scand (B)

1974;82:470-474

19. Stewardson-Krieger P, Gotoff SP: Neonatal meningitis due to group C beta hemobytic streptococcus. J Pediatr

1977;90:103-104

20. Fulginiti VA, Ey JL, Ryan KJ: Recurrent group C strepto-coccal tonsillitis in an adolescent male requiring tonsillec-tomy. Gun Pediatr 1980;19:829-830

21. Schwartz RH, Knerr RJ, Hermansen K, et al: Acute epi-glottitis caused by -hemolytic group C streptococci. Am J Dis Child 1982;136:558-559

22. Noble JT, McGowan K: Group C streptococcal pneumonia in an adolescent. Am J Dis Child 1983;137:1023

23. K#{246}hler W, Cederberg A: Streptococcus zooepidemicus as a cause of human infection. Scand J Infect Dis 1976;8:217-218

24. Duca E, Teodorovici G, Radu C, et al: A new nephritogenic streptococcus. J Hyg 1969;67:691-698

25. Benjamin JT, Perriello VA Jr: Pharyngitis due to group C hemolytic streptococci in children. J Pediatr 1976;89:254-256

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1985;75;114

Pediatrics

PAUL GOLDBERG, STANFORD T. SHULMAN and RAM YOGEV