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The American Jo urnal of Fo rensic Medicine and Pa thology 22(2):177–179, 2001. ©2001 Lippincott Williams & Wilkins, Inc., Philadelphia

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Bacterial infection with Clostridium perfringens in chil-dren less than 2 years of age is frequently associatedwith meningitis, necrotizing gastrointestinal infection,and postoperative infections. However, a review of theliterature reveals no reports of these bacteria infectingthe tonsils. A 9-month old black female was found unre-sponsive at the baby-sitter’s and was rushed to the hos-pital. Shortly after admission to the emergency depart-ment death was pronounced. An autopsy performed onthis otherwise healthy infant revealed shock and acutenecrotizing bacterial tonsillitis. The initial report of thisinfant’s death was questionable sudden infant death syn-drome and questionable smothering. Postmortem cere-brospinal uid, blood, and lung cultures grew purecolonies of C. perfringens . The necrotizing tonsil re-vealed no signicant gross lesions. Microscopically,large numbers of gram-positive rods were easily recog-nized and were compatible with C. perfringens . Becausethe oropharynx is a common portal of entry for infec-tious agents, it is essential to sample tissues of

Waldeyer’s ring and especially the tonsils to nd infec-tious diseases that may become systemic.Key Words: Bacterial tonsillitis— Clostridium perfrin-gens —Sudden infant death syndrome.

Clostridia species are gram-positive, anaerobic,spore-forming bacilli with a wide distribution innature. These bacteria can cause disease by invad-ing tissues and can arise from exogenous or en-

dogenous sources or from the secretion of toxins bythe bacteria. Clostridium perfringens causes foodpoisoning but is also frequently implicated in post-operative infections, especially meningitis, subduralempyema, and neonatal necrotizing enterocolitis.Whether from food poisoning or postoperative in-fection, C. perfringens causes acute illness with se-vere pain and the rapid development of hypotensionand shock (1,2).

This article presents a case study of a 9-month oldinfant with acute necrotizing tonsillitis caused by C.

perfringens . Such a case has not been previously re-ported in the literature. Acute tonsillitis due to C.

perfringens is reportedly rare but may be more com-mon if the oropharyngeal tissues in the neonate andinfant 1 year of age or less are routinely sampled.

CASE REPORT

KG was a 9-month old infant who had a patternof sleeping through the night. She had up-to-dateimmunizations, was eating and drinking normally,and was developmentally on target. The child hadno history of any illnesses, including vomiting, di-arrhea, bloody stools, or respiratory illness.

KG’s mother was scheduled to work two shiftsand took KG to her sister for care during this time.She left KG at this home at 07:30 on the day inquestion and returned 16 hours later.

KG’s mother entered the home and found her sis-ter asleep on a sofa, with KG between her sisterand the back of the sofa. The mother saw that thechild was blue and unresponsive and immediatelycalled 911. Emergency medical technicians foundthe child pulseless and in asystole; however, withresuscitation a pulse was regained.

Acute Necrotizing Bacterial Tonsillitis

With Clostridium perfringens

John E. Gerber, M.D.

Manuscript received March 22, 2000; accepted August 21,2000.

From Forensic Medical, Metropolitan Davidson County,Nashville, Tennessee, U.S.A.

Presented at the National Association of Medical Examiners,Minneapolis, Minnesota, October 16, 1999.

Address correspondence to John E. Gerber, M.D., ForensicMedical, 84 Hermitage Avenue, Nashville, TN 37210, U.S.A.


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KG was taken to Vanderbilt University Chil-dren’s Hospital, where her temperature was 95.6° F.She was admitted and, despite optimal intensivecare, was pronounced dead about 18 hours after911 was dialed.

Following the death of KG, a pediatrician at Van-derbilt Medical Center called the Medical Exam-iner’s ofce and notied the staff of a death thatwas presumed to be caused by positional asphyxia.

Postmortem Examination

Postmortem examination revealed marked pleth-ora with mottling of the skin. There was alsoanasarca. The well-developed 9-month old had nocongenital anomalies and no external or internaltrauma. In addition, there were no petechial hemor-rhages. However, internally there were bilateralpleural effusions of port wine liquid with 100 cc ineach pleural cavity as well as 275 cc of similar uidin the peritoneal cavity. There was a gray duskinessto the maroon appearance of all the organs. In ad-dition, there was generalized lymphadenopathy.Pink liquid was in the small and large intestine, andreddish mucus was in the rectum. There was alsomarked cerebral edema, with a brain weight of 810g (normal, 750 g). Microbiologic postmortem cul-tures of blood, cerebrospinal uid, and lung allgrew pure colonies of C. perfringens bacteria.

Microscopically there was fulminant pulmonaryedema as well as an exudate of red cells into thealveolar spaces. A minimal inammatory inltrate

was also present. A section of tonsil revealed a

necrotizing process with destruction of tonsillar tis-sue and many rod-shaped structures in the paren-chyma. Red cells, neutrophils, and mononuclear in-ammatory cells were also present (Fig. 1). A Gramstain revealed innumerable gram-positive rods, con-sistent with clostridial organisms (Fig. 2).

DISCUSSION

Clostridial bacterial infections or gas gangrenecomplications are well known as complications fromtrauma or surgical procedures. They have been as-sociated with casualties of war, motor vehicle acci-dents, and industrial trauma and in association withneurosurgery, abdominal surgery, or intravenousdrug abuse. However, nontraumatic clostridial in-fection is less commonly associated with specicunderlying disease processes, such as gastrointesti-nal and hematologic malignancies, peripheral vas-cular diseases, and diabetes mellitus, as well as im-munodeciency diseases (3).

A variety of toxins are released from clostridialspecies. At least 17 toxins are produced from C. per-

fringens , the most important of which is an alphatoxin, a lecithinase called phospholipase C, whichcauses the following: lysis of cell membranes, acuterenal failure, and disseminated intravascular coagu-lation. Furthermore, a hyaluronidase called muroxinis synthesized and directly acts on connective tissueto facilitate the spread of infection (1).

Bacterial infection with C. perfringens in chil-

dren less than 2 years is frequently associated with

178 J. E. GERBER

FIG. 1. Low-power ( 10)of tonsil with acute necro-tizing process.


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meningitis, necrotizing gastrointestinal infection,and postoperative infections. However, a review of the literature reveals no reports of these bacteria in-fecting the tonsils (4,5). This could possibly repre-sent the fact that many general and forensic pathol-ogists do not routinely sample tissue fromWaldeyer’s ring in the oropharynx, which includesthe tonsils. During the autopsy in the case under

discussion, the tonsils revealed no gross evidenceof necrosis. It was only because it is this patholo-gist’s routine procedure to sample Waldeyer’s ringin all unexplained infant deaths that C. perfringenswas found.

C. perfringens can easily incubate in spoiledfood in a home setting, and a child could quite sim-ply get access to such food or be fed food that isbeginning to spoil (6,7). This bacterium could ef-fortlessly enter via the oropharynx, which is thepresumed route of entry in the case under discus-sion. Because the oropharynx is a common portalof entry for infectious agents, it is essential to sam-

ple tissues of Waldeyer’s ring and especially thetonsils to nd infectious diseases that may becomesystemic. It could also be another way to be morespecic in identifying childhood diseases that couldbe either grouped in the sudden infant death syn-drome or others of unknown etiology (8,9).

When a hospital or forensic pathologist is pre-sented with a sudden unexpected infant death, rou-

tine sampling of lymphoid tissue from the orophar-ynx is highly recommended.

Acknowledgments: The author thanks Sherry Lewisand Diane Eigsti-Gerber for reviewing and editing thisarticle.

REFERENCES

1. Fmigold SM, George WL. Miscellaneous clostridial infec-tions. In Balows A, Hausler WJ, Lennette EH. Laboratorydiagnosis of infectious diseases, vol 1. New York: Springer-Verlag, 1988:193–201.

2. Burke MP, Opeskin K. Nontraumatic clostridial myonecro-sis. Am J Forensic Med Pathol 1999;20:158–62.

3. Caya JG, Truant AL. Clostridial bacteremia in the non-in-fant pediatric population: a report of two cases and reviewof the literature . Pediatr Infect Dis J 1999;18:291–8.

4. Brook I. Clostridial infection in children. J Med Microbiol1995;42:78–82.

5. Ahtonen P, Lehtonen OP, Kero P, et al. Clostridium perfrin-gens in stool, intra-partum antibiotics and gastrointestinalsigns in a neonatal intensive care unit. Acta Paediatr 1994;83:389–90.

6. Meer RR, Songer JG, Park DL. Human disease associatedwith Clostridium perfringens enterotoxin. Rev Environ Con-tam Toxicol 1997;150:75–94.

7. Lindsay JA. Clostridium perfringens type A enterotoxin(CPE): more than just explosive diarrhea. Crit Rev Micro-biol 1996;22:257–77.

8. Murrell TJ, Murrell WG, Lindsay JA. Sudden infant deathsyndrome (SIDS): are common bacterial toxins responsible,and do they have a vaccine potential? Vaccine 1994;12:365–8.

9. Murrell WG, Stewart BJ, O’Neil C, et al. Enterotoxigenicbacteria in the sudden infant death syndrome. J Med Micro-biol 1993;39:114–27.

ACUTE NECROTIZING BACTERIAL TONSILLITIS 179

FIG. 2. High-power ( 40)of tonsil with neutrophilsand rod-shaped bacteria.

acute necrotizing bacterial tonsillitis with.13

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