Jpn. J. Infect. Dis., 53, 2000

Laboratory and Epidemiology Communications
Fatal Rapidly Progresslng Streptococcal Tわxic Shock‑uke

Syndrome; Case Report
Miki Yokota*, Tadao Hasegawal , Michio Ohtal and Tatunari Satake
Nagoya Ekisaikai Hospital, Department of Clinicopathology,
Shonen‑cho 4‑66, Nakagawa‑ku, Nagoya 45410854 andlNagoya Uun iversiO, Graduate School of Medicine, Department ofMolecular Bacteriology,
Tsurumai‑cho 60, Showa‑ku, Nagoya 466‑8550, A ichi, Japan
Communicated by Hiroshi Yoshikura(Accepted May 26, 2000)

toxic shock‑like syndrome (Strep TSS) (1 ‑2). Cases of Strep

kinase 657 IU/1, blood urea nitrogen 38.5 mg/dl, creatinin
2.6 mg/dl, aspartate aminotransferase 57 IU/I, alanine
aminotransferase 29 IU/1, 1actate dehydrogenase 1245 IU/I.

TSS have been reported with increasing kequency in the pastHis extremities were cold and no obvious dermal manifesta‑

several years in Japan as well as in Europe and No仙Americations were seen. Chest X‑ray revealed mild infiltration in theright lower lobe. He had had 3 years ofmedical histories orThe clinical manifestationsof group A streptococcal infec‑
tion include pharyngltlS, scarlet fever, necrotizing fascitis, and(1, 3‑5).

A 58‑year‑Old man visited the emergency room of ourdiabetes mellitus and atrial fibrillation, and tricuspid valve

hospital at 8:00 p.m. complaining of cough, Sore throat, fever

replacement had been performed a year before. His conditionof 38oC, andjoint pain that had persisted over the previous3

deteriorated despite maximum inotropic support and he dieddays. Physical examination showed no remarkable slgnS andtwo‑and‑a‑half hours after admission. A large amount of blood
was sucked &om his endotracheal tube. Autopsy was performed

he was prescribed medication for a common cold. The next

immediately after death. MacroscopIC examination revealedmornlng at 6:00 a.m., he re山rned to the emergency room

bilateral pulmonary hemorrhage. All of the cardiac valves
including the implanted porcine valve were intact. A small

agaln COmPlainlng Of worsenlng Of general fatigue and hewas advised tovisit the out‑patient clinic of the hospital. Whilewaltlng f♭r examination, he gradually lost his consciousness

fresh clot was found inside the left pulmonary artery trunk.

and fell into a state of cardiopulmonary arrest.AsSoon as

At the time of dissection, Considering the clinical course andcardiopulmonary resuscitation was performed, he was admitted

the macroscopic findings, pulmonary embo)ism was a likely

to仇e intensive care unit. On admission, he was in deep coma

diagnosis. However, We were left feeling slightly skepticaland laboratory data after resuscitation were auollows; bodyof this diagnosis because the size of the clot was too smalltemperature 3 8.2oC, heart rate 1 42/min, blood pressure 1 00/60

and no clots were seen inside the other pulmonary artery trunk.

mm Hg, resplration rate 1 8/min, white blood cell count 2200/

HistologlCally, the pulmonary alveoli were filledwith exu‑Ill, hemoglobin 15. I g/dl, platelet 81000/LLl, total protein 6.8

date, the walls of which were almost intact except fわr mildg/dl, albumin 3.7 g/dl, C reactive protein 9.8 1 mg/dl, creatinin

hemorrhage. However, noinvasion of innammatory eel)s wasobserved. As the Figure shows, many bacteria‑like small*Co汀eSpOnding author: Fax +8 I ‑52‑652‑7783, E‑mail:YOmik

round cells were obseⅣed along the walls of the alveoli. Later

RAV@aol. com

those small cells were found to be gram‑positive cocci with81Jpn. J. Infect. Dis., 53, 2000
too rapid to glVerise to an inflammatory reaction in the lung.
The diagnosis was estabhshed only postmortem by bacterial

culture offrozen specimens. Some acute deaths with unknown
etiology may have been due to infection of this kind.

REFERENCE S
I. Stevens, D. L. (1999): The flesh‑eating bacterium: what's
next? J. Infect. Dis., 179 (Suppl. 2), S366‑S374.

2. Hoge, C. W., Schwartz, B., Talkington, D.F., Breiman,
R. F., MacNeill, E. M. and Englender, S. ∫. (1993): Thechanglng ePidemiology of invasive group A streptococcal
infectionsandthe emergence of streptococcal toxic shock‑1ike syndrome. JAMA 269, 384‑389.
3. Davies, H. D., McGeer, A., Schwartz, B., Green, K.,

Figure. Histology. Pulmonary alveoli were filled withexudateand largenumbers of gram‑positive cocci were observedalong the walls ofCann, D., Simor,A. E., Low, D. E. and the Ontario GroupA Streptococcal Study Group (1 996): Invasive group A

alveoli (Gram stain; × I,000)

streptococcal infections in Ontario, Canada. N. Engl. J.

Med., 335, 547‑554.

gram stain of the tissue. We then performed a culture of thefrozen‑serum stock of the patient. ARer 2 days of incubation,

4. Yoshitaka, S. (1997): Group A streptococcal toxic shock‑Streptococcus pyogenes was isolated at a high concentration.

like syndrome. Sogo Rinshou, 5, 1 578‑1582 (inJapanese).

This strain produced streptococcal pyr?genie exotoxin(Spe)

5. Kiska, D.し., Thiede, B., Caracciolo, ∫., Jordan, M.,

A, B, F, and Mtype 1 andT type I antlgenS.

Johnson, D., Kaplan, E. L., Grunlnger, R. P., Lohr, J. A.,

This case appeared tofulfillthe Centers for Disease Control
and Prevention (CDC) criteria of Strep TSS (6). However,Gillingan, P･ H･and Dermy･ F･ W., Jr･ (1997): Invasive gro.up
A streptococcal infectionsinNorthCarolina: epidem10‑logy, climical features, and genetic and serotype analysis
ofcausative organisms. J. Infect. Dis., 176, 992‑1000.

pulmonary hemorrhage withoutinflammatory reaction as seenin this case appears rare. The commonest respiratory tract

6. Working Group on Severe Streptcoccal Infections ( 1 993):

complication reported in the literahre was pneumonia (3).
Influenzallike symptoms were reported in 20% ( 1). Eighty

Definingthe group A streptococcal toxic shock syndrome;
rationale and consensus definition. JAMA, 269, 390‑39 1.

percent of the patients had climical signsof softtissueinfeCtion(I). Probably the progress of the disease in this patient was82