ACADEMIC EMERGENCY MEDICINE • February 2000, Volume 7, Number 2 169

CLINICAL PRACTICE

Clinicopathological Conference:Multisystem Failure in a Child

LISA CHAN, MD, BRIAN CHINNOCK, MD

RESIDENT CASE PRESENTATION

A 7-year-old Filipino-American female presented tothe emergency department (ED) with a five-dayhistory of lethargy, which began after a day ofswimming. Four days prior to presentation, the pa-tient had a fever to 1027F and abdominal pain. Theparents noted ‘‘big lymph nodes’’ in her neck aswell. Three days prior to presentation, the patientwas seen in an ED and treated for presumptivepharyngitis with amoxicillin and ibuprofen; laterthat day, a truncal rash developed. On the day ofpresentation, the patient complained of continuedfever, lethargy, anorexia, rash, and abdominalpain. She reported three days of emesis and waterydiarrhea three times per day; she denied chestpain or cough. There was no past medical or sur-gical history. The family denied recent travel orhistory of tick bites.

On examination, the patient was in moderatedistress. The blood pressure was 68/26 mm Hg.The heart rate was 140 beats/min. Body tempera-ture was 103.37F. Room-air pulse oximetry was98%. The head, eyes, ears, nose, and throat(HEENT) exam demonstrated bilateral scleral ic-terus and injection, a ‘‘strawberry’’ tongue, fissuredlips, and very dry oral mucosa. On neck exam,there were large, symmetric, mobile, tender sub-mandibular nodes. Heart rate was regular, with nomurmurs or gallop. Lungs were clear to ausculta-tion bilaterally. The abdomen was diffusely tender,but soft. Rectal exam was significant for guaiac-positive stool, but no frank blood. On pelvic exam,there was vaginal hyperemia without vaginal dis-charge. The skin exam showed a macular, ery-

From the Department of Emergency Medicine, University ofArizona at Tucson, Tucson, AZ (LC); and the Department ofEmergency Medicine, UCSF Fresno, Fresno, CA (BC). Dr.Chinnock is now at Texas Tech University Health SciencesCenter, El Paso.Received June 15, 1999; revision received September 21, 1999;accepted October 21, 1999. Presented at the 1999 CPC Com-petition, Boston, MA, May 1999.Section editors: Andy Jagoda, MD, Mt. Sinai School of Medi-cine, New York, NY; and Joseph LaMantia, MD, North ShoreUniversity Hospital, Manhasset, NY.Address for correspondence and reprints: Lisa Chan, MD, 1501North Campbell, PO Box 245057, Tucson, AZ 85724-5057. Fax:520-626-2480; e-mail: lisac8@dakotacom.netA related commentary appears on page 192.

thematous, nonvesicular rash seen mainly acrossthe area covered by the patient’s underpants. Thepalms of the hands were noted to be edematous.

Laboratory testing included electrolytes, with asodium of 129 mEq/L, potassium of 3.6 mEq/L,chloride of 94 mEq/L, and CO2 of 14 mEq/L. Glu-cose was 106 mg/dL, BUN was 91 mg/dL, and cre-atinine was 4.8 mg/dL. White blood cell (WBC)count was 14.2 3 109/L, with 45% segmented neu-trophils and 47% band forms. Hemoglobin was11.6 g/dL and platelets 238 3 109/L. Prothrombintime was elevated at 14.5 sec, with a normal par-tial thromboplastin time. Total bilirubin was 5.3mg/dL; indirect bilirubin was 0.1 mg/dL. The ASTwas 116 IU/L and the ALT 137 IU/L. Amylase wasnormal. Calcium was low at 7.9 mg/dL, with a nor-mal total protein. Urinalysis showed 5–10 WBCs/hpf, with no bacteria or red blood cells. The chestx-ray demonstrated a slightly enlarged cardiac sil-houette with no other abnormalities. The electro-cardiogram showed a sinus tachycardia with non-specific ST–T changes. The abdominal ultrasoundexam was significant for gallbladder and bowelwall edema, no abscess, and a normal appendix.The echocardiogram showed normal ventricularfunction, wall motion, and valve function.

FACULTY DISCUSSION

This 7-year-old Filipino-American female was crit-ically ill with multisystem dysfunction involvingthe cardiovascular, renal, and gastrointestinal sys-tems. Many constitutional symptoms and derma-tologic findings also characterized the illness. Thecardiovascular compromise necessitated immedi-ate resuscitative measures and supportive care, in-cluding intravenous access, pressure support, andcontinuous monitoring. The acute onset of the pa-tient’s signs and symptoms with fever suggestedan infectious etiology. Consequently, a sepsis eval-uation including complete blood count, urinalysis,cultures, plain chest radiography, and initiation ofbroad-spectrum antibiotics was indicated.

Once the patient is stabilized, it is possible todevelop a differential diagnosis that includes con-ditions that cause fever and multisystem dysfunc-tion with cardiovascular collapse. The character-istic skin and mucosal membrane findings mustalso be accounted for. There are five major diag-

170 MULTISYSTEM FAILURE Chan, Chinnock • CPC: MULTISYSTEM FAILURE

TABLE 1. Conditions Manifesting as Fever, MultisystemDysfunction, Cardiovascular Collapse, and Rash in a HealthyChild

Toxic shock syndromeKawasaki diseaseIcteric leptospirosisSevere or septic scarlet feverInfectious mononucleosis

TABLE 2. Clinical Manifestations of Toxic Shock Syndromeand Kawasaki Disease

Toxic Shock Syndrome Kawasaki Disease

Skin and mucosal membranes• Sore throat/tonsillar

hypertrophy• Rash• Strawberry tongue• Fissuring of lips• Conjunctival injection• Vaginal erythema

Cardiovascular system• Hypotension• Tachycardia

Renal• Acute renal failure• Mild pyuria without

bacteriuria

Gastrointestinal system• Abdominal pain• Anorexia• Watery emesis• Jaundice• Elevated liver function tests• Mild hypercoagulability• Gallbladder edema• Bowel wall edema• Hemoculture-positive

Other• Adenopathy• Fever• Fatigue• Peripheral edema• Hyponatremia• Leukocytosis with left shift• Mild anemia• Acidemia

Skin and mucosalmembranes• Sore throat• Rash• Strawberry tongue• Fissuring of lips• Conjunctival injection

Cardiovascular system• Hypotension• Tachycardia

Renal acute renal failure• Mild pyuria without

bacturia

Gastrointestinal system• Abdominal pain• Anorexia• Emesis• Jaundice• Elevated liver function

tests• Mild hypercoagulability• Gallbladder edema• Bowel wall edema• Hemoculture-positive

Other• Adenopathy• Fever• Fatigue• Peripheral edema• Hyponatremia• Leukocytosis without

left shift• Mild anemia• Acidemia

noses that could explain this case scenario (Ta-ble 1).

Toxic shock syndrome (TSS) is a severe, life-threatening syndrome that has been directly as-sociated with toxin-producing Staphylococcus au-reus and Streptococcus pyogenes. The term ‘‘toxicshock-like syndrome’’ is used when S. pyogenes isthe etiologic organism.1,2 The clinical findings instaphylococcal and streptococcal TSS are virtuallyidentical, with the major difference being thatstreptococcal TSS usually develops from a soft-tis-sue infection such as necrotizing fasciitis or cellu-litis.1–3

Toxic shock syndrome could explain many of thecutaneous and mucosal findings described in thispatient. Her sore throat with tonsillar hypertro-phy, strawberry tongue, fissured lips, conjunctivalinjection, vaginal erythema, and rash are all char-acteristic features. The rash described in both var-iants of TSS is a diffuse macular erythroderma.1–3

Table 2 presents the clinical manifestations ofTSS, most of which are present in this patient.However, several clinical features of TSS are notpresent, including dysrhythmias or heart block,pulmonary edema, profuse diarrhea, headache,intermittent confusion without focal neurologicsigns, myalgias, arthralgias, desquamation, andthrombocytopenia or thrombocytosis. Of note, des-quamation usually occurs 6 to 14 days after theonset of the illness and therefore would not be ex-pected at the time this patient presented.1–3

Kawasaki disease (KD) is a generalized vascu-litis of the small and medium arteries.4 It couldalso explain most of the patient’s symptoms (Table2). Kawasaki disease can cause leukocytosis witha left shift and mild anemia, as seen in this pa-tient. However, it usually does not cause renal fail-ure or cardiovascular collapse. The rash of KD ispolymorphous, most commonly noted as irregular,nonpruritic erythematous plaques or morbilliform.Less commonly, the skin manifestation may be ascarlitiniform rash, erythema marginatum, or pus-tules. Erythema of the perineum, which evolvesinto desquamation within 48 hours, has also beenreported.5,6 As with TSS, desquamation occurs latein KD, i.e., during the second and third weeks ofillness; thus, this patient may have presented tooearly in the course of the disease for it to havemanifested.5–7 Other clinical manifestations ofKD that were not present in this patient are car-

diac disease, irritability, lethargy, myalgias, throm-bocytosis, and proteinuria. Reported cardiac ab-normalities in KD include pericardial effusions,myocarditis, congestive heart failure, dysrhyth-mias, valvular disease, and coronary artery le-sions. Although the patient’s chest radiographshowed cardiomegaly, the echocardiogram wasnormal.

Icteric leptospirosis (Weil’s disease) is a life-threatening, multisystem infection that is causedby a spirochete of the genus Leptospira. The rat isthe primary reservoir that affects humans. Afterthe spirochetes infect a rat, they are excreted inthe urine. Humans then become infected whenthey come into contact with contaminated soil orwater. The spirochetes damage the endothelialcells of blood vessels, causing end-organ ischemia,which results in multisystem dysfunction.8,9 Theclinical manifestations of leptospirosis occur in twophases. The first is the septicemic phase, duringwhich multiple systems can be affected (Table 3).8,9

The second phase, the immune phase, involves he-patic dysfunction, renal dysfunction, hemorrhage,and cardiovascular collapse. The patient with lep-

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TABLE 3. Clinical Manifestations of Icteric Leptospirosis

Septicemic phaseCardiac: Bradycardia and hypotension; carditisPulmonary: PneumonitisGastrointestinal: Nausea, vomiting, hepatosplenomegalyNeurologic: Headache, lethargy, intermittent confusion with-

out focal neurologic signsMusculoskeletal: Severe myalgiaSkin, mucous membranes: Conjunctival suffusion; truncal

erythematous maculopapular rash; pharyngitisOther: Fever, chills, malaise, generalized lymphadenopathy,

dehydration

Immune phaseHepatic dysfunction: Right upper quadrant pain, hepato-

megaly, hyperbilirubinemia, modest elevation of liver en-zymes

Renal dysfunction: Hematuria, proteinuria, casts, azotemia,oliguria or anuria

Hemorrhage: Epistaxis, hemoptysis, gastrointestinal and ad-renal bleeding

Cardiovascular collapse

tospirosis may have right upper quadrant pain sec-ondary to hepatomegaly, and high serum bilirubinand liver enzymes. Renal damage may result inazotemia, oliguria, or anuria, with blood, protein,or casts found in the urine.8,9 Icteric leptospiro-sis could explain many of the clinical feature seenin this patient; however, leptospirosis generallycauses altered mental status, headache, and se-vere, debilitating myalgias, which were not re-ported.

Septic scarlet fever (SSF) is caused by S. py-ogenes, though cases caused by S. aureus havebeen reported.2,8,9 Septic scarlet fever can explainsome of the skin and mucosal findings seen in thispatient, such as the strawberry tongue, pharyngi-tis, and rash. When scarlet fever is caused bystreptococcus, the rash is erythematous, finelypunctate, and classically described as being likesand paper. When staphylococcus is the cause, therash is less punctate.9 Fissuring of lips and con-junctival injection are usually not seen in scarletfever. Septic scarlet fever can cause shock andother findings manifested in this patient. However,it usually does not cause renal or liver failure.2,8,9

Clinical findings reported in SSF that were notpresent in this patient are headache, an erythem-atous, finely punctate rash, arthritis, and circum-oral pallor.

Infectious mononucleosis is caused by the Ep-stein-Barr virus (EBV). Clinical findings seen inthis patient that are also reported in mononucleo-sis include pharyngitis, rash, tachycardia, abdom-inal pain, anorexia, watery emesis, jaundice,elevated liver function, adenopathy, fever, andfatigue. However, mononucleosis is often associ-ated with headache, myalgias, hepatomegaly, sple-nomegaly, and atypical lymphocytosis, none ofwhich was reported.10

With the above differential diagnosis in mind,management of this case required continued sup-portive care combined with further diagnostic test-ing. Leptosporosis is diagnosed by isolation of thespirochete or determination of antibody titers inthe blood or urine. Spirochetes can also be recov-ered from the cerebrospinal fluid.8 Although re-sults do not return during the ED stay, a blood orurine sample should be sent for these studies. Athroat culture for streptococcus should also be per-formed, and a blood sample sent for anti-strepto-lysin O titer. In order to diagnose infectious mono-nucleosis, a blood sample should be sent to lookfor lymphocytosis and heterophil antibodies. A rel-ative and absolute lymphocytosis is seen in 39% to75% of patients, with 10% of the total lymphocyteshaving an atypical morphology. During the firstweek of illness, 70% of patients test positive forheterophil antibodies, whereas 85% to 90% testpositive by the third week of illness.10,11

Antibiotics are indicated in the treatment for

TSS, SSF, and leptospirosis. Consequently, itwould have been reasonable to initiate broad-spec-trum antibiotics early in the management of thiscase. Antibiotics have been shown to reduce therecurrence rate of TSS.1,2,8 The antibiotic of choicefor leptospirosis is penicillin G.3,8 The treatment ofKD is intravenous immunoglobulin and salicy-lates.6,7

In order to choose the most likely diagnosisfrom the differential diagnosis list, the patient’sclinical manifestations must be carefully reviewed.Since mononucleosis does not usually result in car-diovascular collapse, renal failure, gastrointestinaledema, or the type of dermatologic manifestationsseen in our patient, it can be eliminated as themost likely diagnosis. Septic scarlet fever also usu-ally does not cause renal failure, gastrointestinaledema, or some of the skin and mucosal findingsseen in our patient; therefore, it also is most likelynot the diagnosis. Icteric leptospirosis would ex-plain the multisystem involvement; however, thepatient does not have the classic myalgia, nor doesleptospirosis present with the skin and mucosalfindings seen in this patient. This leaves TSS andKD as the two most likely culprits. Both can causethe characteristic skin and mucosal findings. Ta-bles 4 and 5 present the criteria necessary for thetwo diagnoses.3,8

This patient seems to fit the criteria for KD.However, one criterion necessary for the diagnosisis the absence of other illness that can account forthe patient’s medical condition. Because the pa-tient also meets the clinical diagnostic criterion forTSS, KD may be ruled out on that basis. The lab-oratory information needed as the fifth criterion ofTSS would not be available during the stay in theED because of the time needed to complete thetests and, therefore, cannot be commented on. In

172 MULTISYSTEM FAILURE Chan, Chinnock • CPC: MULTISYSTEM FAILURE

TABLE 4. Diagnostic Criteria for Kawasaki Disease

Fever

Illness not explained by other known disease process

Presence of a least 4 of the 5 conditions:1. Bilateral conjunctivitis2. Polymorphous rash3. Cervical lymphadenopathy4. Changes of extremities

• Erythema of palms and soles• Edema of hands and feet• Periungual desquamation

5. Changes of the lips and oral mucosa• Dry, red, fissured lips• Strawberry tongue• Oropharhyngeal edema

TABLE 5. Diagnostic Criteria for Toxic Shock Syndrome—All Must Be Present

Body temperature > 38.97C

Hypotension or syncope

Rash

Involvement of 3 of the following organ systems:• Gastrointestinal: Emesis, diarrhea• Musculoskeletal: Severe myalgias or twofold increase in cre-

atine phosphokinase• Mucosal inflammation: Vaginal, conjunctival, pharyngeal er-

ythema• Hepatic: Twofold increase in bilirubin, SGOT, SGPT• Hematologic: More than 100,000 platelets/mm3

• CNS: Disorientation without focal neurologic signs

Negative serologic tests for Rocky Mountain spotted fever, lep-tospirosis, measles, hepatitis B, surface antigen, fluorescentantinuclear antibody, VDRL, and monospot; and negativeblood, urine, and throat cultures

addition, since this patient does have renal failureand cardiovascular compromise, which are seen inTSS but not in KD, TSS is the most likely diag-nosis.

CASE OUTCOME

The patient was given three 20-mL/kg fluid bo-luses of lactated Ringer’s solution over the firsthour, with no improvement in blood pressure. Adopamine drip was begun concurrently with thelast fluid bolus, and was increased to 20 mg/kg/min,with little increase in blood pressure. The patient’sblood pressure finally normalized with the additionof an epinephrine drip. Early administration of an-tibiotics included ceftriaxone for the possibility ofmeningococcemia, oxacillin for the possibility ofTSS, and doxycycline for the possibility of RockyMountain spotted fever or leptospirosis.

After discussion with consultants, a dual diag-nosis of TSS and KD was made because case defi-nition criteria for both diseases were met.12,13 Thepatient was treated with high-dose aspirin andintravenous immunoglobulin (IVIG). Although

IVIG’s efficacy in preventing coronary artery an-eurysms in KD is well known, it may also have arole in the treatment of TSS.14,15 All commerciallyavailable preparations of IVIG have measurablelevels of antibody to TSST-1, the most commontoxin implicated in TSS.16 In addition, animal mod-els have shown IVIG to be protective against thetoxin effect, and there are anecdotal reports ofrapid clinical improvement in TSS patients treatedwith IVIG.17,18

Antibiotic coverage for S. aureus was continuedwith clindamycin, rather than oxacillin. Anecdotalreports and laboratory studies suggest that anti-biotics that inhibit cell wall synthesis, such aspenicillins or cephalosporins, may be inferior toantibiotics such as clindamycin that inhibit pro-tein synthesis.19,20 Inhibiting cell wall synthesisdoes not prevent continued exotoxin production,whereas clindamycin almost completely blocks pro-duction of TSST-1.21

The patient’s fever persisted for one more day,and the blood pressure remained labile. The pa-tient was finally weaned off pressor support afterthree days. Desquamating rash of the palms andsoles began on day 3 of hospitalization. Repeatechocardiography on day 14 of hospitalizationshowed no coronary artery aneurysms. Blood cul-tures (three) and throat, vaginal, and urine cul-tures were negative. Epstein-Barr virus, leptospi-rosis, and rickettsial titers were negative. Theantibody to TSST-1, which confers immunity to thetoxin’s effect, was not present. Although this pa-tient had no obvious risk factors for colonization,between 1% to 4% of healthy individuals withoutrisk factors harbor a TSST-1-producing strain of S.aureus at a cutaneous or mucosal site.16 Of note,neither the rectum nor the nasopharynx of this pa-tient was cultured.

RESIDENT DISCUSSION

The initial laboratory and physical exam findings,as well as the subsequent hospital course, made itdifficult to clearly differentiate whether the patienthad TSS, KD, or both. As stated previously, casedefinition criteria for each were met, and thus thepatient was treated for both diseases. There arethree case reports in the literature of pediatric pa-tients who fulfilled case criteria for both TSS andKD.22–24 In two cases, a 7-year-old and a 13-year-old were initially treated for TSS and later echo-cardiography demonstrated coronary artery aneu-rysms.22,23 In a third case, a 7-month-old infantpresented with symptoms and findings of TSS, andon autopsy was found to have coronary artery vas-culitis.24 An author of one of the case reports la-beled it as a case of ‘‘atypical Kawasaki disease,’’while another author, who reviewed all threecases, labeled them as examples of ‘‘simultaneous

ACADEMIC EMERGENCY MEDICINE • February 2000, Volume 7, Number 2 173

presentation of Kawasaki disease and toxic shocksyndrome.’’ 22,23

Indeed, there is an immunologic basis for bothdiseases to coexist in the same patient. In bothTSS and KD, widespread immune activation andsubsequent multiorgan dysfunction are caused byexpansion of the same specific T-cell group.25,26 InTSS, the agent that causes the immune activation,the superantigen, is most commonly the S. aureus-produced TSST-1.26 Kawasaki disease is also be-lieved to be triggered by a superantigen.25 Effortsto identify the KD superantigen, including at-tempts to implicate TSST-1 as the cause, have beenunrewarding.27,28 The importance of this to theemergency physician is to realize the blurred clin-ical and immunologic lines that separate these dis-eases. The possibility that TSS and KD may occursimultaneously makes it necessary to consider in-stituting treatment for both diseases in certaincase scenarios, as in the one presented.

As is noted above by the faculty discussant, onecriterion necessary for the diagnosis of KD is theabsence of other illness that can account for thepatient’s medical condition. This initially created adiagnostic and management dilemma. It was onlyafter careful consultation with the infectious dis-ease specialists and review of the literature that itwas determined that if a patient fits the criteriafor KD but also has renal or cardiovascular dys-function, as with our patient, KD should not beeliminated as a diagnosis. We think that this is animportant teaching point since the two diseases,KD and TSS, necessitate different treatments inorder to prevent complications. Our treatment ofthis patient with IVIG may have prevented thecoronary artery aneurysms that developed in thethree other patients with simultaneous presenta-tion of both diseases. In addition, if we had consid-ered this patient to simply have atypical KD, wemay have left untreated a toxin-producing strainof S. aureus.

Final diagnosis: concomitant toxic shock syndromeand Kawasaki disease.

Key words. Kawasaki disease; toxic shock syndrome;streptococcal infection; staphylococcal infection.

References

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