Toxic shock syndrome

Postinfluenza Toxic Shock Syndrome (*1)

In 1978, toxic shock syndrome (TSS) was described as a multisystem illness capable of producing fever, hypotension, and rash, with eventual desquamation. [1] The syndrome was later associated with exotoxin-producing Staphyococcus aureus infection usually occurring in women in relation to tampon use. However, non-menstrual TSS has occurred in a variety of other clinical sitations, including respiratory tract infections. There are three reports [2-4] documenting 11 cases in which an influenzalike illness was followed by S aureus respiratory tract infection complicated by TSS. These recently published accounts raise speculation that a syndrome of postinfluenza TSS may be emerging. [4] The following report presents the clinical features of such a case and highlights the importance of respiratory tract involvement in toxic shock syndrome.

CASE REPORT

A 19-year-old man with a four-day history of nonproductive cough, sore throat, and nasal congestion presented with acute deterioration characterized by a productive cough, dyspnea, diarrhea, myalgias, and disorientation. Physical examination revealed an erythematous macular rash over the extremities, chest, and abdomen; pharyngeal erythema with a strawberry tongue; bilateral conjunctival injection; blood pressure 90/50 mm Hg, pulse 150, respirations 30, and temperature 40.6[degrees]C. The abnormal laboratory values included a white blood cell count of 26,000/cu mm, proteinuria, calcium 7.5 mg/dL, creatinine 1.7 mg/dL, aspartate aminotransferase 84 U/L (10-37), alanine aminotransferase 72 U/L (12-39), lactate dehydrogenase 316 U/L (118-242), and creatine kinase 675 U/L (35-185). The arterial blood gas levels on room air demonstrated [Po.sub.2], 44 mm Hg; [Pco.sub.2], 25 mm Hg; and pH, 7.53. The chest x-ray film showed a faint right lower lobe infiltrate (Fig 1) and minimal changes in the left lower lobe. Results of blood, CSF, urine, stool, and throat cultures were negative; purulent sputum produced a pure growth of penicillin-resistent S aureus. Serologic studies were negative for Mycoplasma, Legionella, psittacosis, Rocky Mountain spotted fever, cytomegalovirus, adenovirus, influenza A and C, and parainfluenza. Antiobidies to influenza B were present acutely at a titer of 1:128.

The patient was admitted to the intensive care unit and started on therapy with erythromcyin and nafcillin. He was adequately oxygenated on 50 percent oxygen concentration delivered by face mask and received intravenous fluids, keeping his systolic blood pressure above 100 mm Hg. The symptoms and physical findings showed improvement within four days, and normalization of the laboratory data and chest x-ray film was seen by day 10 of hospitalization. Desquamation of skin over the palms and soles occurred during recovery, appearing most prominently on the sole (Fig. 2). He was discharged in good health on day 12.

DISCUSSION

There is no diagnostic test for toxic shock syndrome. Case definition requires the presence of specific clinical manifestations. The Centers for Disease Control criteria [5,6] include fever, diffuse erythorderma with subsequent desquamation, hypotension, and multisystem involvement. Additionally, blood, throat, and cerebrospinal fluid cultures, as well as serologic studies for Rocky Mountain spotted fever, leptospirosis, and rubeola should be negative if obtained. Positive TSS toxin assays are not necessary for diagnosis. This case fulfills these criteria, including laboratory documentations of systemic illness with elevated creatinine, aspartate aminotransferase, alanine aminotransferase, creatine kinase and thrombocytopenia.

Combining data from this patient and the 11 previously reported cases [2-4] of postinfluenza TSS reveals the following points. The age range was five to 56 years (mean 24) with six males and six females. All had respiratory symptoms and eight of ten had evidence of pneumonia on chest x-ray examination. Two died before hospitalization with no prior chest x-ray examination and their autopsy findings demonstrated tracheitis without pneumonia. [3] Therefore, eight of 12 (67 percent) had evidence of pneumonia. five of five tested had positive cultures or serologies for influenza B. Positive S aureus sputum cultures were seen in 11/11 as a result of purulent tracheitis or pneumonitis. Nine of nine yielded positive TSS toxin assays for either toxin-1 or enterotoxin B. Desquamation, which is an unnecessary criterion for a confirmed case of TSS if the patient dies within two weeks, occurred in seven of 12 (58 percent). The patients who did not display desquamation had died early in their clinical course, so that their findings may not yet have developed. Specific therapeutic regimens were described in four of 12; all of these received antistaphylococcal antibiotics and three of four survived. Overall, fatal outcome was reported in six (50 percent).

These cases appear to define a new syndrome of postinfluenza TSS, although the recognition of this entity may have its origins in antiquity. In fact, before the first such case was reported, Langmuir et al [7,8] theorized that the historic plague of Athens which began in 430 BC was due to toxin-producing S aureus during an influenza epidemic. These authors have suggested the term "Thucydides syndrome" for this disease process in honor of the Athenian general, Thucydides, who documented the effects of the illness extensively. It is of interest that the change or reappearance of bacterial strains and their association with toxic syndromes is not unique to S aureus; rather, this phenomenon has been described most recently with group A streptococcal infections as well. [9,10]

The association of postinfluenza TSS with only influenza B outbreaks may be coincidence. However, this complication of influenza B has now been reported from four geographically separate locations during two different flu seasons and has not been recognized in association with influenza A or other viral illness. Despite the observation that influenza B outbreaks result in milder disease than those caused by influenza A, it appears that the complication of TSS is being seen exclusively with influenza B to date.

Although TSS is an uncommon complication of influenza, a watchful attitude during the influenza season is warranted, perhaps especially when influenza B is prevalent. TSS should be considered in the differential diagnosis of individuals who become critically ill following an initial influenzalike illness, since specific therapy for proven, or unproven but presumed S aureus, may yield a favorable outcome in this highly lethal syndrome.

REFERENCES

[1] Todd J, Fishaut M, Kapral F, Welch T. Toxic-shock syndrome associated with phage-group-I staphylococci. Lancet 1978; 2:1116-18

[2] Wilkins EGL, Nye F, Roberts C, de Saxe M. Probable toxic shock syndrome with primary staphylococcal pneumonia. J Infect 1985; 11:231-32

[3] MacDonald KL, Osterholm MT, Hedberg CW, Schrock CG, Peterson CF, Jentzen JM, et al. Toxic shock syndrome: a newly recognized complication of influenza and influenzalike illness. JAMA 1987; 257;1053-58

[4] Sperber SJ, Francis JB. Toxic shocks syndrome during an influenza outbreak. JAMA 1987; 257:1086-87

[5] Reingold AL, Hargrett NT, Shands KN, Dan BB, Schmid GP, Strickland BY, et al. Toxic shock syndrome surveillance in the United States, 1980 to 1981. Ann Intern Med 1982; 96:875-80

[6] Smith CB, Jacobson JA. Toxic shock syndrome. Disease-a-Month 1986; 32:77-118

[7] Langmuir AD, Worthen TD, Solomon J, Ray CG, Petersen E. The Thucydides syndrome: A new hypothesis for the cause of the plague of Athens. N Engl J Med 1985; 313:1027-30

[8] Langmuir AD, Worthen TD, Solomon J, Ray CG, Petersen E. Reply to Mr. Holladay. N Engl J Med 1986; 315:1172-73

[9] Cone LA, Woodard Dr, Schlievert PM, Tomory GS. Clinical and bacteriologic observations of a toxic shock-like syndrome due to Streptococcus pyogenes. N Engl J Med 1987; 317:146-49

[10] Bartter T, Dascal A, Carroll K, Curley FJ. "Toxic strep syndrome:" A manifestation of group A streptococcal infection. Arch Intern Med 1988; 148:1421-24

(*1) From the United States Air Force Academy Hospital, Colorado Springs, Colorado.

COPYRIGHT 1989 American College of Chest Physicians
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