Case Report

Staphylococcal Toxic Shock Syndrome

M Kare*, A Dang**

Abstract
A 28 year old male presented with fever, tachycardia, generalized lymphadenopathy and diffuse rash over
the body. He failed to respond to intravenous antibiotics and developed cardiogenic shock, multiple organ
failure and died within six hours after hospitalization. Staphylococcus aureus colonies were revealed on blood
culture. ©

Introduction platelet concentrates were infused, dopamine infusion

rate was increased and patient was intubated. But he
S taphylococcal toxic shock syndrome (TSS) is a rare
and potentially fatal multi system dysfunction. The
syndrome occurs primarily due to TSS Toxin-1 (TSS-1)
failed to respond to the line of management and went
into cardiac arrest. Cardiopulmonary resuscitation was
given, but the patient could not be revived and was
elaborated by Staphylococcus aureus (S.aureus). It occurs
declared dead.
in diverse clinical settings, often mimicking common
febrile conditions. The diagnosis depends chiefly on Investigations revealed decreased white blood cell
high degree of clinical suspicion. Thus doctors should count [6000 cells/cmm (myelocytes-10%, stabs-30%,
be familiar with the manifestations of TSS and should neutrophils-36%, lymphocytes-4%, eosinophils-13%,
vigilantly consider the diagnosis in appropriate clinical monocytes-1%] and decreased platelet count (80,000/
setting, as delay in diagnosis and/or in institution of cmm). Blood urea nitrogen (BUN) and SGOT (aspartate
appropriate therapy may result in fatal outcome. aminotransferase) were raised [47 mg/dl and 327 IU/L
respectively]. Rest of the biochemical values were within
Case report normal limits. Urine examination revealed albumin-
A 28 year old male farmer presented to Emergency traces, granular casts-present, pus cells-5-6 per High
Room (ER) with moderate grade fever not associated Power Field (HPF), RBCs-1-2/HPF and epthelial cells-
with chills and rigors for five days and painful swelling 2-3/HPF. Both activated plasma thromboplastin time
of the left leg and right arm for three days. He also (APTT) and prothrombin time (PT) were raised, values
complained of diffuse rash, decreased urinary output, being 1 min 15 secs and 22 secs respectively. Chest
loose motions for two days and breathlessness for one X–ray showed minimal left sided pleural infusion.
day. On examination he was restless and had diffuse Staphylococcus aureus colonies sensitive to oxacillin,
erythematous blanching rash predominantly involving cefazolin and vancomycin were obtained on blood
the trunk and limbs. He had fever (103 oF), warm culture. Smear for malarial parasite (SMP), IgM dengue,
pitting soft tissue edema over left leg and right arm IgM leptospirosis and enzyme linked immuno sorbent
and bilaterally enlarged submandibular, axillary and assay (ELISA) for HIV were negative.
inguinal lymph nodes. Systemic examination revealed Post mortem report of inguinal lymph node and liver
heart rate – 120/min, blood pressure (BP) - 110/40 mm biopsy was inconclusive. Bone marrow examination
Hg, respiratory rate - 40/min with decreased air entry revealed marked myeloid hypercellularity and increase
in left axillary area. The patient was shifted to Intensive in the number of coarse azurophilic granules in the
Coronary Care Unit (ICCU) and treatment was started cytoplasm of myeloid precursors (toxic granules).
with intravenous fluids, ceftriaxone and continuous Staphylococcal toxic shock syndrome was considered
dopamine infusion. Within couple of hours patient had as the cause of death.
altered sensorium, worsening of breathlessness, bilateral
subconjunctival haemorrage and hypotension (BP - Discussion
60/30 mm Hg). Subsequently fresh frozen plasma and Staphylococcal toxic shock syndrome (TSS) was
first described by James Todd and colleagues in 1978
*Consultant, Department of Medicine; **PG Student, Dept. of
Pharmacology, Goa Medical College, Bambolim, Goa.
in children who presented with high fever, headache,
Received : 30.6.2006; Revised : 30.1.2007; confusion, conjunctival hyperemia, scarlatiniform rash,
Re-revised : 01.8.2007; Accepted : 29.12.2007 subcutaneous edema, vomiting, diarrhea, refractory

192 www.japi.org © JAPI  •  VOL. 56  •  MARCH 2008

hypotension, oliguria and acute renal failure. Later on Vbeta “signature”, analysis of which in  vivo during
several reports described this disease in menstruating TSS may facilitate the diagnosis. The test might be
females using tampons in United States. Subsequently impractical in the Indian scenario, henceforth the
there has been many reports of non-menstrual TSS in diagnosis of TSS should be made exclusively on clinical
adults as well as in children.1 grounds and isolation of S. aureus should be tried from
The disease does not show any racial, gender or age body fluids wherever indicated.
bias. The infection may occur in children, men, and non- Case definition of Staphylococcal TSS developed
menstruating women who have undergone surgery2 or by the Centers for Disease Control and Prevention 6
are immunocompromised in some way. includes major criteria, where all 4 conditions must be
TSS is considered to be a superantigen-mediated met i.e. fever: temperature >38.9°C (102°F), rash: diffuse
disease where S. aureus toxins act as superantigens. macular erythroderma, desquamation: 1 to 2 weeks after
These superantigens lead to a massive release of onset of illness, particularly of palms and soles and
cytokines including tumor necrosis factor alpha lastly hypotension: systolic BP <90 mm Hg for adults
(TNF-alpha), interleukin-1 (IL-1) and IL-6 which are or <5th percentile by age for children <16 yr of age or
responsible for a capillary leak syndrome leading to orthostatic syncope and minor criteria, where 3 or more
the development of the clinical signs of TSS.3 TSST-1 of the following multisystems must be involved i.e.
and staphylococcal enterotoxins are the major toxins gastrointestinal: vomiting or diarrhea at onset of illness,
associated with staphylococcal TSS. muscular: severe myalgia or creatine kinase level twice
upper limit of normal for laboratory, mucous membrane:
Risk factors for the development of Staphylococal
vaginal, oropharyngeal, or conjunctival hyperemia.
TSS are tampon use, vaginal colonization with toxin-
renal: BUN or creatinine level at least twice upper
producing S. aureus and lack of serum antibody to
limit of normal for laboratory, or >5 white blood cells
the staphylococcal toxin. Staphylococcal TSS also has
per HPF in absence of urinary tract infection. hepatic:
occurred following use of nasal tampons for procedures
total bilirubin, aspartate aminotransferase, or alanine
of the ears, nose and throat. Infection begins at a site
aminotransferase at least twice upper limit of normal
of minor local trauma, which may be nonpenetrating.
for laboratory, hematologic: platelets <100,000/mm3 and
Cellulitis, subcutaneous abscesses, infected burns and
central nervous system: disorientation or alterations in
pneumonia are some of the non-surgical focal infections
consciousness without focal neurologic signs when fever
associated with TSS. Viral infections such as varicella
and hypotension are absent.
and influenza are sometimes responsible.
Differential diagnosis
Clinical features4 include malaise, myalgias, diarrhea
and chills which often precede the onset of the other 1. Streptococcal TSS: It is virtually identical, with the
physical manifestations of staphylococcal TSS. Fever, major difference being that the portal of entry, which
confusion and lethargy develop soon after the prodromal cannot be proven in at least half the cases.
syndrome and is also associated with symptoms of 2. Leptospirosis (Weil’s disease): Generally causes icterus,
hypovolemic shock related to capillary leakage and headache and severe debilitating myalgias which
diarrhea. Hyperventilation, hypotension, tachycardia were not seen.
and erythematous rash are often seen on physical 3. Dengue shock syndrome: It could present with shock
examination. The rash is usually diffuse macular like state with the development of typical rash
erythroderma. Other signs include strawberry tongue, but on investigating IgM dengue antibody was
conjunctival hyperemia and edema of palms and soles. negative.
Hematologic, hepatic, muscular, renal, gastrointestinal
4. Gram negative septicaemia: Blood culture did not
and central nervous system involvement is common.
show any gram negative organism.
Desquamation usually occurs one to two weeks after
the onset of illness. 5. Pneumococcal pneumonia: Chest X-ray picture was
free of any pulmonary infiltrates making the
Currently, there is no diagnostic test for TSS.
diagnosis of pnemococcal sepsis unlikely.
Identification of TSST-1 producing strains of S. aureus
has been made possible by rapid and easily available Treatment
Reversed Passive Latex Agglutination kit (RPLA) and Treatment consists of immediate and aggressive
other techniques like ELISA and radioimmunoassay; management of hypovolemic shock. To ensure
however these tests do not confirm toxin production adequate perfusion of vital organs, fluid replacement
in vivo. Recent studies show that the analysis of the with large volumes of crystalloid solutions or colloidal
Vbeta repertoire in patients with staphylococcal TSS is a solutions is important and is considered the mainstay
potential diagnostic test.5 Staphylococcal superantigens of treatment. Use of high dose penicillinase resistant
activate specific fractions of the T-cell population by penicillins like oxacillin or flucloxacillin, or β-lactamase
linking the Vbeta domain of the T-cell receptor. Each inhibitor combinations like amoxicillin-clavulanic acid
superantigenic toxin is associated with a characteristic or ampicillin-sulbactam are recommended. Cefazolin
© JAPI  •  VOL. 56  •  MARCH 2008 www.japi.org 193
can be used in patients who are allergic to penicillin. abdominoplasty. Aesthetic Surgery Journal 2007;27:162-66.
Vancomycin or teicoplanin are drugs of choice in case 3. McCormick JK, Yarwood JM, Schlievert PM. Toxic shock
of MRSA. Although corticosteroids were not considered syndrome and bacterial superantigens: an update. Annu Rev
Microbiol 2001;55:77-104.
an effective treatment, recently published case report 7
4. Issa NC, Rodney L Thompson RL. Staphylococcal toxic shock
has highlighted the benefits of methylprednisolone in syndrome. Postgrad Med 2001;110:55-62.
STSS, thereby opening a new window of hope in its
5. MacIsaac CM, Page MA, Biggs BA, Visvanathan K. Staphylococcal
management. toxic shock syndrome: still a problem. The Medical Journal of
Australia (MJA) 2005;182: 651-52.
References 6. CDC. Toxic Shock Syndrome. Fact Sheet. http://www.cdc.gov/
1. Prasad H. V. Raghavendra, Neelima Kharidehal: Staphylococcal ncidod/dbmd/diseaseinfo/ toxicshock_t.htm [Assessed on July
Toxic Shock Syndrome In A 3-Year-Old Male Child. The Internet 22, 2007]
Journal of Infectious Diseases 2006;5:2.
7. Vergis N, Gorard DA. Toxic shock syndrome responsive to
2. Jarrahy R, Roostaeian J, Kaufman MR, Crisera C, Festekjian steroids. J Med Case Reports. 2007;1:5.
JH. A rare case of staphylococcal toxic shock syndrome after

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