Clinics in Dermatology (2005) 23, 148 – 156

Life-threatening eruptions due to infectious agents

Marcia Ramos-e-Silva, MD*, Ana Libia Cardozo Pereira, MD

Sector of Dermatology and Post-Graduation Course, HUCFF-UFRJ and School of Medicine,

Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil

Abstract Some infectious diseases may cause rapidly fatal eruptions that need to be diagnosed and
treated in an early phase for patient survival. The main life-threatening eruptions of infectious etiology
include Rocky Mountain spotted fever, meningococcemia, toxic shock syndrome, streptococcal toxic
shock syndrome, and staphylococcal scalded skin syndrome.
D 2005 Elsevier Inc. All rights reserved.

Introduction infections that have clinical expression due to the presence

of exotoxins in the blood; these are the toxin-mediated
The infectious diseases that develop cutaneous eruption diseases.
have benign course in the majority and often do not require Clinically, the eruptions can be classified as maculopap-
treatment. This is the case of dengue fever, hepatitis, rubella, ular, petechial, diffusely erythematous with scaling, vesico-
parvovirosis, and other viral infections.1 There are, however, bullous-pustular, and nodular.2
some eruptions of infectious etiology that can be fatal if not The clinical knowledge of the main life-threatening
diagnosed and treated precociously. The certainty of the eruption of infectious etiology is very important for their
diagnosis is often damaged by the difficulty of availability of precocious diagnosis, with the consequent immediate
specific laboratorial exams and by the impossibility of institution of efficient treatment. The significantly relevant
obtaining immediate results. The well-detailed anamnesis, mortality and morbidity in those cases are due mainly to the
with questioning about recent travels, contacts with animals delay in the onset of appropriate treatment.3
and other ill people, use of tampons and trauma, and a Other infectious diseases that present themselves as
meticulous physical exam are of great importance for the cutaneous eruption and can lead to life risk, such as the
outlining of the eruption etiology. ehrlichiosis, a bacteremia due to Streptococcus viridans,
Most of the infectious diseases are caused directly by the gonococcemia, epidemic typhus, and rat bite fevers, are
agent’s action; such is the case of Rocky Mountain spotted worth to be mentioned but will not be discussed here. In
fever (RMSF) and meningococcemia. There are also some addition, many diseases that, in general, do not present
complications in clinical practice may have fatal course in
the immunodepressed patient.
* Corresponding author. Rua Sorocaba 464/205 22271-110, Rio de
We shall describe the main life-threatening eruption of
Janeiro, Brazil. Tel.: +55 21 22864632; fax: +55 21 22864632. infectious etiology that attack the immunocompetent patient
E-mail address: [email protected] (M. Ramos-e-Silva). regarding clinical, laboratorial, and treatment aspects; these

0738-081X/$ – see front matter D 2005 Elsevier Inc. All rights reserved.
doi:10.1016/j.clindermatol.2004.06.019
Life-threatening eruptions due to infectious agents 149

are the RMSF, meningococcemia, toxic shock syndrome having presented cutaneous eruption, only 55.9% had
(TSS), streptococcal TSS, and staphylococcal scalded skin involvement of the palms and feet, considered a characteristic
syndrome (SSSS). of the disease, and that the classic triad of fever, eruption, and
headache was only present in 55.3% of the confirmed cases.
Symptoms, such as pain and abdominal distension,
Rocky Mountain spotted fever suggest an acute abdomen, often leading to submit the
patient to undue laparotomy exploitation. Splenomegalia,
The Rocky Mountain spotted fever is an endemic febrile hepatomegalia, and conjunctivitis are common signs, as
disease with an acute course, caused by Rickettsia rickettsii, well as periorbital and peripheral edema.
a Gram-negative bacillus, obligatory intracellular, belonging The involvement of the inferior respiratory tract can
to the Rickettsiacea family.4 It is transmitted accidentally by manifest itself as coughing, lung edema, bacterial pneumo-
tick bites, and the transmitter species involved can vary nia, and lung hemorrhage.11
according with the geographic location. In the United States, Neurological damage, manifested by convulsive crises,
the Dermacentor variabilis, a dog parasite, is more frequent, delirium, ataxia, papilledema, loss of hearing, and coma,
but cases of the disease also exist because of the affects about 2% to 3% of the patients, according to a study
Amblyomma americanum 5 and Dermacentor andersoni. by Linnemann and Janson,9 and reveals a bad prognosis.
In Brazil and remaining countries of South and Central There is also presence of a diffuse vasculitis, similar to
America, Amblyomma cajennense is considered the most that of the Kawasaki disease, that may lead to the decrease
frequent vector.6,7 of the intravascular volume, and consequently, to the drop of
The infection is seasonal, being the end of spring and the blood pressure and shock. After the eruption, hyperpig-
summer as the seasons of more frequent occurrence of the mentation occurs, which can persist for months.8
disease. The reason for this is explained by the fact that in The spotted eruption may be absent in 10% to 15% of
this time of the year, there is a peak in the number of ticks patients who only present visceral damage; this is the
having their largest contact with the human being variant called spotless fever and has the worst prognosis
populations.8 with a mortality of up to 50% of the cases.12
The incidence of the disease is greater in children; The diagnosis of RMSF should always be questioned in
however, the possibility should never be discarded in the feverish patients, with cutaneous eruption and a contact
other age groups. In spite of some studies reporting greater history with ticks. Even in those cases, there is an enormous
incidence in men and in white individuals, this seems to be list of differential diagnoses: meningococcemia, typhoid
related to a larger exposure of that population with areas of fever, measles, disseminated gonococcal infection, second-
tick infestation. ary syphilis, staphylococcal sepsis, drug hypersensitivity,
The interval between the bite of the tick and the idiopathic thrombocytopenic purple, Kawasaki syndrome,
beginning of the symptoms varies from 1 to 12 days, with immune complex vasculitis, leptospirosis, and TSS.6,12
an average of 5 days.9 The beginning is generally sudden, The laboratory examinations offered in most hospitals
with fever, chills, myalgia, and headache. In this phase, only aid in the diagnosis of RMSF. The patients may present
there is still no eruption in most of the cases, being often normochromic and normocytic anemia, with or without
diagnosed as a viral illness. Some patients, except children, leukocytosis or leukopenia. Thrombocytopenia is generally
report having had a strong headache, the worst that they present, as well as the elevated prothrombin time and the
ever had, and this can be a symptom for the diagnosis of partial thromboplastin time. The examination of the
RMSF.6 cerebrospinal fluid can demonstrate pleocytosis and increase
The eruption generally appears 2 to 5 days after onset of of proteins, besides decrease of glucose; these findings,
fever, in spite of cases reporting the simultaneous occurrence although unspecific, may simulate meningococcemia. Other
of both. It is the main characteristic of the disease, and as a systemic damage findings are increase of hepatic enzymes,
rule, appears initially at the extremities, especially at wrists decrease of albumin, and elevation of urea nitrogen in the
and ankles with subsequent progression to palms, feet, blood. The cutaneous biopsy can help the diagnosis, and its
forearms, and trunk. In this phase, the eruption is macular findings correlate with the duration of the disease. The
or maculopapular, with lesions 1 to 3 mm in diameter and Rickettsia causes endothelial damage that, at the beginning,
disappears with compression. After about 2 days, the eruption is a small vessel lymphohistiocytic vasculitis and progresses
gradually becomes petechial, and this progression may occur to leukocytoclasic vasculitis. It is considered as a form of
even after the beginning of the therapy.9 Ecchymoses and septic vasculitis.13 Immunofluorescence can reveal the
gangrene may occur, especially at the extremities such as the etiologic agent in the vessels’ walls. Another very specific
nose, ears, and fingers.10 The involvement of the vulva and method for detection of bacillus in the biopsy is the
scrotum may occur, and in this case, the physician should immunoperoxidase method.14 Many serologic tests are used
always question the possibility of RMSF.8 to confirm the diagnosis of RMSF; however, none of them
Dalton et al, 5 in an epidemiologic work on RMSF with is positive before the first week after the beginning of the
9223 cases, observed that in spite of 80.2% of the patients disease. Therefore, the decision for treatment should not
150 M. Ramos-e-Silva, A. Libia Cardozo Pereira

depend on the result of those tests; thus, their use is incidence in adults and youngsters is increasing consider-
restricted mainly to retrospective diagnosis. The most ably.18 It is more frequent in the lower socioeconomic layers
frequently used at present, because of their greater because of social habits.
sensibility and specificity, are indirect immunofluorescence Its transmission occurs through the respiratory tract.
and latex agglutination. The Weil-Felix test, used previous- Individuals with deficiency of antibody-dependent, comple-
ly, should be abandoned.6 A comparison should be made ment-mediated immune lysis, functional or anatomic asple-
with 2 serologic tests collected in the first and second or nia, deficiency of properdin, and deficiency of terminal
third week of the disease, and there is confirmation of the complement components are prone to meningococcal
disease if there is an increase in this time.9 disease.19 Active or passive exposure to tobacco,20 as well
Being a life-threatening disease, the patient with as viral infections of the upper respiratory tract, is another
suspicion of RMSF should be hospitalized for better risk factor for the meningococcal disease, due to the damage
monitoring of the possible sequels. The drugs of choice to the mechanical and functional integrity of the respiratory
for treatment of RMSF are doxicilin, 100 mg every 12 mucous membrane.
hours administered orally or intravenously, if necessary, or The clinical presentation may vary according to the
tetracycline, 25 to 50 mg/kg per day, divided to be patient’s age group, being less specific in infants. These may
administered every 6 hours. In children, younger than 9 only present signs of general damage, often without
years, and pregnant women, these drugs should not be used symptoms of meningeal attack. Initially, the patient may
because of the risk of developing tooth discoloration. In present symptoms of the upper respiratory tract, accompa-
those cases, the drug used is cloranfenicol, 50 mg/kg per nied by fever and myalgia. About 50% of the patients will
day, divided to be administered every 6 hours. The present meningitis,18 evolving with headache, vomits,
treatment with those drugs should continue for at least 2 anorexia, prostration, and neurological symptoms, such as
days after the fever. Other drugs did not show effectiveness psychomotor agitation, alteration of the level of conscience,
in the treatment of RMSF. Supportive measures, such as signs of Kerning and Brudzinski, nuchal rigidity, and
hydration and monitoring of possible complications, are of convulsive crises. As the meningitis can occur or be
extreme importance. The use of corticoids seems not to concomitant to the sepsis picture, the patient sometimes
show benefits, and use of heparin for disseminated develops an acute picture with evolution to shock in the first
intravascular coagulation is controversial.6,9,12 24 to 36 hours of the disease. In this case, the meningeal
The delay in the onset of the therapeutics is intimately symptoms can be absent and the findings of liquor exam are
related with an increase of mortality. According to Kirkland normal; for those patients, the prognosis is terrible.17 The
et al,15 patients that do not receive antibiotic treatment cutaneous lesions (Figs. 1-3) appear soon at the beginning
before the fifth day of the disease have a 5-fold greater risk of the picture and are characterized mainly by petechia and
of dying than those that received opportune treatment. Risk purpura, which in spite being more frequent in trunk and
factors associated with death include, besides late treatment, extremities, can affect any part of the tegument. At the
advanced age and treatment with cloranfenicol (as compared beginning, the purpuric lesions are small, irregular, slightly
with tetracycline).5 elevated, and painful. Sometimes the lesion becomes
Some patients can develop long-term sequels, whether pustular or nodular.1 Multiple and large hemorrhagic lesions
neurological or not. The main neurological sequels are with widespread distribution were found in patients with
paraparesis; hearing loss; peripheral neuropathy; bladder meningococcemia with worst prognosis.21 In the cases of
and bowel incontinence; cerebellar, vestibule, and motor
dysfunction; and language disorder. The non-neurological
sequels consist of member amputation and scrotal pain after
the necrosis.16

Meningococcemia
Meningococcemia is a severe febrile systemic disease,
caused by Neisseria meningitidis, a Gram-negative encap-
sulated diplococcus. It is classified in at least 13 serogroups
according to the capsular polysaccharide, with the most
frequent being A, B, C, Y, and W135. About 20% of the
young adults present N meningitidis in the oropharynx, but
only 1 in every 1000 to 5000 develop systemic disease.17
It can occur any time of the year, with greater incidence
in winter and early spring. It affects predominantly children
because of their immature immune system; however, its Fig. 1 Cutaneous vasculitis in meningococcal infection.
Life-threatening eruptions due to infectious agents 151

respiratory insufficiency, and blood dyscrasia. The latex

test seeks the detection of antigens of the N meningitidis;
however, its use is now controversial. Polymerase chain
reaction analysis, although still not commercially available
in many countries, allows a rapid identification of the
specific serogroup of the N meningitidis.19 Regarding
histopathology, there is an endothelial damage, with
thrombosis and hemorrhagic areas inside the tissue that
may contain nuclear dust and neutrophils inside and
around the vessels; meningococci can be demonstrated in
the thrombi.27
It is an infectious emergency and thus, the treatment
should not be postponed because in this case, the course will
be fatal. With the arrival of the antibiotic therapy, the
Fig. 2 Severe widespread purpuric lesions in meningococcemia
(courtesy of Tania Cestari, MD). mortality fell significantly, except in fulminating cases in
general associated to massive adrenal hemorrhage (Water-
house-Friderichsen syndrome). The drug of choice for
disseminated purpura, disseminated intravascular coagula- treatment of the meningococcemia is crystalline penicillin,
tion, and failure of multiple organs, it is called purpura 300 to 500.000 U/kg per day, administered intravenously
fulminans. Nielsen et al22 established some criteria to every 4 hours, for at least 7 days. In patients allergic to
differentiate the meningococcemia from other hemorrhagic penicillin, cloranfenicol, 1.0 g intravenous every 6 hours, or
diseases: (1) hemorrhagic lesions of characteristic appear- ceftriaxone, 100 mg/kg per day, can be used. The treatment
ance, (2) universal distribution of skin hemorrhages, (3) should be aided by sensibility test to antibiotics because
maximum diameter of 1 or more skin hemorrhages greater there are cases of penicillin-resistant meningococcemia.
than 2 mm, (4) poor overall condition, and (5) nuchal General measures to reduce the intracranial hypertension
rigidity. Those authors considered that if 2 of the above include avoiding of hyperhydration, raising of head of
criteria are present, the probability of being meningococce- the bed, and inducing osmotic diuresis, and if necessary,
mia is 97%, with a possibility of 12% being false positive. intubation and hyperventilation are also important.17,19
Maculopapular- or exanthema-like eruption can also be The patient with meningococcemia diagnosis should stay
found in the meningococcemia picture, associated or not to in respiratory isolation for 24 hours after beginning of the
hemorrhagic eruption, which does not mean that the disease antibiotic therapy. It is not uncommon that the patients, after
is less serious.23,24 Children with the nonblanching eruption some days of treatment, present fever associated to a picture
confined to the distribution of the superior vena cava are compatible with arthritis. It is the reactive arthritis of
very unlikely to have meningococcal infection.25 immunologic nature and the antibiotic should not be
Other diseases can present damage of the overall state, modified; in this case, aspirin is prescribed as antiinflam-
fever, and hemorrhagic cutaneous eruption, and should matory and analgesic.17
certainly be included in the differential diagnosis of The chemical prophylaxis is indicated for the patients’
meningococcic infection, which are purpura fulminans, intimate contacts and should be administered as early as
vasculitis, RMSF, TSS, enteroviral infection, leptospirosis,
acute bacteremia, and endocarditis.26
The meningococcic infection should always be consid-
ered in the examination of patients with fever and
hemorrhagic eruption, especially in presence of meningitis.
The diagnosis is established by detection of the N
meningitidis through culture in the blood or cerebrospinal
fluid. In some cases, the agent’s presence can be detected
through culture of skin fragment. The blood cell count
shows leukocytosis with deviation to the left, and the
blood sedimentation rate is increased in practically 100%
of the cases. The exam of the cerebrospinal fluid shows
pleocytosis, usually above 500 mm 3 with polymorpho-
nuclear prevalence, reduced glucose, and increase of
proteins. In the liquor bacterioscopy by the Gram method,
the presence of Gram-negative diplococcus is revealed in
about 60% of the cases. The liquor puncture should be Fig. 3 Intravascular coagulation leading to necrosis of the finger
postponed in cases of severe intracranial hypertension, in meningococcemia.
152 M. Ramos-e-Silva, A. Libia Cardozo Pereira

possible. The drug of choice is rifampicin, 600 mg twice a Systemic manifestation such as tachycardia, tachypnea,
day for 2 days for adults, and 20 mg/kg per day divided in and hypotension are usually present at the moment of the
12-hour intervals for children. For pregnant women, first consultation.39 Mental confusion and multiple organ
ceftriaxone 250 mg should be used intramuscularly in a failure can happen later. In cases of nonmenstrual TSS due
single dose. For health professionals, chemical prophylaxis to the surgical wound, the latter can be clean and have no
will only be necessary in cases of orotracheal intubation, signs of infection, postponing the diagnosis.
suction of secretions, and exam of eyegrounds, accom- The Center for Disease Control defines as a case of
plished without mask protection.17,19 TSS a patient with fever; diffuse erythematous eruption,
The quadrivalent vaccine that protects against serous desquamation after 1 to 2 weeks of the onset of the
groups A, C, Y, and W-135 is suitable for patients with disease, particularly in hands and feet (this criterion can be
deficiency of complement, asplenia, residents or individuals absent if the patient dies before its emergence); systemic
traveling to endemic areas, and professionals that work with involvement of at least 3 organs; and negative cultures for
direct exposure risk, besides children in school age.12,17,19 other infectious agents; besides absence of high serology
The vaccine is not effective for children younger than 2 titers for measles, leptospirosis, and RMSF. A case is
years.12 considered suspicious if only desquamation is not pres-
ent.40 In spite of toxicologic and serologic tests not being
part of the Center for Disease Control criteria for diagnosis
Toxic shock syndrome of TSS, the detection of presence of toxigenic strain of S
aureus in absence of acute-phase antibodies may confirm
Toxic shock syndrome is an exotoxin-mediated disease the diagnosis in doubtful cases.41 A culture of suspicious
characterized by fever, eruption, hypotension, involve- places in cases of nonmenstrual TSS can reveal S aureus.42
ment of multiple organs, and finally, desquamation due to The histopathologic findings consist of inflammatory
exotoxin-producing strains of Staphylococcus aureus. It infiltrate with predominance of neutrophils and eosino-
was described initially in 1978 28 and later associated to phils in the perivascular and interstitial area, with foci
the use of sanitary tampons. Cases of nonmenstrual TSS, of spongiosis and necrotic keratinocytes inside the
or without relationship with the use of tampons, were epidermis.27
described in association with the use of barrier contra- The differential diagnosis of TSS includes meningococ-
ceptives, gynecologic surgeries, postpartum, allergic con- cemia, RMSF, scarlet fever, streptococcal TSS, Kawasaki
tact dermatitis, respiratory tract, and cutaneous, visceral, disease, viral exanthema, lupus erythematosus, and adverse
vascular, and odontological infections.29-31 At present, the cutaneous drug eruptions.
number of nonmenstrual cases of TSS exceeds that of The patient with suspicion of TSS should be hospital-
menstrual TSS.32-34 The exotoxins involved in the ized and the treatment begun precociously with antista-
staphylococcal TSS are TSST-1, responsible for about phylococci agents (nafcillin 1.5 g or oxacillin 2.0 g EV
90% of the cases of menstrual TSS,35 enterotoxin B every 4 hours in cases that produce penicillinase). Other
(SEB), and less frequently, enterotoxin C1 (SEC). Those options would be clindamycin, second generation cephalo-
exotoxins act as superantigens, leading to a massive sporin, vancomycin, and fluoroquinolones. In patients
production of cytokines, and consequently, to the clinical using tampons, these should be removed immediately, with
signs of the disease. The patients that develop the irrigation and cleaning of the vagina.39 Supportive meas-
disease, however, seem not to present neutralizing anti- ures such as hydration, use of vasopressors, drainage of
bodies for the toxins, a fact that predisposes them to the abscesses, and cleaning of infected wounds are of extreme
infection.34 importance.
Toxic shock syndrome can come as a potentially fatal The mortality of menstrual TSS is approximately 3% and
disease, characterized by shock and failure of multiple 2- to 3-fold higher for nonmenstrual cases.43 Episodes of
organs or even as a mild picture frequently confused recurrence may occur, especially in patients that do not
clinically with an unspecific viral illness or a gastroenter- develop anti TSST-1 antibodies, after the first episode of
itis.36 There is, in general, a prodromal period of 2 to 3 days TSS.34
with myalgia and indisposition 37 before emergence of high
fever and tachycardia. The cutaneous eruption of TSS is
characterized by macular diffuse and nonpruriginous ery- Streptococcal toxic shock syndrome
thema that can be more intense around the infected area.38
In some cases, there is formation of bullae, papules, The streptococcal toxic shock syndrome (Strep TSS)
petechiae, and pustules,12 besides edema of the extremity, is clinically similar to TSS; however, it is caused by
erythema of the conjunctiva and mucous membranes, and a pyrogenic exotoxin of Streptococcus pyogenes
strawberry tongue. Desquamation of palms and plants (Streptococcus group A), causing early onset of shock
occurs about 2 weeks after the onset of the disease, which and organ failure, and frequently, necrotizing fasciitis
is characteristic. (about 50%).12
Life-threatening eruptions due to infectious agents 153

The patients that develop the disease, similar as in TSS,

seem to lack protecting immunity against the exotoxin,
making them susceptible. Streptococcal pyrogenic exotox-
ins A and B are described as inducers of cytokines, such as
tumor necrosis factor a, interleukin 1b, and interleukin 6,
and are capable to cause the clinical picture found in Strep
TSS. A third pyrogenic exotoxin C (SPEC), streptococcal
superantigens, and mitogenic factors of the streptococci
were also already described as causes of Strep TSS.44
In Strep TSS, the entrance is through the skin in about
80% of the cases, with a soft tissue infection (cellulite,
necrotizing fasciitis, or cutaneous wounds). Cases post-
chickenpox, pharyngitis, peritonitis, phlebitis, and osteomy-
elitis were also described.45
Fig. 5 Staphylococcal scalded skin syndrome in an infant
The clinical aspects are very similar to TSS with high (courtesy of Tania Cestari, MD).
fever, hypotension, mental confusion, failure of multiple
organs, and shock. Its fatal course, however, is more Streptococcus of the A group, many studies try to
frequent with a mortality reaching 30% to 70% of the demonstrate poor positive results when dealing with
cases. The initial manifestation of the disease, in most cases, serious infections, such as necrotizing fasciitis. Clindamy-
is an intense and abrupt pain, without localized infection in cin is presently the drug of choice for treatment of Strep
general in the extremities. The emergence of violaceous TSS. The use of intravenous gamma globulin, although
bulla suggests necrotizing fasciitis or myositis.39 Although a showing good results, mainly if administered at the
erythematosus eruption is possible, as in TSS, the erythema beginning and as auxiliary therapy, still deserves additional
of Strep TSS is in general localized, with or without investigation.49,50 The administration of nonsteroidal anti-
desquamation and strawberry tongue. inflammatory drugs, common in the initial phase of the
Unlike TSS, Strep TSS develops into bacteremia in a disease, should be avoided, because it can contribute to
large number of cases, and, therefore, blood culture is sudden emergence of shock and failure of multiple organs,
normally positive in over more than 50% of the patients.46,47 besides more aggressive infection by inhibition of the
Elevation of creatine phosphokinase level can be indicative neutrophilic function, increase in production of cytokines,
of necrotizing fasciitis or myositis.48 and decrease of the inflammation signs.51
In all patients with high fever and inexplicable strong
muscle-skeletal pain, the doctor should consider the
possibility of a beginning of an infection by Streptococcus Staphylococcal scalded skin syndrome
of the A group,39 because the disease develops in 48 to 72
hours into systemic manifestations with a high mortality Staphylococcal scalded skin syndrome is a superficial
rate. In these cases, the treatment should be started skin blistering disorder caused by the staphylococcal
immediately. The support measures are similar to those exotoxin, exfoliative toxin. It is a disease that basically
for TSS. In spite of penicillin still being a relatively attacks children, presenting benign course in most cases
effective antibiotic in the cases of cutaneous infection by (Figs. 4-6). Despite rare in the adult, when present, it entails

Fig. 4 Discrete SSSS in an infant (courtesy of Tania Cestari, Fig. 6 Staphylococcal scalded skin syndrome in an infant
MD). (courtesy of Gabriela Lowy, MD).
154 M. Ramos-e-Silva, A. Libia Cardozo Pereira

a mortality of 60%52 and may reach 100% in patients with

some previous disease.53
Two exotoxins participate in the pathogenesis of SSSS:
exfoliative toxin A and exfoliative toxin B, but other
exotoxins have also been suggested.54 Those exotoxins act
in the granular zone of the epidermis,55 leading to the
exfoliation. Some authors suggest superantigenic activity of
those exotoxins.56 About 30% of the population presents S
aureus in the skin and mucous membranes as commensal
organisms, and approximately 5% of all strains produce
exfoliative toxin. The S aureus involved in most of the cases
is phase group II.
Although the possibility of damaging the healthy adult,
most of the cases of SSSS in the adult present some
Fig. 8 Scalded skin syndrome in an adult (same patient as in
previous disease, such as renal insufficiency, immunosup- Fig. 7).
pression, alcoholism, malignity, or HIV infection. This
happens because for the development of SSSS, a massive by histopathology, where in the latter, the subepidermal
production of toxins or deficiency in their elimination must cleavage is observed with necrosis of the epidermis.
be present.57 The patient should be hospitalized and the antibiotic
The primary infection begins, in general, in the conjunc- therapy started with the purpose of eradicating the infection
tiva, nasopharynx, ear, urinary tract, or skin, followed by focus. The use of intravenous penicillinase-resistant peni-
skin tenderness and erythemato-scarlatiniform eruption cillin is indicated. Hydroelectrolytic control should be
more pronounced in the flexures. The formation of flaccid rigorous to avoid complications. Adult patients, mainly
bullae occurs in about 24 to 48 hours, preferably in the with previous diseases, should be monitored with extreme
flexures and around orifices. The Nikolsky sign is positive, care due to the high mortality. The local therapy should
and rarely, there is damage of mucous membranes. The consist of compresses and barrier creams. The use of
resulting desquamation reveals an erythematous base of nonsteroidal antiinflammatory drugs was also described as a
rapid healing. In adults, it is frequently followed by predisposing factor to SSSS in the adult for the same
bacteremia and pneumonia,58 favoring a bad prognosis. reasons described for TSS61 (Figs. 7 and 8).
The diagnosis of SSSS is based on 3 criteria59: (1) the Finally, decolonization of chronic carriers of S aureus, as
clinical diagnosis with presence of erythroderma, desqua- well as the decrease in the time of hospitalization and
mation, or formation of bullae; (2) isolation of the S aureus, appropriate antiseptic control of physicians, nurses, and
producer of exfoliative toxin; and (3) the characteristic parents, can significantly decrease SSSS in hospitalized
histopathology that consists of intraepidermal cleavage at patients or in those who have just left the hospital.60
the level of the granular layer. The isolation of the S aureus
can be made from distant places, as mentioned previously,
and serologic tests, with the objective of detecting the toxin, Conclusions
can also be accomplished.60
The main differential diagnosis of SSSS is toxic Infectious diseases that may cause rapidly fatal eruptions
epidermal necrolysis that should be discarded especially must be diagnosed and treated precociously. The diagnosis
is often retarded by the difficulty in performing specific
laboratorial exams and obtaining their immediate results.
The knowledge of the main life-threatening infectious
eruption described in this paper is very important for their
early diagnosis, leading to an immediate institution of an
efficacious therapy.
Of great importance for the etiologic diagnosis of the
eruption is a well-collected anamnesis, which must include
questions about recent travels, animals and ill people
contacts, trauma and use of tampons, as well as a very
meticulous physical exam.
Unfortunately, the delay in establishing the etiologic
diagnosis and the onset of appropriate therapy is frequent
and leads to a relevant mortality and morbidity in the
cases of eruption caused by the infectious diseases
Fig. 7 Scalded skin syndrome in an adult. discussed.
Life-threatening eruptions due to infectious agents 155

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