Varicella is a self limiting disease of childhood.
The incidence of secondary bacterial superinfections such as cellulitis,
septicemia, pneumonia, suppurative arthritis, osteomyelitis, or local
gangrene is usually low(1). We report a case of varicella compli-cated
by celliulitis and scarlet fever. Seven such cases have been reported
before(2-6).
Case Report
A 3-year-old, previously healthy white boy visited a
family doctor on the first day of generalized papulovesicular eruption
invol-ving his face, scalp, trunk, and mouth. A diagnosis of varicella
was made, and nimesulide, a new nonsteroidal anti-inflam-matory drug,
was administered for high fever.
Five days later, he was referred to our clinic for
persistent fever. His body temperature was 39º C, blood pressure was
85/57 mmHg, and there was diffuse blanchable erythema all over his body
which was nonpruritic and most pronounced on the trunk. His face was
flushed and the skin was not tender. The child had circumoral pallor,
tonsillar injection and enlargement, and a strawberry tongue. The
typical vesicles and erosions of varicella were present on the buccal
mucosa, scalp, and his entire body. Small varicella ulcers were also
present on the trunk. Scarlatiniform rash in areas surround-ing
varicella vesicles and small ulcers due to varicella were absent. In
addition, many areas of hard induration (5-10 cm in diameter),
surrounded the ulcers on the trunk (Fig 1).
 |
|
Fig. 1. Hard induration and absence of
scarlatiniform rash around the varicella vesicles and ulcers on
the trunk at admission. |
White blood cell count was 9,000/mm3 with 18% band
forms, 5% segmented neutrophils, 24% lymphocytes, and 3% monocytes;
hemoglobin was 12.1 g/dL; platelet count was 218,000/ mm3; and
erythrocyte sedimentation rate was 105mm/h. Serum electrolytes, blood
urea nitrogen and creatinine levels, liver function tests and urinalysis
were normal. Varicella-zoster virus immunoglobulin G (IgG) and IgM
antibodies detected by enzyme-linked immunosorbent assay were positive.
The wound culture obtained from the ulcers due to varicella revealed
group A beta-hemolytic streptococci (GABHS). The level of
antistreptolysin was not elevated. The clinical and laboratory findings
led to the diagnosis of varicella, superinfection of the skin with
cellulitis due to streptococcal infection, and scarlet fever. Ampicillin
and sulbactam was started. Despite the administration of antibiotics,
the clinical symptoms persisted. On the second day of treatment an
abscess was noticed in the left pectoral region which improved following
surgical drainage. The rash of scarlet fever disappeared within two
days. Staphylococcus aureus was isolated from the abscess, but
further typing was not available. On the seventh day of admission, the
desquamation started which was most pronounced on his trunk, but not
involved the areas of his palms and soles. He was discharged from the
hospital after 10 days of therapy when all lesions became smaller and
the medication was discontinued.
Discussion
Varicella is most frequently complicated by
cellulitis caused by GABHS or S. aureus (6-8). An erythematous
eruption in a febrile child may be caused by drug reaction(s), Kawasaki
syndrome and bacterial toxin mediated illnesses such as toxic shock
syndromes and scarlet fever. A case of chickenpox associated with
Kawasaki syndrome has been previously reported(9).
In our patient the clues for the diagnosis of scarlet
fever were diffuse blanchable erythema, perioral pallor, and a white
strawberry tongue. In addition, his skin was not tender and his face was
flushed. Absence of adenopathy and conjunctivitis ruled out Kawasaki
disease. The blood pressure was normal ruling out shock states. He had
no organ involvement except the skin. The desquamation was also noticed
a few days after subsidence of symptoms and signs. The clinical
diagnosis was confirmed by the recovery of GABHS from skin lesions due
to varicella.
Scarlet fever is caused by streptococcal erythrogenic
toxins from GABHS. The erythema of scarlet fever may be due to a delayed
type hypersensitivity reaction to these toxins. Although there have been
many reported cases of varicella complicated by a secondary infection,
to our knowledge only 7 cases of varicella complicated by scarlet fever
are reported in children. Of those 7 children, in only one had scarlet
fever preceded the exanthem of varicella(2), whereas in two, the
eruption of varicella preceded the exanthem of scarlet fever(3,4), and
the others were not well described(5,6). In our case, cellulitis
associated with scarlet fever developed following varicella rash and
scarlatiniform rash was not present around the varicella vesicles and
ulcers due to varicella. A remarkably similar case was described and the
authors suggested that the inter- feron produced in the varicella
vesicles diffused out in a concentric manner and inhibited the
delayed-type hypersensitivity reaction that was responsible for the
scarlatiniform rash(4).
It was first suggested by Brogan et al(10) that
nonsteroidal anti-inflammatory drugs (NSAIDs) may increase the risk of
invasive GABHS infection in children with varicella. The association
between ibuprofen use and invasive GABHS infection has been
observed(11). In our patient nimesulide may be considered as an
associated factor.
Acknowledgement
The authors would like to thank Dr. Semih Dogan for
review and editorial assistance of this manuscript.
Contributors: TY and AHP drafted the manuscript
and KK critically reviewed the manuscript. TY would act as the guarantor
for the paper.
Funding : None.
Competing interests: None stated.
