Household Transmission of Invasive Group A Streptococcus with Necrotizing Fasciitis
Transcript of Household Transmission of Invasive Group A Streptococcus with Necrotizing Fasciitis
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Submitted April 25, 2003; accepted May 13, 2003
DOI: 10.1080/00365540310012208
Household Transmission of Invasive Group AStreptococcus with Necrotizing FasciitisHENRIK K. LAUSTRUP, ULRIK S. JUSTESEN and COURT PEDERSEN
From the Department of Infectious Diseases, Odense University Hospital, Odense, Denmark
A case of household transmission of invasive group A streptococcus with necrotizing fasciitis is presented. Antibiotic prophylaxis
for close contacts in high-risk groups could be considered.H. K. Laustrup, Kløvervænget 12b-28, DK-5000 Odense C, Denmark (Tel. �/45 6591 7393, e-mail. [email protected])
INTRODUCTION
Streptococcus pyogenes (group A streptococcus, GAS) may
cause a variety of local and systemic infections, including
serious diseases such as streptococcal toxic shock syndrome
and necrotizing fasciitis. Through most of the 20th century
the incidence of severe GAS infections has declined. This
may be due to better socioeconomic conditions or the
introduction of antibiotics, but the reasons are not known
for certain. However, during the late 1980s, an increase in
invasive GAS infections, including necrotizing fasciitis, was
reported. The reason for this is unclear, but serological
typing of group A strains based on antigenic differences in
the M-protein suggests that an increase in the proportion of
virulent organisms may play a role (1). In 1987 Cone et al.
described the streptococcal toxic-like syndrome, an acute
life-threatening complication to group A streptococcal
infections (2). Both the streptococcal toxic-like syndrome
and necrotizing fasciitis may arise following minor skin
trauma, surgical procedures, etc. Mortality rates associated
with necrotizing fasciitis can be more than 40%, despite
antibiotic therapy, surgery and supportive treatment (3).
Underlying conditions such as diabetes, alcohol abuse, skin
abnormalities or wounds, e.g. varicella, may predispose to
invasive GAS (4). The most common streptococcal serotypes
related to GAS necrotizing fasciitis are M1 and M3 (3). It is
well known that non-invasive GAS infections can spread
from person to person. However, person-to-person spread of
invasive GAS causing life-threatening infection has rarely
been reported (5�/7). This report describes transmission of
invasive GAS between family members, clinically manifested
by streptococcal toxin shock syndrome and necrotizing
fasciitis.
CASE REPORT
Case A
A 60-y-old man (patient A) with a known history of high alcohol
consumption attended the emergency room because of pain from his
left hand, diarrhoea, abdominal pain and nausea. Three days earlier
he had cut his hand while doing carpentry at home. On the same day
he consulted his general practitioner, who initiated therapy with
azithromycin. On admission the left hand was diffusely swollen and
painful. There was a minor wound on the back of the hand. There
was no fever but there were signs of shock; systolic blood pressure
414 Case Reports Scand J Infect Dis 35
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was B/55 mmHg and pulse 96 beats/min. Laboratory tests revealed
creatinine levels that were more than 2-fold the normal value. The
absolute white blood cell count was 7.0�/109/l (84% neutrophils
with 13% band forms). C-reactive protein was 148 mg/l. Blood gas
analyses showed acidosis with pH 7.09. Treatment with antibiotics,
cefuroxim, gentamicin and metronidazol, was initiated and after
transferring the patient to the intensive care unit (ICU), treatment
with inotropica was also initiated. 18 h after admission the patient
was treated surgically with debridement and fasciotomy. Bacterio-
logical cultures from the hand yielded S. pyogenes (GAS), T type 1.
Therapy with cefuroxim (the patient was known to be allergic to
penicillin), clindamycin and immunoglobulins (25 g/d for 5 d) was
administered. Signs of adult respiratory distress syndrome and
disseminated intravascular coagulation developed, and therapy was
intensified. The patient developed necrosis of the toes. The condition
improved only slowly. After 1 month on the ICU the patient was
transferred to the ordinary ward and 66 d after admission he was
discharged.
Case B
The day after patient A was admitted, his wife (a 51-y-old female,
patient B) was admitted to hospital. She suffered from swelling and
severe pain of the left hand and forearm, vomiting, diarrhoea and
fever. Bullae and dark blue discoloration were present on the back of
the hand, the arm was swollen and tender, but no fluctuation was
present. On the day before admission she had scraped her hand in a
minor accident. At the time of admission she was awake but with
signs of shock. The systolic blood pressure was B/70 mmHg,
temperature 38.68C and pulse 116 beats/min, and she showed signs
of cyanosis. Therapy with antibiotics, cefuroxim, gentamicin and
metronidazol, was initiated, and the patient was transferred to the
ICU. Laboratory data did not show leucocytosis, the absolute white
blood cell count was 7.7�/109/l (67% neutrophils with 16% band
forms). C-reactive protein was 236 mg/l. No sign of renal involve-
ment was present (creatinine 108 mmol/l). The platelet count was
normal on admission but dropped to 98�/109/l 72 h later.
Intravenous fluids and catecholamines were administered. The arm
was treated surgically with debridement and fasciotomy. Cultures of
tissue fluid and necrotic material from the arm yielded GAS, T type
1. Antibiotic therapy was replaced with clindamycin and penicillin
G. Because of hypotension the patient received dopamine for 24 h.
Two days later she developed signs of adult respiratory distress
syndrome and supplemental oxygen and intubation were needed for
a short period. On the third day she developed a scarlatinous rash.
On the same day therapy with immunoglobulins was initiated (25 g/d
for 5 d). The patient’s condition improved and 16 d after admission
she was transferred to the plastic surgery department for further
treatment.
DISCUSSION
In this case report patients A and B were both infected by
the same invasive S. pyogenes strain, T type 1 (T type 1
corresponds to M type 1). The most likely mode of infection
was transmission from patient A to patient B by direct
contact. Patient B had been taking care of the wound on the
left hand of patient A. Considering the skin wound on her
own hand, she could have been exposed to the S. pyogenes
strain that had already infected her husband. Only the
isolate from patient B was available for further study. The
isolate was tested by polymerase chain reaction to detect the
streptococcal pyogenic exotoxin (spe) genes A, B and C. The
tested isolate possessed the genes speB and speC.
A few case reports have described household transmission
of severe GAS infections (5�/7). Some authors have sug-
gested the use of antibiotic prophylaxis for household
members (7�/9). In meningococcal disease it is recommended
to use antibiotic prophylaxis to household contacts because
of an estimated risk of infection of 2�/4 per 1000 household
contacts (10). With severe GAS infections it is estimated that
the corresponding risk is 3.2 per 1000 household contacts
(95% confidence interval 0.39 to 12 per 1000) (8). A regimen
of penicillin 1�/2 MIE or clindamycin 450�/600 mg 3 times a
day, especially in high-risk groups, e.g. contacts with
varicella, diabetes or alcohol abuse, could be recommended.
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Submitted April 10, 2003; accepted April 14, 2003
DOI: 10.1080/00365540310010967
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