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51.

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. hkl@dadlnet.dk)

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

Scand J Infect Dis 35 Case Reports 415

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