DIAGN MICROBIOLINFECTDIS

1992;15:151-155

151

CASE REPORTS

Group-C -Hemolytic Streptococcal

Bacteremia
Juan Berenguer, Isabel Sampedro,
Emilia Cercenado, Jesus Baraia,
Marta Rodriguez-Cr6ixems, and Emilio Bouza

Group-C jS-hemolytic streptococci (GCBHS) is an uncommon

cause of bacteremia. In a 5-year period, GCBHS accounted for
0.28% of positive blood cultures and 0.35% of bacteremias
documented at our hospital. The incidence of GCBHS bacteremia was 0.05 episodes per 1000 admissions. We were able to
analyze clinical data of 10 of the 13 patients with GCBHS
bacteremias. All but one were adults with significant underlying diseases, and seven episodes were community acquired.
The skin was the portal of entry in only one case. Clinical

syndromes included primary bacteremia (four cases), pneumonia (two cases), endocarditis (two cases), and meningitis,
intraabdominal infection, and metastatic suppurative pericarditis (one episode each). Of 13 isolates, 12 were identified to
species level: six, Streptococcus equisimilis; three S. equi;
two S. dysgalactiae; and one S. zooepidemicus. Resistance
to penicillin was detected in one isolate and none of our isolates displayed penicillin tolerance. Four patients died (40%)
despite appropriate antimicrobial therapy.

INTRODUCTION

by GCBHS has been reviewed recently (Salata et al.,

1989; Arditi et al., 1989). Nevertheless, information
provided is scarce and scattered, has been collected
over prolonged periods of time, and assesses the
subject of bacteremia in only two references (Mohr
et al., 1979; Skogberg et al., 1988). We have, therefore, performed a retrospective analysis of GCBHS
bacteremia as it occurs in a large teaching hospital
over a period of 5 years.

Group-C streptococci are made up of a heterogeneous group of microorganisms that possess Lancefields group-C carbohydrate. They are usually ~-hemolytic on blood agar, but nonhemolytic and ~hemolytic strains may also be observed (Gallis, 1990;
Ruoff, 1988). Group-C ~-hemolytic streptococci
(GCBHS) are recognized as either comensals or pathogens in horses, cattle, swine, and guinea pigs. In
humans, GCBHS may colonize the respiratory,
digestive, and urogenital tract in a small percentage
of healthy individuals. GCBHS is an uncommon cause
of human infection that may occasionally be acquired by exposure to animals or ingestion of raw
animal products (Duma et al., 1969).
The clinical spectrum of human infections caused
From the Department of Clinical Microbiology,Gregorio
Marafi6n General Hospital, Madrid, Spain.
Address reprint requests to Dr. J. Berenguer, Serviciode Microbiologia Clinica, Hospital General Gregorio Marafi6n, C/Dr.
Esquerdo 46, 28007Madrid, Spain.
Received November 28, 1990; revised and accepted January
29, 1991.
1992Elsevier Science Publishing Co., Inc.
655 Avenue of the Americas, New York, NY 10010
0732-8893/92/$5.00

MATERIAL AND METHODS

The Hospital General Gegorio Marah6n is a 2300bed teaching hospital attending a population of
800,000. During the study period (January 1985 to
July 1989), blood cultures were taken and processed
following well-established guidelines (Washington,
1978).
Streptococcal isolates were identified as GCBHS
on the basis of hemolysis in blood agar, Gram stain,
catalase activity, and serogruping by latex agglutination (Streptococcal latex grouping kit, Oxoid,
Hampshire, UK). GCBHS were identified to species
level by means of a commercial kit (API 20 Strep,
Bio M~rieux, Marcy-L'Etoile, France). Antibiotic sus-

J. Berenguer et al.

152

TABLE 1

Epidemiological Data for GCBHS

Bacteremia over a 5-Yr Period
(1985-1989)
Number

Blood cultures
Positive blood cultures
Blood cultures with GCBHS
Number of bacteremias
Bacteremias by GCBHS

74,126
9969
28

13.4
0.28

3707
13

0.35

Hospital admissions
230,034
Bacteremias/1000 admissions
15.1
GCBHS bacteremias/1000 admissions
0.05

ceptibilities [minimum inhibitory and minimum bactericidal concentrations (MIC and MBC, respectively)] were determined following a standardized
broth microdilution technique (NCCLS, 1985).
Clinical charts of the patients with blood isolates
of GCBHS were reviewed, and data were collected
according to a standard protocol. The diagnosis of
bacteremia by GCBHS required the isolation of that
microorganism in at least one blood culture. Bacteremia was considered nosocomially acquired when
the patient had been hospitalized for more than 3
days before the onset of symptoms. Antimicrobial
therapy was considered appropriate when one antibiotic to which the microorganism was susceptible
in vitro was administered intravenously in adequate
dosages.
RESULTS

During the study period, GCBHS was isolated in

0.28% of the blood cultures and accounted for 0.35%
of bacteremias. The incidence of GCBHS bacteremia
was 0.05 per 1000 admissions (Table 1).
We were able to obtain clinical information from
the charts of 10 of 13 patients (Table 2). All but one
of the patients were adults with significant underlying disease. Bacteremia was community acquired
in seven patients. Clinical syndromes associated with
GCBHS bacteremia were diverse. Four patients suffered primary bacteremia. One of these developed
fatal metastatic suppurative pericarditis. Two cases
of pneumonia were found, one community acquired
and the other nosocomial, in the setting of mechanical ventilation. Two other patients, both intravenous drug abusers, suffered tricuspid valve endocarditis with septic lung emboli. Another patient, a
woman with colonic neoplasm, developed bowel
perforation and peritonitis with polymicrobial bacteremia due to GCBHS and Bacteroides fragilis. Finally, a case of acute meningitis was observed in a
boy with postraumatic cerebrospinal fluid leak.

We found no patient with a history of exposure

to animals or ingestion of raw animal products.
However, this information was not invariably requested by the attending physicians.
In two patients, bacteremia was polymicrobial. It
was possible to perform species identification and
antimicrobial susceptibility testing in 12 of 13 GCBHS
isolates (Table 3). One strain was resistant to penicillin (MIC, 4 tx/ml), but, unfortunately, we were not
able to find the clinical record of the patient involved. None of the strains tested exhibited tolerance to penicillin.
Ultimately, four of 10 patients with GCBHS bacteremia died, despite appropriate antimicrobial therapy in nine cases. However, death could be directly
attributed to GCBHS infection in only two patients.

DISCUSSION

With the widespread use of Lancefield grouping, the

apparent frequency of infections by GCBHS has increased. Lancefield grouping is the only reliable laboratory method for the differentiation between
GCBHS and other B-hemolytic streptococci, and if
this method is not employed, then GCBHS may be
misidentified as group A as many of the GCBHS are
bacitracin sensitive (Salata et al., 1989).
Colony morphology permits the division of GCBHS
into two groups: a "large colony type," similar to
Streptococcus pyogenes, and a "minute colony type"
that includes strains of S. anginosus. "Large colony
types" can be further grouped biochemically into
four species: S. equisimilis, S. dysgalactiae, S. equi, and
S. zooepidemicus (Gallis, 1990; Ruoff, 1988).
GCBHS are an uncommon cause of infection and
bacteremia in humans. In Finland, GCBHS accounted for 0.54% of 2207 bacteremias detected in a
single hospital during an 8-year period (Skogberg et
al., 1988). Moreover, in two previously published
surveys, it was found that GCBHS accounted for
K1%-1.16% of streptococcal bacteremias (Duma et
al., 1969; Mohr et al., 1979). Although uncommon,
GCBHS infections are frequently accompanied by
positive blood cultures. In one study that included
31 cases of infection by this microorganism in nine
hospitals, 74% of patients were bacteremic (Salata
et al., 1989). In an outbreak of S. zooepidemicus infection associated with the ingestion of homemade
cheese reported to the Center for Disease Control
(CDC), 16 cases were identified, and the microorganisms was isolated from the blood of the 15 patients (CDC, 1983).
Our experience, as well as that reported by other
authors, permits us to outline some of the typical
characteristics of patients suffering GCBHS bacteremia. It is most frequently a community-acquired

Case R e p o r t

TABLE 2

Case

153

Clinical M a n i f e s t a t i o n s in 10 P a t i e n t s w i t h G C B H S Bacteremia

Age

Sex

60

36

60

82

Underlying
Disease

Place of
Acquisition

Type of
Bacteremia

Alcoholism
cardiomyopathy
Non-Hodgkin
lymphoma
Colonic cardnoma

Community

Primary

Hospital

Primary

Community

Secondary
peritonitis

CHD, COPD

Community

15

CSF leak

Community

32

Community

71

22

IVDA, HIV
infection
Perforated gastric
ulcer
IVDA

42

Hospital

10

33

Ruptured
aneurism (CA)
FMF

Hospital
Community

Community

Blood
Cultures

Complications

Treatment

Outcome

Suppurative
pericarditis
--

GCBHS

Adequate

Death

GCBHS

Adequate

Death

--

GCBHS

Adequate

Cured

Adequate

Cured

Bacteroides
fragilis

Secondary
Pleural
pneumonia
effusion

GCBHS

Secondary
-meningitis
Secondary
Lung emboli
endocarditis
Primary
Septic shock

GCBHS

Adequate

Cured

GCBHS

Adequate

Cured

GCBHS

None

Death

Secondary
Lung emboli
endocarditis
Secondary
-pneumonia
Primary
--

GCBHS

Adequate

Cured

GCBHS

Adequate

Death

GCBHS

Adequate

Cured

Streptococcal
pneumoniae

CHD, chronic heart disease; COPD, chronic obstructive pulmonary disease; CSF, cerebrospinal fuid; IVDA, intravenous drug
abuse; HIV, Human Immunodeficiency Virus; CA, cerebral artery; and FMF, familial mediterranean fever.

disease in a d u l t i n d i v i d u a l s w i t h s o m e t y p e of u n derlying disease such as malignancy, alcoholism, a n d

c h r o n i c l u n g or h e a r t d i s e a s e (Salata et al., 1989;
M o h r et al., 1979; S k o g b e r g et al., 1988). Pediatric
p a t i e n t s s e e m to be less p r o n e to G C B H S b a c t e r e m i a .
W e w e r e able to i d e n t i f y o n l y o n e pediatric case a n d

TABLE 3

a r e c e n t r e v i e w of the literature d i s c l o s e d o n l y 15
r e p o r t e d pediatric cases in w h i c h b l o o d c u l t u r e s
y i e l d e d G C B H S (Arditi et al., 1989).
P r i m a r y b a c t e r e m i a , a p p e a r s to be a c o m m o n
f i n d i n g w i t h G C B H S b o t h in n e u t r o p e n i c a n d n o n n e u t r o p e n i c patients. In f o u r of o u r 10 patients, a

Species I d e n t i f i c a t i o n a n d A n t i m i c r o b i a l Suscepibility T e s t i n g in 12 Strains of G C B H S C a u s i n g

Bacteremia
Penicillin"

MIC (Ixg/ml)

Streptococcus
Species
1
2
3
4
5
6
7
8
9
10
11
12

zooepidemicus
equi
equisimilis
equisimilis
dysgalactiae
dysgalactiae
equisimilis
equisimilis
equi
equisimilis
equi
equisimilis

MIC

MBC

Ery

Van

Chl

Cft

Cip

Imi

Gen

~0.01
~0.01
4
~0.01
~0.01
~0.01
~0.01
~0.01
~0.01
~0.01
~<0.01
0.12

~0.01
~0.01
8
~0.01
~0.01
~0.01
~0.01
~0.01
~0.01
~0.01
~0.01
0.12

~0.01
~0.01
~<0.01
~0.01
~0.01
~0.01
~0.01
0.03
~0.01
~0.01
~0.01
~0.01

0.25
0.25
0.12
0.25
0.25
0.25
0.12
0.25
0.12
0.12
0.25
0.03

2
1
1
2
2
1
2
1
1
1
1
1

~0.01
0.06
1
~0.01
~0.01
~0.01
~0.01
~0.01
~0.01
~0.01
~0.01
0.12

0.25
1
0.25
0.25
0.25
0.25
0.12
0.25
0.5
2
0.25
4

~0.01
~0.01
1
~0.01
<~0.01
~0.01
~0.01
~0.01
~0.01
~0.01
~0.01
0.06

0.25
0.25
0.25
0.5
0.25
0.25
0.5
1
0.25
1
0.5
2

Ery, erythromycin; Van, vancomycin; Chl, chloramphenicol; Cft, cefotaxime; Cip, ciprofloxacin; Imi, imipenem; and Gen, gentamicin.
aMICs and MBCs and Ixg/ml.

154

portal of entry for GCBHS bacteremia could not be

identified, in common with a previously published
series in which this phenomenon occurred in 42%
of the cases (Skogberg et al., 1988).
The skin and soft tissue was found to be the portal
of entry in only one of our patients (10%). Other
authors have reported a well-proven soft tissue of
cutaneous portal of entry in 17%-33% of cases of
GCBHS bacteremia (Mohr et al., 1979; Skogberg et
al., 1988). In our own institution, group A /3-hemolytic bacteremia has a notably higher incidence
in intravenous drug abusers and exhibits a much
higher percentage of cutaneous involvement as well
as a better prognosis (Bern~Ido de Quir6s et al., 1986).
Many of the syndromes associated with GCBHS
Infection were represented in our series. We found
two patients with pneumonia, both of which lacked
some of the features described for this type of infection such as empyema or the tendency to cavitate
(Stamm and Cobbs, 1980; Ekenna et al., 1988). Two
of our patients, both intravenous drug abusers, suffered right-sided endocarditis. These cases and other
reports suggest that GCBHS may be added to the
list of potential pathogens complicating intravenous
drug abuse (Kramer and Ellner, 1988). Under other
circumstances, GCBHS endocarditis frequently pursues a virulent and destructive course with major
emboli to vital organs with associated high mortality
(Salata et al., 1989; Mohr et al., 1979; Raizes et al.,
1987). We observed one patient with suppurative
metastatic pericarditis, a previously described complication of this type of infection (Hanson and Engel,
1981), and two other patients with intraabdominal
infection and cerebrospinal fluid (CSF) leak-related
meningitis, respectively.
Group C streptococci are usually susceptible to
penicillin and several other antimicrobial agents such

J. Berenguer et al.

as third-generation cephalosporins, the newer semisynthetic penicillins, and erythromycin (Rolston et

al., 1982). We were able to perform antimicrobial
susceptibility testing in 12 of 13 strains of GCBHS,
one of which was resistant to penicillin and another
resistant to ciprofloxacin. All the isolates were uniformly sensitive to cefotaxime, imipenem, vancomycin, erythromycin, and chloramphenicol. None
of our strains was tolerant to penicillin, although
this phenomenon has been observed in 8%-94% of
clinical isolates of group C streptococci (Rolston et
al., 1982; Portnoy et al., 1981). This tolerance has
been suggested as the explanation of the poor outcome of serious infections caused by this group of
microorganisms treated with penicillin alone. A synergistic effect of penicillin with gentamicin has been
demonstrated in strains exhibiting tolerance to penicillin. The use of an aminoglycoside in addition to
penicillin as an initial therapy of serious group C
streptococcal infections pending in vitro susceptibility results would, therefore, seem advisable (Rolston et al., 1982).
The infections caused by GCBHS, although rare,
may be extremely severe and associated with a high
mortality (10%-19%) (Salata et al., 1989; Mohr et al.,
1979; Skogberg et al., 1988). The mortality found in
our series (40%), the highest reported to date for
group C infections, reflects the severity of the underlying disease. This grim prognosis suggests that
particular attention should be given to the identification of all non-group A or D blood isolates of Streptococcus.

The authors thank Daphne Coward, who helped us with the

English translation of the manuscript.

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