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Pneumococcal Peritonitis in Adult Patients
Report of 64 Cases With Special Reference to Emergence of Antibiotic Resistance
Olga Capdevila, MD;
Roman Pallares, MD;
Imma Grau, MD;
Fe Tubau, MD;
Josefina Liñares, MD;
Javier Ariza, MD;
Francisco Gudiol, MD
Arch Intern Med. 2001;161:1742-1748.
ABSTRACT
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Background Few data are available regarding pneumococcal peritonitis. We studied
the clinical characteristics of intra-abdominal infections caused by Streptococcus pneumoniae and its prognosis in relation
to antibiotic resistance.
Methods We reviewed all cases of culture-proved pneumococcal peritonitis. Patients
with liver cirrhosis and primary pneumococcal peritonitis were compared with
patients with Escherichia coli peritonitis.
Results Between January 1, 1979, and December 31, 1998, we identified 45 cases
of primary pneumococcal peritonitis in patients with cirrhosis and 19 cases
of secondary (or tertiary) pneumococcal peritonitis. Patients with cirrhosis
and primary pneumococcal peritonitis vs those with primary E coli peritonitis had more frequent community-acquired infection,
73% vs 47%; pneumonia, 36% vs 2%; and bacteremia, 76% vs 33%; and higher attributable
mortality (early mortality), 27% vs 9% (P<.05
for all). Secondary (or tertiary) pneumococcal peritonitis was associated
with upper or lower gastrointestinal tract diseases; in most cases, the infection
appeared after surgery. A hematogenous spread of S pneumoniae from a respiratory tract infection might be the most important origin
of peritonitis; also, S pneumoniae might directly
reach the gastrointestinal tract favored by endoscopic procedures or hypochlorhydria.
There was an increased prevalence of penicillin and cephalosporin resistance
up to 30.7% and 17.0%, respectively, although it was not associated with increased
mortality rates.
Conclusions Primary pneumococcal peritonitis in patients with cirrhosis more often
spread hematogenously from the respiratory tract and was associated with early
mortality. In secondary (and tertiary) pneumococcal peritonitis, a transient
gastrointestinal tract colonization and inoculation during surgery might be
the most important mechanisms. Current levels of resistance were not associated
with increased mortality rates.
INTRODUCTION
STREPTOCOCCUS PNEUMONIAE is a common pathogen
that causes high morbidity and mortality around the world.1-2
It is the most common cause of community-acquired pneumonia and the second
most common cause of purulent meningitis,3-5
but intra-abdominal pneumococcal infections are rarely found.6-9
Primary (or spontaneous) bacterial peritonitis occurs mainly in patients
with liver cirrhosis and is usually caused by gram-negative bacilli.10-12 It is thought that
in most cases the enteric microorganism gains access to the peritoneal cavity
without loss of integrity of the intestinal wall through a mechanism of bacterial
translocation.12-20
In addition, gram-negative bacteria can occasionally reach the peritoneal
cavity by a hematogenous route from a distant primary focus (eg, a urinary
tract infection).21
Primary pneumococcal peritonitis in patients with cirrhosis is usually
associated with a respiratory tract infection such as pneumonia, and, in this
case, the bloodstream (hematogenous spreading) is the most likely route of
peritoneal fluid infection.6-7,22-23
In some patients, a respiratory tract focus is not clinically apparent, and,
in these cases, the gastrointestinal tract has been hypothesized to be a source
of pneumococci.7, 22, 24
However, pneumococci are soluble in bile salts,5
and, therefore, it is unlikely that S pneumoniae
can grow in the normal gastrointestinal tract.
On the other hand, secondary intra-abdominal infection (secondary peritonitis)
is due to the spread of gastrointestinal or genitourinary microorganisms into
the peritoneal space from loss of integrity of the mucosal barrier. These
are often polymicrobial infections and can take the form of generalized peritonitis
or localized peritonitis (localized abscesses).14-15,22
To date, only anecdotal cases of adult patients with secondary pneumococcal
peritonitis have been reported,25-28
and some of them were associated with appendicitis.29-30
The mechanism of the pneumococcus that causes these infections is not clear
because it is not found in the gastrointestinal tract.
There have been reported cases of primary and secondary pneumococcal
peritonitis in prepubertal girls and in postpubertal healthy women, mainly
post partum, after an abortion, after gynecologic procedures, or associated
with intrauterine device use.25-28,31
It is well known that S pneumoniae can colonize in
the vagina and an ascending infection can occur.32-33
In children, colonization in the genitourinary tract with S pneumoniae occurs because of inadequate hygiene or orogenital sexual
abuse.24, 29-30 In
these patients, when no apparent purulent foci in the genitourinary tract
is found, such cases are usually called primary peritonitis.32
The main objectives of the present study were (1) to describe different
types of intra-abdominal infections caused by S pneumoniae; (2) to determine the clinical characteristics, laboratory findings,
and outcomes of patients with liver cirrhosis and primary peritonitis due
to S pneumoniae and to compare them with those infected
by Escherichia coli; and (3) to study antibiotic
resistance in pneumococcal isolates and determine its clinical relevance.
PATIENTS AND METHODS
SETTING AND STUDY DESIGN
The present study was carried out in Bellvitge Hospital, a 1000-bed
teaching hospital for adult patients in Barcelona, Spain. It serves approximately
1 million people and admits more than 26 000 patients per year. This
hospital does not have pediatrics and obstetrics departments.
We reviewed the clinical and microbiological data of all patients who
had a diagnosis of diffused or localized peritonitis and a peritoneal sample
that was positive for S pneumoniae. These patients
were admitted to Bellvitge Hospital between January 1, 1979, and December
31, 1998, and most of them had been cared for and included in a protocol of
invasive pneumococcal
infections by one of us (R.P.).
Patients with liver cirrhosis and primary pneumococcal peritonitis (case
patients) were compared with patients with cirrhosis and primary peritonitis
due to E coli (control patients). For each case patient
we selected a control patient according to the nearest date of positive culture.
If a case or control patient had more than 1 episode of primary peritonitis,
only the first episode was considered.
STUDY VARIABLES AND DEFINITIONS
The diagnosis of liver cirrhosis was established using clinical, laboratory,
and exploratory findings and did not require a liver biopsy with histologic
confirmation. The stage of cirrhosis was determined by the criteria of Pugh
et al.34-35
Primary peritonitis in a patient with cirrhosis was considered when
clinical findings together with biochemical data of peritoneal inflammation
and a positive ascitic fluid culture (for S pneumoniae
[case patients] or E coli [control patients]) were
present, and without any clinical or radiologic data suggesting a surgically
treatable intra-abdominal focus.
Secondary (or tertiary) pneumococcal peritonitis was diagnosed in a
patient with a localized or diffuse suppurative intra-abdominal process together
with a positive culture for S pneumoniae and in whom
an intra-abdominal, surgically treatable source was detected (or in whom the
infection appeared after surgery).
We considered a hospital-acquired peritoneal infection (either primary
or secondary peritonitis) when the episode occurred 48 hours after hospital
admission (or appeared after surgery) and it was not in the incubated period.
Community-acquired infection was considered when it was evident on hospital
admission or within the first 48 hours.
Pneumonia was considered (definitive diagnosis) in a patient with signs
or symptoms of a lower respiratory tract infection and a new pulmonary infiltrate
on chest radiography, together with bacteremia or positive culture from a
lower respiratory tract sample (eg, pleural fluid). We also considered pneumonia
(presumptive diagnosis) in patients with clinical and radiographic findings
compatible with pneumonia, with a positive sputum sample or no respiratory
tract samples available for culture (all of our patients had concomitant positive
ascitic fluid cultures for either S pneumoniae or E coli).
In all patients, demographic characteristics, clinical findings, and
laboratory and medication data were obtained from hospital records or from
previous data recorded in the protocol of invasive pneumococcal infections.
Previous hospitalization was defined as admission to any hospital during
the previous 6 months.
We specifically investigated the performance of endoscopic procedures,
peritoneovenous shunt implementation, or surgery within 1 month of hospital
admission.
Previous antibiotics were considered when the patient received any antibiotic
for prophylaxis or treatment for more than 48 hours during the previous 30
days of peritonitis.
Previous episodes of primary bacterial peritonitis were considered when
they occurred within 1 year of the current hospital admission and by a different
microorganism.
Septic shock was considered in a patient with a systolic blood pressure
below 90 mm Hg and peripheral hypoperfusion together with clinical or bacteriological
evidence of uncontrolled infection.
Antibiotic therapy was prescribed according to the attending physician's
criteria and varied during the study period. The most common empirical antibiotic
regimens were penicillin or ampicillin sodium plus aminoglycosides or aztreonam
during the first years of the 1980s, and since 1986 almost all patients received
a cephalosporin such as cefotaxime sodium or ceftriaxone sodium.
Mortality was considered when the patient died within 30 days of diagnosis
of peritonitis. Attributable mortality (mortality probably related to infection)
was considered when the patient died within 7 days of diagnosis and without
another evident cause of death.
MICROBIOLOGICAL METHODS
Biological samples (eg, blood and peritoneal fluid) were studied at
the Microbiology Laboratory. Strains of S pneumoniae
were identified using standard methods. Ascitic fluid cultures were performed
by the method of bedside inoculation of blood culture bottles with ascites.
Antibiotic susceptibility to penicillin was initially determined with a 1-µg
oxacillin sodium disk using the Kirby-Bauer disk diffusion method, and strains
that showed a zone of inhibition of less than 20 mm were considered nonsusceptible
to penicillin. Minimal inhibitory concentrations (the lowest concentration
that inhibits pneumococcal growth) of isolated strains from 1979 to 1992 were
determined using the agar dilution method in Mueller-Hinton agar supplemented
with 5% sheep blood and containing antimicrobials, as described previously.36 Minimal inhibitory concentrations of isolated strains
from 1993 to 1998 were determined using the microdilution method in Mueller-Hinton
broth supplemented with 5% lysed horse blood, as recommended in the 1992 criteria
of the National Committee for Clinical Laboratory Standards.37
The following 7 antimicrobial agents were tested: penicillin G, ceftriaxone/cefotaxime,
erythromycin, clindamycin, sulfamethoxazole and trimethoprim, tetracycline,
and chloramphenicol. The results of susceptibility tests were evaluated according
to the 1998 criteria of the National Committee for Clinical Laboratory Standards.
STATISTICAL ANALYSIS
Statistical analysis was carried out using a statistical software package
(SPSS for Windows, version 9.0; SPSS Inc, Chicago, Ill). Data are given as
mean ± SD. Continuous variables were compared using the unpaired t test, and categorical variables were compared using  2 or Fisher exact tests when appropriate. Statistical significance was
established at P<.05 (2-tailed). When many variables
were analyzed, and to adjust for multiple comparisons, the Bonferroni adjustment
was used (calculated by dividing  = .05 by  variables).38
RESULTS
At Bellvitge Hospital, during the 20-year study period, we identified
64 patients with intra-abdominal infections caused by S
pneumoniae. During this period, the 64 intra-abdominal pneumococcal
isolates represented 4.3% of a total of 1476 S pneumoniae strains isolated from clinical specimens (all sterile fluid samples;
sputum samples were not included). Comparing 1979 to 1988 with 1989 to 1998,
the percentage of pneumococcal isolates from abdominal samples vs the total
number of sterile fluid samples was 3.6% (22/604) and 4.8% (42/872), respectively
(P = .27).
Of 64 patients with intra-abdominal pneumococcal infections, 45 with
liver cirrhosis had primary pneumococcal peritonitis and the remaining 19
had secondary (or tertiary) pneumococcal peritonitis.
PRIMARY PNEUMOCOCCAL PERITONITIS
Prevalence
We analyzed all patients admitted to Bellvitge Hospital between January
1, 1989, and December 31, 1998, with a diagnosis of chronic liver disease
(n = 7535); approximately 90% of them had liver cirrhosis (an estimated 6871
patients). Primary bacterial peritonitis (of any etiology) occurred in 513
patients (8% of all patients with liver cirrhosis). Primary pneumococcal peritonitis
(30 cases during 1989-1998) represented 5.8% of all primary bacterial peritonitis
and 0.4% of all hospital admissions for liver cirrhosis.
Case-Control Study
Forty-five case patients with primary pneumococcal peritonitis were
compared with 45 control patients with primary peritonitis due to E coli (Table 1).
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Table 1. Clinical Characteristics and Laboratory Findings in Patients
With Liver Cirrhosis and Primary Peritonitis Due to Streptococcus
pneumoniae (Cases) or Escherichia coli (Controls)
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The statistically significant differences between the 2 groups were
that patients with pneumococcal peritonitis were more frequently smokers,
had associated pneumonia, more often had bacteremia, less frequently had a
nosocomial-acquired infection, and had lower ascitic fluid white blood cell
counts (Table 1).
Although not statistically significant, patients with pneumococcal peritonitis
had more associated comorbidities, were more frequently alcohol abusers, received
previous antacid treatment, and had a previous endoscopy. The etiology and
stage of liver cirrhosis were similar in both groups; most patients had an
advanced stage of the disease according to Child-Pugh scores (Table 1).
Mortality in patients with primary pneumococcal peritonitis and E coli peritonitis at 30 days was 47% (21 patients) and
36% (16 patients), respectively (P = .28) (Table 1). Patients with primary pneumococcal
peritonitis had higher attributable mortality than patients with E coli peritonitis: 27% (12 of 45 cases) vs 9% (4 of 45 controls) (P = .05).
During the study, we found a significant decrease in the mortality rate
in both groups. Thus, from 1979-1988 to 1989-1998, mortality decreased in
patients with pneumococcal peritonitis from 73% (11 of 15 patients) to 33%
(10 of 30 patients) (P = .01) and in patients with E coli primary peritonitis from 64% (9 of 14 patients)
to 32% (10 of 31 patients) (P = .04).
SECONDARY (OR TERTIARY) PNEUMOCOCCAL PERITONITIS
We studied 19 patients (age, 59.7 ± 18.6 years; 14 [74%] were
men) with diffuse or focal pneumococcal peritonitis in whom an apparent source
of the infection was detected; they were divided into upper and lower abdominal
infections.
Upper Abdominal Infection
The 12 patients with upper abdominal pneumococcal infections had associated
gastroduodenal or pancreaticobiliary tract disease.
Of 7 patients with gastroduodenal ulcer (perforated or bleeding), in
1 case S pneumoniae was isolated in pure culture
at the time of initial surgery and in the remaining 6 cases the microorganism
was iso lated 4 to 31 days after surgery (4 had polymicrobial infection).
Of the other 5 patients, 3 were admitted to the hospital because of
an exacerbation of chronic pancreatitis, and during hospitalization a pancreatic
pseudocyst or abscess was diagnosed; S pneumoniae
was isolated from a sample obtained from scanning guided puncture 12 to 46
days after hospitalization (none of these patients underwent previous surgery).
The other 2 patients were admitted to the hospital because of biliary tract
neoplasm (n = 1) or pancreatic neoplasm (n = 1). The patient with a diagnosis
of pancreatic neoplasm underwent surgery on hospital admission, and S pneumoniae grew in pure culture from an exudate obtained
from a perineoplasm abscess. The patient with biliary tract neoplasm was admitted
to the hospital for elective surgery; 11 days later, an intra-abdominal abscess
was detected in which S pneumoniae grew in pure culture.
Lower Abdominal Infection
Of 7 patients with lower pneumococcal abdominal infections, 6 were admitted
to the hospital for elective surgery (5 with intestinal neoplasm and 1 with
Gardner syndrome). The intra-abdominal infection appeared 5 to 20 days after
surgery (in 4 of the 6 cases, S pneumoniae was isolated
in pure culture). The last patient is a postpartum woman who was admitted
to the hospital because of abdominal pain and fever and was diagnosed as having
an intra-abdominal abscess in which S pneumoniae
grew in pure culture.
Predisposing Factors
Most patients with secondary pneumococcal peritonitis had some predisposing
factors for pneumococcal infection or colonization. Of 19 patients, alcohol
abuse was present in 14 (74%), liver cirrhosis in 2 (11%), chronic bronchitis
or chronic obstructive pulmonary disease in 7 (37%), and clinical and radiologic
findings suggestive of a lower respiratory tract infection coinciding with
or preceding the intra-abdominal pneumococcal infection in 5 (26%). Only 4
patients (21%) underwent previous endoscopy, and 8 (42%) had previous antacid
treatment.
Treatment and Mortality
All but one patient required drainage (surgically or by scanning guide
puncture); this was a patient with cirrhosis who died (see the following paragraph).
All but 3 patients received antibiotic therapy; these 3 patients recovered
with only surgical drainage.
Two (11%) of 19 patients died, both within 3 days of diagnoses of pneumococcal
infection. One of them, a 73-year-old man with liver cirrhosis in an advanced
stage, had a polymicrobial infection after surgery for a perforated gastric
ulcer; a culture from an abdominal fluid puncture grew S pneumoniae and Pseudomonas aeruginosa (resistant
to initial therapy with ceftriaxone and clindamycin); no surgical drainage
could be performed. The second patient was a 78-year-old man with chronic
obstructive pulmonary disease and gastrointestinal tract bleeding secondary
to duodenal ulcer who developed a polymicrobial infection after surgery in
which grew S pneumoniae and Morganella
morganii; he died despite surgical drainage and antibiotic therapy
(amoxicillin and clavulanate potassium plus tobramycin sulfate).
ANTIBIOTIC RESISTANCE
Overall, in the abdominal pneumococcal isolates (n = 64) we found an
increase in penicillin resistance during the study: 14% (2 of 14 strains)
between 1979 and 1985, 33% (5 of 15 strains) between 1986 and 1991, and 40%
(14 of 35 strains) between 1992 and 1998 (P = .05).
The mortality rate did not differ significantly between patients infected
with penicillin-resistant and penicillin-susceptible strains (Table 2). Only 4 patients had resistance to cefotaxime/ceftriaxone,
and one of them died.
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Table 2. Mortality Rates in Patients With Primary and Secondary Peritonitis
Due to Streptococcus pneumoniae According to MICs
of Penicillin and Cefotaxime/Ceftriaxone*
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Table 3 shows our experience
with antibiotic resistance in 1095 pneumococcal blood isolates during 2 different
periods. There was increased prevalence of penicillin, cephalosporin, and
macrolide resistance and decreased tetracycline and chloramphenicol resistance.
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Table 3. Trends in Antibiotic Resistance in 1095 Blood Isolates of Streptococcus pneumoniae*
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COMMENT
We suggest a comprehensive classification of pneumococcal peritonitis
(Table 4). Most patients with
pneumococcal peritonitis can be included in 1 of 3 categories: (1) primary
peritonitis associated with liver cirrhosis, nephrotic syndrome, or chronic
renal failure and continuous ambulatory peritoneal dialysis; (2) secondary
(or tertiary) peritonitis associated with gastrointestinal disease (or after
surgery); and (3) peritonitis in young women with or without an apparent genitourinary
focus.
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Table 4. Classification of Peritonitis Caused by Streptococcus pneumoniae
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To date, most cases of pneumococcal peritonitis have occurred in patients
with liver cirrhosis.7, 9 According
to different studies,10-11,39
of all cases of primary peritonitis in patients with cirrhosis, 1% to 11%
are caused by S pneumoniae. However, pneumococcus
rarely causes secondary (or tertiary) peritonitis, and there have been only
anecdotal reports of well-documented secondary (or tertiary) pneumococcal
peritonitis associated with gastrointestinal disease8-9,29-30
or in young women.5, 22-28,33
Herein, we found that in patients with cirrhosis, the mechanism of spread
and prognosis are the 2 most important differences between primary peritonitis
due to S pneumoniae and primary peritonitis due to E coli.
In patients with cirrhosis and primary peritonitis due to E coli, the most important mechanism is thought to be translocation
from the gastrointestinal tract, and, in some cases, it can be due to a bacteremic
spread from a distant focus (eg, urinary tract infections). On the other hand,
the mechanism of primary pneumococcal peritonitis in patients with cirrhosis
is controversial because S pneumoniae is not found
in the gastrointestinal tract, probably because this microorganism is soluble
in bile salts that avoid bacterial growth.5
However, we can speculate that hematogenous spreading might be important.
Thus, in our study, 16 patients (36%) had associated pneumonia, and, in these
cases, hematogenous spread from the respiratory tract could be suggested.7 In addition, other patients who develop pneumococcal
peritonitis are those without an apparent respiratory tract infection but
who are at higher risk of S pneumoniae oropharyngeal
colonization (eg, smokers and alcoholics) and who were recently subjected
to previous endoscopic procedures. Transient bacteremia can occur after endoscopy.40
Recent studies41-46
have shown that short-term prognosis in patients with cirrhosis and primary
bacterial peritonitis (most cases caused by Enterobacteriaceae) has improved
during the past decade, probably as a consequence of early diagnosis and better
therapeutic approaches. Thus, mortality from primary bacterial peritonitis
(all cases) decreased from more than 75% in the 1970s to about 40% in the
1990s.13-14,17, 21-22,47
We also found a decreased mortality rate during recent years in patients with
either pneumococcal or E coli primary peritonitis.
In our study, we found a higher 30-day mortality rate in patients with
pneumococcal peritonitis compared with those with E coli peritonitis, but this difference did not reach statistical significance
(Table 1). Moreover, patients
with pneumococcal peritonitis had higher attributable mortality (27%) than
those with peritonitis due to E coli (9%). We can
speculate that S pneumoniae might be more virulent
than E coli and that pneumococcal peritonitis is
often associated with pneumonia, which can be complicated with respiratory
failure and septic shock. We did not find that patients with pneumococcal
peritonitis had a more advanced stage of cirrhosis.
Of note is the high number of nosocomial-acquired pneumococcal and E coli peritonitis in our study. Despite the fact that
these microorganisms are usually components of the patient's own flora (acquired
in the community), in recent years patients with cirrohsis have a long life
expectancy and might develop peritonitis during hospitalization for other
reasons. However, we cannot exclude that some of these microorganisms were
transmitted from inpatients or hospital personnel.
Table 3 shows trends in
antibiotic resistance during the past 2 decades. We observed significant increases
in cases with intermediate or resistant penicillin, cephalosporin, and macrolide.
We did not find a correlation between the minimal inhibitory concentrations
of penicillin and cephalosporin and mortality rates (Table 2). This is also found with other nonmeningeal pneumococcal
infections48 and might be because levels of ß-lactams
achieved in serum and ascitic fluid are much higher than minimal inhibitory
concentrations.
In cases of secondary peritonitis, the infection might occur as a result
of loss of integrity of the gastrointestinal tract wall (eg, perforation of
gastric ulcer or colonic neoplasm).14 Secondary
peritonitis caused by S pneumoniae has rarely been
reported.9 We identified 19 cases of secondary
(or tertiary) pneumococcal peritonitis associated with upper or lower gastrointestinal
tract diseases.
Although S pneumoniae is not a component of
gastrointestinal tract flora, we can speculate that in some circumstances
the microorganisms might become part of the transient gastric flora. Despite
not being well documented, upper abdominal transient colonization by S pneumoniae might occur in patients with low gastric acidity
who had oropharyngeal colonization by S pneumoniae,
and particularly in patients subjected to endoscopic procedures.
In lower abdominal infections, the pneumococcal colonization is more
difficult to explain, and we found in the literature only a few cases of acute
appendicitis caused by S pneumoniae.9, 29-30
In our study, we identified 6 patients with colonic diseases and pneumococcal
peritonitis, and in all cases the infection appeared after surgery. In cases
of pneumococcal peritonitis that occur after surgery (tertiary peritonitis),
one can speculate that the microorganism might also be inoculated during the
surgical procedure from the oropharyngeal flora of the surgical personnel.
In conclusion, the main characteristics of primary pneumococcal peritonitis
in patients with cirrhosis (compared with E coli
peritonitis) were the hematogenous spread from the respiratory tract and the
higher attributable mortality rate. Perhaps, in some cases, S pneumoniae might directly reach the gastrointestinal tract from the
oropharynx favored by endoscopic procedures or achlorhydria. In secondary
(and tertiary) pneumococcal peritonitis, the origin of the pneumococcus is
unclear, but transient gastrointestinal tract colonization and inoculation
during surgical procedures might be the most important causes. Mortality was
not related to penicillin and cephalosporin resistance.
AUTHOR INFORMATION
Accepted for publication December 4, 2000.
This study was supported in part by grant FIS 97/0716 from the National
Health Service, Madrid, Spain, and from the Agencia d'Avaluacio de Tecnologia
Medica, Generalitat de Catalunya, Barcelona, Spain.
Corresponding author: Roman Pallares, MD, Fundacio August Pi i Sunyer,
Hospital de Bellvitge, Feixa Llarga s/n, 08907 L' Hospitalet, Barcelona, Spain
(e-mail: rpallares{at}bell.ub.es).
From the Infectious Disease Service (Drs Capdevila, Pallares, Grau,
Ariza, and Gudiol) and Microbiology Service (Drs Tubau and Liñares),
Hospital de Bellvitge and University of Barcelona, Barcelona, Spain.
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