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Journal of Clinical Microbiology, September 1999, p. 3074-3075, Vol. 37, No. 9
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Peritonitis Caused by Haemophilus
parainfluenzae in a Patient Undergoing Continuous Ambulatory
Peritoneal Dialysis
Carmen
Betriu,1,*
Francisco
Coronel,2
Pilar
Martin,2 and
Juan J.
Picazo1
Department of Clinical
Microbiology1 and Department of
Nephrology,2 Hospital Clínico San
Carlos, 28040 Madrid, Spain
Received 8 February 1999/Returned for modification 26 April
1999/Accepted 14 June 1999
 |
ABSTRACT |
We report a case of peritonitis in a patient undergoing continuous
ambulatory peritoneal dialysis. Haemophilus parainfluenzae biotype III was recovered in pure culture from dialysis fluid.
 |
CASE REPORT |
Peritonitis is a common complication
of continuous ambulatory peritoneal dialysis (CAPD), with two-thirds of
patients developing peritonitis during the first year of dialysis
(8). Three cases of CAPD peritonitis due to
Haemophilus parainfluenzae have been reported (1, 3,
10), and none of these mentions bacteremia.
A 44-year-old patient with chronic renal failure, probably due to
nephrosclerosis, started on CAPD in April 1997. He had a history of
coronary disease treated by angioplasty and stent implantation, peripheral arteriopathy with left femoral stenosis, and long-term arterial hypertension. The patient was in good health from the beginning of CAPD treatment and had no episodes of peritonitis. He was
admitted to our Peritoneal Dialysis Unit in November 1998 with
abdominal pain and cloudy peritoneal fluid. The day before admission he
developed diarrhea. On admission he was afebrile, and the peritoneal
fluid was cloudy and contained 1,860 leukocytes/mm3 with
80% polymorphonuclear neutrophils (PMN). Physical examination revealed
marked abdominal distension, increased bowel sounds, and abdominal
tenderness. The peritoneal catheter exit site was of normal appearance.
A blood test revealed 10,710 leukocytes/mm3 with 66% PMN,
a hematocrit value of 42%, and a hemoglobin concentration of 13.1 g. As the patient was afebrile, blood cultures were not collected.
After taking samples of dialysis fluid for Gram staining and culture,
teicoplanin and cefotaxime were administered intraperitoneally.
H. parainfluenzae biotype III was recovered in
pure culture from dialysis fluid, although no organisms were detected
on a Gram stain of the centrifuged sample. Five-milliliter samples of
fluid were inoculated in each of two blood culture bottles of the
Bactec system NR 860 (Johnston Laboratories, Inc., Towson, Md.)
Subcultures were performed on blood agar and chocolate agar, which were
incubated in a CO2-enriched atmosphere at 37°C, and on
Brucella agar incubated in an anaerobic atmosphere. Gram-negative coccobacilli grew after 24 h on chocolate agar. They were
identified as H. parainfluenzae on the basis of V-factor
requirement and absence of hemolysis. Identification of the isolate to
species level was confirmed and biotyping was performed by using
growth-independent rapid biochemical tests of the API NH system
(bioMérieux, Marcy l'Etoile, France). Susceptibility to
antimicrobial agents was determined by a broth microdilution procedure
(Sensititre; Radiometer, Copenhagen, Denmark) performed according to
the guidelines of the National Committee for Clinical Laboratory
Standards (6). The isolate was
-lactamase positive and
susceptible to amoxicillin-clavulanate, cefotaxime, and chloramphenicol
at the following MICs: 2/1,
0.06 µg/ml, and
2 µg/ml,
respectively. With the culture identification of H. parainfluenzae, cefotaxime was continued for a total of 10 days,
but teicoplanin was stopped. The patient responded well to this
treatment, and symptoms disappeared 2 days after therapy was started.
We investigated the presence of H. parainfluenzae in the
patient's feces and throat swab. This organism was not isolated.
Unlike surgical peritonitis, CAPD peritonitis is usually caused by a
single organism, and bacteremia is extremely rare (8, 9,
11). Microorganisms causing CAPD peritonitis usually originate in
the skin but could also originate in either the upper respiratory tract
or the bowel. Coagulase-negative staphylococci are the most commonly
identified agents, accounting for 40 to 60% of all positive cultures,
followed by S. aureus and streptococci (10 to 20% each). Members of the family Enterobacteriaceae accounted for 5 to
20% of all positive cultures, nonfermentative gram-negative rods
accounted for 3 to 15%, and gram-positive rods accounted for 2 to 4%.
Values for mixed bacteria, fungi, mycobacteria, and anaerobes are
generally <5% (11).
H. parainfluenzae is a commensal organism of the upper
respiratory tract and has also been isolated from the urogenital tracts of children and adults. H. parainfluenzae can colonize the
gastrointestinal tract; this fact is supported by some observations
(2, 4, 5). The characterization of the iron-repressible
outer-membrane proteins of H. parainfluenzae showed that
they are closely related to those of enteric bacteria (5);
these proteins may serve as adhesins, allowing colonization of the
intestinal tract mucosa (2). Furthermore, H. parainfluenzae is dependent for growth upon V factor, which is
supplied by intestinal flora. In a study of Haemophilus
species in the human gastrointestinal tract, Megraud et al.
(4) found that most of the strains isolated from the appendices were H. influenzae (77%) whereas 60% of the
strains from the stools were H. parainfluenzae. This
microorganism is an uncommon agent of human infections and has
occasionally been associated with upper respiratory tract infections,
endocarditis, osteomyelitis, psoas abscess, retroperitoneal abscess,
peritonitis, urinary infections, liver abscess, and biliary tract
infections. It is a very rare cause of CAPD peritonitis (1, 3,
10).
The three sites most frequently associated with CAPD infections are the
catheter exit site, the subcutaneous peritoneal catheter tunnel in the
abdominal wall, and the peritoneum itself (11). This episode
is an unusual case of CAPD peritonitis. The source of H. parainfluenzae was not identified. Considering that this organism
is a normal inhabitant of the human respiratory tract and may also
colonize the gastrointestinal tract, we suggest that, in our case, the
entry of H. parainfluenzae into the peritoneal cavity could
have been by two routes: (i) through touch contamination during
dialysate exchanges, or (ii) by transmural migration of H. parainfluenzae from the gastrointestinal tract, as some studies have indicated for Escherichia coli (7).
We believe that Haemophilus species should be considered
possible etiologic agents of CAPD peritonitis. These organisms have fastidious nutritional requirements. H. parainfluenzae
requires V factor (NAD) and growth in the laboratory only when it is
provided with medium, such as chocolate agar. The low incidence of
Haemophilus species in CAPD peritonitis could be explained,
in part, by the fact that the majority of laboratories do not include
plating the peritoneal fluid to a medium to ensure the growth of these microorganisms.
 |
FOOTNOTES |
*
Corresponding author. Mailing address: Department of
Clinical Microbiology, Hospital Clínico San Carlos, Plaza
Cristo Rey s/n, 28040 Madrid, Spain. Phone: 341 3303486. Fax: 341 3303478. E-mail: cbetriu{at}efd.net.
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Journal of Clinical Microbiology, September 1999, p. 3074-3075, Vol. 37, No. 9
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.