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Journal of Clinical Microbiology, June 1999, p. 2084-2086, Vol. 37, No. 6
Departments of Laboratory
Medicine1 and Internal
Medicine,
Received 12 January 1999/Returned for modification 9 February
1999/Accepted 9 March 1999
Helicobacter fennelliae (formerly Campylobacter
fennelliae) has been reported to cause bacteremia in homosexual
men with or without human immunodeficiency virus (HIV) infection. We
report here a 48-year-old, non-HIV-infected, heterosexual man with
diabetes mellitus and cirrhosis of the liver who developed bacteremia
and septic shock due to H. fennelliae. The patient was
treated successfully initially with intravenous ampicillin-sulbactam
and ceftazidime, followed by ampicillin-sulbactam only. These agents
were active in vitro against the isolate by E-test results. To our
knowledge, this is the first documented case of septic shock due to
H. fennelliae in a non-HIV-infected, heterosexual,
immunocompromised patient.
Helicobacter fennelliae,
formerly known as Campylobacter fennelliae, has been
isolated from rectal swabs of asymptomatic and symptomatic (proctitis,
proctocolitis, or enteritis) homosexual men with or without human
immunodeficiency virus (HIV) infection (7, 8, 11, 13, 15,
16). Bacteremia caused by this organism in HIV-infected patients
has also been previously reported (8, 9, 11). We describe
here an immunocompromised patient with bacteremia associated with
septic shock due to H. fennelliae. To our knowledge, this is
the first documented case of septic shock due to H. fennelliae in a non-HIV-infected heterosexual patient.
Case report.
A 48-year-old heterosexual man with cirrhosis of
the liver and diabetes mellitus was hospitalized with a 2-week history
of fever, progressive abdominal fullness, and dyspnea. Disseminated Penicillium marneffei infection involving the lung
(pneumonia and pleural effusion), peritoneum (peritonitis and ascites),
and lymph nodes (cervical lymphadenitis) was diagnosed. His HIV
antibody test results by enzyme immunoassay (ICE* HIV-1.O.2; Murex
Biotech Limited, Dartford, United Kingdom) and Western blot (NEW
LAV-BLOT 1; Sanofi Diagnostics Pasteur, Marnes-La-Coquette, France)
were negative. He received amphotericin B treatment (1 mg/kg of body weight/day), and his condition remained stable. Unfortunately, 3 weeks
after initiation of amphotericin B treatment (accumulative dose, 650 mg), high fever (40°C) accompanying shaking chills, drowsiness,
dyspnea, and hypotension (systolic blood pressure, 60 mm Hg) developed.
Laboratory data revealed leukocytosis, lactic acidosis, and
deterioration of renal and liver functions. A chest radiograph showed
complete resolution of previous pneumonic patches and pleural effusion,
and there were no gastrointestinal symptoms. The patient was
transferred to the medical intensive care unit and was treated
empirically with ampicillin-sulbactam (6 g/day) and ceftazidime (6 g/day). Two sets of blood cultures obtained on the day of septic shock
yielded large, elongated, gram-negative rods with spiral or helical
morphology (Fig. 1) from two BACTEC 6A
bottles (Becton Dickinson, Sparks, Md.) after 5 days of incubation. During treatment with ampicillin-sulbactam and ceftazidime for 5 days
and ampicillin-sulbactam (6 g/day) only for another 9 days, the fever
gradually subsided and clinical symptoms resolved. Blood cultures drawn
2 days after completion of antibiotic therapy were sterile. Stool and
rectal swab cultures for H. fennelliae were obtained after
the notification of positive blood cultures. The patient received a
total of 2 g of amphotericin B, followed by itraconazole (400 mg/day) for another 3 months for P. marneffei infection. He
was well at follow-up 6 months after discharge.
Microbiology.
The bacterium recovered had a positive culture
signal with growth indexes of 45 and 42, respectively, in two BACTEC 6A
aerobic bottles but no growth in two BACTEC 7A anaerobic bottles. Upon subculture to Trypticase soy agar supplemented with 5% sheep blood, CDC blood agar, and chocolate agar (BBL Microbiology Systems), no
growth was found after 48 h of incubation at 25 or 37°C under ambient air, CO2 incubator, or anaerobic conditions. When
incubating in a microaerobic atmosphere (5% O2, 10%
CO2, 85% N2), the bacterium grew well at
37°C (but did not grow at 25 or 42°C) on both CDC blood agar and
chocolate agar. Poor growth was noted on Trypticase soy agar
supplemented with 5% sheep blood. Scanty growth at 37°C and no
growth at 42°C on CAMPY BAP (containing the following five antimicrobial agents: cephalothin [15 µg/ml], trimethoprim [5 µg/ml], polymyxin [2.5 U/ml], vancomycin [10 µg/ml], and
amphotericin B [2 µg/ml]; BBL Microbiology Systems) was found after
a 48-h incubation in a microaerobic atmosphere. Colonies on chocolate agar were 2 to 3 mm in diameter and were gray, convex, and circular with a hypochlorite smell. Isolates were gram-negative curved or
helical bacilli and were positive for both oxidase and catalase reactions. Nitrate reduction, hippurate hydrolysis, urease reactions, and H2S production in triple sugar iron agar (BBL
Microbiology Systems) were negative. The organism was susceptible to
cephalothin (30-µg disk) and nalidixic acid (30-µg disk). Cellular
morphotypes, growth characteristics, biochemical profiles, and
susceptibility results for the above two agents were in agreement with
those of H. fennelliae (7, 14, 16). Stool and
rectal swab cultures for this organism on chocolate agar and CDC blood
agar plates at 37°C under microaerobic conditions after 5 days of
incubation grew moderate amounts of several species of bacteria and
yeasts but were negative for H. fennelliae.
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Septic Shock Due to Helicobacter
fennelliae in a Non-Human Immunodeficiency Virus-Infected
Heterosexual Patient
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FIG. 1.
Gram-negative helical bacilli in a BACTEC 6A aerobic
bottle cultured from a blood specimen of a 48-year-old, heterosexual,
non-HIV-infected patient with septic shock (Gram stain with 1%
carbolfuchsin as counterstain; magnification, ×1,000).
3%) of hexadecanoic acid
(16:0), octadecenoic acid (18:1), tetradecanoic acid (14:0),
octadecanoic acid (18:0), and dodecanoic acid (12:0) and small amounts
(
3%) of 3-hydroxytetradecanoic acid (3-OH-14:0). The chromatogram
(Lambert group E) of the isolate can be differentiated from that for
Helicobacter cinaedi by the presence of 3-OH-14:0 and the
absence of 3-OH-12:0 (3-hydroxydodecanoic acid) (10, 12).
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FIG. 2.
Gas chromatogram of cellular fatty acid methyl esters of
H. fennelliae. See the text for compound abbreviations and
designations.
-lactamase negative by cefinase disk (BBL Microbiology Systems). The MICs of the
seven agents were identical on the two media and were as follows:
ampicillin-sulbactam, 0.38 µg/ml; ceftazidime, 0.75 µg/ml; ceftriaxone, 0.094 µg/ml; ciprofloxacin, 0.5 µg/ml; clarithromycin, 4 µg/ml; trimethoprim-sulfamethoxazole, 0.5 µg/ml; gentamicin, 1.5 µg/ml.
This is the first documented case of H. fennelliae
bacteremia in a non-HIV-infected patient or in a heterosexual patient
and the first reported case of septic shock due to infection caused by
this organism. The nearly complete resolution of systemic fungal infection prior to acquisition of H. fennelliae, the absence
of other newly developed infections, and the patient's apparent
response to antimicrobial therapy suggest that H. fennelliae
caused the severe septic complication. Though ours was not an AIDS
patient or an HIV-infected homosexual or bisexual man, his underlying immunoincompetence due to cirrhosis of the liver and diabetes mellitus,
as well as preexisting disseminated fungal infections, might have
contributed to the occurrence of bacteremia complicated with septic
shock caused by this organism.
The portal of entry of H. fennelliae in our patient was not
readily apparent. H. cinaedi has been reported to gain
access to the host through the gastrointestinal tract or via direct
inoculation into skin (cellulitis) and joints (arthritis) (1, 3,
6, 11, 13). This organism is found in 8% of stool cultures from homosexual men without diarrhea, but it is not found in stool cultures
from heterosexual men and women (2, 14). Despite the
original association between H. cinaedi bacteremia and
diarrhea, gastrointestinal symptoms have rarely been encountered in
patients with bacteremia due to H. fennelliae or H. cinaedi (1, 14). Our patient had no gastrointestinal
symptoms or skin and soft-tissue lesions prior to or during the
bacteremic episode, and microbiological investigations of fecal
specimens and rectal swab samples were all negative for the organism.
Several investigators have noted difficulty in initial staining of
H. cinaedi and H. fennelliae in blood culture
bottles (2, 11). In these studies, the organisms were
demonstrated only upon dark-field examination or acridine orange
staining smears. We did not experience difficulty visualizing these
organisms in the nonradiometric BACTEC blood culture system
(6). However, the replacement of safranin by 1%
carbolfuchsin in the Gram-staining preparation improved visualization
of these organisms.
Susceptibility tests for H. cinaedi or H. fennelliae are not standardized. However, a wide variety of
antimicrobial agents, including ceftriaxone, gentamicin, rifampin,
doxycycline, and ciprofloxacin have in vitro activity against these
organisms and have also been demonstrated to be effective in vivo
(2, 6, 11-13). The susceptibility pattern of our isolate
partly agreed with the previous observations of H. fennelliae.
In conclusion, this report describes H. fennelliae
bacteremia in a non-HIV-infected heterosexual man and demonstrates the capacity of this organism to cause septic shock. H. fennelliae should be considered in clinical contexts, including
HIV-infected homosexual men with proctocolitis or bacteremia and
patients with other immunocompromised conditions manifesting bacteremia
with or without severe septic complications.
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FOOTNOTES |
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* Corresponding author. Mailing address: Department of Laboratory Medicine, National Taiwan University Hospital, No. 7 Chung-Shan South Rd., Taipei, Taiwan. Phone: 886-2-23562149. Fax: 886-2-23224263. E-mail: luhkt{at}ha.mc.ntu.edu.tw.
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Journal of Clinical Microbiology, June 1999, p. 2084-2086, Vol. 37, No. 6
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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