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CID 1998;27 (December)
Brief Reports
1533
hemoglobin level, hematocrit, platelet count, and results of blood
chemistry and urinalysis were all within normal limits, and cultures
of blood were negative.
Empiric antimicrobial therapy was initiated with iv vancomycin,
1,000 mg every 12 hours, and iv aztreonam, 2 g every 8 hours. The
patient was afebrile within 24 hours of the incision-and-drainage
procedure and aztreonam was subsequently discontinued. On the
10th day of antimicrobial therapy, a febrile reaction to vancomycin
prompted a change in therapy to ciprofloxacin, 750 mg every 12
hours, for an additional week. Within another 3 weeks, the patient
had returned to his full-time gastroenterology practice. A followup MRI scan confirmed resolution of the septic synovitis.
C. striatum is a nonsporulating, non-acid-fast, pleomorphic,
gram-positive rod that is aerobic and facultatively anaerobic. The
organism appears striated on gram-stained preparations. Excluding
the case we describe, only 22 cases of infection due to C. striatum
have been reported.
The organism is normally found in the nose, mucous membranes,
and the skin of the arms, forehead, and cheeks, and is isolated most
often from the upper half of the body. Corynebacterium jeikeium in
contrast, colonizes the axillary, inguinal, and anal areas of the skin.
Men are predisposed to bacteremia due to Corynebacterium species,
probably because the sebum content of their skin is higher than that
of women, and thus provides more fat and fatty acids for growth of
lipophilic diphtheroids. Previous reports of septic arthritis caused by
other corynebacteria included infections due to Corynebacterium xero-
sis, Corynebacterium pyogenes, Corynebacterium haemolyticum, Corynebacterium kutscheri, Corynebacterium group D2, and two nonspeciated corynebacteria.
With the exception of the most resistant strains, C. jeikeium and
Corynebacterium urealyticum, most Corynebacterium species are
susceptible to penicillin, ampicillin, cephalosporins, aminoglycosides, vancomycin, rifampin, and the fluoroquinolones.
Detection of Specific Cellular Immune Response to
Bartonella henselae in a Patient with Cat Scratch Disease
ing days, erythema nodosum of the left leg and arm, arthritis of
the left ankle joint, and conjunctivitis of the right eye developed.
Reiter’s syndrome was suspected and testing for HLA-B27-antigen
was positive. Cultures of stool, urine, and cervical smear specimens
did not reveal any pathogens. The patient was treated with oral
Clinical presentation of infection due to Bartonella henselae
ranges from a relatively mild lymphadenopathy with few additional
symptoms, seen in cat scratch disease (CSD), to life-threatening
systemic disease in immunocompromised individuals [1]. The
more severe clinical manifestation in immunocompromised hosts
points to a role of T cells in the pathogenesis of these infections.
We describe a patient with CSD and Reiter’s syndrome, whose
cellular immune response to B. henselae was investigated by using
a lymphoproliferation assay.
A 27-year-old woman presented with a 4-week history of inguinal lymphadenopathy, and a 1-week history of fever. Despite therapy with trimethoprim-sulfamethoxazole for 10 days, the lymph
node had continued to enlarge. Therefore, she was admitted to
the hospital. Physical examination was unremarkable except for a
tender, dolent, 8-cm 1 4-cm right inguinal lymph node and cat
scratch lesions on the right leg. She had acquired a young stray
cat during her holiday in Sicily 3 months earlier. Serologies for
common agents of lymphadenopathy were negative. Fine needle
aspiration of the lymph node yielded sterile pus. During the follow-
Reprints or correspondence: Dr. Mardjan Arvand, Institut für Infektionsmedizin, Abteilung für Medizinische Mikrobiologie und Infektionsimmunologie, Universitätsklinikum Benjamin Franklin, Freie Universität Berlin, Hindenburgdamm 27, D-12203 Berlin, Germany.
Clinical Infectious Diseases 1998;27:1533–4
q 1998 by the Infectious Diseases Society of America. All rights reserved.
1058–4838/98/2706–0036$03.00
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Lawrence A. Cone, Noel Curry, Moxelle A. Wuestoff,
Stephen J. O’Connell, and John F. Feller
Departments of Medicine, Orthopedic Surgery, Pathology, and
Radiology, Eisenhower Medical Center, Rancho Mirage, California
References
1. Watkins DA, Chahine A, Creger RJ, Jacobs MR, Lazarus HM. Corynebacterium striatum: a diphtheroid with pathogenic potential. Clin Infect Dis
1993; 17:21 – 5.
2. Rufael DW, Cohn SE. Native valve endocarditis due to Corynebacterium
striatum: case report and review. Clin Infect Dis 1994; 19:1054 – 61.
3. Weiss K, Labbe AC, Laverdiere M. Corynebacterium striatum meningitis:
case report and review of an increasingly important Corynebacterium
species. Clin Infect Dis 1996; 23:1246 – 48.
4. National Committee for Clinical Laboratory Standards. Susceptibility testing criteria and QC parameters: approved guidelines. NCCLS document
M23A. Wayne, Pennsylvania: National Committee for Clinical Laboratory Standards, 1995.
Figure 1. Stimulation of peripheral blood lymphocytes of the patient (black bars) and of two representative healthy donors (white and
hatched bars) with heat-killed Bartonella henselae in the indicated
concentrations. Proliferation was determined after incubation for 5
days. Results are presented as stimulation index (thymidine uptake
after antigen stimulation divided by the spontaneous uptake).
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1534
Brief Reports
CID 1998;27 (December)
doxycycline and prednisolone for 4 weeks. All symptoms resolved
except for the adenopathy; the lymph node erupted spontaneously
on day 17 and revealed pus, which was sent to our laboratory to
be evaluated for B. henselae. A fistula that developed at the incisional area healed within a few weeks. She was discharged from
the hospital on day 22 and did well thereafter.
B. henselae DNA was isolated from the lymph node aspirate
by using PCR amplification of citrate synthase gene and restriction
fragment length polymorphism (RFLP) analysis [2]. Culture for
Bartonella species performed on solid agar media and incubated
for up to 6 weeks did not yield B. henselae. Serology was performed by using an indirect fluorescence assay (MRL, Cypress,
CA). Diagnostics serum samples collected at 2 and 6 weeks and
8 months after admission yielded titers of 256, 128, and 32, respectively, for IgG antibodies to B. henselae.
Peripheral blood lymphocytes were evaluated for B. henselae–
specific stimulation using a whole-blood lymphoproliferation
assay [3]. Heparinized blood was collected from the patient 2
weeks after admission, and blood samples from five healthy donors
were analyzed in parallel. Heat-killed B. henselae (ATCC [American Type Culture Collection] 49793) was used as a specific stimulus, whereas lectin mitogens served as positive controls. We found
a specific proliferation of the patient’s lymphocytes upon stimulation with B. henselae, whereas lymphocytes from the five healthy
donors did not respond to equivalent stimulation (figure 1).
To our knowledge, there are no data available concerning
B. henselae –specific cellular immune responses in vitro in patients
with CSD. The CSD skin test used previously as one of four
criteria for clinical diagnosis of CSD [4] determined a delayed-
type hypersensitivity to tissue homogenates containing the (at that
time) unknown agent of CSD. The skin test antigen is, however,
not commercially available and tissue homogenates bear the risk
of transmitting pathogens. Thus, an in vitro lymphoproliferation
assay might be a useful diagnostic adjunct, especially in cases for
which serologic results are equivocal. (After preparing this article,
we studied the peripheral blood lymphocytes of another CSD patient, and found, as described in this report for the first time, a
Bartonella-specific proliferation of her cells.)
Mycoplasma pneumoniae and Second-Degree Heart Block
SaO2 88%. Laboratory evaluation revealed the following values:
WBCs, 15,600/mm3 (80% neutrophils); hemoglobin, 10 g/dL; and
C-reactive protein, 226 mg/L. Blood electrolyte (potassium, sodium, and calcium), blood urea and nitrogen, and creatinine levels
and platelet counts were normal. Cultures of blood were sterile,
and serological investigations were negative for antibodies to Chlamydia and Legionella species and HIV. Conversely, a serology
for Mycoplasma pneumoniae with use of EIA was positive according to the following results: on the first serum sample (hospital
day 2), positive for IgM antibodies with IgG antibodies; and on
the second sample (20 days later), a significant increase in IgG
antibodies coinciding with the strong decrease in IgM. An electrocardiogram showed no abnormality on the first hospital day. According to the clinical, biological, and radiographic findings, atypical pneumonia was diagnosed, and the initial treatment consisted
of iv erythromycin and iv cefotaxime. Oxygen was delivered at a
rate of 8 L per minute.
On the second hospital day, the patient experienced dizziness
and was bradycardic. An electrocardiogram showed a slow ventricular rate (45/minute) and a constant long PR space (36 milliseconds), with one narrow QRS complex observed every two P nodes.
In addition, we noted the absence of a bundle branch block, which
was compatible with a second-degree heart block. A 24-hour
Holter electrocardiogram showed episodical Luciani-Wenckebach
period (figure 1). Transthoracic echocardiography was normal. On
the basis of the positive initial serological findings (IgM), the heart
block was determined to be of infectious origin; cefotaxime therapy
was discontinued. Because of the patient’s excellent tolerance of
the bradycardia, the probable nodal level of the heart block (narrow
Cardiac manifestations of infection due to Mycoplasma pneumoniae have been described previously in association with myocarditis and pericarditis [1–3]. M. pneumoniae infections have
been associated with nonspecific electrocardiographic modifications and are not believed to be responsible for potentially serious
high-level heart blocks. Herein we describe a patient with seconddegree heart block associated with M. pneumoniae.
A 45-year-old man was admitted to our intensive care unit because of mild respiratory distress, fever (temperature, 39.87C),
myalgia, cough, and diarrhea. At the time of admission, his blood
pressure was 120/85 mm Hg, his pulse was 85/minute, and his
respiratory rate was 27/minute. One week before admission, he
had a mild illness with cough and fever. He had no history of
cardiovascular disease, and had not been taking any medications.
A chest radiograph demonstrated bilateral interstitial infiltrates.
Arterial blood gas determinations while the patient was breathing
room air included the following values: pH, 7.43; PaO2, 8.32 kPa;
PaCO2, 4.29 kPa; bicarbonate, 19.5 mmol/L; base excess, 2.5; and
Reprints or correspondence: Dr. Antoine Veillard Baron, Service de Reanimation Medicale, Hôpital Ambroise Pare, 9 Avenue Charles de Gaulle, 92100,
Boulogne-Billancourt, France.
Clinical Infectious Diseases 1998;27:1534–5
q 1998 by the Infectious Diseases Society of America. All rights reserved.
1058–4838/98/2706–0037$03.00
/ 9c5c$$de50
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Mardjan Arvand, Martin E. A. Mielke, Klaus Sterry,
and Helmut Hahn
Institut für Infektionsmedizin, Universitätsklinikum Benjamin Franklin,
Freie Universität Berlin, and Abteilung für Innere Medizin,
Grunewaldklinik, Berlin, Germany
References
1. Anderson B, Sims K, Regnery R, et al. Detection of Rochalimaea henselae
DNA in specimens from cat scratch disease patients by PCR. J Clin
Microbiol 1994; 32:942 – 8.
2. Norman AF, Regnery R, Jameson P, Greene C, Krause DC. Differentiation
of Bartonella-like isolates at the species level by PCR-restriction fragment length polymorphism in the citrate synthase gene. J Clin Microbiol
1995; 33:1797 – 803.
3. Leroux M, Schindler L, Braun R, Doerr HW, Geisen HP, Kirchner H. A
whole-blood lymphoproliferation assay for measuring cellular immunity
against herpes viruses. J Immunol Methods 1985; 79:251 – 62
4. Carithers HA, Carithers CM, Edwards RO. Cat-scratch disease, its natural
history. JAMA 1969; 207:312 – 6.
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