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Radiological Case of the Month
Mirzada Kurbasic, MD;
V. Faye Jones, MD;
Charles M. Maxfield, MD
From the University of Louisville School of Medicine, Department of Pediatrics (Drs Kurbasic and Jones), and Kosair Children's Hospital, Department of Pediatric Radiology (Dr Maxfield), Louisville, Ky.
Arch Pediatr Adolesc Med. 1999;153:761-762.
A 2-YEAR-OLD BOY presented with a 6-week history of enlarged lymph nodes in his right axilla and arm. Other symptoms included a temperature of 38.8°C, a mild cough, abdominal pain, and decreased activity and appetite. Prior chest radiographs had revealed bilateral pulmonary opacities in the upper lobes. Previous outpatient therapy with antimicrobials had shown no response. The patient lives in a rural area and has a kitten and 2 dogs. The family reported no knowledge of exposure to tuberculosis or other transmissible diseases.
Physical examination revealed tender, mobile, 1- to 2-cm, nonfluctuant lymph nodes in the right axilla, mid arm, and epitrochlear regions. The liver and spleen were mildly enlarged. Linear erythematous excoriations were present on the right side of the chest and a healing papular lesion was observed on the dorsum of the right arm.
Computed tomography of the chest was performed and the results are shown in Figure 1, Figure 2, and Figure 3. Results of a purified protein derivative test were negative. Laboratory studies including fungal and Bartonella species serology tests were inconclusive. Excisional biopsy of the lymph node of the mid arm was performed.
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Figure 1.
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Figure 2.
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Figure 3.
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Denouement and Discussion: Atypical Cat-scratch Disease
Figure 1. A 2-cm lymph node in the right axilla (arrow).
Figure 2. Lytic lesion of the left first rib (arrow).
Figure 3. Nodular lesion in the left upper lobe (arrow).
The lymph node biopsy revealed granulomatous inflammation with fungal hyphae; a diagnosis of Bartonella henselae infection was confirmed using polymerase chain reaction on the lymph node specimen.
Cat-scratch disease (CSD) is a relatively common bacterial infection occurring all over the world. In the United States, it is estimated that 22,000 to 24,000 cases occur each year with 2000 patients requiring hospitalization.1-2 Although CSD is considered a childhood disease, 20% of the cases occur in people aged 20 years or older.3 Sixty percent of cases occur in men; the preponderance of patients are white.3-4 Cat-scratch disease occurs most frequently in the fall and winter.3
Wear et al5 were the first to definitively identify a bacterium as the etiologic agent in CSD. This organism was designated Afipia felis. More recently, other studies indicated Bartonella (formerly Rochalimaea henselae, a fastidious, slow-growing, gram-negative organism) as the major causative agent of CSD.6-7
Cat-scratch disease can affect all organ systems and cause a variety of clinical manifestations. Lymphadenopathy is the most common presentation, occurring in more than 80% of cases.3 Axillary lymph nodes, followed by cervical and mandibular nodes, are most commonly involved. Mild systemic symptoms may also be present. Additionally, 5% to 20% of patients are seen with more atypical presentations.3 These include Parinaud oculoglandular syndrome, encephalopathy/encephalitis, radiculopathy, rashes, pneumonitis, and osteolytic lesions.
Pulmonary involvement is a rare complication of CSD occurring in less than 1% of cases.8 The severity of the disease process varies from mild to severe and some patients require assisted ventilation. Abbasi9 reported 4 cases, all of which had pleural involvement as well as parenchymal disease. Typically, exudative pleural fluid is present, which may require drainage. Complete recovery is usual.
Osteomyelitis is also seen in less than 1% of cases of CSD.10-11 It has been reported that direct extension from an adjacent involved lymph node is the causative mechanism, but hematogenous spread is also likely.10 Any region of the skeleton may be affected. Bone biopsy will show granulomatous inflammation with central necrosis.12 Imaging studies such as computed tomography, magnetic resonance imaging, or bone scans are helpful to identify the lesion but are not specific.13
Historically, diagnosis was based on meeting 3 of 4 criteria: history of an intimate exposure to a healthy cat (especially a kitten) and an inoculation site, regional adenopathy with sterile pus, a positive cat-scratch test> result, and a lymph node biopsy showing granulomas and abcessess. Currently, a more definitive diagnosis ispossible using enzyme-linked immunosorbent assay for IgM and IgG and indirect immunofluorescent assay, but sensitivity and specitivity varies among laboratories. The identification of B henselae as the most common causative agent for CSD makes the role of culture more promising.2 Polymerase chain reaction assay is more sensitive than culture and establishes the diagnosis very early.4, 14
Most people with CSD require no therapy. The lymphadenopathy associated with this infection spontaneously resolves in 2 to 4 months. Needle aspiration of the suppurated lymph node may be necessary to relieve pain, but it rarely needs to be repeated.
Antimicrobial therapy is controverial. Most studies have not demonstrated any significant alteration in the course of the disease when it is used. However, in patients who are severely ill or immunosuppressed, rifampin, trimethoprim-sulfamethoxazole, ciprofloxacin, and parenteral gentamicin sulfate have been shown to be effective in some cases.2, 15-16 In patients with bacillary angiomatosis, erythromycin and doxycycline are considered the first and second line of treatment, respectively.2
Control of the disease is directed at prevention. Cats, particularly kittens, are the major source of infection from B henselae. Avoidance of bites and scratches from these animals or prompt cleaning if they occur is imperative.
AUTHOR INFORMATION
Accepted March 10, 1998.
Reprints: Mirzada Kurbasic, MD, Department of Pediatrics, University of Louisville School of Medicine, Louisville, KY 40292.
REFERENCES
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1. Jackson LA, Perkins BA, Wenger JD. Cat scratch disease in the United States: an analysis of three national databases. Am J Public Health. 1993;83:1707-1711.
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2. Shenep JL. Cat scratch disease and Bartonella henselae infections in children. Pediatr Ann. 1996;25:518-523.
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3. Klein JD. Cat scratch disease. Pediatr Rev. 1994;15:348-353.
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5. Wear DJ, Margilein AM, Hadfield TL, Fisher GW, Schlagel CJ, King FM. Cat scratch disease: a bacterial infection. Science. 1983;221:1403-1405.
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6. Relman DA, Loutit JS, Schmidt TM, Falkow S, Tompkins LS. The agent of bacillary angiomatosis. N Engl J Med. 1990;323:1573-1580.
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7. Relman DA. The identification of uncultured microbial pathogens. J Infect Dis. 1993;168:1-8.
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8. Margileth AM. Cat scratch disease. Adv Pediatr Infect Dis. 1993;8:1-21.
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9. Abbasi S. Pulmonary manifestations of cat scratch disease. Pediatr Infect Dis J. 1995;14:547-548.
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10. Carithers HA. Cat scratch disease associated with an osteolytic lesion. AJDC. 1983;137:968-970.
11. Walterspiel JN, Nimityongskul P. Positive bone scan in cat scratch disease. Pediatr Infect Dis J. 1987;6:944-945.
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12. Muszynski MJ, Eppes S, Riley HD. Granulomatous osteolytic lesion of the skull associated with cat scratch disease. Pediatr Infect Dis J. 1987;6:199-201.
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13. Hopkins KL, Simoneaux SF, Patrick LE, Wyly JB, Dalton MJ, Snitzer JA. Imaging manifestations of cat scratch disease. AJR Am J Roentgenol. 1996;166:435-438.
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14. Anderson BA, Sims K, Regnery R, et al. Detection of Rochalimaea henselae DNA in specimens from cat scratch disease patients by PCR. J Clin Microbiol. 1994;32:942-948.
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15. Collipp PJ. Cat scratch disease: therapy with trimethoprim-sulfamethoxazole. AJDC. 1992;146:397-399.
16. Bogue CW, Wise JD, Gray GF, Edwards KM. Antibiotic therapy for cat-scratch disease? JAMA. 1989;262:813-816.
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SECTION EDITOR: BEVERLY P. WOOD, MD
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
Index of Suspicion
Bhansali et al.
Pediatr. Rev. 2005;26:143-147.
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