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Transverse Myelitis in 2 Patients With Bartonella henselae Infection (Cat Scratch Disease) (in comes Army Pathology) (Seen that before! CR)

Posted By: CrystalRiver
Date: Thursday, 4-Jan-2018 23:11:54
www.rumormillnews.com

In Response To: Co-culture of human fibroblasts and Borrelia burgdorferi enhances collagen and growth factor mRNA (very scientific/for nerds) (CrystalRiver)

Transverse Myelitis in 2 Patients With Bartonella henselae Infection (Cat Scratch Disease) (in comes Army Pathology) (Seen that before! CR)

https://academic.oup.com/cid/article/45/4/e42/428639

Issue Cover
Volume 45 Issue 4
15 August 2007
Article Contents
Abstract
Acknowledgments
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Transverse Myelitis in 2 Patients With Bartonella henselae Infection (Cat Scratch Disease)
Peter Baylor Anastasia Garoufi Themistoclis Karpathios Jon Lutz Jeffrey Mogelof Dennis Moseley
Clinical Infectious Diseases, Volume 45, Issue 4, 15 August 2007, Pages e42–e45, https://doi.org/10.1086/519998
Published: 15 August 2007 Article history
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Abstract
Cat scratch disease is usually a benign, self-limiting condition. Neurological manifestations are uncommon and may consist of encephalopathy, seizures, and coma. This report describes 2 cases of transverse myelitis: 1 case in a 46-year-old man who had lymph node biopsy and serological testing results that were positive for Bartonella henselae and 1 case in a 13-year-old adolescent boy who had serological testing results that were positive for B. henselae. These are 2 of the only 3 cases of transverse myelitis associated with cat scratch disease that have been reported since the causative organism was first reported.
Topic: seizures coma cat-scratch disease adolescent bartonella henselae transverse myelitis neurologic manifestations serologic tests infection lymph node biopsy encephalopathy
Issue Section: Brief Reports
Cat scratch disease (CSD) is caused by a gram-negative bacillus, Bartonella henselae [1]. It usually produces a mild, self-limiting illness characterized by regional lymphadenopathy, malaise, and fever. Encephalopathy accounts for 80% of the neurological manifestations of CSD [2]. To our knowledge, there have only been 6 reports of transverse myelitis associated with CSD to date [3,4,5,6,7–8]. This report describes 2 patients with CSD-associated transverse myelitis.

Patient 1.In May 1997, a 46-year-old man, who had a 3–4-week history of intermittent fever, night sweats, and 5.5-kg weight loss, visited our evaluation unit 4 days after developing a large, painful swelling in the right groin. He stated that he had received several cat scratches in the weeks previous to hospitalization. The mass was explored, found to be an enlarged lymph node, and excised. The following day, the patient complained of numbness in the right foot and difficulty voiding. Catheterization yielded 900 mL of urine. The next morning, the patient was unable to walk. Examination revealed a temperature of 37.2° C, which subsequently increased to 39.4° C; a pulse of 80 beats/min; and blood pressure of 150/92 mm Hg. An incomplete sensory level was noted at T5 to light touch; pain sensation was absent below this level. The patient had flaccid areflexic paraplegia, except for minimal movement of the right foot and toes.

The following laboratory values were noted: a hemoglobin level of 14.9 g/dL and a WBC count of 10,000 cells/mm3 (with 42% neutrophils, 21% band forms, 21% lymphocytes, 12% monocytes, and 4% eosinophils). Chest radiograph, urinalysis, and blood chemistry analysis findings were normal, except for a lactate dehydrogenase level of 266 mU/mL (normal range, 91–180 mU/mL). Results of cranial CT without contrast were normal. MRI of the cervicothoracic spine revealed a faint, poorly defined C5–C7 central cord hyperintensity on sagittal T2-weighted images without focal cord enlargement, consistent with an inflammatory process. Lumbar puncture yielded an RBC count of 100 cells/mm3, a WBC count of 47 cells/mm3 (with 70% lymphocytes, 26% monocytes, and 4% neutrophils), a protein level of 58 mg/dL, and a glucose level of 67 mg/dL. Results of culture and stain of CSF samples were negative for bacteria, fungi, and acid-fast bacilli. Testing of CSF samples for cryptococcal antigen yielded negative results. Purified protein derivative skin testing yielded negative results, as did serological testing for coccidioidomycosis, HIV infection, Lyme disease, antinuclear antibodies, and syphilis.

Light microscopic examination of the lymph node revealed severe necrotizing granulomatous inflammation, with prominent areas of central necrosis and microabscess formation. Results of acid-fast and methenamine silver staining were negative, but staining with Dieterli's silver revealed small scattered organisms, which upon review at the Armed Forces Institute of Pathology (Washington, DC) and study using Warthin-Starry stain, appeared to be myriad branched bacilli of CSD. Serum immunofluorescent IgM and IgG antibody titers to B. henselae were 1 : 32 (normal titer, <1 : 16) and 1 : 128 (normal titer, <1 : 64), respectively (measured at Associated Regional and University Pathologists, Salt Lake City, UT). No antibodies to B. henselae were detected in CSF samples. The total IgG level in CSF samples was elevated at 7.1 mg/dL (normal range, 2–4 mg/dL). PCR of CSF samples for Bartonella species (performed at the Armed Forces Institute of Pathology) yielded negative results. A second measurement obtained 2–3 weeks later revealed a serum titer of IgG to B. henselae of 1 : 512 (normal titer, <1 : 64).

After the MRI study and before the Armed Forces Institute of Pathology report, the patient received empirical treatment with methylprednisone and intravenous immunoglobulin for 4 days. After confirmation of the diagnosis of CSD, the patient was treated with doxycycline and rifampin for 2 months. When seen for a follow-up visit 4 months after his initial presentation, the patient was much improved and was walking with a walker. Fourteen months later, he used only a cane. Physical examination revealed lower extension hyperreflexia, bilateral Babinski signs, and moderate weakness of both legs (left leg, 3/5; right leg, 4/5).

Patient 2.A 13-year-old adolescent boy presented with right axillary lymphadenopathy and a cutaneous skin lesion 1 week after a cat scratch [7]. One week after the initial presentation, fever, anorexia, and headaches developed. On day 17 after the cat scratch, the patient complained of dysesthesias, abdominal pain, and sensory impairment below T8–T10. Difficulty walking was quickly followed by paralysis of the legs and urinary retention. Examination of CSF samples revealed a WBC count of 300 cells/mm3 (with 70% lymphocytes and 30% neutrophils), a glucose level of 53 mg/dL, and a protein level of 90 mg/dL.

Treatment was initiated with ceftazidime and netilmicin administered intravenously for 10 days. Dexamethasone was administered intravenously for 5 days. Fever subsided by day 3 of treatment. On day 4 of treatment, a second lumbar puncture revealed a decrease in the WBC count to 80 cells/mm3 (with 50% neutrophils), a protein level of 29 mg/dL, and a glucose level of 85 mg/dL. The neurological symptoms began to resolve on day 7. Walking unaided was possible by day 12 after treatment initiation. Bladder function improved, and lymphadenopathy decreased. Six weeks later, the patient had recovered completely. Titers of antibody to B. henselae were 1 : 128 on admission, 1 : 512 at day 15, and 1 : 32 at 6 months (normal titer, <1 : 64). Titers to Bartonella quintana were 1 : 512 on admission and at day 15 and 1 : 32 at 6 months (normal titer, <1 : 64). The titer to Bartonella elizabethae was 1 : 32 in all samples (normal titer, <1 : 64). Serological examination was performed by indirect fluorescent antibody at the Centers for Disease Control and Prevention (Atlanta, GA). The diagnosis of CSD with transverse myelitis in patient 2 was based on the history, clinical findings, and antibody titers. Biopsy of the lymph node was not performed.

Discussion.The etiology of CSD as a bacterial infection was confirmed with the discovery of pleomorphic bacilli in the lymph nodes of a patient with CSD in 1983 [9]. B. henselae was first identified by culture of lymph nodes samples from patients with CSD in 1993 [10]. In a report from California, 81 (40%) of 205 cats tested had B. henselae bacteremia [11]. We now know that B. henselae resides in the digestive tract of the cat flea, B. henselae organisms are excreted in the feces of the cat flea, the claws of the cat become contaminated with the organism when the cat scratches itself in an effort to rid itself of the organism, and cat scratches transmit the infection to humans [12]. A strong correlation exists between PCR results of pus aspirate samples from lymph nodes of patients who have positive skin test results for CSD and high B. henselae antibody titers [13]. In 1995, Dalton et al. [14] reported that 86 (95%) of 91 patients who met strict criteria for the diagnosis of CSD had titers of ⩾1 : 64 to either B. henselae or B. quintana. More recently, it was reported that some of the serological tests are not as sensitive as initially believed [15]. Extensive cross-reactivity occurs between B. henselae and B. quintana; patients with CSD typically have high titers to both organisms [16].

Pathologic examination reveals a necrotizing granulomatous inflammatory process that may resemble the process found with fungal or mycobacterial infection or tularemia [1]. Warthin-Starry staining of involved lymph nodes reveals the small pleomorphic organisms, which although nondiagnostic, provide strong evidence of CSD. A high antibody titer to Bartonella species is useful diagnostically.

Both patients were exposed to young cats. Both patients had positive serological test results. Patient 1 had a lymph node biopsy result that revealed findings that were consistent with the causative organisms that were found on Warthin-Starry staining.

Transverse myelitis is one of the neurological manifestations of CSD. In a review of 62 patients with acute transverse myelitis, Berman et al. [17] found that 37% of the patients had had a viral or bacterial infection 5–21 days before presentation. Antecedent infection was found in one-third of the patients with acute transverse myelitis in the study by Hoffman [18]. In another review, myelitis was preceded by a febrile illness in 25 (81%) of 31 patients [19].

Since the discovery that B. henselae infection was the cause of CSD in 1993 [9], the case report presented here is the first case of transverse myelitis associated with CSD in which organisms consistent with features of B. henselae (as demonstrated by Warthin-Starry staining) were found in the involved lymph node.

Six cases of transverse myelitis due to CSD were reported in the literature before our first case described herein [3,4,5,6,7–8]. Since the discovery of the causative agent in 1993 [9], only 1 case of transverse myelitis due to B. henselae has been reported, but in that case, no pathologic examination results documenting the presence of B. henselae were available [8]. The patient reported by Karpathios et al. [7], in whom the diagnosis was confirmed serologically, was included in a large series from Greece; no pathologic examination results documenting the presence of B. henselae were available. The features of the 7 patients with CSD-associated transverse myelitis are summarized in table 1.

Table 1
Characteristics of 7 patients with cat scratch disease (CSD)–associated transverse myelitis.
View largeDownload slide
Characteristics of 7 patients with cat scratch disease (CSD)–associated transverse myelitis.
Whether the pathogenesis of myelitis is because of direct invasion of the spinal cord by B. henselae or because of an immune-mediated postinfectious process is uncertain. Examination of CSF samples from patients with CSD-associated transverse myelitis reveals a normal glucose level, slightly elevated protein level, and moderate pleocytosis, usually of lymphocytes (table 1). Patient 1 could have had another cause of myelitis; however, in view of the rapid onset of paraparesis associated with detection of Bartonella species in the lymph node, it seems likely that CSD was the cause. The failure to detect Bartonella nucleic acids in the CSF samples of patient 1 does not exclude the possibility that transverse myelitis was caused by Bartonella [15]. The preferred drug for treatment of this infection is azithromycin [20].

Acknowledgments

We thank Dr. J. E. Koehler, for helpful discussion of therapy and her review of the manuscript, and Dr. A. Arvin, who was the first physician to suggest that myelitis was attributable to cat scratch disease.

Potential conflicts of interest.All authors: no conflicts.

References

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----------------------------------------
Lot of symptoms like I had

Many Blessings,
CrystalRiver





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