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Two different genotypes of Bartonella henselae in children with cat-scratch disease and their pet cats.

Two genotypes (I and II) of Bartonella henselae are involved in cat-scratch disease (CSD). Lymph node biopsies were taken from 3 children suffering from CSD, and blood cultures were obtained from their pet cats. Cat-scratch disease was confirmed serologically, histologically and by detection of B. henselae DNA in all 3 lymph nodes by PCR. Bartonella henselae grew in all cats' blood cultures. The first 2 children were siblings. Both children and their pet cats were infected with B. henselae genotype II, and the third patient and her cat were infected with B. henselae genotype I. In all cases, there were no essential differences in the clinical manifestations of the infection caused by these 2 genotypes of B. henselae.

Adolescent↗

Isolated splenic cat scratch disease in an immunocompetent adult woman.

We report a case of isolated splenic cat scratch disease in an immunocompetent woman. The clinical presentation of prolonged fever, night sweats, weakness, and intrasplenic lesions was highly suggestive of lymphoma. This is the second reported case of isolated splenic cat scratch disease in an adult and the first in a healthy adult.

Adult↗

Cat-scratch disease with paravertebral mass and osteomyelitis.

The case of a 9-year-old girl with cat-scratch disease (CSD) complicated by development of a paravertebral mass and osteomyelitis is presented. Following multiple scratches and inguinal lymphadenopathy, she developed back pain, and imaging demonstrated a paravertebral mass with evidence of osteomyelitis involving vertebra T9. The diagnosis was made on the basis of detection of Bartonella henselae by use of molecular techniques on an aspirate from the vertebral column and supportive serology for infection with B. henselae. Eleven other cases of this unusual manifestation associated with CSD have been reported in the literature and are reviewed. The patient was treated with gentamicin, followed by rifampicin and trimethoprim-sulfamethoxazole, orally and made a favorable recovery over 7 months. This is comparable with other case reports, regardless of the choice of antibiotic therapy. CSD in immunocompetent hosts is not always self-limiting, and tissues beyond the lymph nodes can be involved.

Bartonella henselae↗

Hepatosplenic cat-scratch disease in children: selected clinical features and treatment.

We reviewed 19 cases of hepatosplenic cat-scratch disease at Texas Children's Hospital (Houston). The range of the patients' ages was 2 years 4 months to 11 years 8 months. The chief complaint was fever for all patients. The duration of fever before diagnosis was 7 to 56 days (mean, 22 days). Abdominal pain was present in 13 patients (68%). Thirteen children were treated with rifampin alone, and three received rifampin therapy plus gentamicin or trimethoprim-sulfamethoxazole. Once rifampin therapy was initiated alone or in combination, improvement was noted within 1 to 5 days (mean, 2.6 days) for patients who had had prolonged fever the duration of which before rifampin therapy averaged 3 weeks. The most common dosage and duration for our patients were 20 mg/[kg x d] every 12 hours and 14 days, respectively. Rifampin should be considered in the initial antimicrobial treatment of hepatosplenic cat-scratch disease.

Animals↗

Monoclonal antibodies to Afipia felis--a putative agent of cat scratch disease.

Twelve hybridoma clones producing monoclonal antibodies to Afipia felis, a putative causative agent of cat scratch disease, were derived from BALB/c mice immunized with A felis. All 12 monoclonal antibodies were species-specific for A felis and reacted with lipopolysaccharide antigens of A felis. These monoclonal antibodies belong to immunoglobulin (Ig) G1, IgG2a, IgG2b, IgG3, and IgM isotypes. All monoclonal antibodies reacted with both agar-grown A felis and tissue culture-propagated A felis. Formalin fixation did not alter the reactivity of the antigen with the monoclonal antibodies. These monoclonal antibodies could be a useful tool for investigation of the disputed role of A felis in cat scratch disease.

Animals↗

Hepatosplenic cat-scratch disease and abdominal pain.

BACKGROUND: There have been several recent reports that cat-scratch disease (CSD) causes a multiplicity of atypical clinical syndromes. We recently diagnosed hepatosplenic CSD in a child who was seen with fever and abdominal pain. We report this case and 10 other patients with hepatosplenic CSD and highlight the importance of abdominal pain in this clinical entity. METHODS: This was a retrospective review of charts of patients with a diagnosis of cat-scratch disease at Egleston Children's Hospital between January, 1985, and June, 1996. From these cases patients with hepatosplenic CSD were selected for study. RESULTS: Seven children (64%) had significant abdominal pain, and in three children abdominal pain was their chief complaint. All children in the study had pathologic evidence of CSD or elevated titers of antibodies to Bartonella henselae. Ultrasound examination showed that all children had microabscesses in the spleen, and eight had abscesses in the liver. CONCLUSIONS: One of the most remarkable findings in this large series of cases of hepatosplenic CSD was that 64% of the patients complained of abdominal pain. All children in this study received antibiotics. It was our clinical impression that once antibiotics had been started, the patients appeared to improve very quickly. With an increased index of suspicion, the use of B. henselae serology and an abdominal ultrasound examination, the diagnosis of this underrecognized disease might be more readily made.

Abdominal Pain↗

Cat-scratch encephalopathy presenting as status epilepticus and lymphadenitis.

A five-year-old male was admitted to the hospital with generalized seizures. Enlarged lymph nodes raised the suspicion of cat-scratch disease. The diagnosis was confirmed by a positive history of a cat bite, typical histopathologic findings in the biopsy of the lymph nodes, and a positive skin test. Brain CT scan and LP were repeatedly normal. The clinical course was remarkable for recurrent episodes of status epilepticus refractory to usual anticonvulsant therapy and prolonged encephalopathy consisting of mental confusion, hemiparesis, tremor, chorea, and vomiting. All neurologic symptoms gradually resolved within nine months, without sequelae. Cat-scratch encephalopathy should be suspected in a child presenting with status epilepticus and enlarged lymph nodes. Aggressive and prolonged anticonvulsant therapy is strongly recommended.

Brain Diseases↗

Inguinal bubo due to cat-scratch disease.

A case of suppurative inguinal bubo due to cat-scratch disease in a young Caucasian man is described. The bubo was thought to have followed a laceration on the leg that occurred while the man was working in a slaughterhouse. The evidence for cat-scratch disease is considered, and its differentiation from other possible diagnoses, in particular lymphogranuloma venereum, is discussed.

Adult↗

Treatment of cat-scratch disease.

Cat-scratch disease is an infection caused by Bartonella henselae, a fastidious gram-negative bacillus acquired from exposure to an infected kitten or cat. The most common manifestation of human disease is lymphadenitis. Atypical forms of infection include Parinaud oculoglandular syndrome, stellate neuroretinitis, persistent fever without localizing signs, hepatosplenic infection, encephalopathy, osteomyelitis, and endocarditis. Immunocompromised individuals with B. hensalae infection may develop bacillary angiomatosis, bacillary peliosis, and relapsing bacteremia with fever syndrome. The bacillus is susceptible to several antibacterial agents in vitro, including penicillins, cephalosporins, aminoglycosides, tetracyclines, macrolides, quinolones, trimethoprim and sulfamethoxazole, and rifampin. Greatest clinical efficacy has been observed following treatment with rifampin, ciprofloxacin, gentamicin, trimethoprim and sulfamethoxazole, clarithromycin, and azithromycin. In one placebo-controlled study, azithromycin therapy was associated with more rapid diminution in size of infected lymph nodes. The majority of cases of cat-scratch disease occurring in normal hosts do not require anti-infective therapy for resolution of infection.

Animals↗

Disseminated cat scratch disease with vertebral osteomyelitis and epidural abscess.

A 5-year-old boy with cat scratch disease presented with fever of unknown origin and osteomyelitis of the thoracic spine and epidural abscess. He did not have localizing signs or symptoms. Computed tomography of the abdomen, which was initially negative, showed hepatosplenic disease. Cat scratch disease has variable systemic presentations and should be included in the differential diagnosis of fever of unknown origin if an epidemiologic risk factor is present.

Animals↗

Dermatologic manifestations and update of cat scratch disease.

Cat scratch disease is a relatively common cause of chronic (three weeks or longer) lymphadenopathy, with 80% of cases occurring in children and adolescents. This self-limited infection caused by a small, gram-negative, pleomorphic bacillus has been identified in ocular granuloma, skin inoculation lesions, and lymph node specimens. Dermatologic manifestations observed prospectively in 908 patients included primary cat scratch inoculation papules, pustules or rarely, vesicles. Occasionally, enanthematous mucous membrane (oral, ocular) primary inoculation lesions were observed. About 5% of patients have generalized macular, maculopapular, morbilliform, and rarely petechial, usually nonpruritic exanthem. Rarely, erythema nodosum or multiforme and ecchymoses with petechial rashes are seen. Thrombocytopenic purpura is extremely uncommon. Unusual manifestations such as the oculoglandular syndrome of Parinaud, encephalopathy, or severe systemic disease occur in about 10% of patients. Management consists of symptomatic treatment and occasional aspiration of a suppurative node. The disease usually resolves spontaneously in two to four months.

Adolescent↗

Cat-scratch disease: a review of the literature.

Cat-scratch disease (CSD) is a common cause of chronic lymphadenopathy (especially regional) that primarily affects children and adolescents. The clinical diagnosis of CSD is based on the presence of three of four criteria, which may include a positive CSD skin test. Usually a benign, self-limiting disease, CSD may sometimes have atypical manifestations and serious complications, particularly in immunocompromised hosts. Cat-scratch disease is now known to be caused by a small, gram-negative, pleomorphic bacterium. Antibiotics are dramatically effective against CSD in immunocompromised patients, but are not [corrected] of proven benefit in typical cases. Most patients recover with only symptomatic treatment. This article reviews the history of CSD research, clinical features of typical and atypical CSD, and current topics of interest in CSD research, especially in the areas of diagnosis and treatment.

Anti-Bacterial Agents↗

[Three children with systemic cat scratch disease].

Three girls with systemic cat scratch disease, aged 10, 13 and 9 years, were reported. They presented a prolonged fever and back pain in the early stage of the disease, and had no regional lymphadenopathy. Two of them had hepatosplenic granulomas, one with multiple 5 mm hypoechoic lesions in the liver and spleen, and the other with a single 2.5 cm hypodense lesion in the left hepatic lobe. The latter patient underwent a partial left hepatic lobectomy. All patients had elevated titers of antibodies to Bartonella henselae. Polymerase chain reaction detected B. henselae DNA in tissue specimens of the patient who underwent a hepatic lobectomy. Cat scratch disease should be recognized as a cause of fever of unknown origin because the prevalence of B henselae infection might be higher in Japan.

Adolescent↗

[A case of cat scratch disease with encephalopathy].

We report an atypical case of cat scratch disease (CSD), accompanied with encephalopathy that is a rare complication of CSD. A 17-year old man consulted a doctor for his right axillary lymphadenopathy. The history of his contact with cats and the sign of lymphnode swelling and fever suggested a suspect of cat scratch disease. Administration of ampicillin improved his clinical symptoms, but a few days later he suddenly fell into coma after an episode of convulsion. The CT scan of the brain and laboratory tests showed no significant findings except the slightly elevated cell counts and concentration of protein in his cerebrospinal fluid. He was referred to our hospital on the next day for further examinations and treatments for his coma of unknown cause. The physical examination on admission revealed slight neck stiffening and hypertonicity of his right lower limb, but radiological and laboratory tests showed no significant findings. He gradually recovered from his coma without apparent sequelae in three weeks. Indirect fluorescence antibody titers for CSD in his serum showed a significant elevation to 1:160 of IgM and 1:512 of IgG, and his clinical features were compatible to these of CSD with complications of the central nervous system.

Adolescent↗

Cat scratch disease: a bacterial infection.

Histopathologic examination of lymph nodes from 39 patients with clinical and pathological criteria for cat scratch disease revealed delicate pleomorphic Gram-negative bacilli in 34 of the 39 nodes. They were within the walls of capillaries in or near areas of follicular hyperplasia and within microabscesses. They were best seen with the Warthin-Starry silver impregnation stain. Organisms in lymph node sections exposed to convalescent serum from three patients and to immunoperoxidase stained equally well with all three samples. The organisms did not react with hyperimmune sera to Legionella pneumophila nor to several species of Rickettsia. These bacilli appear to be the causative agents of cat scratch disease.

Cat-Scratch Disease↗

Intracellular growth of Afipia felis, a putative etiologic agent of cat scratch disease.

The organism Afipia felis, which is though to be an etiologic agent of cat scratch disease, is a gram-negative rod that is clearly seen in infected tissue but is very difficult to isolate from clinical specimens; there has been only one report to date of the successful isolation and maintenance of the bacterium on artificial medium. We have found that A. felis will attach, invade via phagocytosis, and multiply intracellularly within the phagosomes of primary human monocytes and HeLa cells. Once in the cell, the bacterium appears to change morphologically, becoming longer and more pleomorphic, and loses its ability to grow on an artificial medium. Unique proteins have been identified in both the intra- and extracellular variants of A. felis. Convalescent-phase sera from patients with cat scratch disease react poorly with intracellular and extracellular bacteria, suggesting a poor humoral response. The tissue culture protocol presented has been used to isolate 14 new strains of A. felis and has for the first time permitted study of the pathogenesis of this unique organism.

Blotting, Western↗

Cellular fatty acid compositions of an unidentified organism and a bacterium associated with cat scratch disease.

The cellular fatty acid composition of a gram-negative bacterium associated with cat scratch disease was determined by capillary gas chromatography-mass spectrometry (GC-MS). The fatty acid profile of this organism was distinct from those of other bacteria we have tested and was characterized by an unknown acid which was identified as 11-methyloctadec-12-enoic acid. The position of the branched methyl group in this acid was established by GC-MS of the reduced acid, and the location of the double bond was confirmed by GC-MS analysis of dimethyl disulfide derivatives. Another clinical isolate with no known relationship to cat scratch disease but with similar morphological and biochemical features had a similar fatty acid profile, including 11-methyloctadec-12-enoic acid.

Cat-Scratch Disease↗