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A case of cat scratch disease with a submental mass as the initial symptom has been presented. The disease should be considered in the evaluation of swellings and masses of the cervicofacial region. However, because of the benign course of cat scratch disease, other more serious disease processes must be ruled out before establishing the diagnosis of cat scratch disease.
Cat-scratch disease is a zoonotic infection characterized by a skin papule at the site of the scratch followed by regional lymphadenitis. Recently, small gram-negative pleomorphic bacilli were demonstrated in sections of lymph node from patients with the disease. We now report identical bacteria in the primary inoculation site of three patients with cat-scratch disease. Lymph nodes from two of these patients also contained the same bacilli. Identical bacteria in both skin and lymph nodes from these patients are further evidence that the bacilli are the cause of cat-scratch disease. In early infections, biopsy of the primary site of inoculation and demonstration of bacilli may replace excision and histologic examination of lymph node in establishing the diagnosis of cat-scratch disease.
A case of encephalopathy complicating cat-scratch disease has been described. Neurologic signs manifested by convulstions and stupor appeared ten days after epitrochlear lymphadenopathy. The clinical course gradually improved over the next few days and recovery was complete. The spinal fluid was normal. The skin test with CSD antigen was positive. In all cases of encephalopathy developing within six weeks following the appearance of unexplained lymphadenopathy, the diagnosis of cat-scratch disease should be entertained. The importance of the cat-scratch disease antigen in diagnosis is emphasized.
BACKGROUND: Cat-scratch disease, or CSD, results from inoculation of the gram-negative bacillus Bartonella henselae via a cat's scratch. A regional lymphadenitis, which usually is cervical, develops and may progress to suppuration. It is necessary to differentiate CSD from other lymphadenopathies. CASE DESCRIPTION: A patient who had close contact with a cat subsequently developed a localized, suppurative cervical lymphadenitis. As B. henselae was identified in 1992, the authors were able to confirm the existence of CSD serologically. Surgical drainage resulted in a successful resolution of the disease process. CLINICAL IMPLICATIONS: As patients with CSD may be seen in the dental office, an awareness of its symptomatology can prevent unnecessary dental intervention and facilitate early treatment.
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Bartonella henselae is an etiologic agent of cat-scratch disease and, in immunocompromised patients, of bacillary angiomatosis and other severe syndromes. Cat-scratch disease usually presents as lymphadenopathy, which resolves spontaneously within 2-4 months. The utility of antibiotic therapy remains controversial. In Tyrol four cases of human cat-scratch disease were diagnosed in children in 1994, yielding a prevalence of 0.7/100,000 per year. A 3-year-old boy had lymphadenitis coli since one year despite antituberculosis therapy which was initiated because of the histopathological picture and a positive tuberculin reaction (despite negative mycobacteria-cultures and -PCR). Two girls, age 9 and 13 years, had lymphadenitis at upper or lower extremities after cat-scratches from kittens. A 13-year-old boy presented with febrile illness and right hip pain, computer tomography revealed an osteolytic lesion; symptoms subsided within 3 weeks. Diagnosis of cat-scratch disease is based on cat contact, negative studies for other similar diseases, characteristic histopathologic features (if available), and results of an indirect immunofluorescence test (antigen: Houston-1 isolate, ATCC 49882). We believe that the availability of this serological test will increase the number of diagnosed cases of human Bartonella henselae infections.
Ocular and neuro-ophthalmic manifestations of cat scratch disease are not uncommon. The association of anterior optic neuritis with retinal lesions suggests neuroretinitis, which is highly suggestive of cat scratch disease. A new case is described.
Encephalitis in cat scratch disease is uncommon and usually reversible. The patient with cognitive impairment and severe memory disorder did not improve after a 30 month follow up. MRI revealed disseminated lesions in the white matter of the cerebral hemispheres.
Cat-Scratch Disease (CSD) is a benign lymphadenitis that may progress to severe or recurrent forms, and it is occasionally associated with morbidity. Between January of 1998 and March of 1999, forty-three suspected CSD patients were assessed in the Hospital Cayetano Heredia and the Instituto de Salud del Niño, in Lima, Peru. Twelve patients had a confirmed diagnosis, 8 of whom were women, and the mean age was 10 years old. The majority (53%) of the cases were encountered in the summer. All patients reported having had contact with cats. Fever, malaise, lymphadenopathy and skin lesions were the most frequent clinical features. Twelve patients had indirect immunofluorescence antibody test titers of between 1/50 and 1/800 for Bartonella henselae and Bartonella clarridgeiae. Two lymph node biopsies were histologically compatible with CSD. No positive blood cultures could be obtained. This is the first Peruvian prospective study able to identify B. henselae and B. clarridgeiae in pediatric patients.
Cat-scratch disease (CSD) is a common cause of regional lymphadenopathy. We describe 2 children with an unusual presentation of disseminated CSD, the first one presenting with persistent fever, multilocular abscesses in liver and spleen as well as osteolytic lesions in the lumbar spine and the second one with portal vein thrombosis and severe ascites.
Cat-scratch disease (CSD) is an infection caused by a gram-negative bacillus known as Bartonella Henselae. Hepatosplenic disease occurs in only 0.3-0.7% of patients. In this report we describe a 7-year-old male presented with a 4-week history of fever, after diagnosis of CSD with regional lymphoadenitis. Ultrasonography and tomography identified hepatic and splenic abscesses. Antibiotic treatment for three months was associated with resolution of lesions. In Patients affected by CSD, ultrasonography and tomography permit to identify hepatic and/or splenic lesions, indicating systemic CSD.
Because the causative bacterium of cat scratch disease has not been definitively cultured or fully characterized, the authors have studied its ultrastructure in lymph node biopsies from two patients using glutaraldehyde-fixed tissue. In both specimens, the organisms were invariably extracellular, forming small groups within bundles of collagen fibrils. Their appearance was similar in necrotic and viable regions of the nodes, although in the latter sites they could not be identified by light microscopic examination with the Warthin-Starry stain. The bacteria were pleomorphic rods, and, despite faint gram-negative staining, their walls were consistently thick and homogeneous.
A case report of cat-scratch disease manifest as submandibular lymphadenopathy has been presented. The etiology, histopathology, symptoms, diagnosis, treatment, and complications of cat-scratch disease have been discussed. Cat-scratch disease should be considered in the differential diagnosis of all equivocal cases of unilateral lymphadenopathy of the head and neck.
BACKGROUND: Cat-scratch disease (CSD) is mostly contracted by children and young adults. To our knowledge, CSD in elderly patients has never been characterized, and it may be underrecognized in this age group. METHODS: The study population included all patients with CSD diagnosed at our reference laboratory during 1991-2002. Demographic, clinical, and laboratory data for patients with CSD aged >or=60 years (elderly group) were compared with data for patients with CSD aged <60 years (nonelderly group). RESULTS: There were 846 immunocompetent patients with CSD included in this study. Fifty-two patients (6%) were >or=60 years old. Lymphadenopathy was less common in elderly patients than in nonelderly patients (76.5% vs. 94.4%; P<.001), and general malaise was more frequent in elderly patients (70.8% vs. 51.4%; P=.009). Atypical CSD was more common in elderly patients than in nonelderly patients (32.7% vs. 13.6%), including endocarditis (odds ratio [OR], 61.6; P<.001), encephalitis (OR, 6.3; P=.013), and fever of unknown origin (OR, 7.3; P<.001). The time period from onset of symptoms to diagnosis was >6 weeks for 29.5% of elderly patients versus 13.3% of nonelderly patients (P=.003). CONCLUSIONS: CSD affects elderly persons as well as nonelderly persons, but clinical features differ between the patient groups. Atypical CSD, including endocarditis, is more frequent in elderly than in nonelderly patients. Conversely, lymphadenitis, the hallmark of typical CSD, is often absent in elderly patients. Lack of awareness among clinicians may delay the diagnosis of CSD in elderly persons and result in unnecessary and often invasive diagnostic procedures.
CONTEXT: Cat scratch disease (CSD) commonly occurs secondary to Bartonella henselae infection, and the diagnosis has traditionally been made by microscopic findings, the identification of organisms by cytochemistry, and clinical history. However, cytochemical analysis tends to be very difficult to interpret, and histology alone may be insufficient to establish a definitive diagnosis of CSD. OBJECTIVE: To demonstrate the presence of B henselae in tissue suspected of involvement by CSD, using a novel polymerase chain reaction (PCR) assay. DESIGN: Isolates of B henselae (American Tissue Culture Collection 49793) and Afipia felis (American Tissue Culture Collection 49714) were cultured on blood agar and buffered charcoal yeast extract agar, respectively. DNA was isolated from these organisms and from formalin-fixed, paraffin-embedded tissue sections with involvement by CSD (8 patients). Negative controls included water, human placental tissue, and lymph node specimens from 6 patients with reactive lymphoid hyperplasia and from 2 patients with granulomatous lymphadenitis. A primer complementary to B henselae citrate synthase gltA gene sequence was designed to perform a seminested PCR amplification. For restriction fragment length polymorphism analysis, PCR products were digested by TaqI restriction enzyme and analyzed by gel electrophoresis. RESULTS: Seminested PCR analysis of the cultured isolates of B henselae, but not of A felis, showed specific amplification. However, nonnested PCR did not provide consistently positive results in tissue sections with CSD. Therefore, we used a seminested PCR, which revealed positivity in all of the cases with clinicopathologic diagnoses of CSD. None of the negative controls showed positivity. Restriction enzyme provided confirmation of the specific PCR amplification of the B henselae sequence. CONCLUSIONS: Since the amplification product has a low molecular size (<200 base pairs), this assay is useful for detection of B henselae in formalin-fixed, paraffin-embedded tissues. The seminested PCR protocol described here can be used for rapid and reliable confirmation of B henselae in samples that are histologically suggestive of CSD.
BACKGROUND: Cat scratch disease (CSD) is a relatively common cause of chronic lymphadenopathy in the USA. In the present paper the authors describe recent advances in the understanding of this disorder focusing on etiology, clinical aspects, diagnostic management, and therapy. ETIOLOGY: Rochalimaea henselae and Afipia felis, two gram-negative bacteria, have recently been isolated from lymph node tissue of patients suffering from CSD. The current literature reveals that Rochalimaea henselae seems to be the most probable agent responsible for CSD. Serum samples from CSD patients' cats have shown titers of 1:64 or higher for antibodies to Rochallmaea henselae. EPIDEMIOLOGY: The incidence of CSD in the USA is between 0.77 and 9.3 per 100,000 per year. The incidence of CSD in Europe is unknown, but the prevalence of antibodies to Rochalimaea henselae among cats is comparable. CLINICAL MANIFESTATIONS: Most common symptoms of CSD are regional lymphadenopathy, fever, and malaise. Other manifestations occur in about 5% of patients and include encephalitis, granulomatous hepatitis, and Parinaud's oculoglandular syndrome. Fatal complications and irreversible sequelae have not been reported. DIAGNOSIS: To establish the diagnosis of CSD, the presence of regional lymphadenopathy, cat contact, and papula are required. Additional procedures include indirect fluorescent antibody assays and PCR. THERAPY: Up to now there is no standard therapy for CSD. Antibiotic treatment, however, might be considered for CSD patients with severe symptoms. Rifampicin, ciprofloxacin, trimethoprim sulfamethoxazole, and gentamicin are known to be effective antibiotic agents.
Serum bile acid concentrations were measured after food had been withheld for 12 hours (fasting serum bile acid [FSBA] concentration) and 2 hours after a meal (post-prandial serum bile acid [PSBA] concentration) using a direct enzymatic procedure in 108 cats clinically suspected of having hepatobiliary disease. In all cats, liver tissue was examined histologically to confirm the diagnosis. Twenty-six cats did not have histologic evidence of hepatobiliary disease and served as controls. The remaining 82 cats had hepatobiliary disease including hepatic lipidosis (n = 20), portosystemic vascular anomaly (n = 24), hepatic necrosis (n =13), hepatic neoplasia (n = 8), or cholestatic hepatic disease(n = 17). Sensitivity and specificity of measuring FSBA and PSBA concentrations were calculated for each test alone and when results were interpreted in combination (ie, in series and in parallel), and were compared with sensitivity and specificity of routinely used serum biochemical tests, including measuring serum activities of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and gamma-glutamyltransferase, and measuring serum concentrations of cholesterol, BUN, and total bilirubin. When tests were considered individually, determination of FSBA and PSBA concentrations had higher specificity than did the other tests (using a cutoff of 15 mumol/L for FSBA concentration and of 20 mumol/L for PSBA concentration). Determination of PSBA concentration had the highest sensitivity of all single tests in cats with hepatic lipidosis, portosystemic vascular anomaly, or cholestasis; determination of alanine aminotransferase activity or PSBA concentration had the highest sensitivity for cats with hepatic necrosis.(ABSTRACT TRUNCATED AT 250 WORDS)