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Results for “CAT SCRATCH DISEASE”

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PubMed2005

[Erythema nodosum and adenopathy in a 15-year-old boy: uncommon signs of cat scratch disease].

UNLABELLED: Erythema nodosum rarely occurs in childhood and can be caused by cat scratch disease, as a result of agent Bartonella henselae. We report the case of a teenager who presented erythema nodosum and bilateral inguinal adenitis. Cat scratch disease diagnosis was confirmed by anti-Bartonella henselae serologies. Despite an appropriate antibiotic therapy, evolution was unfavourable with adenitis abcédation requiring surgical drainage. CONCLUSION: Erythema nodosum in children must let think to cat scratch disease among others etiologies.

Abscess↗
PubMed1995

Prolonged Bartonella bacteremia in cats associated with cat-scratch disease patients.

Recent evidence supports a causal relationship between Bartonella (Rochalimaea) henselae, cat-scratch disease (CSD), and bacillary angiomatosis. Cats appear to be the primary reservoir. Blood from 19 cats owned by 14 patients diagnosed with CSD was cultured. Blood samples from cats owned by veterinary students (n = 25) having no association with CSD or bacillary angiomatosis were cultured as controls. Eighty-nine percent (17 of 19) of cats associated with CSD patients and 28% (7 of 25) of controls were bacteremic with Bartonella species (chi-square = 16.47; P < 0.001). Twenty-three isolates were characterized as B. henselae, while one isolate from the cat of a CSD patient appeared to be a new Bartonella species. Thirteen cats remained culture positive during the ensuing 12-month period. Our results support the conclusion that B. henselae is the predominant species involved in CSD and is transmitted by cats. The incidence of Bartonella bacteremia in control cats suggests that B. henselae bacteremia is prevalent among the domestic cat population in the United States.

Adolescent↗
PubMed1982

Cat-scratch disease simulating malignant lymphoma.

A six-year-old girl with induration, swelling and discoloration of the lower eyelid, a temporal mass, preauricular adenopathy and enlarged parotid gland, underwent biopsy, She was initially diagnosed as having a malignant disorder of histiocytic origin. All lesions resolved without therapy. Further evaluation revealed that the child had oculoglandular cat-scratch disease. Cat-scratch disease should be added to the list of nonmalignant disorders which may simulate a malignant neoplasm in its clinical and histologic appearance. Recognition of this fact is important in order to avoid erroneous diagnosis, unnecessary procedures and hazardous therapy.

Cat-Scratch Disease↗
PubMed1991

Cat-scratch disease. Acute encephalopathy and other neurologic manifestations.

Seventy-six patients with neurologic complications of cat-scratch disease are discussed. Encephalopathy occurred in 61, while 15 had either cranial or peripheral nerve involvement. The average age of the patients with encephalopathy was 10.6 years (range, 1 to 66 years), and almost twice as many males as females were affected in contrast to patients with uncomplicated cat-scratch disease, in which the ratio was almost equal. Fever was not documented in 50% of patients with encephalopathy and only 26% had temperatures higher than 39 degrees C. Convulsions occurred in 46% and combative behavior in 40%. Lethargy with or without coma was accompanied by variable neurologic signs. Results of laboratory studies, including imaging of the central nervous system, were inconsistent and nondiagnostic. Biopsy tissue from 14 patients showed histopathologic findings compatible with cat-scratch disease. The "English-Wear bacillus" was demonstrated by the Warthin-Starry stain in 10 of 14 skin or lymph node specimens. Of the 15 patients without encephalopathy, two children with facial nerve paresis displayed cranial nerve symptoms and/or signs, 10 patients had cat-scratch disease neuroretinitis, and three women had peripheral neuritis. All 76 patients recovered within 12 months; 78% recovered within 1 to 12 weeks. There were no neurologic sequelae. Treatment consisted of control of convulsions and supportive measures. Commonly used antibiotics administered to more than half of the patients were apparently ineffective.

Adolescent↗
PubMed1997

[Cat-scratch disease: historical, clinical, phylogenetic and taxonomic aspects].

The cat-scratch disease (CSD) is known as a nosological entity since 1950. It was diagnosed by the clinical symptoms, epidemiologic data, and the intracutaneous test of Hanger and Rose. The aetiologic agent is Bartonella (formerly Rochalimaea) henselae occurring in thirty to fifty percent of healthy cats. The gramnegative alpha-2-proteobacteria cause the CSD but also fever in healthy humans. Patients suffering from AIDS show bacillary angiomatosis, bacillary peliosis hepatis, endocarditis, and septicemia. There is an open question for other aetiologic agents causing CSD as cofactors. For example, Afipia felis is found to a certain extent from patients suffering from CSD. Furthermore, Rothia dentocariosa was isolated in lymphnodes of CSD patients, and also other grampositive rods may play an important role together with B. henselae in CSD.

AIDS-Related Opportunistic Infections↗
PubMed1998

Hypercalcemia due to endogenous overproduction of active vitamin D in identical twins with cat-scratch disease.

CONTEXT: The extrarenal synthesis of active vitamin D sterols has a central causative role in the hypercalcemia associated with various granulomatous diseases. OBJECTIVE: To study the calcium metabolism in patients with cat-scratch disease who have hypercalcemia. DESIGN: Case report. SETTING: University hospital in Barcelona, Spain. PATIENTS: Two identical twins who developed asymptomatic hypercalcemia during the acute phase of cat-scratch disease. MAIN OUTCOME MEASURES: Serial measures of calcium homeostasis and metabolism over a 2-month period. RESULTS: On admission and 6 and 7 days later, both patients were found to have increased levels of serum and urinary calcium, serum phosphate, and serum 1,25-dihydroxyvitamin D [1,25(OH)2D], whereas they had normal values of serum 25-hydroxyvitamin D and urinary cyclic adenosine monophosphate and decreased serum concentrations of intact parathyroid hormone. Sixteen and 20 days after admission, these abnormalities had resolved without treatment. A direct correlation was observed between the serum 1,25(OH)2D levels and both the serum and 24-hour urinary calcium concentrations. Also, the concentrations of calcium and 1,25(OH)2D paralleled the clinical activity of the infectious disease over the period these parameters were measured. CONCLUSIONS: Our cases provide evidence that cat-scratch disease can produce hypercalcemia through the unregulated production of the metabolite 1,25(OH)2D. Cat-scratch disease should be added to the list of granuloma-forming diseases that are responsible for 1,25(OH)2D-mediated hypercalcemia.

Adolescent↗
PubMed2006

[Hepatosplenic localization of cat scratch disease: two cases in immunocompetent adult patients].

INTRODUCTION: Cat-Scratch Disease (CSD) is a well-recognized benign cause of localized lymphadenopathy, which often recovers spontaneously. However systemic clinical presentations are described in immunodeficient adults (bacillary angiomatosis, bacillary splenitis) and are less common in immunocompetent ones. EXEGESIS: We report two cases of disseminated CSD in immunocompetent patients, presenting hepatosplenic nodules, associated in the second case with an endocarditis. CONCLUSION: Bartonella serology must be achieved in case of hepatosplenic nodules with fever. Treatment of disseminated CSD in immunocompetent adults is still empirical and recovery can occur without antibiotherapy when endocarditis is not associated.

Aged↗
PubMed2005

Macular hole in cat scratch disease.

PURPOSE: To report the development of a macular hole as a complication of cat scratch disease. DESIGN: Case report. METHODS: A 10-year-old girl was seen with unilateral neuroretinitis from serologically confirmed cat scratch disease. Twelve days later, she developed a macular hole in the involved eye. Fundus photography and optical coherence tomography (OCT) were obtained at presentation and after the development of a macular hole. RESULTS: Fundus photography and OCT on presentation revealed a nasal neurosensory detachment and multiple inflammatory foci throughout the macula, including a subfoveal lesion. Fundus photography and OCT 12 days later revealed the development of a partial posterior vitreous detachment and a full thickness macular hole. CONCLUSIONS: Macular hole should be included among posterior segment complications of cat scratch disease. In this case, the macular hole was associated with partial vitreous detachment and a preexisting subfoveal lesion, likely representing an inflammatory focus.

Antibodies, Bacterial↗
PubMedDate not supplied

Cat scratch disease and acquired immunodeficiency disease: diagnosis by transmission electron microscopy.

A 33-year-old, homosexual, cat-owning, African-American man with human immunodeficiency virus infection by positive serologic tests and acquired immunodeficiency syndrome by CD4 lymphocyte count alone (39 cells/mL) presented with a one-year history of intermittent fever, weight loss, and generalized lymphadenopathy. A malignant lymphoma was suspected clinically. Light microscopic study of a left inguinal lymph node biopsy specimen revealed effacement of the lymph node architecture by a diffuse infiltrate of large, atypical reticulum cells, loose, patchy granulomatous inflammation, diffuse hyaline fibrosis, diffusely proliferated blood vessels, and multifocal degeneration and necrosis. Lymph follicles were absent and lymphocytes were moderately depleted. Microorganisms were not seen in lymph node sections stained with special histochemical stains (including the Warthin-Starry stain). These light microscopic changes were considered suggestive of a malignant lymphoma, especially Hodgkin's disease. The diagnosis of cat scratch disease (CSD) became apparent only after transmission electron microscopic study of the lymph node revealed clusters of small, pleomorphic bacteria in degenerated collagenous tissue and in blood vessel walls. This case illustrates the value of transmission electron microscopy in making the diagnosis of CSD, especially when light microscopic changes are superimposed on those of late human immunodeficiency virus infection of the lymph node.

Acquired Immunodeficiency Syndrome↗