[Encephalopathy in cat scratch disease].
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UNLABELLED: Cat-scratch disease is a frequent but innocuous cause of chronic lymphadenopathy in children. Numerous atypical forms have been described. We report three cases of acute sight impairment revealing a cat-scratch disease. BACKGROUND: A 13 year-old boy and two girls aged 10 and 13 suffered from a sudden bilateral sight impairment with papillary edema, with fever in two cases. Neurological examinations, X-rays and lumbar puncture results were found normal. However, all patients were tested positive to Bartonella Henselae. Antibiotic and anti-inflammatory treatments were efficient in two cases. CONCLUSION: Cat-scratch disease can be characterized by an isolated and acute sight impairment with a stellate neuroretinitis. The potency of antibiotic treatments is debatable.
Forty-four female American Shorthair cats with inflammatory uterine disease or infertility were evaluated. Data collected included age, month of diagnosis, housing, reproductive history, results of bacteriologic culture of uterine specimens, serum concentrations of estrogen, progesterone, and prolactin and histopathologic features of the ovaries and uterus. Histologically, the ovaries of 19 cats were dominated by active or cystic follicles, whereas 25 cats had luteal-phase ovaries. Of the 25 cats with active corpora lutea, 20 had either recently weaned litters (n = 11) without subsequent exposure to a male cat, or had been housed individually for lengthy periods (n = 9). The finding of active corpora lutea under these circumstances indicates that in queens, ovulation may occur by mechanisms not involving coitus. Prominent, active corpora lutea on the ovaries were associated with adenomatotic proliferative changes in the superficial and glandular epithelium of the uterus and with myometrial hyperplasia, compared with the uterus of cats with follicular ovaries (P less than 0.01). Serum progesterone concentration greater than or equal to 1.87 ng/ml was consistently associated with luteal-phase ovaries. Serum progesterone values less than or equal to 0.15 ng/ml were consistently associated with follicular-phase ovaries. Escherichia coli was the organism most commonly isolated from uterine contents.
Etiology, epidemiology and clinical symptoms of Mollaret's disease, also known as Cat-scratch disease, were described. Four cases of treated patients were presented. One patient with a history of type I Diabetes mellitus presented clinical symptoms of Mollaret's disease, however, after investigation he was finally diagnosed with malignant lymphoma and was given chemotherapy. In other cases some symptoms were also doubtful, but the final diagnoses were made upon positive results of serological reactions and all patients recovered completely after a few week antibiotic treatment. All patients had frequent contacts with cats. A significant divergence between the results of histopathological, serological and ultrasonographic findings lead to a conclusion that a certain diagnosis of Cat-scratch disease can only be made with the use of positive results of serological reactions.
The prominent clinical manifestation of cat scratch disease is regional lymphadenopathy at the site of the cat scratch or bite, associated with fever or general symptoms. A serological study of 540 patients with either lymphadenopathy, persistent fever, or pet ownership disclosed that 30 (16.1%) of the 186 patients with a serological diagnosis of cat scratch disease had no regional lymphadenopathy, and in these 30 patients, the absence of lymphadenopathy was closely related to the presence of persistent fever, fever of unknown origin, or systemic complications. Physicians should be alert to cat scratch disease that is not associated with lymphadenopathy to enable prompt diagnosis and treatment.
BACKGROUND: Cat scratch disease neuroretinitis is caused by infection by Bartonella henselae. To demonstrate B. henselae infection, serologic examination is commonly used, but sometimes serologic examination is not adequate for correct diagnosis. Here we present a case of cat scratch disease neuroretinitis confirmed by polymerase chain reaction in addition to serologic examination. CASE: A 55-year-old woman, presenting with headache and high fever, had noticed visual disturbance. The best-corrected visual acuity in her right eye was 0.01. Meningitis, optic neuritis and retinitis were observed and she was treated with oral prednisolone. After repeated questioning, the patient remembered being scratched by a cat. Systemic examination focusing on B. henselae infection was conducted and B. henselae-specific immunoglobulin (Ig) G, but not IgM, was detected in both serum and cerebrospinal fluid. To confirm B. henselae infection, polymerase chain reaction (PCR) analysis using cerebrospinal fluid was performed and the presence of B. henselae-specific DNA was demonstrated. From these results, we diagnosed cat scratch disease neuroretinitis and treated the patient with minocycline hydrochloride together with prednisolone. Following this treatment regimen, the patient's condition improved, and the best-corrected visual acuity in her right eye increased to 0.6 five months after the onset. CONCLUSION: The PCR technique is useful to correctly diagnose cat scratch disease neuroretinitis, if patients exhibit marginal data on B. henselae-specific antibody titer.
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.
The historic, physical, laboratory, and histologic findings for 74 cats with chronic renal disease were reviewed. Most cats were older, and no breed or sex predilection was detected. This most common clinical signs detected by owners were lethargy, anorexia, and weight loss. Dehydration and emaciation were common physical examination findings. Common laboratory findings were nonregenerative anemia, lymphopenia, azotemia, hypercholesterolemia, metabolic acidosis, hyperphosphatemia, and isosthenuria. The most common morphologic diagnosis was chronic tubulointerstitial nephritis of unknown cause. The other pathologic diagnoses were renal lymphosarcoma, renal amyloidosis, chronic pyelonephritis, chronic glomerulonephritis, polycystic renal disease, and pyogranulomatous nephritis secondary to feline infectious peritonitis.
Cat-scratch disease (CSD) initially was described in 1931, but the etiologic agent (Bartonella henselae) was not elucidated until decades later. This disease is the most common cause of chronic lymphadenopathy among children and adolescents, characteristically manifesting as subacute regional lymphadenitis with an associated inoculation site due to a cat scratch or bite, often accompanied by fever. The hallmark histologic lesion is granulomatous inflammation with a central stellate microabscess. Numerous atypical manifestations of CSD have been described, and these often lack the characteristic superficial lymphadenopathy and inoculation site papule. These atypical forms may be misdiagnosed initially as other infectious processes or neoplasms. We present a review of the history and epidemiologic features of CSD, describe common and unusual clinicopathologic manifestations, and discuss current diagnostic modalities.
A cytauxzoon-like agent caused fatal disease in 4 domestic cats from separate, rural, heavily wooded premises in southwestern Missouri. Clinical signs included lethargy; pale, icteric mucous membranes; fever; and dehydration. One case of fatal cytauxzoonosis occurred in early September, 1973, and another in September, 1974. Two additional cases were detected in June, 1975. Tick infestations were reported from a variety of animals, including cats, on all premises. Necropsy revealed generalized icterus and petechial and ecchymotic hemorrhages over the surfaces of the heart and lungs. The pericardial sac was distended with clear yellow serous fluid. Large numbers of schizonts characteristic of Cytauxzoon spp were discovered in specimens of liver, lung, spleen, and lymph nodes of all cats. Infection of vascular endothelial cells, a characteristic of cytauxzoonosis, was observed in all organs examined. Piroplasms or ring forms of the agent were observed in erythrocytes of affected cats.
Shortly after adopting a 6-week-old cat, a veterinarian was bitten on the left index finger. Within 3 weeks, he developed headache, fever, and left axillary lymphadenopathy. Initial blood cultures from the cat and veterinarian were sterile. Repeat cultures from the cat grew Bartonella-like organisms with lophotrichous flagella. Sera from the veterinarian were not reactive against Bartonella henselae, B. quintana, or B. elizabethae antigens but were seroreactive (reciprocal titer, 1,024) against the feline isolate. Sequential serum samples from the cat were reactive against antigens of B. henselae (titer, 1,024), B. quintana (titer, 128), and the feline isolate (titer, 2,048). Phenotypic and genotypic characterization of this and six additional feline isolates, including microscopic evaluation, biochemical analysis, 16S rRNA gene sequencing, DNA-DNA hybridization, and PCR-restriction fragment length polymorphism of the 16S gene, 16S-23S intergenic spacer region, and citrate synthase gene identified the isolates as B. clarridgeiae. This is the first report of cat scratch disease associated with B. clarridgeiae.
OBJECTIVE: To describe a clinical syndrome of cat scratch disease caused by Rochalimaea henselae, including methods for isolation of the organism from tissue and for identification. DESIGN: Case series. SETTING: U.S. Air Force referral hospital infectious diseases clinic. PATIENTS: Two previously healthy patients. MAIN MEASUREMENTS AND RESULTS: Two immunocompetent patients who had handled cats developed unilateral upper-extremity adenitis associated with a distal papular lesion and fever. The adenitis and distal lesions persisted and progressively worsened. Cultures of the involved lymph nodes from both patients grew R. henselae, a recently described organism associated with bacillary angiomatosis and peliosis hepatis in human immunodeficiency virus-infected patients and with bacteremia in immunocompromised and immunocompetent hosts. The organism was characterized as oxidase negative and X-factor dependent and had a characteristic pattern in analysis of whole-cell fatty acids differing from Afipia felis, a bacterium that has been associated with cat scratch disease. The identity of the isolate was confirmed by analysis of whole-cell fatty acids using gas chromatography and by amplification of the citrate synthetase gene sequence and analysis of the polymerase chain reaction-amplified product. The organisms were broadly susceptible to a variety of antimicrobials by broth microdilution; however in-vitro resistance to first-generation cephalosporins correlated with clinical failure of therapy. CONCLUSION: Rochalimaea henselae can be a cause of cat scratch disease in immunocompetent patients.
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.
PURPOSE: We studied an unusual ocular manifestation of cat scratch disease. METHODS: We examined a patient who had a serous retinal detachment of the macula with vision loss out of proportion to her retinal findings. RESULTS: The patient was found to have cat scratch disease by antibody titers. CONCLUSION: Cat scratch disease should be considered in patients with a serous neurosensory retinal detachment of the macula and a history of cat exposure or systemic signs or symptoms consistent with the disease.
Cats with lesions involving either the cerebral cortex or thalamus (forebrain) often have a characteristic group of neurologic deficits. When these deficits, in part or in toto, are recognized, consideration should be given to diseases that preferentially involve this area of the brain. Certain diseases that characteristically affect the forebrain are discussed here. Seizures are discussed as a separate entity at the conclusion of this chapter. Other diseases that also may involve the forebrain, but often cause additional lesions in other areas of the brain, are collectively discussed under the subheading of multifocal neurologic disease in Multiple Neurologic Deficits: Inflammatory Diseases (page 426) and Multiple Neurologic Deficits: Noninfectious Diseases (page 440).
Brush cytology was used as a diagnostic aid in 85 cats affected with chronic intranasal disease. Fifty-three of these cases, sampled over a five-year period, were included in this study, while the other cases were excluded due to poor cellularity of the cytological samples (nine cases) or a lack of histological or follow-up data (23 cases). Thirty-six brush samples were classified by cytology as inflammatory. Subsequent histological examination revealed a false negative diagnosis of neoplasia in six cats, two of which had malignant tumours (one adenocarcinoma and one lymphoma), the remaining four having benign tumours (two adenomas and two osteochondromas). Seventeen samples were classified by brush cytology as neoplastic. This was confirmed in 16 of these cases by histology or follow-up (nine epithelial malignant tumours, six lymphomas and one osteosarcoma). In the remaining case, a false positive diagnosis of lymphoma was made. The procedure had an overall 86.8 per cent (46/53) agreement between the diagnosis of inflammatory conditions versus neoplasia, with a sensitivity of 72.7 per cent, a specificity of 96.8 per cent, a predictive value of a positive test of 94.1 per cent and a predictive value of a negative test of 83.3 per cent.
Generally cat-scratch disease is a benign inflammatory adenopathy. The Authors describe an atypical form of this disease, characterized by persistent fever and splenic granulomatosis requiring a diagnostic and therapeutic prolonged effort. They point out the important role of new immuno-fluorescent techniques to exactly identify the bacterium--Bartonella henselae--causing cat-scratch disease and suggest to include cat-scratch disease among the causes of unknown origin fever.