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PubMed1989

Antibiotic therapy for cat-scratch disease?

Cat-scratch disease is usually a benign, self-limited disease that causes regional lymphadenopathy. Occasionally, it may present with systemic symptoms and have a prolonged course. To date, antibiotic therapy has not been proved to be of value. We describe three patients with cat-scratch disease who were treated successfully with gentamicin sulfate. Two patients had extensive hepatic involvement, and one patient had regional lymphadenopathy. All three patients responded within 48 hours to intravenous gentamicin. Extensive follow-up has shown no recurrence of symptoms. These cases suggest that gentamicin may be efficacious in shortening the course of cat-scratch disease. Prospective, randomized trials should be performed to confirm these results.

Cat-Scratch Disease↗

PubMed1985

Cat scratch disease. Report of a case with hepatic lesions and a brief review of the literature.

An unusual case of cat scratch disease with large hepatic defects is presented. We describe a previously healthy 16-yr-old black man presenting with a neck mass, hepatosplenomegaly, and systemic symptoms. Pathology of the neck mass revealed a lymph node with chronic inflammation and focal necrosis. An abnormal computed tomography scan showed large hepatic defects which were confirmed at peritoneoscopy; biopsy specimens are described. Routine and special stains for bacteria and fungi were all negative. Serologic studies were unremarkable but a cat scratch skin test was positive. Follow-up examinations revealed resolution of all findings. Cat scratch disease should be considered in the differential diagnosis of diseases causing lymphadenopathy, systemic symptoms, and hepatic (and splenic) defects.

Adolescent↗

PubMed1987

Cat-scratch disease.

Cat-scratch disease is a self-limited disease associated with contact with cats that causes regional lymphadenopathy in children and young adults. Recently identification of the probable causative organism, a gram-negative, non-acid-fast coccobacillus, has been achieved through special staining techniques from skin inoculation sites and involved lymph tissue. Differential diagnosis includes a variety of other infectious diseases and neoplasms. Diagnosis of cat-scratch disease can be made by presence of typical clinical findings, history of exposure to cats, results of skin testing to cat-scratch antigen, and in some circumstances, biopsy or fine-needle aspiration from skin inoculation site or involved lymph nodes. Future developments awaiting culture of the suspected bacterium include a vaccine for prevention, rapid diagnostic methods, and antimicrobial testing.

Cat-Scratch Disease↗

PubMed1995

Cat scratch disease in two children presenting with fever of unknown origin: imaging features and association with a new causative agent, Rochalimaea henselae.

OBJECTIVE: To report the clinical course, imaging findings, and method of diagnosis of two patients with systemic manifestations of cat scratch disease, presenting with fever of unknown origin. DESIGN: Case study. PATIENTS: Two children with fever of unknown origin who had multiple lesions in the liver and spleen, shown on ultrasound, computed tomography, and magnetic resonance imaging. Initial diagnoses were Kawasaki disease (case 1) and metastatic neuroblastoma (case 2). RESULTS: Biopsy material showed granulomatous hepatitis in both patients. The diagnoses were confirmed by positive assays for Rochalimaea henselae, currently thought to be the causative agent of cat scratch disease. CONCLUSION: Cat scratch disease presenting as fever of unknown origin is now well described and can be more readily diagnosed because of the availability of new serologic assays, as well as polymerase chain reaction assays for R henselae DNA in tissue specimens.

Bartonella henselae↗

PubMed1996

[Visceral localizations of cat-scratch disease in an immunocompetent patient].

Locoregional expression of cat scratch disease is well known, but despite advances in microbiology over the last 10 years leading to the description of two new bacteria (Afipia felis, Bartonella henselae) the infective agent responsible for cat scratch syndrome remains unknown. Until the 80s, only one systemic disease was attributed to infection with a germ in the Bartonella genus: trench fever. With the onset of the AIDS epidemic, new clinical syndromes caused by Bartonella bacteria have been described: bacillary angiomatosis, hepatic peliosis, cases of recurrent septicemia, cases of endocarditis, etc. More recently, atypical forms of cat scratch disease including systemic diseases have been reported in immunocompetent subjects. Although quite rare (1% of the cases), such types of expression can raise questions as to diagnosis both in terms of clinical signs and in terms of bacteriological findings. Clinical and experimental data do not provide a clear direction for treatment but would suggest that prolonged use of aminoglycosides is useful.

Adult↗

PubMed1997

Cat-scratch disease and related clinical syndromes.

Bartonella (Rochalimaea) henselae is a common cause of cat-scratch disease. This newly identified bacterium is also the cause of several other clinical syndromes, including bacillary angiomatosis, bacillary peliosis hepatitis and splenitis, and acute and relapsing bacteremia. A high percentage of young cats carry B. henselae. Fortunately, serious complications of B. henselae infections are rare in immunocompetent patients. Cat-scratch disease is usually a self-limited illness that does not necessarily require antibiotic therapy. Severe or persistent cases respond well to several antibiotics, including erythromycin and doxycycline. Cat-scratch disease should be included in the differential diagnosis of serious neurologic disease, particularly when regional lymphadenopathy develops suddenly in a previously healthy patient who owns a cat. Treatment of uncomplicated central nervous system disease is generally supportive. Antibiotic therapy is reserved for patients with atypical or severe involvement, including encephalopathy and retinitis. Other internal and cutaneous manifestations of B. henselae infection have recently been described. These potentially life-threatening infections respond well to antibiotic therapy, even in immunocompromised patients.

Angiomatosis, Bacillary↗

PubMedDate not supplied

[Atypical cat-scratch disease: a case report of splenic granulomatosis].

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.

Anti-Bacterial Agents↗

PubMed2005

Differential effects of ambient temperature and humidity on allogrooming, self-grooming, and scratching in wild Japanese macaques.

This study presents data on the effects of variations in ambient temperature and humidity on behaviors related to the care of the pelage (allogrooming, self-grooming, and scratching) in wild Japanese macaques (Macaca fuscata yakui). The amount of time monkeys spent allogrooming was essentially unaffected by variations in ambient temperature and relative humidity. Frequency of scratching and, to a lesser extent, time spent self-grooming significantly increased when ambient temperature and/or relative humidity increased. These results are interpreted in relation to the differences in ultimate function that exist between allogrooming (with both hygienic and social functions) and self-grooming and scratching (with a solely hygienic function).

Analysis of Variance↗

PubMed1994

Inhibitory effects of salmon calcitonin on the tail-biting and scratching behavior induced by substance P and three excitatory amino acids.

We have examined the effects of salmon calcitonin (SCT), injected into the cerebral ventricle (i.c.v.), on the tail-biting and scratching behavior induced by the intrathecal injection of different types of nociceptive agents, i.e., substance P, N-methyl-D-aspartate (NMDA), kainate (KA), and quisqualate (Quis). Tail-biting and scratching behavior induced by the 4 substances was significantly inhibited by SCT (i.c.v.) in the same manner: the dose-response curves were U-shaped, and the most effective dose was 0.1 IU/mouse in all cases. SCT did not, however, completely inhibit tail-biting and scratching behavior. At its most effective dose, the percent inhibition of substance P-, NMDA-, KA- and Quis-induced behavior were 77.9%, 40.2%, 49.4%, and 52.9%, respectively. These results suggest that SCT has the inhibitory effects of substance P- and glutamate receptor agonists-induced nociceptive response in vivo.

Afferent Pathways↗

PubMed1992

Induction of fos expression by activity in the spinal rhythm generator for scratching.

Fos expression was evaluated immunohistochemically in L7-S1 spinal segments after inducing fictive scratching in paralysed, unanaesthetized, decerebrate cats. The activity was induced by cutaneous stimulation of the pinna on one side and recorded from peripheral nerves. A cumulative duration of scratching of 60 to 90 min was effective in inducing fos expression. Most Fos-positive neurones were found in the dorsolateral part of the ventral horn and in the intermediate region of the spinal cord on the scratching side. In sham-operated animals the finding of Fos-positive neurones in these areas was very rare.

Animals↗

PubMed1994

Differential ability of tachykinin NK-1 and NK-2 agonists to produce scratching and grooming behaviours in mice.

Potent and selective NK-1 and NK-2 agonists as well as compounds with lower selectivity and affinity for NK-1 binding sites were compared in their ability to produce scratching and grooming behaviours when injected intracerebroventricularly in mice. Septide, an agonist with a low affinity for NK-1 binding sites, [Sar9, Met(O2)11]SP and to a lesser extent [Pro9]SP, two potent and selective NK-1 agonists were the most effective drugs in stimulating these behaviours. Only high doses of [Apa9,10]SP and [Lys5, Tyr7, Pro8]NKA(4-10), two agonists with low affinity for NK-1 binding sites, produced scratching and grooming responses. Similarly, only high doses of [Lys5, MeLeu9, NLe10]NKA(4-10), a potent NK-2 agonist, produced grooming behaviour. When coinjected with the endopeptidase enzyme inhibitor phosphoramidon, the effects of [Apa9,10]SP, [Lys5, Tyr7, Pro8]NKA(4-10) and [Pro9]SP were markedly enhanced. Analyses of the potency of the different agents to displace 3H-SP binding in mouse subcortical structures revealed that the affinities of the agonists for NK-1 receptors are similar to those previously reported in rat brain. The efficacy of the agonists at producing behavioural responses was not equivalent to their potency to bind to central NK-1 receptors. These findings therefore suggest that a stimulation of NK-1 but also non classical NK-1 receptors are involved in the induction of scratching and grooming behaviours.

Animals↗

PubMed1991

Age dependence of 5-methoxytryptamine-induced hindlimb scratching in rats.

The influence of age on hindlimb scratching induced in rats by the serotonin agonist, 5-methoxytryptamine (5-MeOT), was studied. The 5-MeOT-induced scratching was strongest in 30-day-old rats and least in 90-day-old rats. Sex hormones do not play a role in these differences since treatment of young male rats with testosterone propionate did not change the scratching response. The same age dependence was found for female rats as for males.

5-Methoxytryptamine↗

PubMed1995

Scratching behavior induced by pruritogenic but not algesiogenic agents in mice.

We compared the behavioral effects of treatment with pruritogenic and algesiogenic agents in mice. The animals were given subcutaneous injections of pruritogenic agents, compound 48/80 (3-100 micrograms), substance P (10-300 micrograms) and histamine (3-300 micrograms), and algesiogenic agents, capsaicin (30 and 100 micrograms) and dilute formalin (5 mg of formaldehyde), into the rostral back, and scratching of the injected site by the hind paws was counted. Compound 48/80 and substance P dose dependently elicited the scratching behavior, but histamine, capsaicin and dilute formalin were without significant effects at the doses examined. These results suggest that compound 48/80- and substance P-induced scratching of the injected site is due to itch, but not to pain. The data did not provide support for the idea that histamine produces itch in the mouse.

Animals↗

PubMed1987

Pilocarpine-induced reciprocal hindlimb scratching in mice.

Intrathecal (IT) administration of pilocarpine (0.25-2.0 micrograms) to mice produced a vigorous and dose-related reciprocal hindlimb scratching response that lasted for 10-15 minutes. Neither the intracerebroventricular administration of pilocarpine at up to 10 times the intrathecal ED90 dose nor the subcutaneous administration of 10 mg/kg pilocarpine caused as robust an effect as IT administration. The reciprocal hindlimb scratching produced by the ED90 dose of pilocarpine (2 micrograms, IT) was antagonized in a dose-related manner by simultaneous IT administration of atropine (ID50 = 0.002 micrograms), methysergide (ID50 = 1.89 micrograms), the substance P antagonist [D-Pro2,D-Trp7,9]-SP (ID50 = 4.94 micrograms), and the putative neurokinin B antagonist [D-Pro2,D-Trp6,8,Nle10]-NK (ID50 = 3.33 micrograms), but not by yohimbine (5 micrograms), phentolamine (2 micrograms), or naloxone (2.5 micrograms). These results suggest that pilocarpine-induced reciprocal hindlimb scratching is mediated spinally, that the effect is produced by an action of pilocarpine on muscarinic receptors in the spinal cord, and that neurokinin, and perhaps 5-HT, mechanisms might also be involved.

Animals↗

PubMed1995

Control of Sarcoptes scabiei var. suis with ivermectin: influence on scratching behaviour of fattening pigs and occurrence of dermatitis at slaughter.

The behaviour of fattening pigs, the occurrence of erythematous papular dermatitis in pigs at slaughter and the effects of treatment for mange with ivermectin at the start of the fattening period were evaluated at ten farms. At each farm, trial pigs were randomly allotted to a control or a treated group. At the start of the trial, the control group was injected intramuscularly with 5 mg kg-1 levamisole, and the treated group was injected subcutaneously with 300 micrograms kg-1 ivermectin. Skin scrapings, taken from each pig before medication at the start of the trial, and at slaughter, were examined for presence of sarcoptic mites. Pig behaviour was monitored at 2 week intervals from Week 5 to Week 13 of the trial. Carcasses of trial pigs were inspected for dermatitis at slaughter. Low to moderate Sarcoptes scabiei var. suis infestations were demonstrated at the start of the trial on five farms (S+ farms). At slaughter, the mean percentage of Sarcoptes-positive pigs per pen on S+ farms was 34.8% (range 11-60%) for the control group as compared with 0.5% (range 0-2.7%) for the ivermectin-treated group (P < 0.01). No S. scabiei was recovered from any pig at any time from the five other farms (mange-free (S-) farms). The low initial levels of mange in the controls at S+ farms resulted in a consistently high scratching index. Ivermectin treatment resulted in a significantly (P < 0.01) lower prevalence of scratching, comparable with the prevalence observed at S- farms. High prevalences of generalized dermatitis at slaughter were observed in control pigs from all S+ farms. Ivermectin treatment resulted in much lower prevalences, reflected in a significantly (P < 0.01) lower grand mean dermatitis index per pen for this group as compared with the controls. The majority of pigs from both treatment groups at all S- farms were free of papular lesions. These results indicate that low levels of sarcoptic mange at the start of fattening, left untreated, will result in a high prevalence of scratching during the fattening period and high prevalences of Sarcoptes and dermatitis at slaughter. Treatment with ivermectin at the start of fattening results in behaviour and dermatitis prevalences similar to those observed in mange-free herds.

Animal Husbandry↗

PubMed2005

DPP IV inhibitor blocks mescaline-induced scratching and amphetamine-induced hyperactivity in mice.

Dipeptidyl peptidase IV (DPP IV) is a ubiquitous membrane-bound enzyme that cleaves the two N-terminal amino acids from peptides with a proline or alanine residue in the second position from the amino end. Potential substrates for DPP IV include several neuropeptides, suggesting a role for DPP IV in neurological processes. We have developed a potent DPP IV inhibitor (IC50 = 30 nM), 1-(2-amino-3-methyl-butyryl)-azetidine-2-carbonitrile (AMAC), which has shown efficacy in two established models of psychosis: mescaline-induced scratching and amphetamine-induced hyperactivity. In the mescaline-induced scratching model, AMAC treatment before mescaline administration reduced the number of scratching paroxysms by 68% (P < 0.01). The compound showed a dose-dependent effect, inhibiting significantly at 6, 20 and 60 mg/kg (37%, 39% and 68%, respectively). In the amphetamine-induced hyperactivity model, 50 and 60 mg/kg AMAC, given before injection of amphetamine, significantly reduced hyper-locomotion by 65% and 76%, respectively. Additionally, AMAC showed no significant activity in binding assays for 20 receptors thought to be involved in the pathology of schizophrenia, including dopamine, serotonin and glutamate. A structurally similar analog, 1-(2-dimethylamino-3-methyl-butyryl)-azetidine-2-carbonitrile (DAMAC), that does not inhibit DPP IV, was inactive in both models. Taken together, these data suggest that the antipsychotic effects of AMAC are the result of DPP IV inhibition.

Amphetamine↗

PubMed2006

12(S)-HPETE induces itch-associated scratchings in mice.

The itch-associated responses evoked by intradermal injection of 12(S)-HPETE and leukotriene B4 were compared in ICR-mice. 12(S)-HPETE and leukotriene B4 (0.01-0.2 nmol/site) induced scratching of the injected site, respectively; the dose-responses were a peak at 0.05 nmol/site (12(S)-HPETE) or 0.03 nmol/site (leukotriene B4). The scratching response by 12(S)-HPETE (0.05 nmol/site) started within 1 min, peaked in the first 10 min period, had almost subsided by 25 min whereas the effect of leukotriene B4 peaked in the second 10 min. The effect of leukotriene B4 is slightly stronger than that of 12(S)-HPETE in 40 min of count. The scratching induced by 12(S)-HPETE was inhibited by capsaicin, naltrexon, and LY255283. These results suggest the possibility that 12-lipoxygenase product can be added to a new member of an endogenous itch mediator in the skin.

Animals↗

PubMed2006

A novel scratching approach for measuring age-related changes in the in situ toughness of bone.

A scratch test using a nanoindentation system was proposed in this study to assess the age-related changes in the in situ toughness of bone matrix at ultrastructural levels. A tissue removal energy density (u(r)) was defined and estimated as the work done by the scratch (U(T)) divided by the total volume of the scratch groove (u(s)). The value of u(s) was used as a relative measure of the in situ toughness of the tissue. Human cortical bone specimens obtained from middle-aged (between 49 and 59 years old) and elderly groups (over 69 years old) were tested using this technique. A significant difference in the estimated removal energy density (u(s)) in the secondary osteons was found between the middle-aged and elderly groups (5.49+/-0.696 vs. 4.09+/-1.30 N/mm(2), respectively).

Aged↗