Stephanofilariasis in beef cattle - case report / Estefanofilariose em bovinos de corte - relato de caso

Stephanofilariasis is an ulcerative dermatitis caused by nematodes that affect cattle in several countries in the world. However, it has not been described in beef cattle in Brazil. The objective of this study is to describe three cases of stephanofilariasis, which occurred in beef cows in the municipality of Ipê, RS, Brazil. The disease was characterized by pruritic, ulcerated and crusty seasonal lesions present in the cranial region of the udder. The diagnosis was confirmed by analyses of secretions stained smears and by direct optical microscopic examination of the sediment and the treatment was effectively carried out with topical trichlorphon. This report indicates that stephanofilariasis should be included as a differential diagnosis for dermatopathies in beef cattle in Brazil.(AU)

A estefanofilariose é uma dermatite ulcerativa causada por nematódeos que acometem bovinos em vários países do mundo, no entanto não tem sido descrita em bovinos de corte no Brasil. O objetivo do trabalho é a descrição de três casos de estefanofilariose em vacas de corte ocorridos no município de Ipê, RS. A enfermidade foi caracterizada por lesões sazonais pruriginosas, ulceradas e crostosas, presentes na região cranial do úbere. O diagnóstico foi confirmado pela análise dos esfregaços corados das secreções e por exame direto do sedimento em microscopia óptica, e o tratamento foi realizado de maneira eficaz com triclorfon tópico. Este relato demonstra que a estefanofilariose deve ser incluída como diagnóstico diferencial nas dermatopatias em bovinos de corte no Brasil.(AU)

Chronic renal failure in equine due to ascending pyelonephritis predisposed by cauda equina syndrome: case report / Insuficiência renal crônica em equino devido à pielonefrite ascendente predisposta por síndrome da cauda equina: relato de caso

Descreve-se o caso de uma égua, da raça Campeiro, utilizada como doadora de embriões, que apresentava quadros de cistite recorrente e incontinência urinária. Os sinais clínicos evoluíram para emagrecimento progressivo, anorexia, apatia e isolamento do plantel. Ao exame físico, foi identificada hipotonia da cauda, hipoalgesia da região perineal, flacidez retal e vesical, compatíveis com sinais relacionados à síndrome da cauda equina. Exames complementares laboratoriais, exame ultrassonográfico e necropsia confirmaram o diagnóstico de insuficiência renal crônica (IRC), a qual foi atribuida à pielonefrite ascendente. O exame de urocultura demonstrou crescimento de bactérias do gêneroStreptococcus sp. Este é um caso raro em equinos em que a disfunção de neurônio motor inferior propiciou o desenvolvimento de processo infeccioso no trato urinário, progredindo para um quadro crônico renal incompatível com a vida.(AU)

Descreve-se o caso de uma égua, da raça Campeiro, utilizada como doadora de embriões, que apresentava quadros de cistite recorrente e incontinência urinária. Os sinais clínicos evoluíram para emagrecimento progressivo, anorexia, apatia e isolamento do plantel. Ao exame físico, foi identificada hipotonia da cauda, hipoalgesia da região perineal, flacidez retal e vesical, compatíveis com sinais relacionados à síndrome da cauda equina. Exames complementares laboratoriais, exame ultrassonográfico e necropsia confirmaram o diagnóstico de insuficiência renal crônica (IRC), a qual foi atribuida à pielonefrite ascendente. O exame de urocultura demonstrou crescimento de bactérias do gênero Streptococcus sp. Este é um caso raro em equinos em que a disfunção de neurônio motor inferior propiciou o desenvolvimento de processo infeccioso no trato urinário, progredindo para um quadro crônico renal incompatível com a vida.(AU)

Systemic toxic reaction due to multiple honeybee stings in equine: Case report / Reação tóxica sistêmica devido a múltiplas ferroadas de abelha em equino: relato de caso

Accidents caused by insects of the Hymenoptera are rarely described in large animals. The attacks caused by honeybee (Apis mellifera) may cause severe consequences and its intensity changes according to the number of stings. Local and systemic reactions can occur, including progression to death. This report describes a case of honeybee attack on an equine, which took place in the city of Lages, in the state of Santa Catarina, Brazil. In the clinical assessment the horse showed apathy, anorexia, head and pectoral edemas, dyspnea, icteric mucosa, increased mandibular lymph nodes and darkened urine. The blood count showed anemia and serum biochemical tests suggested, muscular and hepatic lesions. The urinalysis test indicated hemoglobinuria and increased clotting time. Treatment included lactate Ringer's solution fluid therapy, furosemide, promethazine, corticosteroids and 20% mannitol solution. Hot and cold compresses were applied alternately on areas with edema. There was a satisfactory response to treatment and the animal was discharged after 30 days in veterinary hospital. The description of honeybee sting accidents in large animals is important because of the evolution that can lead to death. The early approach associated with appropriate treatment, avoiding the worsening of the lesions is fundamental for the recovery of the patient.(AU)

Os acidentes causados por insetos da ordem Hymenoptera são raramente descritos em grandes animais. Os ataques provocados por abelhas (Apis mellifera) causam consequências graves, e sua intensidade varia de acordo com a quantidade de ferroadas. Reações locais a sistêmicas podem ocorrer, incluindo a evolução para a morte. Este relato descreve um caso de ataque por abelhas em equino, ocorrido no município de Lages, SC. No exame clínico, o equino apresentava apatia, anorexia, edema de cabeça e região peitoral, dispneia inspiratória, mucosas ictéricas, linfonodos mandibulares aumentados e urina de coloração marrom-escura. O hemograma evidenciou anemia hemolítica, e os exames de bioquímica sérica sugeriram lesão muscular e lesão hepática. A urinálise demonstrou hemoglobinúria, e o tempo de coagulação apresentava-se aumentado. Como tratamento, foram administrados solução de ringer com lactato, furosemida, prometazina, corticosteroides e solução de manitol a 20%. Compressas quentes e frias foram aplicadas alternadamente sobre as áreas de edema. Houve adequada resposta ao tratamento instituído e o animal recebeu alta hospitalar após 30 dias de internamento. A descrição de casos de acidentes por picadas de abelhas em grandes animais é importante devido à evolução, que pode levar à morte. A abordagem precoce associada ao tratamento adequado, evitando o agravamento das lesões, é fundamental para a recuperação do paciente.(AU)

Excretion of mutagens, nicotine and its metabolites in urine of cigarette smokers.

Urine samples from 26 cigarette smokers on a restricted diet were collected in the late afternoon. Urine extracts on XAD-2 resin were tested for mutagenicity in the microsuspension assay using Salmonella typhimurium strain TA98 in the presence of metabolizing and deconjugating enzymes. Levels of urinary nicotine plus metabolites and cotinine were determined. Eighteen samples were clearly mutagenic, i.e. capable of doubling the number of spontaneous revertants at one of the assayed doses of urine. Urinary mutagenic activity ranged from 193 to 8462 net revertants/mmol of creatinine, while urinary nicotine plus metabolites and cotinine levels varied from 0.007 to 1.366 and from 0.011 to 0.297 mg/mmol creatinine. Urine samples with nicotine metabolite levels of < 0.33, 0.33- < 0.66 and > 0.66 mg/mmol creatinine had mean values +/- SD of mutagenic activity of 490 +/- 222 (n = 10), 964 +/- 560 (n = 9) and 2692 +/- 2807 (n = 7) revertants/mmol of creatinine, respectively, the statistical comparison between the groups being positive (Mann-Whitney U-test, P < 0.05). The mutagenic activity of urine samples from smokers correlated well with urinary nicotine plus metabolite levels (r = 0.658, P < 0.01). A less close correlation was found between urinary mutagenic activity and other indicators of tobacco smoke exposure, such as urinary cotinine (r = 0.504, P < 0.05), number of cigarettes smoked during the day of urine collection (r = 0.399, P < 0.05) and machine smoking-derived nicotine deliveries of the total number of cigarettes smoked (number of cigarettes multiplied by the nicotine content of each cigarette, as indicated by the manufacturer; r = 0.439, P < 0.05). These results suggest that the mutagenic activity of smokers' urine may be predicted by the urinary level of nicotine plus metabolites. The low degree of reliability of many presumptive indicators of exposure to tobacco smoke and the different urinary excretion kinetics of tobacco smoke mutagens with respect to cotinine (a frequently used biomarker for monitoring exposure to tobacco smoke) are both emphasized.

Mutagenicity and contents of polycyclic aromatic hydrocarbons in new high-viscosity naphthenic oils and used and recycled mineral oils.

Mutagenic activity on the Ames test was evaluated in 15 samples of naphthenic high-viscosity mineral oils and 12 samples of used lubricants (recovered and pooled) and their recycled products. Bacterial mutagenesis was assayed using both the standard technique and Blackburn's modification. The contents of polycyclic aromatic hydrocarbons (PAH) was also evaluated, as polynuclear aromatic fraction (PAF) and total PAH, determined respectively with the semi-quantitative dimethylsulphoxide-refractive index method and the Grimmer method. Only four samples (three acid-treated naphthenic oils and one recycled fraction of a used oil) showed mutagenic activity higher than 6 revertants/mg of oil, considered by Blackburn and coworkers as indicating a potential carcinogenic risk for these compounds. Limited mutagenicity was found in all used and recycled oils, but also in samples of acid- or solvent-treated oils. No hydrogen-treated naphthenic oils turned out to have any mutagenic activity. PAF contents of oils were closely correlated with those of total PAH (n = 15, r = 0.83; n = 12, r = 0.91; p < 0.01 for both naphthenic and used/recycled oils respectively). No recycled oil had high PAF contents. Eleven samples had PAF contents higher than 3%, the arbitrary danger threshold suggested by the CONCAWE (1988). Of these 11 samples, the majority were acid-treated products, although there was one hydrogen-treated oil and one used and recycled oil. No mutagenic activity could be demonstrated in almost half the oils with PAF > 3%. In this study, the presence of mutagens was not correlated wither with PAF or with total or mutagenic PAH. The difficulty of predicting the mutagenicity of mineral oils is stressed. Most naphthenic and some recycled oils clearly have components which inhibit the metabolizing system in the bacterial mutagenesis test, with consequent possible false negative results.

Urinary excretion of mutagens in coke oven workers.

The influence of occupational exposure to polycyclic aromatic hydrocarbons (PAHs) on urinary mutagenic activity was assessed in 75 coke oven workers, using a highly sensitive bacterial mutagen technique (extraction with C18 resin and liquid micro-preincubation test on strain TA98 of Salmonella typhimurium in the presence of metabolizing and deconjugating enzymes). Exposure to PAHs was assessed according to the urinary excretion of 1-pyrenol; the main confounding factors were checked by the number of cigarettes smoked per day and the levels of nicotine and its metabolites in urine, or by ascertaining whether recommended dietary restrictions had been followed. Of the 20 urine samples which turned out to be positive (producing at least double the number of spontaneous revertants), 19 (95%) belonged to smokers. Only one non-smoker had obvious urinary mutagenic activity, and was highly exposed occupationally to PAHs (urinary 1-pyrenol of 3.930 mumol/mol of creatinine). Of the five urine samples from subjects who had not followed the recommended diet, two (40%) were clearly mutagenic. Multiple regression analysis (n = 67) showed that the presence of samples positive for urinary mutagenic activity depended only on smoking habits, if this confounding factor was assessed according to the number of cigarettes smoked per day, while the significant influence of exposure to PAH could be shown when the confounding factor was objectively estimated according to the urinary levels of nicotine and its metabolites. Assessment of the mutagenic potency of urinary extracts (net revertants/mmol creatinine) confirmed the strong influence of smoking habits on urinary mutagenic activity (all smokers 2156 +/- 2691 versus non-smokers 939 +/- 947 net revertants/mmol creatinine; Mann-Whitney test: P < 0.01). In smokers highly exposed to PAHs, greater excretion of mutagens with respect to low-exposure smokers was revealed (3548 +/- 4009 versus 1552 +/- 1227 net revertants/mmol creatinine; Mann-Whitney test: P < 0.01). Multiple regression analysis showed that the mutagenic potency of urinary extracts of coke oven workers depended on exposure to PAHs, tobacco smoking habits, and consumption of fried, grilled or barbecued meat. Increased urinary mutagenic activity strengthens epidemiological evidence of the increased risk of renal and urinary tract tumours in these workers. The presence of mutagenic metabolites in urine as a result of occupational exposure to PAH may be demonstrated only by using highly sensitive techniques for assessing urinary mutagenic activity in studies which include careful checking of the main confounding factors.

Mutagens in indoor air particulate.

Twenty-seven extracts of airborne particulate from domestic environments, both in the absence of sources of pollution and during activities such as smoking tobacco, using a fireplace, and cooking using grills and barbecues, and eight control samples of outdoor particulate were tested using the Salmonella/microsome assay on strains TA98 and TA98NR. Dust levels and mutagenic activity in the indoor environments turned out to be very low in the absence of polluting sources, with highest mean values in winter of less than 0.1 mg/m3 and 6 and 12 revertants/m3, respectively without and with S9. The specific mutagenic activity of indoor dust ranged from 22 and 137 revertants/mg, with a contribution of nitroarene compounds of about 50%, indicating that, in city indoor air, the main cause of background particulate pollution is very probably penetration of traffic fumes from the outside. In contrast, in a country house far from traffic, very low dust and mutagenicity levels were found, without the influence of nitroarene compounds. The presence of autochthonous polluting sources, such as tobacco smoke and fumes from cooking and wood or charcoal burning, greatly increased indoor dust levels, especially during cooking operations, which reached 25.5 and 31.6 mg/m3. The particulate produced by the various indoor pollution sources showed varying specific mutagenic activities. The highest values were found for fumes produced by burning charcoal and wood, smoking tobacco, and cooking foods with high animal protein contents. Mutagens responsible were mainly direct-acting in the case of fumes from burning wood or charcoal, and required mammalian metabolic activation in the case of fumes from tobacco and meat, with a lower contribution (maximum 33%) of nitroarenes than in urban particulate.

Urinary excretion of 1-pyrenol in automotive repair workers.

The urinary excretion of a pyrene metabolite was evaluated in 65 automotive repair workers whose skin was exposed to used mineral oils, and in 41 controls. Pyrene contents were determined in oily material taken from cloths used to clean various types of engines (n = 8) and were found to vary (mean +/- SD) from 2.8 +/- 0.4 ppm for dirty matter obtained from diesel truck engines to 9.3 +/- 8.2 ppm for that from petrol car engines. Tobacco smoking and polycyclic aromatic hydrocarbon (PAH)-rich diets were considered as confounding factors. At both the beginning and the end of the working week, the values of urinary 1-pyrenol were slightly higher in exposed subjects (0.178 +/- 0.150 and 0.194 +/- 0.135 mumol/mol creatinine on Monday and Friday, respectively) than in controls (0.124 +/- 0.090 mumol/mol creatinine) (Mann-Whitney test, z = 2.741, P < 0.01). The urinary 1-pyrenol values were higher in both smoking and non-smoking subjects than in controls. The highest values were found in urinary samples of smokers exposed to used mineral oils (0.259 +/- 0.201 mumol/mol creatinine). In non-smoking workers (n = 40), post-shift 1-pyrenol values were 0.154 +/- 0.105 mumol/mol creatinine, as against 0.083 +/- 0.042 mumol/mol creatinine for the 19 non-smoking controls (Mann-Whitney test, z = 2.765, P < 0.01). In automobile repair workers, urinary 1-pyrenol values before the beginning of the weekly workshift did not differ substantially from those measured at the end of the week, not being related to the subjective degree of dirty skin as stated by workers.(ABSTRACT TRUNCATED AT 250 WORDS)

[The urinary mutagenicity test in monitoring exposure to aromatic polycyclic hydrocarbons in workers in the aluminum industry]. / Test di mutangenicità urinaria nel monitoraggio dell'esposizione ad idrocarburi policiclici aromatici di lavoratori dell'industria di alluminio.

The sensitivity of 3 urinary mutagenicity tests was assayed: the plate test, the fluctuation test and the micropreincubation test, in order to assess their possible use in monitoring human exposure to polycyclic aromatic hydrocarbons (PAH). Urine samples from workers of an anode production plant exposed to coal tar and from psoriatic patients undergoing treatment with coal-tar ointments were tested for mutagenic activity on strain TA98 Salmonella typhimurium, in the presence of the microsome fraction and deconjugating enzymes. Parallelly, the urinary concentration of PAH metabolites or one of their trace metabolites, 1-hydroxypyrene, was determined. Increased levels of PAH metabolites were observed in the urine of anode production workers after a work shift compared with controls. Results of the plate test and the fluctuation test performed on urine of exposed subjects, both smokers and nonsmokers, showed mutagenicity values similar to the controls. Much higher 1-hydroxypyrene concentrations were found in the urine of psoriatic patients treated with coal tar than in post-shift urine of anode production workers. The urine of the former was also mutagenic in the 3 mutagenicity tests used. The minimum mean dose of PAH metabolites was calculated, expressed as quantity of 1-hydroxypyrene, that would give a mutagenic response in the 3 tests: the micropreincubation test was found to be about 100 times more sensitive than the plate test and about 30 times more sensitive than the fluctuation test. The theoretical minimum urinary concentration of 1-hydroxypyrene detectable by each test was determined: the micropreincubation test was 15 times more sensitive than the plate test and 7 times more sensitive than the fluctuation test.(ABSTRACT TRUNCATED AT 250 WORDS)

Sensitivity of different bacterial assays in detecting mutagens in urine of humans exposed to polycyclic aromatic hydrocarbons.

The urine mutagenicity and excretion of 1-hydroxypyrene (1-OH PYR) in non-smoking psoriatic patients treated topically with coal-tar-based ointments were analysed in order to find the most appropriate procedure for monitoring occupational PAH exposure. The bacterial mutagenicity assays used were the plate incorporation, macro-scale fluctuation and microsuspension tests, all on Salmonella typhimurium strain TA98 in the presence of S9 mix and beta-glucuronidase. The sensitivities of the three assays in detecting mutagenic urinary PAH metabolites were compared. The efficiencies of XAD-2 and C18 resins for concentrating PAH urinary mutagens were evaluated in the microsuspension assay. The plate and fluctuation tests on XAD-2 urine extracts were shown to be insufficiently sensitive to detect low urinary levels of mutagens, being positive on urine samples with very high PAH metabolite content, estimated as more than 30 micrograms/g of creatinine of 1-OH PYR. The microsuspension assay on XAD-2 or, even better, on C18 urine extracts was very sensitive in detecting up to 5 micrograms/g of creatinine of 1-OH PYR. It therefore seems to be applicable to the biological monitoring of most occupational low exposures to coal tar.

The mutagenic activity and polycyclic aromatic hydrocarbon content of mineral oils.

Naphthenic distillates (raw or acid-treated) and motor and emulsifiable aluminium rolling oils were tested for mutagenicity in the Salmonella/microsome assay using the TA98 and TA100 strains. The polycyclic aromatic hydrocarbon (PAH) content of oil samples was also determined in parallel. In the presence of metabolic activation, both untreated and acid-treated naphthenic distillates were found to be mutagenic on a modified Ames test. One untreated sample showed the highest value of mutagenic potency (50 net revertants/mg oil for strain TA98). The PAH content of naphthenic distillates was about 10% (w/w) and was slightly reduced by sulfuric acid/earth treatment (1%). Non-mutagenic paraffin- and solvent-extracted crankcase oils became active, both with and without enzyme activation, after long use as gasoline engine lubricants, whereby their PAH content doubled (from 1.5% to 3%, w/w). A refined emulsifiable mineral oil also became directly mutagenic in both Salmonella strains after prolonged use in an aluminium hot-rolling mill. As the PAH levels found in used rolling oils was very low, we cannot explain their mutagenic activity. Mutagenicity was greatly reduced following careful cleaning of the oil bath and of the entire rolling machine. The present data reveal both the potential risk of occupational exposure to unrefined or mildly treated oils and the formation of mutagens in highly refined oils if the latter are used at high temperatures. The formation of mutagens in oils used in the metal-working industry can be prevented by careful industrial hygiene measures.

[Identification of genotoxic compounds used in leather processing industry]. / Identificazione di composti genotossici utilizzati nella lavorazione delle pelli.

The release of mutagens from 7 carbon black-based leather dyes and from leather samples at various stages of finishing was determined. After vigorous treatment with toluene, 4 commercial dyes yelded mutagenic extracts on Salmonella typhimurium in the presence of microsomal enzymes. Only in one case were the responsible chemicals identified as polycyclic aromatic hydrocarbons. The low bioavailability of mutagens contained in carbon black and their low mutagenic activity suggest that the risk associated with the use of these dyes is probably negligible. Soxhlet extracts with ethanol from finished leather were mutagenic on strain TA98 of Salmonella typhimurium in the absence of S9 mix. Analysis of extracts of leather samples at various intermediate stages of processing showed that mutagenic activity was detectable after the colouring process. The responsible compound was identified as a nitroazo dye (Colour Index: Acid Brown 83), with a mutagenic potential of about 4 revertant/micrograms. Eighteen commercial tannins containing mainly Cr(III) sulphates were assessed for genotoxicity. Most were contaminated with Cr(VI), a known mutagenic and carcinogenic agent, at levels sufficient to induce an increased frequency of SCE (sister chromatid exchanges) in mammalian cells (CHO, chinese hamster ovary) tested in vitro.

[Leather azo dyes: mutagenic and carcinogenic risks]. / I coloranti azoici per cuoio: rischio mutageno e cancerogeno.

The paper reviews the carcinogenicity and mutagenicity data on azo dyes used in the leather industry. Two water soluble benzidine-based dyes were classified as "probably carcinogenic to humans" by the International Agency for Research on Cancer (IARC). No other dyes have been evaluated by the IARC. Of the 48 azo dyes assayed in the Salmonella/microsome test, 20 gave positive results. Attention is drawn to the important role of the in vivo metabolism of azo compounds, which includes a preliminary reduction of the azo bonds and subsequent release of the aromatic amines of the dye. A useful assay (Prival test) for evaluating the mutagenic properties of azo dyes involves a reductive step that permits the release of any genotoxic agents present in the compounds. A list of leather azo dyes is furnished that are considered as potentially harmful due to the presence of a carcinogenic aromatic amine (benzidine, p-aminobenzene and derivatives) in their formulae.

[Urinary excretion of mutagens and cisplatin among the nursing staff at a medical oncology department exposed to cytostatic drugs]. / Escrezione urinaria di mutageni e cisplatino nel personale infermieristico dei reprti di oncologia media esposto a farmaci citostatici.

Exposure to cytostatic drugs was assessed in a group of 9 nurses employed in a hospital cancer therapy department by measuring the post-shift levels of urinary mutagens and cis-platinum. A slight but significant increase in urinary mutagenic activity compared to 11 controls was observed in the non-smokers: the mean values of mutagenic activity on the Ta100 strain in the presence of both microsomal and deconjugating enzymes were 4418 +/- 1186 and 2468 +/- 1681 respectively. Conversely, the urinary platinum concentration was below the detection limit of the analytical method (10 micrograms/l) in all samples. The increased urinary mutagenic activity in the exposed group can probably be attributed to the absorption of cyclophosphamide either during preparation and administration of the drug, or due to accidental contact with contaminated biological fluids, in view of the fact that the level of mutagens in urine samples from cyclophosphamide-treated patients is extremely high (up to 319,478 revertants/g creatinine in the case we examined).