Lesão traumática facial em cão - reconstrução cirúrgica com retalho de transposição rotacional / Facial traumatic injury in a dog - surgical reconstruction with rotational transposition flap

Background: Bite injuries are commonly found in small animal clinics, especially in male dogs, due to their habits of fighting and territorial disputes. In general, the lesions are treated with the use of compresses and bandages, however, it is extremely important to carefully evaluate the site, in order to carry out the appropriate treatment. In cases of tissue loss, an increasingly used practice is reconstructive surgery, which launches alternatives for treatment through flaps and skin grafts, promoting healing and satisfactory aesthetic repair. This report describes the case of a dog with a facial bite, treated with reconstructive surgery. Case: A 5-year-old male mixed-breed dog, with a body mass of 5 kg, was treated and submitted to a physical examination, due to the owner's complaint that he had been attacked by another dog, causing a bite on the face. On physical examination, the animal showed normal vital parameters, except for mild hyperthermia due to rectal temperature (39.5°C). On the face, it was possible to observe a lacerative lesion in the temporomandibular and masseteric regions, with loss of skin and muscle, in addition to having an aspect of infection and necrosis. To describe the hematological profile, a blood count was performed, showing no changes. In the biochemical tests, the present alteration was a slight increase in Alkaline Phosphatase (393.8 IU/L). Surgical treatment was indicated through facial reconstruction with a skin graft. After performing the antisepsis, the lesion was debrided, the edges were regularized and the injured tissue was curetted. For reconstruction of the defect, we used a flap obtained through a perpendicular incision at the base of the ear, in a caudal direction, and this flap was pulled and transposed over the wound. Flap synthesis was performed with 3-0 nylon thread. After surgery, a compressive bandage was performed, which was removed after 24 h. It was indicated to avoid exertion in the area and to return in 10 days for the evaluation of the surgery and removal of the stitches. Discussion: Traumatic injuries in animals are being increasingly reported, with male and non-neutered dogs being the most prevalent patients. This report is in line with other studies, with the patient's profile being a male dog, with an average age, in line with the literature. In general, in certain types of wounds, the affected animals can develop sepsis and even progress to death, however, in this case the patient did not show changes in vital parameters and in hematological tests. Reconstructive surgeries are performed with the aim of correcting skin defects and knowledge of the available techniques is important. It is also necessary to carry out a good planning, in order to avoid complications in the trans and postoperative period. In the present case, we chose to use a flap obtained through an incision perpendicular to the base of the ear, transposing it over the wound, in addition to relieving tissue tension through skin divulsion, increasing its elastic potential. The use of bandages is considered extremely important for the success of the surgical procedure, as it provides an efficient barrier against infections, trauma and adhesions. However, we emphasize the need to use ointments, gauzes and bandages concomitantly, in order to have the desired success in the postoperative period. In addition to proper surgical techniques, pain management and infection control are important for patient recovery. It is important to use non-steroidal anti-inflammatory drugs and opioids to obtain analgesia, in addition to antibiotic therapy before and after surgery. The reported case demonstrated that lesions in dogs with skin loss can be reconstructed using skin flaps, with an excellent recovery and good prognosis, as was the case with the patient in this report.

Myonecrosis caused by Clostridium septicum in a horse from Southern Brazil / Mionecrose causada por Clostridium septicum em um cavalo do sul do Brasil

Clostridial myonecrosis is a highly fatal infectious disease of the muscle that is caused by pathogenic clostridia. When it occurs in equine muscle, the infection can cause a variety of clinical signs. The present report described a case of acute myonecrosis caused by Clostridium septicum in a horse, which had a favorable clinical evolution. A 6-year-old mare was admitted to a veterinary hospital due to increased volume and lameness in the left pelvic limb after an intramuscular injection of an anti-inflammatory drug. The diagnosis of myonecrosis caused by C. septicum was based on clinical and laboratory findings. The animal showed significant improvement after 5 months of treatment and was discharged from the hospital. There is very limited information regarding myonecrosis caused by C. septicum in horses in Brazil; our study showed that early diagnosis and prompt appropriate treatment can ensure significant improvement and recovery of affected animals.

Mionecroses clostridiais são doenças altamente fatais, causadas por uma ou mais espécies de Clostridium sp. patogênicos. Entretanto, no músculo equino, a infecção pode produzir uma variedade de lesões e sinais clínicos. O presente relato descreve um caso de mionecrose aguda em um cavalo causada por Clostridium septicum, que apresentou uma evolução clínica favorável. Uma égua de seis anos foi internada em um hospital veterinário devido a um aumento de volume e claudicação no membro pélvico esquerdo, observado após injeção intramuscular de anti-inflamatório. O diagnóstico de mionecrose por C. septicum foi baseado nos achados clínicos e laboratoriais. Houve uma melhora significativa do animal após cinco meses de tratamento, permitindo que o mesmo fosse liberado do hospital veterinário. Considerando que as informações sobre C. septicum causadores de mionecroses em cavalos no Brasil são muito limitadas, este relato demonstra que o diagnóstico precoce e a implementação adequada do tratamento podem garantir uma melhora significativa e a recuperação dos animais afetados.

Downer cow syndrome causing rhabdomyolysis and acute renal failure in a 17-month-old Guzerá heifer / Síndrome da vaca caída causando rabdomiólise e insuficiência renal aguda em uma novilha Guzerá de 17 meses

The downer cow syndrome (DCS) is characterized by an alert cow showing inability or reluctance to stand for 12 hours or more. This paper reported clinical, laboratory, and pathological findings in a Guzerá heifer with rhabdomyolysis, pigmenturia and acute renal failure following DCS. A 17-month-old Guzerá heifer was transported via a 350-km ride in a truck and showed sternal recumbency and severe difficulty in standing and walking. Neurological examination was unremarkable, and the heifer presented normal response to cranial nerves and spinal cord tests. Rectal palpation revealed a 5-month gravid uterus. No other abnormalities were noted in the pelvis or around the coxofemoral joints. Biochemical abnormalities included extremely high muscular enzyme activities (creatine phosphokinase and aspartate aminotransferase) and high creatinine levels. Urinalysis revealed blackish and cloudy urine, proteinuria, and a positive occult blood test. Spinal cord ultrasonography showed no abnormalities. This report highlighted an uncommon clinical presentation (myoglobinuria) and pathological findings in a heifer with DCS as a consequence of severe compressive muscle damage. Practitioners and producers must be aware of the risk of careless road transportation for long distances of cattle, especially obese cows, avoiding unnecessary suffering and expenses due to DCS.

A síndrome da vaca caída (SVC) é caracterizada por um bovino alerta que mostra incapacidade ou relutância em permanecer em estação por 12 horas ou mais. O objetivo deste trabalho é relatar os achados clínicos, laboratoriais e patológicos em uma novilha Guzerá com rabdomiólise, pigmentúria e insuficiência renal aguda após a SVC. Uma novilha da raça Guzerá, de 17 meses de idade, foi transportada de caminhão por 350 km e apresentou decúbito esternal, grande dificuldade para assumir estação e caminhar. O exame neurológico não demonstrou alterações, e a novilha possuía resposta normal aos testes de nervos cranianos e medula espinhal. A palpação retal revelou útero grávido de cinco meses. Nenhuma outra anormalidade foi observada na pelve ou na região das articulações coxofemorais. As anormalidades bioquímicas incluíram atividades de enzimas musculares (creatina fosfoquinase e aspartato aminotransferase) extremamente aumentadas e níveis elevados de creatinina. A urinálise revelou urina enegrecida e turva, proteinúria e teste de sangue oculto positivo. O exame ultrassonográfico da medula espinhal não apresentou anormalidades. Este relato evidencia uma apresentação clínica (mioglobinúria) e achados patológicos incomuns em uma novilha com SVC em consequência de extensa lesão muscular compressiva. Veterinários e produtores devem estar atentos aos riscos do transporte rodoviário descuidado por longas distâncias de bovinos, especialmente vacas obesas, evitando assim sofrimento e despesas desnecessárias decorrentes da SVC.

Spontaneous poisoning by Baccharis vulneraria Backer in cattle

ABSTRACT: Baccharis vulneraria Backer is a sub-shrub frequently found in southern Brazil, which leads to gastrointestinal tract intoxication. The objective of this study is to describe epidemiological, clinical and anatomopathological aspects of two cases of B. vulneraria poisoning in cattle. Two bovines from two different municipalities in the Itajaí Valley, Santa Catarina, Brazil were necropsied and performed the histopathological evaluation and botanical classification of the plant found in the pasture. Bovine 1 had dehydration, ruminal atony, diarrhea, congested mucous membranes and hypothermia for 20 hours, and died during clinical care. At necropsy, there was moderate multifocal detachment and reddening of the forestomachs mucosa. Bovine 2 presented anorexia, dry feces, ruminal atony, vocalization and muscle tremors for ten days, unresponsive to treatments, evolving to death. At necropsy were seen loosening of the mucosa with marked diffuse reddening and transmural edema. The microscopic exam revealed degeneration, necrosis, vesiculation, and detachment of the forestomachs mucosa, associated with moderate multifocal neutrophilic infiltrate (Bovine 1); marked diffuse transmural necrosis, edema, hemorrhage, and marked fibrinous exudation (Bovine 2). A large amount of B. vulneraria was found in the pastures, with signs of consumption. In this report, a case of subacute evolution of B. vulneraria poisoning was observed, since the poisoning by this plant is usually acute. More knowledge about poisoning by this plant is necessary for the prevention and control, avoiding new mortality cases.

RESUMO: Baccharis vulneraria Backer é um subarbusto frequentemente encontrado no sul do Brasil, que leva a um quadro de intoxicação nocivo ao trato gastrointestinal. O objetivo deste trabalho é descrever aspectos epidemiológicos, clínicos e anatomopatológicos de dois casos de intoxicação por B. vulneraria em bovinos. Foram necropsiados dois bovinos de dois municípios do Vale do Itajaí, Santa Catarina, Brasil, com avaliação histopatológica dos órgãos e classificação botânica dos exemplares da planta localizada nos piquetes. No exame clínico do Bovino 1 foram constatados desidratação, atonia ruminal, diarreia, mucosas congestas e hipotermia durante 20 horas, com morte durante atendimento clínico. Na necropsia, havia desprendimento e avermelhamento multifocais moderados na mucosa dos proventrículos. Já o Bovino 2 teve manifestações clínicas de anorexia, fezes secas, atonia ruminal, vocalização e tremores musculares por 10 dias, não responsivas a tratamento, evoluindo para óbito. Na necropsia, havia desprendimento da mucosa dos proventrículos, com avermelhamento e edema transmural difusos acentuados. No exame histológico havia degeneração e necrose da mucosa proventricular, vacuolização e desprendimento do epitélio, infiltrado neutrofílico multifocal moderado (Bovino 1), e necrose transmural difusa acentuada, edema, hemorragia e exsudação fibrinosa acentuados (Bovino 2). Grande quantidade de B. vulneraria foi encontrada nas pastagens dos bovinos, com sinais de consumo. É relatado um caso de evolução subaguda de intoxicação por B. vulneraria, visto que a intoxicação por essa planta geralmente tem curso agudo. Conhecimentos acerca desta planta são necessários para prevenção e controle da intoxicação, evitando novos casos de mortalidade.

Necrose tissular em equino associada ao uso de fenilbutazona / Tissue necrosis in equine associated with use of phenylbutazone

Background: Wounds that occur with tissue necrosis and that result from the application of medications through the most diverse accesses are described as drug skin medical embolism or Nicholas syndrome in human medicine, with wide description. In veterinary medicine, this subject has not yet been described extensively and specifically in veterinary medicine, especially regarding to wounds that occurred after the application of non-intravenous medications in horses, even though these lesions are recurrent in the clinical routine. This report aims to describe a case of skin necrosis in a horse, due to phenylbutazone infection. Case: A 7 year-old Mangalarga Marchador horse, weighing 400 kg, was admitted to the Veterinary Hospital for Large Animals of the Universiade Federal Rural do Rio de Janeiro (UFRRJ), with a history of phenylbutazone injection to the left side of the neck. The animal had an extensive wound on the neck and face on the left side and was characterized by the presence of cold and devitalized skin, with a hardened and parched appearance and that easily detached. During the anamnesis, a single administration of 10 mL of a non-steroidal anti-inflammatory drug based on phenylbutazone was reported intramuscularly for about 10 days to control the pain resulting from the claudication present for 14 days. The medication was administered in the region of the lateral border of the neck, on the left side. After drug administration, the animal presented an increase in volume at the application site. After 24 h, the lesion spread from the inoculation region, extending to the head and chest of the animal. During debridement, it was found that the lesion did not reach the underlying muscle tissue. In addition to the wound, the animal had upper eyelid palsy, lower lip, and auricular ptosis. Treatment with surgical debridement of devitalized tissue, topical application of ozonated sunflower oil, ketanserin, and a free skin graft was instituted. During hospitalization, the animal had a corneal ulcer in the left eye with an unfavorable prognosis due to paralysis of the upper eyelid, with enucleation of the affected eyeball. The animal was under veterinary care for 180 days and was discharged when his wound was already in an advanced stage of healing. Discussion: The history of the application of phenylbutazone intramuscularly and the location and characteristics of the lesion presented by the patient in the present report suggest that this animal presented aseptic tissue necrosis resulting from the administration of non-steroidal anti-inflammatory drugs, phenylbutazone. Although aseptic tissue necrosis, better known as Nicolau's syndrome or drug embolism cutis, is widely characterized and described in this species, there are studies in the literature that reproduce the syndrome in pigs and rabbits. Phenylbutazone was able to cause arterial damage, mainly in the tunica intima of the artery in which the medication was administered, with perivascular inflammatory infiltrate and subsequent skin necrosis at the site of administration. In addition to the skin lesion, the animal started to show signs compatible with the left facial nerve lesion, evidenced by the immobility of the upper eyelid and labial and ear ptosis. This resulted in corneal ulceration and subsequent enucleation. The animal also developed chewing difficulty in the first months of hospitalization. This dysfunction may be due to a lesion of the mandibular nerve, responsible for innervating the masticatory muscles and the oral mucosa. However, the animal showed improvement in this aspect, no longer showing this condition after 90 days of hospitalization. The treatment used was successful in healing the wound.

Natural and experimental salinomycin poisoning associated with the use of florfenicol in pigs

ABSTRACT: This study describes the spontaneous and experimental salinomycin poisoning associated with the use of florfenicol and warns about the effects of the administration of antibiotics to animals that receive ionophores in the feed as growth promoters. A batch with 1,200 finishing pigs fed a diet containing 30ppm of salinomycin received florfenicol (60ppm via feed) to control respiratory diseases. Twenty-seven pigs had difficulty walking, tip-toe walking, muscle tremors, and anorexia seven days after the start of treatment. Twenty-two animals died, 10 recovered, and two were sent to the Laboratory of Animal Pathology of CAV-UDESC to be necropsied. The experimental reproduction of the disease was carried out to clarify the possible influence of florfenicol on salinomycin poisoning using 12 pigs divided into four groups with three animals each, treated for 16 days with diets containing no additives (Group 1), 50ppm of salinomycin (Group 2), 40ppm of florfenicol (Group 3), and 50ppm of salinomycin and 40ppm of florfenicol (Group 4). Only animals in Group 4 became ill. The clinical disease was reproduced from the ingestion of 24.67mg/kg/LW of salinomycin and 19.74mg/kg/LW of florfenicol. Both natural and experimental salinomycin poisoning associated with the use of florfenicol caused a condition of myopathy characterized in histology by hyaline degeneration and floccular necrosis of skeletal fibers, with macrophage infiltrate, associated with the figures of regeneration in skeletal muscles and multifocal areas of the proliferation of fibroblasts, being more intense in the longissimus dorsi and semimembranosus muscles. Therefore, florfenicol can cause the accumulation of ionophore salinomycin in the animal organism, resulting in a condition of toxic myopathy.

RESUMO: O presente trabalho descreve as intoxicações espontânea e experimental por salinomicina associada ao uso de florfenicol e alerta sobre os efeitos da administração de antibióticos aos animais que recebem ionóforos na ração como promotores de crescimento. Um lote com 1.200 suínos em fase de terminação, alimentados com ração contendo 30ppm de salinomicina, recebeu florfenicol (60ppm via ração) para o controle de doenças respiratórias. Sete dias após o início do tratamento, 27 suínos apresentaram dificuldade de locomoção, caminhar em brasa, tremores musculares e anorexia. Vinte e dois animais morreram, 10 recuperaram-se e dois foram encaminhados ao Laboratório de Patologia Animal (CAV-UDESC) para serem necropsiados. Para esclarecer a possível influência do florfenicol na toxicidade da salinomicina foi realizada a reprodução experimental da doença utilizando 12 suínos, divididos em 4 grupos com 3 animais cada, tratados por 16 dias com rações contendo: Grupo 1 = sem aditivos, Grupo 2 = 50ppm de salinomicina, Grupo 3 = 40ppm de florfenicol e Grupo 4 = 50ppm de salinomicina e 40ppm de florfenicol. Somente os animais do Grupo 4 adoeceram. A doença clínica foi reproduzida a partir da ingestão de 24,67mg/kg/PV de salinomicina e 19,74 mg/kg/PV de florfenicol. Tanto a intoxicação natural quanto a experimental por salinomicina associada ao uso de florfenicol provocaram um quadro de miopatia caracterizado na histologia por degeneração hialina e necrose flocular das fibras esqueléticas, com infiltrado macrofágico, associada às figuras de regeneração na musculatura esquelética e áreas multifocais de proliferação de fibroblastos, sendo mais intensas nos músculos longissimus dorsi e semimembranoso. Conclui-se que, o florfenicol tem a capacidade de ocasionar o acúmulo do ionóforo salinomicina no organismo animal, resultando em um quadro de miopatia tóxica.

Penile fractures in young bulls raised in feedlots in Southern Brazil

Background: Penile fracture is a pathology of young cattle that perform precocious and disordered breeding. The incompatibility of height between males and females and sodomy between males cause a great pressure on the sigmoid flexure and retractor muscle of the penis, which are the main causes and sites of organ injury. This study aimed to describe the epidemiological and pathological aspects of penile fractures observed in young bulls raised in pre-export feedlots (PEFs) in southern Brazil. Cases: In 2 PEFs located in the municipalities of Pelotas (property 1) and Capão do Leão (property 2), 3 male cattle [1 from property 1 and 2 from property 2] presented subcutaneous edema in the foreskin and perineum, associated with dysuria. The evolution of the clinical picture was approximately 20 days in all cases, with evolution to death. The bovine necropsied on property 1 had an increased volume and inguinal edema, involving the penis and scrotal sac. Necrosis of the subcutaneous tissue and local musculature was also observed. The testicles were surrounded by the necrotic tissue, and the right testis was swollen, with flaccid parenchyma adhering to the tunica albuginea. In the necropsy of 1 bull from property 2, an increase in the inguinal volume was observed, with an extensive area of necrosis and edema extending from the prepuce to the caudal musculature of the scrotal sac. There were also marked varicosis in the sigmoid flexure and necrosis of the adjacent region, without the involvement of the corpus cavernosum. During the necropsy of the 2 young bulls, fragments of organs from the abdominal, thoracic, and brain cavities were collected and fixed in 10% buffered formalin. From the bull of the property 2, an anatomical piece consisting of the penis, prepuce, and testicles was also collected and fixed in 10% buffered formalin. After 48 h, the tissue samples were cleaved, embedded in paraffin, cut into 3-µm-thick sections, and stained using hematoxylin and eosin (HE). A histological evaluation of the penile lesions in both cattle revealed intense hemorrhage, congestion, and necrosis of the muscles and tissues adjacent to the corpus cavernosum. In addition to areas of dystrophic calcification, neutrophil and macrophage infiltration was also observed. In the bull from the property 1, an intense edema and proliferation of fibrous tissue surrounding the urethra were noted. There were also marked tubular degeneration and intense infiltration of neutrophils, lymphocytes, and macrophages in the inner portion of the tunica albuginea. Discussion: In the present cases, the diagnosis was based on epidemiological data associated with clinical signs and pathology. The macroscopic lesions observed were probably due to the involvement of blood vessels adjacent to the penis, which suffered trauma during sodomy mating among cattle. These lesions have been described in other reports of this pathology and in diseases, such as acropostitis-phimosis, fibropapilloma of the glans, preputial abscess, and urolithiasis, and the differential diagnosis of these diseases must be carried out, as they have different etiologies. In the bulls of the present study, no lesions were observed in the corpus cavernosum, and this condition was attributed to the presence of varicosis and accumulation of urine in the prepuce, due to the difficulty in exposing the penis. Histologically, there were intense hemorrhage, congestion, and necrosis of the muscles and tissues adjacent to the corpus cavernosum, with the infiltration of neutrophils and macrophages, and areas of dystrophic calcification. The presence of necrotic lesions in tissues adjacent to the penis may be related to hypoxia, vascular lesions, or the action of chemical elements present in the urine. In both cases, vascular lesions were present, which were attributed to the main triggering factor for the disease.

Accidental monensin poisoning in buffaloes in Bahia, Brazil

ABSTRACT: Monensin is an ionophore antibiotic (IA) widely used for growth promotion and weight gain in the production of ruminants. However, it has caused intoxication in several species, including buffaloes, mainly because of the ignorance or disrespect of the recommendations for use in each animal species. The objective of this study was to describe, for the first time, clinical-epidemiological and anatomopathological data of an outbreak of accidental poisoning by monensin in buffalos and rediscuss the recommendation of the use of IA in the production of this species. The outbreak affected 21 adult buffaloes after consumption of remains from a feed formulated on the farm and whose constituents were mixed by hand. Clinical and first death signs were observed 24 hours after ingestion of this food. In general, the clinical picture was characterized by muscle weakness, tremors, difficulty in locomotion, and decubitus. Fifteen buffaloes presented clinical signs of poisoning (71.5% morbidity), followed by death (100% lethality), after acute to subacute evolution ( 24h to 96h). Laboratory tests indicated elevated serum activity of creatine phosphokinase and aspartate aminotransferase enzymes. Three buffaloes underwent necropsy, and samples from several organs were collected for histopathological examination. The main injuries found were hyaline degeneration and multifocal segmental necrosis in the skeletal and cardiac striated muscles (myopathy and degenerative-necrotic multifocal multifocal-necrotic cardiopathy). The diagnosis was confirmed by the toxicological evaluation of suspected ration remains, which detected 461.67mg/kg of monensin. The death of 71.5% buffaloes in this lot occurred due to a succession of errors, which included faults in the formulation of the ration and, above all, due to the use of monensin in a highly sensitive species. Despite the possible beneficial effects of IA use as a dietary supplement for buffaloes, we are of the opinion that IAs should never be used in bubalinoculture since any increment in production does not compensate for the imminent risk of death due to a small safety margin for this species and the absence of antidotes.

RESUMO: Monensina é um antibiótico ionóforo (AI) amplamente empregado na produção de ruminantes para promoção de crescimento e ganho de peso, mas que tem causado intoxicação em diversas espécies, incluindo os búfalos, principalmente, pelo desconhecimento ou desrespeito das recomendações de uso e às particularidades de cada espécie animal. Objetivou-se descrever, pela primeira vez na Bahia, dados clínico-epidemiológicos e anatomopatológicos de um surto de intoxicação acidental por monensina em búfalos e rediscutir a recomendação do uso de AI na produção de bubalinos. O surto acometeu um lote de 21 búfalos adultos após consumo de sobras de uma ração para bovinos formulada na fazenda e cujos constituintes eram misturados à mão. Os sinais clínicos e primeiros óbitos foram observados 24 horas após a ingestão dessa ração. O quadro clínico, em geral, se caracterizou por fraqueza muscular, tremores, dificuldade de locomoção e decúbito. Quinze búfalos apresentaram sinais clínicos de intoxicação (morbidade 71,5%), seguido de morte (letalidade 100%), após evolução aguda a subaguda ( 24h até 96h). Exames laboratoriais indicaram acentuada elevação na atividade sérica das enzimas CPK e AST. Três búfalos foram necropsiados, sendo coletadas amostras de diversos órgãos para exame histopatológico. A principal lesão encontrada foi degeneração hialina e necrose segmentar multifocal nos músculos estriados esqueléticos e cardíacos (miopatia e cardiopatia degenerativo-necrótica tóxica multifocal polifásica). O diagnóstico foi confirmado pela avaliação toxicológica das sobras da ração suspeita, que detectou 461,67mg/kg de monensina. A morte de 71,5% dos búfalos deste lote ocorreu devido a uma sucessão de erros, que incluíram falhas na formulação da ração e, sobretudo, devido ao uso da monensina em uma espécie altamente sensível. Enfatizamos que, apesar dos possíveis efeitos benéficos do uso AIs como suplemento dietético para bubalinos, somos da opinião que os AIs nunca devem ser empregados na bubalinocultura, uma vez que os eventuais incrementos na produção não compensam o risco iminente de morte, devido a pequena margem de segurança para essa espécie e a inexistência de antídotos.

Bothrops envenomation in dogs: local and systemic manifestations

Background: Snakebite envenoming is a condition that affects humans and domestic animals worldwide. Identification of the snake species involved in the envenomation is infrequent. Bothrops envenomation presents typical clinicopathological features. This report describes epidemiological, clinical, and pathological data of 2 cases of Bothrops envenomation in dogs, including the first case of Bothrops moojeni snake striking a domestic animal in Brazil. Cases: Case 1. A dog was witnessed to have a Bothrops moojeni snakebite on a farm. In the first 24 h, acute lameness, pain, diffuse swelling, focal bleeding at the left forelimb, and increased whole-blood clotting time were observed in the envenomed dog. Polyvalent antivenom was administered in addition to fluid therapy, analgesics, corticosteroids, and antibiotics. On the 5th day, the animal presented spontaneous bleeding at the wound site, thrombocytopenia, and increased whole-blood clotting time. An additional dose of polyvalent antivenom was administered, and local treatment at the snakebite site was initiated. After 13 days, the dog showed no clinical or laboratory changes and recovered entirely. Case 2. A mongrel dog was taken for a necropsy to determine the cause of death. Grossly, major findings included swelling in the nasal plane that extended to the neck and dissecting hemorrhage in the subcutaneous tissue and adjacent musculature. Hemorrhages were observed in the heart, parietal pleura, left forelimb, lumbar region, and perirenal tissue. Marked necrosis and disruption of small blood vessels and lymphatics within the deep dermis and subcutaneous tissue were the main microscopic findings close to the snakebite site. Additionally, degeneration and necrosis of muscle fibers and dissecting hemorrhage were observed in the head and neck tissues surrounding the snakebite site. Kidneys showed marked interstitial hemorrhage and acute tubular nephrosis. Discussion: Bothrops envenoming is characterized by local (hemorrhage, dermonecrosis, and myonecrosis) and systemic (coagulative disorders, systemic hemorrhage, and acute kidney injury) changes due to the effect of the main venom components such as phospholipase A2 and metalloproteinases. These changes are hallmarks for the bothropic envenomation, supporting the diagnosis in cases 1 and 2. In case 1, the dog developed a Bothrops moojeni snakebite envenomation, but the immediate treatment with antivenom allowed a favorable outcome. In case 2, gross and microscopic findings supported the presumptive diagnosis of fatal bothropic envenomation. A marked local reaction such as swelling, pain, bleeding, bruising, and tissue necrosis was observed in case 1. In case 2, the most significant local changes were swelling and edema at the head and neck, hemorrhage in the subcutaneous tissue, and adjacent musculature. Systemic effects were observed clinically as spontaneous bleeding, thrombocytopenia, increased whole-blood clotting time (Case 1), systemic hemorrhages, and acute tubular nephrosis (Case 2). A proper treatment probably prevented the development of acute renal failure in Case 1. Herein, we show the first case of accidental snakebite envenomation by B. moojeni in a dog in Brazil. Information is scarce on the identification of venomous snake species striking domestic animals. Fast detection of well-determined clinical and pathological findings of Bothrops envenomation is essential for a correct diagnosis, therapeutics, and a good prognosis, even in cases with an unknown history.

Macracanthorhynchus hirudinaceus em uma porca da Província de El Oro - Equador / Macracanthorhynchus hirudinaceus in a sow in El Oro Province - Ecuador

Background: Macracantorhincosis is a zoonotic disease resulting from inadequate sanitary conditions, which occurs in pigs infected by acanthocephalic helminths called Macracanthorhynchus hirudinaceus. The eggs of these parasites are resistant to cold, high temperatures and can survive up to 3 years in the soil. They are consumed by dung beetles of the Scarabeidae family causing the parasite to evolve into its infective form, the cystacanth. The pig becomes infected after ingestion of either larvae or adult forms of these coleoptera. This work describes a case report of macracantorhincosis found in a pig from the canton of Zaruma located in the province of El Oro, Ecuador. Case: One sow, approximately 24-month-old, weighing 30 kg, presented cachexia, muscle weakness, pale oral and ocular mucosa and a body temperature above 39.4°C. The animal had a bulge on the ventral side of the neck, which evolved causing progressive discomfort to the point that the animal stopped eating. The sow was dewormed for 3 consecutive days. Fifteen days later, the animal had convulsions and muscle tremors, and died some hours after the symptoms started. During necropsy procedure, pale digestive tract membranes and nodules with fibrin were observed in the small intestine (jejunum), which was incised and the presence of parasites adhered to the granulomas detected. Two granulomas for morphological and histological studies and stool samples for coproparasitic test were collected. The collected parasites were fixed in a 10% buffered formalin solution, cross-sections were made and routinely processed for histological studies. The 5 µm thick sections were stained using the hematoxylin and eosin (HE) technique. The parasite's action involves perforation of the intestinal wall though its proboscis causing peritonitis and enteritis. Other conditions in intestinal dissection such as necrotic areas, inflammation of the submucosa and adult parasites adhered to the intestinal mucosa were also observed. The coproparasitic examination was performed using the flotation and sedimentation techniques. The coproparasitic test detected dark colored feces, semi-solid consistency and the presence of Macracanthorhynchus hirudinaceu eggs. In the histological evaluation of the cross section of the parasite, the presence of circular and longitudinal muscle fibers and lemniscus with their constrictor muscles was observed. Cuticle, hypodermis with tapered fibers and a large number of developing mature eggs were also reported. Discussion: There is no pathognomonic symptomatology about this parasitosis and peritonitis can be generated by intestinal perforations. The findings at necropsy were ulcerations, inflammation in the small intestine and the presence of numerous nodules in the serous layer, where there was penetration of the parasite's proboscis. When fixed to the mucosa, these parasites cause ulcerations, inflammation and necrosis in the wall of the small intestine. The hypodermic layer is thicker than the muscular layer and the presence of leminis with their constricting muscles are typical features of acanthocephalus. It is considered appropriate to carry out epidemiological studies on the prevalence of the parasite Macracanthorhynchus hirudinaceus at pig farming system in the region, in order to determine the main risk factors. In Ecuador, cases of this disease in humans have not yet been reported, but have already been described in other countries, so the presence of this parasite in family swine farming may be considered a zoonotic-type risk factor.

Polymyositis associated with brainstem signs in a dog

Background: Polymyositis is a generalized inflammatory myopathy which can lead to rhabdomyolysis. This affection may have several origins, including degenerative, metabolic, autoimmune, infectious, inflammatory, ischemic, traumatic, by drug use, induced by toxins and also of idiopathic origin. Diagnosis is made with seric dosage, electrodiagnostic tests and muscle biopsy. Lesions in the rostral oblong medulla may affect the central vestibular system, and there may be signs such as opisthotonos, nystagmus, and strabismus. The aim of this report is to describe a case of a mixed breed dog with manifestation of polymyositis associated with brainstem signs of probable idiopathic origin. Case: A 5-year-old mixed breed male dog was attended with opisthotonos episodes for 2 days, and pelvic limbs extension and thoracic limbs flexion that lasted 10 to 20 min at intervals of approximately 1 h. The animal was anorexic and had also presented one episode of emesis. Upon neurological examination, ventromedial strabismus and Horner's syndrome was observed on the right side, besides vertical nystagmus, flaccid tetraparesis and absence of proprioception in the four limbs. Biochemical analyses revealed creatine kinase (CK) increased (2,433.9 UI/L - reference: 1.5-28.4 UI/L), and urinalysis showed dark color and presence of occult blood without, however, erythrocyturia. Electrocardiogram (ECG) showed QS wave and deviation of the electrical axis. Treatment with prednisolone (1 mg/kg, BID), phenobarbital (2 mg/kg, BID), maropitant citrate (1 mg/kg in 2 doses), and crystalloid fluid therapy (50 mL/kg/day) were prescribed. On the 4th day, the dog was more active and feeding without a tube, so it recommended keep the treatment at home. On the 10th day, the animal had proprioception present on the 4 limbs and normorexia. Biochemical analyses and urinalysis showed no alterations, but normochromic normochromic anemia with thrombocytopenia and leukocytosis by neutrophilia showed in blood count exam. PCR to Ehrlichia canis, Hepatozoon sp., and Babesia canis resulted negative. On the 15th day, blood count, biochemical analyses and urinalysis showed no alterations. Neurological examination revealed only positional vertical nystagmus. which remained as a sequel. Discussion: Polymyositis may be accompanied by rhabdomyolysis, characterized by acute muscle necrosis, increased CK and myoglobinuria. The animal had polymyositis of acute onset, with myoglobinuria and elevated CK values, whose presentation included myalgia and muscle weakness. In humans, polymyositis is accompanied by changes in electrocardiographic tracing without clinical alterations. In dogs, the first report that showed cardiac involvement was compatible with myocarditis. The changes in ECG in the present case was attributed to failure in myocardial electrical conduction. The patient also showed signs of brainstem and central vestibular system injuries. Stress myopathy, intoxication, snakebite, infectious, and metabolic diseases were discarded leading to a clinical suspicion as idiopathic origin. Similar to a published case, the patient of this report received symptomatic and supportive treatment, being discharged from the hospital 20 days after the onset of clinical signs. Thus, polymyositis may be accompanied by signs indicative of brainstem injury. Patients with rhabdomyolysis require intense monitoring due to the high risk of developing acute renal failure. Since no causative agent was identified, symptomatic treatment combined with the prevention of possible complications were fundamental for the maintenance of the animal's life.

Kukoamine A activates Akt/GSK-3ß signaling pathway to inhibit oxidative stress and relieve myocardial ischemia-reperfusion injury

Purpose: Myocardial ischemia/reperfusion (MI/R) injury refers to a pathological condition of treatment of myocardial infarction. Oxidative stress and inflammation are believed to be important mechanisms mediating MI/R injury. Kukoamine A (KuA), a sperm, is the main bioactive component extracted from the bark of goji berries. In this study, we wanted to investigate the possible effects of KuA on MI/R injury. Methods: In this experiment, all rats were divided into sham operation group, MI/R group, KuA 10 mg + MI/R group, KuA 20 mg + MI/R group. After 120 min of ischemia/reperfusion treatment, left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), maximal rates of rising and fall of left ventricular pressure (±dp/dtmax), and ischemic area were detected. Serum samples of rats in each group were collected. The enzyme activities of catalase (CAT), glutathione peroxidase (GSH-PX), superoxide dismutase (SOD), levels of malondialdehyde (MDA), CK muscle/brain (CK-MB), tumor necrosis factor (TNF), interleukin-1ß (IL-1ß), and interleukin-6 (IL-6) were detected using enzyme-linked immunosorbent assay (ELISA). The apoptosis of myocardium in each group was detected according to the instructions of the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The expressions of mammalian target of glycogen synthase kinase-3ß (GSH-3ß) and protein kinase B (Akt) mRNA level in myocardial tissues were detected via reverse transcription-polymerase chain reaction (RT-PCR). Results: MI/R rats showed a significant increase in oxidative stress and inflammation. In addition, we showed that KuA significantly improved the myocardial function such as LVSP, left ventricular ejection fraction, +dp/dt, and -dp/dt. Here, it attenuated dose-dependent histological damage in ischemia-reperfused myocardium, which is associated with the enzyme activities of SOD, GSH-PX, and levels of MDA, IL-6, TNF-α, L-1ß. Conclusions: KuA inhibited gene expression of Akt/GSK-3ß, inflammation, oxidative stress and improved MR/I injury. Taken together, our results allowed us to better understand the pharmacological activity of KuA against MR/I injury.

Spontaneous poisoning by Baccharis vulneraria Backer in cattle / Intoxicação espontânea por Baccharis vulneraria Backer em bovinos

Baccharis vulneraria Backer is a sub-shrub frequently found in southern Brazil, which leads to gastrointestinal tract intoxication. The objective of this study is to describe epidemiological, clinical and anatomopathological aspects of two cases of B. vulneraria poisoning in cattle. Two bovines from two different municipalities in the Itajaí Valley, Santa Catarina, Brazil were necropsied and performed the histopathological evaluation and botanical classification of the plant found in the pasture. Bovine 1 had dehydration, ruminal atony, diarrhea, congested mucous membranes and hypothermia for 20 hours, and died during clinical care. At necropsy, there was moderate multifocal detachment and reddening of the forestomachs mucosa. Bovine 2 presented anorexia, dry feces, ruminal atony, vocalization and muscle tremors for ten days, unresponsive to treatments, evolving to death. At necropsy were seen loosening of the mucosa with marked diffuse reddening and transmural edema. The microscopic exam revealed degeneration, necrosis, vesiculation, and detachment of the forestomachs' mucosa, associated with moderate multifocal neutrophilic infiltrate (Bovine 1); marked diffuse transmural necrosis, edema, hemorrhage, and marked fibrinous exudation (Bovine 2). A large amount of B. vulneraria was found in the pastures, with signs of consumption. In this report, a case of subacute evolution of B. vulneraria poisoning was observed, since the poisoning by this plant is usually acute. More knowledge about poisoning by this plant is necessary for the prevention and control, avoiding new mortality cases.

Baccharis vulneraria Backer é um subarbusto frequentemente encontrado no sul do Brasil, que leva a um quadro de intoxicação nocivo ao trato gastrointestinal. O objetivo deste trabalho é descrever aspectos epidemiológicos, clínicos e anatomopatológicos de dois casos de intoxicação por B. vulneraria em bovinos. Foram necropsiados dois bovinos de dois municípios do Vale do Itajaí, Santa Catarina, Brasil, com avaliação histopatológica dos órgãos e classificação botânica dos exemplares da planta localizada nos piquetes. No exame clínico do Bovino 1 foram constatados desidratação, atonia ruminal, diarreia, mucosas congestas e hipotermia durante 20 horas, com morte durante atendimento clínico. Na necropsia, havia desprendimento e avermelhamento multifocais moderados na mucosa dos proventrículos. Já o Bovino 2 teve manifestações clínicas de anorexia, fezes secas, atonia ruminal, vocalização e tremores musculares por 10 dias, não responsivas a tratamento, evoluindo para óbito. Na necropsia, havia desprendimento da mucosa dos proventrículos, com avermelhamento e edema transmural difusos acentuados. No exame histológico havia degeneração e necrose da mucosa proventricular, vacuolização e desprendimento do epitélio, infiltrado neutrofílico multifocal moderado (Bovino 1), e necrose transmural difusa acentuada, edema, hemorragia e exsudação fibrinosa acentuados (Bovino 2). Grande quantidade de B. vulneraria foi encontrada nas pastagens dos bovinos, com sinais de consumo. É relatado um caso de evolução subaguda de intoxicação por B. vulneraria, visto que a intoxicação por essa planta geralmente tem curso agudo. Conhecimentos acerca desta planta são necessários para prevenção e controle da intoxicação, evitando novos casos de mortalidade.

Spontaneous poisoning by Baccharis vulneraria Backer in cattle / Intoxicação espontânea por Baccharis vulneraria Backer em bovinos

Baccharis vulneraria Backer is a sub-shrub frequently found in southern Brazil, which leads to gastrointestinal tract intoxication. The objective of this study is to describe epidemiological, clinical and anatomopathological aspects of two cases of B. vulneraria poisoning in cattle. Two bovines from two different municipalities in the Itajaí Valley, Santa Catarina, Brazil were necropsied and performed the histopathological evaluation and botanical classification of the plant found in the pasture. Bovine 1 had dehydration, ruminal atony, diarrhea, congested mucous membranes and hypothermia for 20 hours, and died during clinical care. At necropsy, there was moderate multifocal detachment and reddening of the forestomachs mucosa. Bovine 2 presented anorexia, dry feces, ruminal atony, vocalization and muscle tremors for ten days, unresponsive to treatments, evolving to death. At necropsy were seen loosening of the mucosa with marked diffuse reddening and transmural edema. The microscopic exam revealed degeneration, necrosis, vesiculation, and detachment of the forestomachs' mucosa, associated with moderate multifocal neutrophilic infiltrate (Bovine 1); marked diffuse transmural necrosis, edema, hemorrhage, and marked fibrinous exudation (Bovine 2). A large amount of B. vulneraria was found in the pastures, with signs of consumption. In this report, a case of subacute evolution of B. vulneraria poisoning was observed, since the poisoning by this plant is usually acute. More knowledge about poisoning by this plant is necessary for the prevention and control, avoiding new mortality cases.(AU)

Baccharis vulneraria Backer é um subarbusto frequentemente encontrado no sul do Brasil, que leva a um quadro de intoxicação nocivo ao trato gastrointestinal. O objetivo deste trabalho é descrever aspectos epidemiológicos, clínicos e anatomopatológicos de dois casos de intoxicação por B. vulneraria em bovinos. Foram necropsiados dois bovinos de dois municípios do Vale do Itajaí, Santa Catarina, Brasil, com avaliação histopatológica dos órgãos e classificação botânica dos exemplares da planta localizada nos piquetes. No exame clínico do Bovino 1 foram constatados desidratação, atonia ruminal, diarreia, mucosas congestas e hipotermia durante 20 horas, com morte durante atendimento clínico. Na necropsia, havia desprendimento e avermelhamento multifocais moderados na mucosa dos proventrículos. Já o Bovino 2 teve manifestações clínicas de anorexia, fezes secas, atonia ruminal, vocalização e tremores musculares por 10 dias, não responsivas a tratamento, evoluindo para óbito. Na necropsia, havia desprendimento da mucosa dos proventrículos, com avermelhamento e edema transmural difusos acentuados. No exame histológico havia degeneração e necrose da mucosa proventricular, vacuolização e desprendimento do epitélio, infiltrado neutrofílico multifocal moderado (Bovino 1), e necrose transmural difusa acentuada, edema, hemorragia e exsudação fibrinosa acentuados (Bovino 2). Grande quantidade de B. vulneraria foi encontrada nas pastagens dos bovinos, com sinais de consumo. É relatado um caso de evolução subaguda de intoxicação por B. vulneraria, visto que a intoxicação por essa planta geralmente tem curso agudo. Conhecimentos acerca desta planta são necessários para prevenção e controle da intoxicação, evitando novos casos de mortalidade.(AU)

Accidental monensin poisoning in buffaloes in Bahia, Brazil / Intoxicação acidental por monensina em búfalos na Bahia, Brasil

Monensin is an ionophore antibiotic (IA) widely used for growth promotion and weight gain in the production of ruminants. However, it has caused intoxication in several species, including buffaloes, mainly because of the ignorance or disrespect of the recommendations for use in each animal species. The objective of this study was to describe, for the first time, clinical-epidemiological and anatomopathological data of an outbreak of accidental poisoning by monensin in buffalos and rediscuss the recommendation of the use of IA in the production of this species. The outbreak affected 21 adult buffaloes after consumption of remains from a feed formulated on the farm and whose constituents were mixed by hand. Clinical and first death signs were observed 24 hours after ingestion of this food. In general, the clinical picture was characterized by muscle weakness, tremors, difficulty in locomotion, and decubitus. Fifteen buffaloes presented clinical signs of poisoning (71.5% morbidity), followed by death (100% lethality), after acute to subacute evolution (<24h to 96h). Laboratory tests indicated elevated serum activity of creatine phosphokinase and aspartate aminotransferase enzymes. Three buffaloes underwent necropsy, and samples from several organs were collected for histopathological examination. The main injuries found were hyaline degeneration and multifocal segmental necrosis in the skeletal and cardiac striated muscles (myopathy and degenerative-necrotic multifocal multifocal-necrotic cardiopathy). The diagnosis was confirmed by the toxicological evaluation of suspected ration remains, which detected 461.67mg/kg of monensin. The death of 71.5% buffaloes in this lot occurred due to a succession of errors, which included faults in the formulation of the ration and, above all, due to the use of monensin in a highly sensitive species. Despite the possible beneficial effects of IA use as a dietary supplement for buffaloes, we are of the opinion that IAs should never be used in bubalinoculture since any increment in production does not compensate for the imminent risk of death due to a small safety margin for this species and the absence of antidotes.

Monensina é um antibiótico ionóforo (AI) amplamente empregado na produção de ruminantes para promoção de crescimento e ganho de peso, mas que tem causado intoxicação em diversas espécies, incluindo os búfalos, principalmente, pelo desconhecimento ou desrespeito das recomendações de uso e às particularidades de cada espécie animal. Objetivou-se descrever, pela primeira vez na Bahia, dados clínico-epidemiológicos e anatomopatológicos de um surto de intoxicação acidental por monensina em búfalos e rediscutir a recomendação do uso de AI na produção de bubalinos. O surto acometeu um lote de 21 búfalos adultos após consumo de sobras de uma ração para bovinos formulada na fazenda e cujos constituintes eram misturados à mão. Os sinais clínicos e primeiros óbitos foram observados 24 horas após a ingestão dessa ração. O quadro clínico, em geral, se caracterizou por fraqueza muscular, tremores, dificuldade de locomoção e decúbito. Quinze búfalos apresentaram sinais clínicos de intoxicação (morbidade 71,5%), seguido de morte (letalidade 100%), após evolução aguda a subaguda (<24h até 96h). Exames laboratoriais indicaram acentuada elevação na atividade sérica das enzimas CPK e AST. Três búfalos foram necropsiados, sendo coletadas amostras de diversos órgãos para exame histopatológico. A principal lesão encontrada foi degeneração hialina e necrose segmentar multifocal nos músculos estriados esqueléticos e cardíacos (miopatia e cardiopatia degenerativo-necrótica tóxica multifocal polifásica). O diagnóstico foi confirmado pela avaliação toxicológica das sobras da ração suspeita, que detectou 461,67mg/kg de monensina. A morte de 71,5% dos búfalos deste lote ocorreu devido a uma sucessão de erros, que incluíram falhas na formulação da ração e, sobretudo, devido ao uso da monensina em uma espécie altamente sensível. Enfatizamos que, apesar dos possíveis efeitos benéficos do uso AIs como suplemento dietético para bubalinos, somos da opinião que os AIs nunca devem ser empregados na bubalinocultura, uma vez que os eventuais incrementos na produção não compensam o risco iminente de morte, devido a pequena margem de segurança para essa espécie e a inexistência de antídotos.

Natural and experimental salinomycin poisoning associated with the use of florfenicol in pigs / Intoxicação natural e experimental por salinomicina associada ao uso de florfenicol em suínos

This study describes the spontaneous and experimental salinomycin poisoning associated with the use of florfenicol and warns about the effects of the administration of antibiotics to animals that receive ionophores in the feed as growth promoters. A batch with 1,200 finishing pigs fed a diet containing 30ppm of salinomycin received florfenicol (60ppm via feed) to control respiratory diseases. Twenty-seven pigs had difficulty walking, tip-toe walking, muscle tremors, and anorexia seven days after the start of treatment. Twenty-two animals died, 10 recovered, and two were sent to the Laboratory of Animal Pathology of CAV-UDESC to be necropsied. The experimental reproduction of the disease was carried out to clarify the possible influence of florfenicol on salinomycin poisoning using 12 pigs divided into four groups with three animals each, treated for 16 days with diets containing no additives (Group 1), 50ppm of salinomycin (Group 2), 40ppm of florfenicol (Group 3), and 50ppm of salinomycin and 40ppm of florfenicol (Group 4). Only animals in Group 4 became ill. The clinical disease was reproduced from the ingestion of 24.67mg/kg/LW of salinomycin and 19.74mg/kg/LW of florfenicol. Both natural and experimental salinomycin poisoning associated with the use of florfenicol caused a condition of myopathy characterized in histology by hyaline degeneration and floccular necrosis of skeletal fibers, with macrophage infiltrate, associated with the figures of regeneration in skeletal muscles and multifocal areas of the proliferation of fibroblasts, being more intense in the longissimus dorsi and semimembranosus muscles. Therefore, florfenicol can cause the accumulation of ionophore salinomycin in the animal organism, resulting in a condition of toxic myopathy.

O presente trabalho descreve as intoxicações espontânea e experimental por salinomicina associada ao uso de florfenicol e alerta sobre os efeitos da administração de antibióticos aos animais que recebem ionóforos na ração como promotores de crescimento. Um lote com 1.200 suínos em fase de terminação, alimentados com ração contendo 30ppm de salinomicina, recebeu florfenicol (60ppm via ração) para o controle de doenças respiratórias. Sete dias após o início do tratamento, 27 suínos apresentaram dificuldade de locomoção, "caminhar em brasa", tremores musculares e anorexia. Vinte e dois animais morreram, 10 recuperaram-se e dois foram encaminhados ao Laboratório de Patologia Animal (CAV-UDESC) para serem necropsiados. Para esclarecer a possível influência do florfenicol na toxicidade da salinomicina foi realizada a reprodução experimental da doença utilizando 12 suínos, divididos em 4 grupos com 3 animais cada, tratados por 16 dias com rações contendo: Grupo 1 = sem aditivos, Grupo 2 = 50ppm de salinomicina, Grupo 3 = 40ppm de florfenicol e Grupo 4 = 50ppm de salinomicina e 40ppm de florfenicol. Somente os animais do Grupo 4 adoeceram. A doença clínica foi reproduzida a partir da ingestão de 24,67mg/kg/PV de salinomicina e 19,74 mg/kg/PV de florfenicol. Tanto a intoxicação natural quanto a experimental por salinomicina associada ao uso de florfenicol provocaram um quadro de miopatia caracterizado na histologia por degeneração hialina e necrose flocular das fibras esqueléticas, com infiltrado macrofágico, associada às figuras de regeneração na musculatura esquelética e áreas multifocais de proliferação de fibroblastos, sendo mais intensas nos músculos longissimus dorsi e semimembranoso. Conclui-se que, o florfenicol tem a capacidade de ocasionar o acúmulo do ionóforo salinomicina no organismo animal, resultando em um quadro de miopatia tóxica.

Accidental monensin poisoning in buffaloes in Bahia, Brazil / Intoxicação acidental por monensina em búfalos na Bahia, Brasil

Monensin is an ionophore antibiotic (IA) widely used for growth promotion and weight gain in the production of ruminants. However, it has caused intoxication in several species, including buffaloes, mainly because of the ignorance or disrespect of the recommendations for use in each animal species. The objective of this study was to describe, for the first time, clinical-epidemiological and anatomopathological data of an outbreak of accidental poisoning by monensin in buffalos and rediscuss the recommendation of the use of IA in the production of this species. The outbreak affected 21 adult buffaloes after consumption of remains from a feed formulated on the farm and whose constituents were mixed by hand. Clinical and first death signs were observed 24 hours after ingestion of this food. In general, the clinical picture was characterized by muscle weakness, tremors, difficulty in locomotion, and decubitus. Fifteen buffaloes presented clinical signs of poisoning (71.5% morbidity), followed by death (100% lethality), after acute to subacute evolution (<24h to 96h). Laboratory tests indicated elevated serum activity of creatine phosphokinase and aspartate aminotransferase enzymes. Three buffaloes underwent necropsy, and samples from several organs were collected for histopathological examination. The main injuries found were hyaline degeneration and multifocal segmental necrosis in the skeletal and cardiac striated muscles (myopathy and degenerative-necrotic multifocal multifocal-necrotic cardiopathy). The diagnosis was confirmed by the toxicological evaluation of suspected ration remains, which detected 461.67mg/kg of monensin. The death of 71.5% buffaloes in this lot occurred due to a succession of errors, which included faults in the formulation of the ration and, above all, due to the use of monensin in a highly sensitive species. Despite the possible beneficial effects of IA use as a dietary supplement for buffaloes, we are of the opinion that IAs should never be used in bubalinoculture since any increment in production does not compensate for the imminent risk of death due to a small safety margin for this species and the absence of antidotes.(AU)

Monensina é um antibiótico ionóforo (AI) amplamente empregado na produção de ruminantes para promoção de crescimento e ganho de peso, mas que tem causado intoxicação em diversas espécies, incluindo os búfalos, principalmente, pelo desconhecimento ou desrespeito das recomendações de uso e às particularidades de cada espécie animal. Objetivou-se descrever, pela primeira vez na Bahia, dados clínico-epidemiológicos e anatomopatológicos de um surto de intoxicação acidental por monensina em búfalos e rediscutir a recomendação do uso de AI na produção de bubalinos. O surto acometeu um lote de 21 búfalos adultos após consumo de sobras de uma ração para bovinos formulada na fazenda e cujos constituintes eram misturados à mão. Os sinais clínicos e primeiros óbitos foram observados 24 horas após a ingestão dessa ração. O quadro clínico, em geral, se caracterizou por fraqueza muscular, tremores, dificuldade de locomoção e decúbito. Quinze búfalos apresentaram sinais clínicos de intoxicação (morbidade 71,5%), seguido de morte (letalidade 100%), após evolução aguda a subaguda (<24h até 96h). Exames laboratoriais indicaram acentuada elevação na atividade sérica das enzimas CPK e AST. Três búfalos foram necropsiados, sendo coletadas amostras de diversos órgãos para exame histopatológico. A principal lesão encontrada foi degeneração hialina e necrose segmentar multifocal nos músculos estriados esqueléticos e cardíacos (miopatia e cardiopatia degenerativo-necrótica tóxica multifocal polifásica). O diagnóstico foi confirmado pela avaliação toxicológica das sobras da ração suspeita, que detectou 461,67mg/kg de monensina. A morte de 71,5% dos búfalos deste lote ocorreu devido a uma sucessão de erros, que incluíram falhas na formulação da ração e, sobretudo, devido ao uso da monensina em uma espécie altamente sensível. Enfatizamos que, apesar dos possíveis efeitos benéficos do uso AIs como suplemento dietético para bubalinos, somos da opinião que os AIs nunca devem ser empregados na bubalinocultura, uma vez que os eventuais incrementos na produção não compensam o risco iminente de morte, devido a pequena margem de segurança para essa espécie e a inexistência de antídotos.(AU)

Natural and experimental salinomycin poisoning associated with the use of florfenicol in pigs / Intoxicação natural e experimental por salinomicina associada ao uso de florfenicol em suínos

This study describes the spontaneous and experimental salinomycin poisoning associated with the use of florfenicol and warns about the effects of the administration of antibiotics to animals that receive ionophores in the feed as growth promoters. A batch with 1,200 finishing pigs fed a diet containing 30ppm of salinomycin received florfenicol (60ppm via feed) to control respiratory diseases. Twenty-seven pigs had difficulty walking, tip-toe walking, muscle tremors, and anorexia seven days after the start of treatment. Twenty-two animals died, 10 recovered, and two were sent to the Laboratory of Animal Pathology of CAV-UDESC to be necropsied. The experimental reproduction of the disease was carried out to clarify the possible influence of florfenicol on salinomycin poisoning using 12 pigs divided into four groups with three animals each, treated for 16 days with diets containing no additives (Group 1), 50ppm of salinomycin (Group 2), 40ppm of florfenicol (Group 3), and 50ppm of salinomycin and 40ppm of florfenicol (Group 4). Only animals in Group 4 became ill. The clinical disease was reproduced from the ingestion of 24.67mg/kg/LW of salinomycin and 19.74mg/kg/LW of florfenicol. Both natural and experimental salinomycin poisoning associated with the use of florfenicol caused a condition of myopathy characterized in histology by hyaline degeneration and floccular necrosis of skeletal fibers, with macrophage infiltrate, associated with the figures of regeneration in skeletal muscles and multifocal areas of the proliferation of fibroblasts, being more intense in the longissimus dorsi and semimembranosus muscles. Therefore, florfenicol can cause the accumulation of ionophore salinomycin in the animal organism, resulting in a condition of toxic myopathy.(AU)

O presente trabalho descreve as intoxicações espontânea e experimental por salinomicina associada ao uso de florfenicol e alerta sobre os efeitos da administração de antibióticos aos animais que recebem ionóforos na ração como promotores de crescimento. Um lote com 1.200 suínos em fase de terminação, alimentados com ração contendo 30ppm de salinomicina, recebeu florfenicol (60ppm via ração) para o controle de doenças respiratórias. Sete dias após o início do tratamento, 27 suínos apresentaram dificuldade de locomoção, "caminhar em brasa", tremores musculares e anorexia. Vinte e dois animais morreram, 10 recuperaram-se e dois foram encaminhados ao Laboratório de Patologia Animal (CAV-UDESC) para serem necropsiados. Para esclarecer a possível influência do florfenicol na toxicidade da salinomicina foi realizada a reprodução experimental da doença utilizando 12 suínos, divididos em 4 grupos com 3 animais cada, tratados por 16 dias com rações contendo: Grupo 1 = sem aditivos, Grupo 2 = 50ppm de salinomicina, Grupo 3 = 40ppm de florfenicol e Grupo 4 = 50ppm de salinomicina e 40ppm de florfenicol. Somente os animais do Grupo 4 adoeceram. A doença clínica foi reproduzida a partir da ingestão de 24,67mg/kg/PV de salinomicina e 19,74 mg/kg/PV de florfenicol. Tanto a intoxicação natural quanto a experimental por salinomicina associada ao uso de florfenicol provocaram um quadro de miopatia caracterizado na histologia por degeneração hialina e necrose flocular das fibras esqueléticas, com infiltrado macrofágico, associada às figuras de regeneração na musculatura esquelética e áreas multifocais de proliferação de fibroblastos, sendo mais intensas nos músculos longissimus dorsi e semimembranoso. Conclui-se que, o florfenicol tem a capacidade de ocasionar o acúmulo do ionóforo salinomicina no organismo animal, resultando em um quadro de miopatia tóxica.(AU)

Clinical, sonographic and anatomopathological aspects of ovarian teratoma in a heifer / Aspectos clínicos, ultrassonográficos e anatomopatológicos do teratoma ovariano em uma novilha

Teratomas rarely occur in domestic species, especially in cattle. These tumors originate in fetal life and are characterized by rapid growth, which justifies their frequent detection in young animals. This study reported a case of ovarian teratoma in a heifer. On physical examination, the main signs identified were apathy, abdominal distention and tension, empty rumen, and mushy diarrhea. During rectal palpation, a mass was identified in the pelvic region, which was suggestive of cysts on ultrasound examination. The animal underwent laparotomy, followed by euthanasia due to a poor prognosis. At necropsy, a 54 x 43 x 52 cm (length x width x thickness) tumor was observed in the right ovary with multiple cystic areas, in addition to masses associated with multiple adhesions of the intestinal loops and peritonitis. On histopathology, muscle, cartilage, bone, nervous and epithelial tissue, glands, hair with follicles, were identified in the affected ovary. There was mixed inflammation and foci of necrosis observed with a complete absence of ovarian architecture in both the ovaries. Infiltrations were identified in the lymph nodes and mesenteric vessels. Glandular ducts were seen from the serosa to the intestinal mucosa. A locally infiltrative and expansile ovarian teratoma was diagnosed accordingly. It is considered that this kind of tumor can induce abdominal distension and absence of estrus in previously healthy, non-pregnant heifers.

Os teratomas são tumores raros nas espécies domésticas, sobretudo em bovinos. Esses tumores são caracterizados por crescimento rápido e origem durante a vida fetal, o que justifica seu diagnóstico frequente em animais jovens. O presente trabalho relata um caso de teratoma ovariano em uma novilha. No exame físico, os principais sinais identificados foram apatia, distensão e tensão abdominal, rúmen vazio e diarreia pastosa. Durante a palpação retal, uma massa foi identificada na região pélvica. Ao exame ultrassonográfico, a massa era sugestiva de cistos. O animal foi submetido a laparotomia, seguido de eutanásia devido ao mau prognóstico. Na necropsia foi observado um tumor de 54 x 43 x 52 cm (comprimento x largura x espessura) no ovário direito com múltiplas áreas císticas, além de massas associadas à múltiplas aderências das alças intestinais e peritonite. Na histopatologia foram identificados no ovário acometido a presença de tecidos muscular, cartilaginoso, ósseo, nervoso e epitelial, com glândulas, pelos e folículos. Havia inflamação mista e focos de necrose com ausência completa de arquitetura ovariana em ambos os ovários. Infiltrações foram identificadas em linfonodos e vasos mesentéricos. Ductos glandulares foram vistos desde a serosa até mucosa intestinal. Diagnosticou-se um teratoma ovariano localmente infiltrativo e expansivo. Considera-se que este tumor pode induzir distensão abdominal e ausência de estro em novilhas previamente sadias e não gestantes.

Intoxicação por lasalocida em bezerros búfalos no Estado do Pará, Brasil / Lasalocid poisoning in buffalo calves in the state of Pará, Brazil

Background: Ionophore antibiotics are food additives with coccidiostatic or antimicrobial action; they are also used as growth promoters, ruminal pH regulators, volatile fatty acid molar modifiers, and methanogenesis reducers. However, these compounds have the potential to cause microbial resistance, in addition to the risk of intoxication. Ionophore poisoning may be caused by excessive intake, sensitivity of certain animal species, and concomitant use with other drugs. In Brazil, cases of ionophore poisoning in buffalos are rare. This study aims to describe the epidemiological, clinical, and pathological findings of lasalocid poisoning in buffalo calves. Case: A visit was made to a farm in the municipality of Mojú, Pará state to care for Murrah buffalo calves. After weaning, the buffalos were grazed in paddocks with Panicum spp., and received a supplement of mineral, protein, and vitamin. This supplement contained, per kg, 250 g PB, 50 g Ca, 20 g P, 8 g S, 39 g Na, 20 mg Co, 557 mg Cu, 200 mg Fe, 12.4 mg Se, 2040 mg Zn, 0.19 mg biotin, 26750 IU of vitamin A, 4175 IU of vitamin D, 155 IU of vitamin E and 300 mg/kg of lasalocid. The product was made available to all calves, at 1-2 g/kg body weight (BW), according to the manufacturer's recommendations. Older calves were raised together with those less than 30 days old; as a result, the older calves tended to eat more, which could lead to a supplementation consumption of more than 1 kg body weight per animal per day. It was reported that between 40 and 60 days after the introduction of this supplement, 16 calves fell ill and died due to apathy, motor instability, tremors, and distended neck. The herd had a mortality rate of 33.3%. Two calves underwent a necroscopic examination at the Pathology Section of the Veterinary Institute of the Federal University of Pará. Macroscopic examination revealed extensive pale areas in the skeletal muscles, myocardium, and tongue. Fragments of these muscles and various organs were collected, fixed in 10% buffered formalin, processed according to the routine histological technique, and stained with hematoxylin-eosin and Masson's trichrome stain. Microscopic examination of the histologic samples revealed foci of muscle atrophy and necrosis characterized by an increase in cytoplasmic eosinophilia associated with the loss of stretch marks, and hyperchromatic nuclei that were displaced to the periphery. The necrosis of the muscle fibers was highlighted by Masson's trichrome staining. Discussion: The diagnosis of lasalocid poisoning in buffalo calves was based on epidemiological data, clinical findings, results of macroscopic and histopathological examination, and based on the estimated ionophore intake, obtained directly from the supplement label and by the calf's handler. Based on the absence of stratification of the calves by similarity of age and because the buffalo calves older than 30 days could eat more than 1 kg of the supplement (containing 300 mg/kg of lasalocid), it was possible to estimate the intake of lasalocid per kg CP (body weight). Therefore, the intake of lasalocid by a 70-kg buffalo calf in approximately 90 days and daily supplement consumption between 1 and 1.5 kg would be between 4.2 and 6.4 mg/kg of body weight. This report reinforces that notion that buffalo calves should never ingest ionophores; however, if necessary, strict protocols must be followed to avoid poisoning in these animals. This study highlighted the fact that stratification of buffaloes by different age groups during feeding became a risk factor that allowed greater consumption by older animals; this led to the estimated consumption of 4.2-6.4 mg/kg of lasalocid.