Hematological, clinical and epidemiological aspects of Hepatozoon canis infection by parasitological detection in dogs from the rural area of Sousa, Paraíba, Brazil / Aspectos hematológicos, clínicos e epidemiológicos da infecção por Hepatozoon canis por detecção parasitológica em cães da zona rural de Sousa, Paraíba, Brasil

Hepatozoonosis is caused by protozoa of the genus Hepatozoon. In dogs, the infection is caused mainly by Hepatozoon canis, and there are a few descriptions of the prevalence of this infection in the Northeast region of Brazil, especially in the semi-arid region. Therefore, we aimed to determine the prevalence of Hepatozoon canis infection in dogs in the rural area of Sousa, Paraíba, Brazil, as well as to determine the possible clinical and epidemiological aspects of this infection. Ninety-eight dogs in the rural zone of the municipality of Sousa that were at least 4 months old were evaluated, regardless of their breed or gender. Clinical examinations were carried out, and samples of systemic and peripheral blood were collected to determine the presence of the parasite in blood smears and carry out hemograms. In addition, epidemiological questionnaires about animal health and food management were completed. The prevalence of H. canis infections in dogs was 8.1% (8/98). There were three main changes in the hematological status: thrombocytopenia, anemia and hyperproteinemia, mainly related to percentage of leukocyte infection 5%, and also to the presence of clinical signs such as mucopurulent secretion, lymphadenomegaly, dry skin, pale mucous membranes, and lean or cachectic body score.(AU)

A hepatozoonose é causada por protozoários do gênero Hepatozoon. Em cães, a infecção ocorre principalmente por Hepatozoon canis, sendo escassas as descrições de prevalências desta infecção na região Nordeste do Brasil, sobretudo no Semiárido. Com isso, o trabalho objetivou determinar a prevalência da infecção por Hepatozoon canis em cães da zona rural do município de Sousa, Paraíba, Brasil, como também determinar possíveis sinais clínicos e aspectos epidemiológicos relacionados à esta infecção. Foram avaliados 98 cães da zona rural do município de Sousa, independentemente da raça ou sexo, com idade superior a quatro meses. Foram realizados exames clínicos e colhidas amostras de sangue sistêmico e periférico para a pesquisa do parasito em esfregaços sanguíneos e hemogramas. Além disso, foram preenchidos questionários epidemiológicos acerca do manejo sanitário e alimentar dos animais. A prevalência de cães positivos para H. canis foi de 8,1% (8/98). Foram observados três principais alterações no quadro hematológico, sendo trombocitopenia, anemia e hiperproteinemia, principalmente relacionadas ao percentual de leucócitos infectados 5%, e também à presença de sinais clínicos, como secreção mucopurulenta, linfadenomegalia, pelos ressecados, mucosas hipocoradas e escore corporal magro ou caquético.(AU)

Anemia hemolítica imunomediada associada à micoplasmose em um cão / Associated immunomediated hemolytic anemia mycoplasmosis in a dog

A anemia hemolítica imunomediada (AHIM) é uma reação de hipersensibilidade tipo II onde ocorre o aumento da destruição das hemácias. Ela pode ser dividida em primaria, caracterizada por não ter uma causa subjacente, e em secundária, pode ser causada por agentes infecciosos, como a micoplasmose, neoplasias, medicamentos e transfusões. O objetivo desse trabalho foi realizar uma análise clínica e laboratorial de um cão com anemia hemolítica imunomediada decorrente da Mycoplasma spp. Uma cadela da raça Pit Bull, com 05 meses de idade, foi levada ao hospital apresentando vômitos, diarreia e anorexia. No exame físico, foi possível observar a presença de carrapatos e mucosas ictéricas. Nos exames hematológicos foi possível evidenciaras alterações morfológicas de hemácias que caracterizavam anemia hemolítica imunomediada e a presença do parasita Mycoplasma spp. Nas análises bioquímicas se observou níveis séricos aumentados de creatinina e ureia. Pode-se concluir que, a observação de Mycoplasma spp. em esfregaços sanguíneos associada às alterações morfológicas eritrocitárias são de relevante importância para o diagnóstico de AHIM, auxiliando assim na instituição da melhor conduta terapêutica, contribuindo para o prognóstico do paciente.

Immune-mediated hemolytic anemia (AHIM) is a type II hypersensitivity reaction, where red blood cell destruction occurs or increases. It can be divided into primary, characterized by not having an underlying cause, and secondary, which can be caused by infectious agents, such as mycoplasmosis, neoplasms, drugs and transfusions. The objective of this work was to perform a clinical and laboratory analysis of a dog with immune-mediated hemolytic anemia due to Mycoplasma spp. A five-months-old female Pit Bull dog was taken to the hospital presenting vomiting, diarrhea and anorexia. On physical examination, it was possible to observe the presence of ticks and icteric mucous membranes. In hematological exams, it was possible to show morphological changes in red blood cells that characterize immune-mediated hemolytic anemia and the presence of the parasite Mycoplasma spp. In the biochemical analyzes it was observed increased serum levels of creatinine and urea. It can be concluded that the observation of Mycoplasma spp. in blood vessels associated with erythrocyte morphological changes are of relevant importance for the diagnosis of AHIM, thus assisting in the practice of a better method of therapy, contributing to the patient's prognosis.

Anemia hemolítica imunomediada associada à micoplasmose em um cão / Associated immunomediated hemolytic anemia mycoplasmosis in a dog

A anemia hemolítica imunomediada (AHIM) é uma reação de hipersensibilidade tipo II onde ocorre o aumento da destruição das hemácias. Ela pode ser dividida em primaria, caracterizada por não ter uma causa subjacente, e em secundária, pode ser causada por agentes infecciosos, como a micoplasmose, neoplasias, medicamentos e transfusões. O objetivo desse trabalho foi realizar uma análise clínica e laboratorial de um cão com anemia hemolítica imunomediada decorrente da Mycoplasma spp. Uma cadela da raça Pit Bull, com 05 meses de idade, foi levada ao hospital apresentando vômitos, diarreia e anorexia. No exame físico, foi possível observar a presença de carrapatos e mucosas ictéricas. Nos exames hematológicos foi possível evidenciaras alterações morfológicas de hemácias que caracterizavam anemia hemolítica imunomediada e a presença do parasita Mycoplasma spp. Nas análises bioquímicas se observou níveis séricos aumentados de creatinina e ureia. Pode-se concluir que, a observação de Mycoplasma spp. em esfregaços sanguíneos associada às alterações morfológicas eritrocitárias são de relevante importância para o diagnóstico de AHIM, auxiliando assim na instituição da melhor conduta terapêutica, contribuindo para o prognóstico do paciente.(AU)

Immune-mediated hemolytic anemia (AHIM) is a type II hypersensitivity reaction, where red blood cell destruction occurs or increases. It can be divided into primary, characterized by not having an underlying cause, and secondary, which can be caused by infectious agents, such as mycoplasmosis, neoplasms, drugs and transfusions. The objective of this work was to perform a clinical and laboratory analysis of a dog with immune-mediated hemolytic anemia due to Mycoplasma spp. A five-months-old female Pit Bull dog was taken to the hospital presenting vomiting, diarrhea and anorexia. On physical examination, it was possible to observe the presence of ticks and icteric mucous membranes. In hematological exams, it was possible to show morphological changes in red blood cells that characterize immune-mediated hemolytic anemia and the presence of the parasite Mycoplasma spp. In the biochemical analyzes it was observed increased serum levels of creatinine and urea. It can be concluded that the observation of Mycoplasma spp. in blood vessels associated with erythrocyte morphological changes are of relevant importance for the diagnosis of AHIM, thus assisting in the practice of a better method of therapy, contributing to the patient's prognosis.(AU)

Erliquiose canina - relato de caso / Ehrlichiosis canine - case report

Canine ehrlichiosis is a disease caused by species of genus Ehrlichia with great importance in veterinary. The clinical signs as well as haematological changes are variable and it is necessary to use other more specific diagnostic methods. The present work reports the case of a female dog, SRD, presenting hyperthermia, convulsion, uveitis, nystagmus, myoclonus, ataxia, prostration and lymphadenitis. The necropsy report was suggestive of ehrlichiosis.

Erliquiose canina - relato de caso / Ehrlichiosis canine - case report

Canine ehrlichiosis is a disease caused by species of genus Ehrlichia with great importance in veterinary. The clinical signs as well as haematological changes are variable and it is necessary to use other more specific diagnostic methods. The present work reports the case of a female dog, SRD, presenting hyperthermia, convulsion, uveitis, nystagmus, myoclonus, ataxia, prostration and lymphadenitis. The necropsy report was suggestive of ehrlichiosis.(AU)

Investigations on the role of insulin and scorpion antivenom in scorpion envenoming syndrome

Acute myocardiopathy in alloxan treated experimental dogs and rabbits was induced by subcutaneous (SQ) injection of scorpion venom from Mesobuthus tamulus concanesis, Pocock. Envenoming resulted in an initial transient hypertension (180-320 mm Hg.) followed by hypotension. Simultaneous administration of venom and species-specific scorpion antivenom (SAV) prevented hypertension and hypotension. Hypotension did not occur when SAV was given 60 min after envenoming. Blood glucose, triglycerides, cholesterol, amylase, insulin, glucagon, cortisol, hematocrit, mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), platelet count, red blood cell (RBC) count, hemoglobin (Hb), 2,3-diphosphoglycerate (2,3-DPG), and glutathione levels were increased 60 and 90 min after envenoming. Total white blood cell (WBC) count was reduced 60 min and increased 90 min after envenoming. Simultaneous administration of venom and SAV did not alter Hb, MCHC, and packed cell volume (PCV) levels, or ECG, and cardiovascular, biochemical, metabolic, and hormonal changes. Hematological parameters were reversed when SAV was given 30 and 60 min after envenoming. PCV, Hb, and MCHC values returned to normal 120 min after SAV. Alloxan-treated dogs showed increased blood glucose, cholesterol, glucagon, cortisol levels; reduced glycogen content of liver, cardiac and skeletal muscles; and reduced insulin levels and insulin/ glucagon ratio (I/G ratio). Envenoming in the alloxan pre-treated dogs further increased these levels and reduced tissue glycogen content, insulin levels, and I/G ratio. Administration of 4 U of insulin to alloxan pre-treated envenomed rabbits caused a biochemical and clinical improvement and increased glycogen content of all tissues in comparison with the values from those administered with SAV to alloxan pre-treated envenomed animals. SAV administration to envenomed alloxan pre-treated rabbits did not cause clinical or biochemical improvement. Severe scorpion envenoming causes an autonomic storm with a massive release of catecholamines and other counter-regulatory hormones; changes in insulin secretion resulting in fuel energy deficits producing multi-system-organ-failure (MSOF); and death. Administration of either insulin or SAV (through the release of insulin) appears to be the physiological basis for the control of the metabolic support to control the adverse effects triggered by counter-regulatory hormones.

Investigations on the role of insulin and scorpion antivenom in scorpion envenoming syndrome

Acute myocardiopathy in alloxan treated experimental dogs and rabbits was induced by subcutaneous (SQ) injection of scorpion venom from Mesobuthus tamulus concanesis, Pocock. Envenoming resulted in an initial transient hypertension (180-320 mm Hg.) followed by hypotension. Simultaneous administration of venom and species-specific scorpion antivenom (SAV) prevented hypertension and hypotension. Hypotension did not occur when SAV was given 60 min after envenoming. Blood glucose, triglycerides, cholesterol, amylase, insulin, glucagon, cortisol, hematocrit, mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), platelet count, red blood cell (RBC) count, hemoglobin (Hb), 2,3-diphosphoglycerate (2,3-DPG), and glutathione levels were increased 60 and 90 min after envenoming. Total white blood cell (WBC) count was reduced 60 min and increased 90 min after envenoming. Simultaneous administration of venom and SAV did not alter Hb, MCHC, and packed cell volume (PCV) levels, or ECG, and cardiovascular, biochemical, metabolic, and hormonal changes. Hematological parameters were reversed when SAV was given 30 and 60 min after envenoming. PCV, Hb, and MCHC values returned to normal 120 min after SAV. Alloxan-treated dogs showed increased blood glucose, cholesterol, glucagon, cortisol levels; reduced glycogen content of liver, cardiac and skeletal muscles; and reduced insulin levels and insulin/ glucagon ratio (I/G ratio). Envenoming in the alloxan pre-treated dogs further increased these levels and reduced tissue glycogen content, insulin levels, and I/G ratio. Administration of 4 U of insulin to alloxan pre-treated envenomed rabbits caused a biochemical and clinical improvement and increased glycogen content of all tissues in comparison with the values from those administered with SAV to alloxan pre-treated envenomed animals. SAV administration to envenomed alloxan pre-treated rabbits did not cause clinical or biochemical improvement. Severe scorpion envenoming causes an autonomic storm with a massive release of catecholamines and other counter-regulatory hormones; changes in insulin secretion resulting in fuel energy deficits producing multi-system-organ-failure (MSOF); and death. Administration of either insulin or SAV (through the release of insulin) appears to be the physiological basis for the control of the metabolic support to control the adverse effects triggered by counter-regulatory hormones.