Thromboembolism in a bitch - diagnosis by infrared thermography

Background: Thermography is a noninvasive, non-contact, painless, and non-ionizing imaging technique that records cutaneous thermal patterns generated by infrared emission of the surface. The surface heat is closely related to dermal microcirculation. Thromboembolism is responsible for important changes in the thermal pattern of the body surface due to physical obstruction of blood flow, being the main complication in immune-mediated hemolytic anemia. The aim of this paper is to report a dog with thrombus in his left forelimb secondary to idiopathic hemolytic anemia, whose diagnostic screening was performed through infrared thermography. Case: A 9-year-old mixed breed bitch was referred to a veterinary hospital with a history of emesis, diarrhea and dark-colored urine for 2 days. The complete blood count showed hypochromic macrocytic anemia (hematocrit [HTC] 28%, reference: 37 to 55%) with the presence of nucleated erythrocyte (14/100 leukocytes, reference: 0 to 5/100 leukocytes), polychromasia and spherocytes. Leukocytosis (28,300 mm³, reference: 6,000 to 17,000 mm³) by neutrophilia with left deviation and toxic granulations was also present, in addition to hemoglobinuria at urine exam. Therefore, treatment for immune-mediated hemolytic anemia (IMHA) was instituted. After 2 days, the animal returned with acute functional impairment of the left forelimb. Physical examination revealed that the limb was cold, without pulse, proprioception, reflexes, and deep pain. New blood analyses revealed decreased hematocrit (HTC 17%, reference: 37 to 55%), and increased total leukocyte number (57,000 mm3, reference: 6,000 to 17,000 mm³). Infrared thermography revealed an important temperature difference between the limbs, with the affected limb temperature considerably lower (31.3ºC) when compared to the contralateral limb (35.0ºC). Thermography showed the site of the thrombus in the medial portion of the limb (cephalic vein), where the catheter had been placed for fluid therapy. Due to the severity of the condition, the bitch was submitted to amputation surgery, which occurred without complications. The patient had a good response to treatment, with decreased signs of hemolysis and hypercoagulability. The medications were slowly withdrawn, and the clinical discharge occurred after 4 weeks. Discussion: In humans, thermography has been widely used in the assessment of thrombotic diseases, contributing to diagnosis, localization, and prognosis. In veterinary medicine, however, the use of this tool in the diagnosis of thromboembolism is still rare. The difference of 3.7°C between the affected and contralateral limb was objectively verified using thermography. A minimum difference of 2.4°C between limbs has high sensitivity and specificity for diagnosing thromboembolism and occurs due to the reduction in local blood flow. In the present case this tool was essential for the anatomical location of the thrombus, which was in the middle third of the forearm, and allowed an adequate surgical planning. It is known that the main complication of IMHA is thromboembolism. Its predisposing factors include venous stasis, endothelial damage, and hypercoagulability, being exacerbated by cage confinement, decubitus and presence of a peripheral venous catheter. The reported case corroborates at least one of these factors since it had a peripheral venous catheter in the left forelimb, which later showed absence of pulse, spinal reflexes, pain and proprioception. The thermography showed to be an objective, rapid and non-invasive tool to diagnose and precisely locate the thrombus, which allowed for adequate treatment and surgical planning for the case. To the best of our knowledge, this is the first report about use of thermography to diagnose thromboembolism secondary to immune-mediated hemolytic anemia in a dog.

Thalassemia, a human blood disorder / Talassemia, uma doença do sangue humano

A group of inherited blood defects is known as Thalassemia is among the world's most prevalent hemoglobinopathies. Thalassemias are of two types such as Alpha and Beta Thalassemia. The cause of these defects is gene mutations leading to low levels and/or malfunctioning α and β globin proteins, respectively. In some cases, one of these proteins may be completely absent. α and β globin chains form a globin fold or pocket for heme (Fe++) attachment to carry oxygen. Genes for alpha and beta-globin proteins are present in the form of a cluster on chromosome 16 and 11, respectively. Different globin genes are used at different stages in the life course. During embryonic and fetal developmental stages, γ globin proteins partner with α globin and are later replaced by β globin protein. Globin chain imbalances result in hemolysis and impede erythropoiesis. Individuals showing mild symptoms include carriers of alpha thalassemia or the people bearing alpha or beta-thalassemia trait. Alpha thalassemia causes conditions like hemolytic anemia or fatal hydrops fetalis depending upon the severity of the disease. Beta thalassemia major results in hemolytic anemia, growth retardation, and skeletal aberrations in early childhood. Children affected by this disorder need regular blood transfusions throughout their lives. Patients that depend on blood transfusion usually develop iron overload that causes other complications in the body systems like renal or hepatic impairment therefore, thalassemias are now categorized as a syndrome. The only cure for Thalassemias would be a bone marrow transplant, or gene therapy with currently no significant success rate. A thorough understanding of the molecular basis of this syndrome may provide novel insights and ideas for its treatment, as scientists have still been unable to find a permanent cure for this deadly disease after more than 87 years since it is first described in 1925.

Um grupo de defeitos sanguíneos hereditários é conhecido como talassemia e está entre as hemoglobinopatias mais prevalentes do mundo. As talassemias são de dois tipos, como talassemia alfa e beta. As causas desses defeitos são as mutações genéticas que levam a níveis baixos e/ou proteínas de globina com mau funcionamento, respectivamente. Em alguns casos, uma dessas proteínas pode estar completamente ausente. As cadeias de globina α e β formam uma dobra ou bolsa de globina para a fixação de heme (Fe ++) para transportar oxigênio. Os genes das proteínas alfa e beta globina estão presentes na forma de um cluster nos cromossomos 16 e 11, respectivamente. Diferentes genes de globina são usados em diferentes estágios do curso de vida. Durante os estágios de desenvolvimento embrionário e fetal, as proteínas γ globina se associam à α globina e, posteriormente, são substituídas pela proteína β globina. Os desequilíbrios da cadeia de globina resultam em hemólise e impedem a eritropoiese. Indivíduos que apresentam sintomas leves incluem portadores de talassemia alfa ou as pessoas com traços de talassemia alfa ou beta. A talassemia alfa causa condições como anemia hemolítica ou hidropsia fetal fatal, dependendo da gravidade da doença. A beta talassemia principal resulta em anemia hemolítica, retardo de crescimento e aberrações esqueléticas na primeira infância. As crianças afetadas por esse distúrbio precisam de transfusões de sangue regulares ao longo da vida. Os pacientes que dependem de transfusão de sangue geralmente desenvolvem sobrecarga de ferro que causa outras complicações nos sistemas do corpo, como insuficiência renal ou hepática, portanto as talassemias agora são classificadas como uma síndrome. A única cura para as talassemias seria um transplante de medula óssea ou terapia genética sem atualmente uma taxa de sucesso significativa. Uma compreensão completa da base molecular dessa síndrome pode fornecer novos insights e ideias para seu tratamento, [...].

Thalassemia, a human blood disorder / Talassemia, uma doença do sangue humano

Abstract A group of inherited blood defects is known as Thalassemia is among the world's most prevalent hemoglobinopathies. Thalassemias are of two types such as Alpha and Beta Thalassemia. The cause of these defects is gene mutations leading to low levels and/or malfunctioning α and β globin proteins, respectively. In some cases, one of these proteins may be completely absent. α and β globin chains form a globin fold or pocket for heme (Fe++) attachment to carry oxygen. Genes for alpha and beta-globin proteins are present in the form of a cluster on chromosome 16 and 11, respectively. Different globin genes are used at different stages in the life course. During embryonic and fetal developmental stages, γ globin proteins partner with α globin and are later replaced by β globin protein. Globin chain imbalances result in hemolysis and impede erythropoiesis. Individuals showing mild symptoms include carriers of alpha thalassemia or the people bearing alpha or beta-thalassemia trait. Alpha thalassemia causes conditions like hemolytic anemia or fatal hydrops fetalis depending upon the severity of the disease. Beta thalassemia major results in hemolytic anemia, growth retardation, and skeletal aberrations in early childhood. Children affected by this disorder need regular blood transfusions throughout their lives. Patients that depend on blood transfusion usually develop iron overload that causes other complications in the body systems like renal or hepatic impairment therefore, thalassemias are now categorized as a syndrome. The only cure for Thalassemias would be a bone marrow transplant, or gene therapy with currently no significant success rate. A thorough understanding of the molecular basis of this syndrome may provide novel insights and ideas for its treatment, as scientists have still been unable to find a permanent cure for this deadly disease after more than 87 years since it is first described in 1925.

Resumo Um grupo de defeitos sanguíneos hereditários é conhecido como talassemia e está entre as hemoglobinopatias mais prevalentes do mundo. As talassemias são de dois tipos, como talassemia alfa e beta. As causas desses defeitos são as mutações genéticas que levam a níveis baixos e/ou proteínas de globina com mau funcionamento, respectivamente. Em alguns casos, uma dessas proteínas pode estar completamente ausente. As cadeias de globina α e β formam uma dobra ou bolsa de globina para a fixação de heme (Fe ++) para transportar oxigênio. Os genes das proteínas alfa e beta globina estão presentes na forma de um cluster nos cromossomos 16 e 11, respectivamente. Diferentes genes de globina são usados ​​em diferentes estágios do curso de vida. Durante os estágios de desenvolvimento embrionário e fetal, as proteínas γ globina se associam à α globina e, posteriormente, são substituídas pela proteína β globina. Os desequilíbrios da cadeia de globina resultam em hemólise e impedem a eritropoiese. Indivíduos que apresentam sintomas leves incluem portadores de talassemia alfa ou as pessoas com traços de talassemia alfa ou beta. A talassemia alfa causa condições como anemia hemolítica ou hidropsia fetal fatal, dependendo da gravidade da doença. A beta talassemia principal resulta em anemia hemolítica, retardo de crescimento e aberrações esqueléticas na primeira infância. As crianças afetadas por esse distúrbio precisam de transfusões de sangue regulares ao longo da vida. Os pacientes que dependem de transfusão de sangue geralmente desenvolvem sobrecarga de ferro que causa outras complicações nos sistemas do corpo, como insuficiência renal ou hepática, portanto as talassemias agora são classificadas como uma síndrome. A única cura para as talassemias seria um transplante de medula óssea ou terapia genética sem atualmente uma taxa de sucesso significativa. Uma compreensão completa da base molecular dessa síndrome pode fornecer novos insights e ideias para seu tratamento, já que os cientistas ainda não conseguiram encontrar uma cura permanente para essa doença mortal depois de mais de 87 anos desde que foi descrita pela primeira vez em 1925.

Thalassemia, a human blood disorder / Talassemia, uma doença do sangue humano

A group of inherited blood defects is known as Thalassemia is among the world's most prevalent hemoglobinopathies. Thalassemias are of two types such as Alpha and Beta Thalassemia. The cause of these defects is gene mutations leading to low levels and/or malfunctioning α and β globin proteins, respectively. In some cases, one of these proteins may be completely absent. α and β globin chains form a globin fold or pocket for heme (Fe++) attachment to carry oxygen. Genes for alpha and beta-globin proteins are present in the form of a cluster on chromosome 16 and 11, respectively. Different globin genes are used at different stages in the life course. During embryonic and fetal developmental stages, γ globin proteins partner with α globin and are later replaced by β globin protein. Globin chain imbalances result in hemolysis and impede erythropoiesis. Individuals showing mild symptoms include carriers of alpha thalassemia or the people bearing alpha or beta-thalassemia trait. Alpha thalassemia causes conditions like hemolytic anemia or fatal hydrops fetalis depending upon the severity of the disease. Beta thalassemia major results in hemolytic anemia, growth retardation, and skeletal aberrations in early childhood. Children affected by this disorder need regular blood transfusions throughout their lives. Patients that depend on blood transfusion usually develop iron overload that causes other complications in the body systems like renal or hepatic impairment therefore, thalassemias are now categorized as a syndrome. The only cure for Thalassemias would be a bone marrow transplant, or gene therapy with currently no significant success rate. A thorough understanding of the molecular basis of this syndrome may provide novel insights and ideas for its treatment, as scientists have still been unable to find a permanent cure for this deadly disease after more than 87 years since it is first described in 1925.(AU)

Um grupo de defeitos sanguíneos hereditários é conhecido como talassemia e está entre as hemoglobinopatias mais prevalentes do mundo. As talassemias são de dois tipos, como talassemia alfa e beta. As causas desses defeitos são as mutações genéticas que levam a níveis baixos e/ou proteínas de globina com mau funcionamento, respectivamente. Em alguns casos, uma dessas proteínas pode estar completamente ausente. As cadeias de globina α e β formam uma dobra ou bolsa de globina para a fixação de heme (Fe ++) para transportar oxigênio. Os genes das proteínas alfa e beta globina estão presentes na forma de um cluster nos cromossomos 16 e 11, respectivamente. Diferentes genes de globina são usados em diferentes estágios do curso de vida. Durante os estágios de desenvolvimento embrionário e fetal, as proteínas γ globina se associam à α globina e, posteriormente, são substituídas pela proteína β globina. Os desequilíbrios da cadeia de globina resultam em hemólise e impedem a eritropoiese. Indivíduos que apresentam sintomas leves incluem portadores de talassemia alfa ou as pessoas com traços de talassemia alfa ou beta. A talassemia alfa causa condições como anemia hemolítica ou hidropsia fetal fatal, dependendo da gravidade da doença. A beta talassemia principal resulta em anemia hemolítica, retardo de crescimento e aberrações esqueléticas na primeira infância. As crianças afetadas por esse distúrbio precisam de transfusões de sangue regulares ao longo da vida. Os pacientes que dependem de transfusão de sangue geralmente desenvolvem sobrecarga de ferro que causa outras complicações nos sistemas do corpo, como insuficiência renal ou hepática, portanto as talassemias agora são classificadas como uma síndrome. A única cura para as talassemias seria um transplante de medula óssea ou terapia genética sem atualmente uma taxa de sucesso significativa. Uma compreensão completa da base molecular dessa síndrome pode fornecer novos insights e ideias para seu tratamento, [...].(AU)

Thalassemia, a human blood disorder

Abstract A group of inherited blood defects is known as Thalassemia is among the worlds most prevalent hemoglobinopathies. Thalassemias are of two types such as Alpha and Beta Thalassemia. The cause of these defects is gene mutations leading to low levels and/or malfunctioning and globin proteins, respectively. In some cases, one of these proteins may be completely absent. and globin chains form a globin fold or pocket for heme (Fe++) attachment to carry oxygen. Genes for alpha and beta-globin proteins are present in the form of a cluster on chromosome 16 and 11, respectively. Different globin genes are used at different stages in the life course. During embryonic and fetal developmental stages, globin proteins partner with globin and are later replaced by globin protein. Globin chain imbalances result in hemolysis and impede erythropoiesis. Individuals showing mild symptoms include carriers of alpha thalassemia or the people bearing alpha or beta-thalassemia trait. Alpha thalassemia causes conditions like hemolytic anemia or fatal hydrops fetalis depending upon the severity of the disease. Beta thalassemia major results in hemolytic anemia, growth retardation, and skeletal aberrations in early childhood. Children affected by this disorder need regular blood transfusions throughout their lives. Patients that depend on blood transfusion usually develop iron overload that causes other complications in the body systems like renal or hepatic impairment therefore, thalassemias are now categorized as a syndrome. The only cure for Thalassemias would be a bone marrow transplant, or gene therapy with currently no significant success rate. A thorough understanding of the molecular basis of this syndrome may provide novel insights and ideas for its treatment, as scientists have still been unable to find a permanent cure for this deadly disease after more than 87 years since it is first described in 1925.

Resumo Um grupo de defeitos sanguíneos hereditários é conhecido como talassemia e está entre as hemoglobinopatias mais prevalentes do mundo. As talassemias são de dois tipos, como talassemia alfa e beta. As causas desses defeitos são as mutações genéticas que levam a níveis baixos e/ou proteínas de globina com mau funcionamento, respectivamente. Em alguns casos, uma dessas proteínas pode estar completamente ausente. As cadeias de globina e formam uma dobra ou bolsa de globina para a fixação de heme (Fe ++) para transportar oxigênio. Os genes das proteínas alfa e beta globina estão presentes na forma de um cluster nos cromossomos 16 e 11, respectivamente. Diferentes genes de globina são usados em diferentes estágios do curso de vida. Durante os estágios de desenvolvimento embrionário e fetal, as proteínas globina se associam à globina e, posteriormente, são substituídas pela proteína globina. Os desequilíbrios da cadeia de globina resultam em hemólise e impedem a eritropoiese. Indivíduos que apresentam sintomas leves incluem portadores de talassemia alfa ou as pessoas com traços de talassemia alfa ou beta. A talassemia alfa causa condições como anemia hemolítica ou hidropsia fetal fatal, dependendo da gravidade da doença. A beta talassemia principal resulta em anemia hemolítica, retardo de crescimento e aberrações esqueléticas na primeira infância. As crianças afetadas por esse distúrbio precisam de transfusões de sangue regulares ao longo da vida. Os pacientes que dependem de transfusão de sangue geralmente desenvolvem sobrecarga de ferro que causa outras complicações nos sistemas do corpo, como insuficiência renal ou hepática, portanto as talassemias agora são classificadas como uma síndrome. A única cura para as talassemias seria um transplante de medula óssea ou terapia genética sem atualmente uma taxa de sucesso significativa. Uma compreensão completa da base molecular dessa síndrome pode fornecer novos insights e ideias para seu tratamento, já que os cientistas ainda não conseguiram encontrar uma cura permanente para essa doença mortal depois de mais de 87 anos desde que foi descrita pela primeira vez em 1925.

Acute erythroid leukemia in a cat infected with feline leukemia virus

Background: Erythroid leukemia is a myeloproliferative hematopoietic disorder considered acute when there is a predominance of blasts in the bone marrow. It is frequently reported in cats infected with feline leukemia virus, but it is unclear whether this virus is involved in the oncogenesis. The clinical signs in cats are anorexia, apathy, weight loss, with evolution from 2 weeks to 2 months, pale mucous membranes, hemorrhages, ascites, salivation, and dyspnea due to pleural effusion. This affection responds little to chemotherapy with an unfavorable prognosis. The aim of this study is to report a case of a feline leukemia virus infected cat with the onset of severe hemolytic anemia. Case: A 8-year-old male mixed breed cat was attended with a history of anorexia, oligodipsia, apathy, progressive weight loss, and yellowish color of urine for 7 days. Laboratorial exams showed anemia (with metarubricytes, acanthocytes and ghost cells), leukocytosis and FeLV reagent test. The cat underwent treatment with methylprednisolone acetate and supportive care. One day later, the animal returned with icteric mucous membranes, and emesis. A blood count was performed that found worsening anemia, increased leukocytosis, and lymphocytosis. Abdominal ultrasound showed cholangiohepatitis and lymphadenomegaly in mesenteric lymph nodes. Treatment was started with ondansetron, metronidazole, and amoxicilin with potassium clavulanate. The cat returned after 3 days and laboratorial exams revealed worsening of blood parameters, so blood transfusion was performed. After 2 days, the patient started with dyspnea and hypothermia, that evolved to cardiorespiratory arrest. The body was sent to necropsy and histopathology, where blast cells and rubricytes were found in blood vessels of various organs. The bone marrow was markedly cellular with complete disappearance of adipose tissue. Most of the cells were blasts with abundant and eosinophilic cytoplasm, central nucleus with finely dotted chromatin and a large nucleolus. There were rubricytes, which made possible to confirm acute erythroid leukemia as a morphological diagnosis. Discussion: The clinical signs observed in acute erythroid leukemia are lethargy, inappetence, fever, splenomegaly, mild lymphadenomegaly, associated with leukocytosis, severe anemia, and thrombocytopenia. The reported animal presented signs similar to those described in the literature except that there was no change in platelet counts. The diagnosis of leukemia was reached after histopathology, and it is made when is observed more than 30% of myeloblasts and monoblasts together or when the blast cells count including rubriblasts is greater than 30%. Although chemotherapy, the prognosis is usually poor. It is essential to perform the myelogram for the diagnosis of myeloid leukemias in vivo. In this report, we only achieve final diagnosis after the cat's death, due to the aggressive behavior of the disease. Clinicians must be aware of the likely development of acute erythroid leukemia whenever a feline leukemia virus infected cat presents hemolytic anemia to get an early diagnosis, since this is an extremely aggressive disease, to propose prompt chemotherapy and give the patient a longer survival period.

Aspectos da hemoplasmose em búfalos: revisão bibliográfica / Aspects of hemoplasmosis in buffaloes: literature review / Aspectos de la hemoplasmosis en búfalos: revisión de la literatura

Búfalos são animais rústicos que podem ser explorados para a produção de carne ou leite. Estes animais são susceptíveis a enfermidades que também acometem outras espécies de ruminantes, principalmente os bovinos. Entretanto, acredita-se que os bubalinos sejam mais resistentes a algumas doenças, mas ainda há poucos estudos epidemiológicos abrangendo doenças infecciosas como a hemoplasmose em búfalos. A hemoplasmose é causada por micoplasmas hemotrópicos ou hemoplasmas, que são bactérias gram-negativas causadoras de anemia hemolítica em hospedeiros imunocomprometidos. Mycoplasma wenyonii e 'Candidatus Mycoplasma haemobos' são as principais espécies de hemoplasmas que podem infectar búfalos. A transmissão da doença ocorre principalmente por meio de vetores artrópodes hematófagos ou por via iatrogênica. O diagnóstico de animais infectados é realizado por meio da Reação em Cadeia da Polimerase (PCR). Medidas de prevenção e controle são essenciais para o controle desta enfermidade nos rebanhos bubalinos.

Buffalo are rustic animals that can be exploited for meat or milk production. These animals are susceptible to diseases that also affect other species of ruminants, especially cattle. However, it is believed that buffalo are more resistant to some diseases, but there are still few epidemiological studies covering infectious diseases such as hemoplasmosis in buffaloes. Hemoplasmosis is caused by hemotropic mycoplasmas or hemoplasmas, which are gram-negative bacteria that cause hemolytic anemia in immunocompromised hosts. Mycoplasma wenyonii and 'Candidatus Mycoplasma haemobos' are the main hemoplasma species that can infect buffaloes. Transmission of the disease occurs mainly via hematophagous arthropod vectors or iatrogenically. The diagnosis of infected animals is made by Polymerase Chain Reaction (PCR). Prevention and control measures are essential for the control of this disease in buffalo herds.

Los búfalos son animales rústicos que pueden ser explotados para la producción de carne o leche. Estos animales son susceptibles de contraer enfermedades que también afectan a otras especies de rumiantes, especialmente al ganado vacuno. Sin embargo, se cree que los búfalos son más resistentes a algunas enfermedades, pero todavía hay pocos estudios epidemiológicos sobre enfermedades infecciosas como la hemoplasmosis en búfalos. La hemoplasmosis está causada por micoplasmas hemotrópicos o hemoplasmas, que son bacterias gram negativas que causan anemia hemolítica en huéspedes inmunodeprimidos. Mycoplasma wenyonii y 'Candidatus Mycoplasma haemobos' son las principales especies de hemoplasma que pueden infectar a los búfalos. La transmisión de la enfermedad se produce principalmente a través de vectores artrópodos hematófagos o de forma iatrogénica. El diagnóstico de los animales infectados se realiza mediante la reacción en cadena de la polimerasa (PCR). Las medidas de prevención y control son esenciales para controlar esta enfermedad en los rebaños de búfalos.

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)

Thromboelastometry assessment of mycophenolate mofetil effect on thrombotic risk in dogs with primary and secondary immune-mediated hemolytic anemia and by Erhlichia canis infection / [Avaliação por tromboelastometria do efeito do micofenolato de mofetila no risco trombótico em cães com anemia hemolítica imunomediada primária e secundária à infecção por Erhlichia canis]

This study aimed to identify, by means of thromboelastometry assessment, altered thrombotic risk in dogs with primary and secondary IMHA by E. canis infection after initiating the immunosuppressive therapy with mycophenolate mofetil. The animals' screening was based on complete blood count (CBC), biochemical and urine tests. Dogs with moderate to severe anemia (hematocrit ≤ 25%) which showed symptoms of immune-mediated hemolysis, such as spherocytosis, positive saline agglutination, bilirubinuria and/or hemoglobinuria, were included. Blood and urine samples were collected at two different moments. The first sample (M1) was collected at the time of diagnosis, when hematocrit was lower or equal to 25% before treatment with mycophenolate mofetil (Accord ®); the second sample (M2) was collected after treatment with mycophenolate mofetil, when hematocrit was greater or equal to 30%. Five out of the twelve animals selected died before the end of the study. No reduction in thrombotic risk was observed in the animals treated with mycophenolate mofetil. The animals that presented hypocoagulation at the time of diagnosis showed the worst prognosis, and their reticulocyte count displayed a better prognostic value than their erythrocytes count at the time of diagnosis.(AU)

O objetivo deste estudo foi esclarecer se há alteração do risco trombótico em cães com anemia hemolítica imunomediada primária e secundária a E.canis, avaliado por meio da tromboelastometria, após início de tratamento com micofenolato de mofetila. A seleção dos animais foi baseada na avaliação de hemograma, exame bioquímico e urinálise. Cães com anemia moderada a severa (hematócrito ≤ 25%), com sinais de hemólise imunomediada, como esferocitose, aglutinação em salina positivo, bilirrubinúria e/ ou hemoglobinúria, foram incluídos. As amostras de sangue e urina foram coletadas em dois momentos diferentes. A primeira amostra (M1) foi coletada no momento do diagnóstico, quando o hematócrito era igual ou inferior a 25%, sem fazer uso do micofenolato de mofetila (Accord®), e o segundo momento (M2), após tratamento com micofenolato de mofetila, quando o hematócrito era igual ou maior que 30%. Doze animais foram selecionados, cinco morreram antes do término do estudo. Não houve diminuição do risco trombótico entre os animais tratados com micofenolato de mofetila; os animais que apresentaram menor coagulabilidade apresentaram pior prognóstico, e a contagem de reticulócitos apresentou melhor valor prognóstico do que a contagem de hemácias no momento do diagnóstico.(AU)

Anemia hemolítica imunomediada medicamentosa em uma cadela / Immune-mediated hemolytic anemia in a bitch triggered by drugs

Background: Immune-mediated hemolytic anemia (IMHA) is characterized by an autoimmune response with production of auto-antibodies and destruction of erythrocytes resulting in anemia. Primary IMHA is referred to a condition when the cause is unknown (idiopathic), whereas secondary IMHA involves changes in red blood cells caused by the action of drugs, neoplasms, or infectious diseases. The diagnosis can be made through changes in the blood count, usually of a regenerative character, Coombs test, and autoagglutination test. The present study aimed to report a case of drug-induced hemolytic anemia, with emphasis on the clinical signs, diagnostic methods, and treatment, in a female dog. Case: A 9-year-old mixed-breed bitch weighing 29.6 kg was referred to the Veterinary Medical Teaching Hospital (HCVUFRGS) with a previous diagnosis of gallbladder mucocele that was unresponsive to clinical treatment. After laboratory tests, cholecystectomy was performed, and the procedure required conversion from laparoscopic to open cholecystectomy. Therapy included administration of amoxicillin, dipyrone, tramadol hydrochloride, and meloxicam. Three days after surgery, the dog presented with apathy, lethargy, hyporexia, and a pale and subicteric mucosa. The patient developed hypochromic macrocytic anemia with reticulocytosis, spherocytosis, anisocytosis, and leukocytosis with neutrophilia. The result of the autoagglutination test was positive, confirming the diagnosis. All medications were suspended, and immunosuppressive treatment with dexamethasone was included, with a subsequent switch to prednisolone. After 10 days of treatment, the patient experienced significant improvement, and therapy was discontinued. Discussion: Based on the patient's history, the cause of the IMHA was secondary to drug administration, and it is not possible to distinguish if it was due to one or a combination of drugs, as they were all started and stopped simultaneously. The patient had hypothyroidism, which may have contributed to the production of antibodies against TSH receptors, blocking the hormone's action, thereby causing tissue damage due to T cell-mediated cytotoxicity and the effect of cytokines. The pale and subicteric mucosa, apathy, weakness, lethargy, exercise intolerance, and dyspnea resulted from extravascular hemolysis and bilirubin released from erythrocyte rupture with a subsequent decrease in the number of red blood cells, leading to oxygen transport deficiency. The diagnosis is based on the blood count and results of autoagglutination supported by the response to immunosuppressive therapy. Anemia results in increased production and release of precursor cells from the bone marrow, accompanied by reticulocytosis and increased mean corpuscular volume (MCV) and mean corpuscular hemoglobin concentration (MCHC). The treatment of IMHA consists of supportive care and immunosuppressive therapy with corticosteroids to ensure suppression of the immune system, preventing response against erythrocytes. Initially, tramadol hydrochloride, dipyrone, and amoxicillin with potassium clavulanate were suspended to interrupt the cause of IMHA, and administration of dexamethasone in an immunosuppressive dose was started. Therefore, it is important to include drug-induced IMHA in the differential diagnosis of patients who present with anemia after using medications. Early diagnosis, initiation of therapy, and adequate care were important factors for the recovery of the animal.

Clinical, hematological, blood gasometric and electrolytic changes in dogs receiving whole blood transfusions

Blood transfusion is a tool capable of saving lives. Patients undergoing blood transfusion usually present several alterations in the acid-base and electrolyte balance, aggravating the condition of critically ill patients. Some studies have demonstrated haematological alterations in certain species that received whole blood transfusions, however, few studies have evaluated acid base and electrolyte changes in dogs undergoing whole blood haemotherapy. The aim of this study was to analyze clinical, hematological, blood gas and electrolyte changes in anemic dogs after whole blood transfusion. Twenty nine dogs transfused due to anemia were enrolled in the study. Donors blood was collected in a transfusion bag containing citrate phosphate adenine dextrose and stored up to 24 h. Blood collections and evaluations were made before and 24 h after the transfusion. Data distribution normality was tested by the Shapiro Wilk Test. The means of the variables were compared by paired t-test. It was observed an increase in diastolic blood pressure and a reduction in heart rate (P < 0.05). There was a not significant increase in systolic blood pressure, temperature, and a reduction in respiratory rate per minute. Erythrocyte, haemoglobin and haematocrit averages were significantly increased after blood transfusion (P < 0.05). It was observed a reduction in the mean values of pH (P < 0.05), potassium (P > 0.05) and ionized calcium (P > 0.05) and an increase in the mean partial pressure of carbon dioxide (pCO2 ) (P < 0.001), bicarbonate (P > 0.05) and sodium (P < 0.05). The probable cause of anemia was monocytic ehrlichiosis (14/29), visceral leishmaniasis (1/29), babesiosis (1/29), co-infection of Ehrlichia canis and Leishmania infantum (2/29), co-infection of E. canis and Babesia vogeli (1/29). It was not possible to determine the etiology of the anemia in ten dogs. Heart rate significantly reduced after transfusion, probably because of the increase in hematocrit, hemoglobin and erythrocyte values. It may be justified by the displacement of extravascular fluid to the intravascular space. Mean values of systolic blood pressure were slightly elevated before transfusion and remained elevated afterwards, while diastolic and mean arterial pressure increased significantly after transfusion. These changes may be due to the morbid condition and may be influenced by many other factors. Haematocrit, haemoglobin and erythrocyte values increased significantly after transfusion, according to what was observed in other studies. The significant reduction in pH and increase in pCO2 reflects the compensatory mechanism for metabolic acidosis to increase ventilation, leading to pCO2 reduction and changes in pH. The reduction in pH due to the contact of the collected blood with conservative solutions is one of the main changes thar occurs during blood storage. It was described significantly lower pH in dogs' whole blood samples stored for more than 24 h in vacutainer plastic containing CPDA-1. We may assume there was no intense pH reduction in the present study because the bags were stored for up to 24 h. Although not statistically significant, the increase of pO2 mean reflects the improvement of tissue oxygen perfusion. It was observed a significant increase in sodium ions. The mean sodium ion concentration before transfusion was very close to the maximum reference value. Hyperkalaemia was not observed, nor was there significant reduction of potassium ions after transfusion. Several studies report hyperkalaemia and transfusion-associated cardiac arrests in humans, associated with infusion of large volumes of blood. Whole blood transfusion increased erythrogram values and did not negatively affect the electrolyte or acid-base status, representing a safe and useful tool in the intensive care of small animals.(AU)

Infecção verdadeira por Capillaria hepatica em cão / True infection by Capillaria hepatica in a dog

Background: Capillaria hepatica is a nematode, zoonotic, with worldwide distribution. The main hosts are rodents, nevertheless other mammals can be affected. Although the parasite has high affinity for the liver, it rarely causes a hepaticdisease in domestic animals and humans. The diagnosis is difficult and usually a biopsy is required. The treatment is difficult and is based in anti-helminthic and corticoid, but prevention is the best strategy against the disease. The aim of thepresent report is to describe a case of hepatic capillariosis in a dog approaching the clinical signs, diagnosis and therapeutic.Case: A 12-year-old Brazilian Terrier bitch, with a history of visit to the farm and regular hunting of rats, frogs, birds andother wild animals, was attended with hyporexia and apathy. At the physical exam the dog presented elevation of rectaltemperature, intense jaundice and abdominal pain. In the biochemical exams was noticed a slight increase in globulins anda sharp increase in alkaline phosphatase (AP), total, direct and indirect bilirubin, suggesting a liver injury. In the ultrasonographic exam, hepatomegaly with dispersed hyperechoic areas were observed, suggesting hepatic steatosis. The patientwas treated with ursodesoxicolic acid and S-adenosil metionin for 30 consecutive days, showing a clinic improvement.Two months after the end of the treatment the animal worsened, showing jaundice, ascites, motor incoordination, weakness, difficulty in food and water ingestion and changes in the mental state. In the complete blood count was observed amacrocytic hypochromic regenerative anemia, leukocytosis with neutrophilia and monocytosis and thrombocytopenia.In biochemical exams was detected decrease in creatinine and albumin and increase in alanine aminotransferase and AP,suggesting hepatopathy by biliary obstruction. There were performed exams for leishmania and ehrlichiosis that testednegative. In the ultrasonographic exam it...

Infecção verdadeira por Capillaria hepatica em cão / True infection by Capillaria hepatica in a dog

Background: Capillaria hepatica is a nematode, zoonotic, with worldwide distribution. The main hosts are rodents, nevertheless other mammals can be affected. Although the parasite has high affinity for the liver, it rarely causes a hepaticdisease in domestic animals and humans. The diagnosis is difficult and usually a biopsy is required. The treatment is difficult and is based in anti-helminthic and corticoid, but prevention is the best strategy against the disease. The aim of thepresent report is to describe a case of hepatic capillariosis in a dog approaching the clinical signs, diagnosis and therapeutic.Case: A 12-year-old Brazilian Terrier bitch, with a history of visit to the farm and regular hunting of rats, frogs, birds andother wild animals, was attended with hyporexia and apathy. At the physical exam the dog presented elevation of rectaltemperature, intense jaundice and abdominal pain. In the biochemical exams was noticed a slight increase in globulins anda sharp increase in alkaline phosphatase (AP), total, direct and indirect bilirubin, suggesting a liver injury. In the ultrasonographic exam, hepatomegaly with dispersed hyperechoic areas were observed, suggesting hepatic steatosis. The patientwas treated with ursodesoxicolic acid and S-adenosil metionin for 30 consecutive days, showing a clinic improvement.Two months after the end of the treatment the animal worsened, showing jaundice, ascites, motor incoordination, weakness, difficulty in food and water ingestion and changes in the mental state. In the complete blood count was observed amacrocytic hypochromic regenerative anemia, leukocytosis with neutrophilia and monocytosis and thrombocytopenia.In biochemical exams was detected decrease in creatinine and albumin and increase in alanine aminotransferase and AP,suggesting hepatopathy by biliary obstruction. There were performed exams for leishmania and ehrlichiosis that testednegative. In the ultrasonographic exam it...(AU)

Atypical spleen hemophagocytic histiocytic sarcoma in a dog

Background: The histiocytic sarcoma (HS) complex is a set of malignant neoplasms originating from interstitial dendritic cells or macrophages. When it involves macrophages of the splenic red pulp and bone marrow, it is referred to as hemophagocytic histiocytic sarcoma (HHS). HHS behaves more aggressively than HS and is usually fatal. HHS can be diagnosed by cytological and histopathological examination of neoplastic tissue. HHS is confirmed by immunohistochemistry using an anti-CD11d antibody. This neoplasm is often confused with immune-mediated hemolytic anemia or Evans syndrome due to erythrophagocytosis and platelet consumption. The clinical presentation of the animals progresses with evident anemia and thrombocytopenia, leading to signs such as prostration, inappetence, and pale mucosa, making diagnosis challenging and often late. This study aimed to report the clinic-pathological aspects of a canine with atypical hemophagocytic splenic HS. Case: A 4-year-old male Shih-Tzu canine was referred to the Veterinary Hospital with a history of prostration and anorexia. Pale mucous membranes were observed on physical examination. Blood tests revealed non-regenerative anemia, leukopenia, and thrombocytopenia. Serum protein levels were below the reference values for the species in biochemical examinations. Hemoparasitosis was suspected; however, the result of the polymerase chain reaction was negative. Abdominal ultrasound revealed a splenomegaly with heterogeneous parenchyma and a slightly irregular surface, but no visible mass in the spleen. Due to the difficulty of stabilizing the patient, even after successive transfusions, the animal underwent exploratory laparotomy with medial access and posterior splenectomy. Subsequently, the spleen was surgically removed, fixed in 10% buffered formalin, and processed routinely. Macroscopically, it had an irregular reddish-brown capsular surface. Histopathological examination of the spleen revealed a densely cellular neoplasm composed of round to spindle cells (histiocytes) arranged haphazardly in variably sized sheets separating the pre-existing spleen stroma. These histopathological findings were consistent with a histiocytic malignant neoplasm. Immunohistochemical analysis was performed to better define the origin of the histiocytic neoplasm. Neoplastic cells showed positive immunostaining of more than 80% of tumor cells for the CD11d antibody and weak immunostaining for CD11c and lysozyme. The patient survived for less than 30 days after the first hospital visit. Discussion: The diagnosis of HHS was based on the histological characteristics and positive immunostaining of more than 80% of the tumor cells for the CD11d antibody. HHS is an extremely aggressive and rare tumor that affects elderly dogs of any breed. In this study, HHS had atypical histologic characteristics, in which erythrophagocytosis and hemosiderin were not observed within macrophages. HHSs arise from macrophages of the red pulp of the spleen or bone marrow and express the b2 integrin, CD11d, and have low expression of CD1 and CD11c, which are predominantly expressed by non-hemophagocytic HS. The hematological and biochemical changes observed in this case were similar to those described in other dogs with HHS. Treatment of HHS is only palliative. Erlichia ewingii, E. canis, Anaplasma phagocytophilum, A. platys, Borrelia burgdorferi, Dirofilaria immitis, Leishmania infantum and immune-mediated hemolytic anemia are the main differential diagnoses because they cause anemia and thrombocytopenia accompanied by splenomegaly.

Micoplasmose em felino doméstico, FeLV (+), relato de caso / Mycoplasmosis in feline domestic, FeLV (+), case report / Micoplasmosis en felino doméstico, FeLV (+), caso clínico

Mycoplasma spp. são bactérias pleomórficas que parasitam a superfície das hemácias de várias espécies domésticas, sendo o Mycoplasma haemofelis, a espécie mais frequente nos felinos. Este parasito é reponsável pela micoplasmose felina, também chamada de micoplasmose haemotrópica felina (MHF) e de anemia infecciosa felina, que pode causar um quadro de anemia hemolítica aguda ou crônica. O objetivo deste trabalho, foi relatar o caso de um felino doméstico, apresentando na avaliação clínica, mucosas ictéricas e os linfonodos submandibulares aumentados de volume. Foi realizado teste rápido para diagnóstico de FIV/FeLV, onde constatou-se que o paciente era FeLV (+), sendo este, um fator de risco para o desenvolvimento da micoplasmose. No eritrograma, evidenciou-se diminuição do hematócrito, hemácias e hemoglobina. O exame bioquímico, indicou aumento de ALT, ureia e bilirrubina total. Para diagnóstico definitivo, foi realizado pesquisa de hemoparasitos, pela técnica de esfregaço sanguíneo corado, onde observou-se na superfície das hemácias, a presença de estruturas eosinofílicas na forma de cocos, característicos do gênero Mycoplasma.

Mycoplasma spp. they are pleomorphic bacteria that parasitize the surface of red blood cells of several domestic species, Mycoplasma haemofelis being the most frequent species in cats. This parasite is responsible for feline mycoplasmosis, also called feline haemotropic mycoplasmosis (MHF) and feline infectious anemia, which can cause acute or chronic hemolytic anemia. The aim of this study was to report the case of a domestic feline, presenting in the clinical evaluation, jaundiced mucous membranes and enlarged submandibular lymph nodes. A rapid test was performed for the diagnosis of FIV / FeLV, where it was found that the patient was FeLV (+), which is a risk factor for the development of mycoplasmosis. The erythrogram showed a decrease in hematocrit, red blood cells and hemoglobin. Biochemical examination indicated an increase in ALT, urea and total bilirubin. For a definitive diagnosis, a survey of hemoparasites was carried out, using the stained blood smear technique, where the presence of eosinophilic.

Mycoplasma spp. son bacterias pleomórficas que parasitan la superficie de los glóbulos rojos de varias especies domésticas, siendo Mycoplasma haemofelis la especie más frecuente en gatos. Este parásito es responsable de la micoplasmosis felina, también llamada micoplasmosis hemotrópica felina (MHF) y anemia infecciosa felina, que puede causar anemia hemolítica aguda o crónica. El objetivo de este trabajo fue informar el caso de un felino doméstico, presentando en la evaluación clínica, membranas mucosas con ictericiay ganglios linfáticos submandibulares agrandados. Se realizó una prueba rápida para el diagnóstico de FIV / FeLV, donde se encontró que el paciente era FeLV (+), que es un factor de riesgo para el desarrollo de micoplasmosis. El eritrograma mostró una disminución en el hematocrito, los glóbulos rojos y la hemoglobina. Para un diagnóstico definitivo, se realizó una encuesta de hemoparásitos, utilizando la técnica de frotis de sangre teñida, donde se observó la presencia de estructuras eosinofílicas en formade cocos, características del género Mycoplasma, en la superficie de los glóbulos rojos.

Micoplasmose em felino doméstico, FeLV (+), relato de caso / Mycoplasmosis in feline domestic, FeLV (+), case report / Micoplasmosis en felino doméstico, FeLV (+), caso clínico

Mycoplasma spp. são bactérias pleomórficas que parasitam a superfície das hemácias de várias espécies domésticas, sendo o Mycoplasma haemofelis, a espécie mais frequente nos felinos. Este parasito é reponsável pela micoplasmose felina, também chamada de micoplasmose haemotrópica felina (MHF) e de anemia infecciosa felina, que pode causar um quadro de anemia hemolítica aguda ou crônica. O objetivo deste trabalho, foi relatar o caso de um felino doméstico, apresentando na avaliação clínica, mucosas ictéricas e os linfonodos submandibulares aumentados de volume. Foi realizado teste rápido para diagnóstico de FIV/FeLV, onde constatou-se que o paciente era FeLV (+), sendo este, um fator de risco para o desenvolvimento da micoplasmose. No eritrograma, evidenciou-se diminuição do hematócrito, hemácias e hemoglobina. O exame bioquímico, indicou aumento de ALT, ureia e bilirrubina total. Para diagnóstico definitivo, foi realizado pesquisa de hemoparasitos, pela técnica de esfregaço sanguíneo corado, onde observou-se na superfície das hemácias, a presença de estruturas eosinofílicas na forma de cocos, característicos do gênero Mycoplasma.(AU)

Mycoplasma spp. they are pleomorphic bacteria that parasitize the surface of red blood cells of several domestic species, Mycoplasma haemofelis being the most frequent species in cats. This parasite is responsible for feline mycoplasmosis, also called feline haemotropic mycoplasmosis (MHF) and feline infectious anemia, which can cause acute or chronic hemolytic anemia. The aim of this study was to report the case of a domestic feline, presenting in the clinical evaluation, jaundiced mucous membranes and enlarged submandibular lymph nodes. A rapid test was performed for the diagnosis of FIV / FeLV, where it was found that the patient was FeLV (+), which is a risk factor for the development of mycoplasmosis. The erythrogram showed a decrease in hematocrit, red blood cells and hemoglobin. Biochemical examination indicated an increase in ALT, urea and total bilirubin. For a definitive diagnosis, a survey of hemoparasites was carried out, using the stained blood smear technique, where the presence of eosinophilic.(AU)

Mycoplasma spp. son bacterias pleomórficas que parasitan la superficie de los glóbulos rojos de varias especies domésticas, siendo Mycoplasma haemofelis la especie más frecuente en gatos. Este parásito es responsable de la micoplasmosis felina, también llamada micoplasmosis hemotrópica felina (MHF) y anemia infecciosa felina, que puede causar anemia hemolítica aguda o crónica. El objetivo de este trabajo fue informar el caso de un felino doméstico, presentando en la evaluación clínica, membranas mucosas con ictericiay ganglios linfáticos submandibulares agrandados. Se realizó una prueba rápida para el diagnóstico de FIV / FeLV, donde se encontró que el paciente era FeLV (+), que es un factor de riesgo para el desarrollo de micoplasmosis. El eritrograma mostró una disminución en el hematocrito, los glóbulos rojos y la hemoglobina. Para un diagnóstico definitivo, se realizó una encuesta de hemoparásitos, utilizando la técnica de frotis de sangre teñida, donde se observó la presencia de estructuras eosinofílicas en formade cocos, características del género Mycoplasma, en la superficie de los glóbulos rojos.(AU)

Anemia hemolítica imunomediada primária em cães - Revisão de literatura / Primary immune-mediated hemolytic anemia in dogs - Literature review / Anemia hemolítica inmunomediada primaria en perros ­ Revisión de literatura

A anemia hemolítica imunomediada (AHIM) é o distúrbio imunológico de maior prevalência em cães. Caracteriza-se como uma hipersensibilidade do tipo II, que leva a destruição prematura de hemácias. Dentre as principais complicações, o estado de hipercoagulabilidade predispondo a coagulação intravascular disseminada e tromboembolismo pulmonar é a mais importante, sendo a causa de óbito em mais de 80% dos casos. O diagnóstico é realizado a partir da exclusão de outras causas para anemia e por meio da constatação de um ou mais desses sinais: anemia moderada a grave (hematócrito <25-35%), evidências de hemólise (hemoglobinemia, hemoglobinúria ou hiperbilirrubinemia) e presença de anticorpos na hemácia (caracterizado a partir da auto-aglutinação, esferocitose, teste de Coombs positivo ou citometria de fluxo). O tratamento é direcionado à supressão da resposta imune, sendo os corticosteroides e os imunossupressores, os fármacos de predileção.(AU)

Immune-mediated hemolytic anemia (IMHA) is the most prevalent immune disorder among dogs. It is characterized as type II hypersensitivity, leading to premature destruction of red blood cells. Among the main complications, hypercoagulability predisposing to disseminated intravascular coagulation and pulmonary thromboembolism is the most important, being the cause of death in more than 80% of the cases. The diagnosis is made by excluding other causes for anemia and the presence of one or more of these signs: moderate to severe anemia (hematocrit <25-35%), evidence of hemolysis (hemoglobinemia, hemoglobinuria or hyperbilirubinemia) and presence of antibodies in the erythrocyte (characterized by self-agglutination, spherocytosis, positive Coombs test, or flow cytometry). Treatment is directed to suppression of the immune response, with corticosteroids and immunosuppressants the drugs of predilection.(AU)

La anemia hemolítica inmunomediada (AHIM) es el disturbio inmunológico con mayor prevalencia en perros. Es definido como una hipersensibilidad tipo II, que lleva a destrucción prematura de hematíes. Dentro de las principales complicaciones, el estado de hipercoagulabilidad que predispone a coagulación intravascular diseminada y tromboembolismo pulmonar es el más importante, siendo la causa de muerte en más de 80% de los casos. El diagnóstico se realiza excluyendo otras causas de anemia y confirmando una o más de las siguientes alteraciones: anemia moderada a grave (hematocrito <25-35%), evidencias de hemolisis (hemoglobinemia, hemoglobinuria o hiperbilirrubinemia) y presencia de anticuerpos en hematíes (caracterizado a partir de autoaglutinación, esferocitosis, test de Coombs positivo o citometría de flujo). El tratamiento se basa en la supresión de la respuesta inmune, siendo los cortico esteroides y los inmunosupresores los fármacos de elección.(AU)

Crise hemolítica em um cão com hepatite crônica associada ao cobre / Hemolytic crisis in a dog with copper-associated chronic hepatitis

Background: Copper is an essential micronutrient for the body to function properly. However, although it is a vital element,an excess of copper in the body is extremely toxic. Copper toxicity has been reported mainly in sheep. In dogs, clinicopathological signs of toxicity are characterized by chronic liver failure. This means that the hemolytic crisis so commonin sheep is a condition rarely associated with toxicity in dogs, so there are very few descriptions of this condition in theveterinary literature. The purpose of this report is to describe a case of hemolytic crisis in a dog with copper-associatedchronic hepatitis.Case: A medium-sized 6-year-old bitch was brought to the Veterinary Hospital of the Federal University of Santa Maria,with clinical presentation of apathy, anorexia and red urine. A physical examination revealed mildly jaundiced mucosaand dark brown urine. A urinalysis indicated the presence of protein, bilirubin and occult blood. The blood count revealedhypochromic macrocytic anemia, leukocytosis due to left shift neutrophilia and thrombocytopenia. Serum biochemistryshowed elevated levels of alanine aminotransferase and alkaline phosphatase. The animal was given a blood transfusiondue to the severity of her anemia, but her clinical condition worsened and she died, whereupon her body was sent for necropsy. This necropsy revealed conspicuous signs of jaundice, splenomegaly and altered liver and kidney color. The liverwas brownish, with its natural surface firm and slightly irregular. The kidneys were diffusely blackened. The urine wasdark brown. Fragments of different organs were collected, fixed in 10% buffered formalin solution, routinely processedfor histopathology and stained with hematoxylin and eosin. A histological dissection of the liver showed the hepatic lobesdissected by fibrosis, forming islands of hepatocytes and numerous lymphocytes and...

Crise hemolítica em um cão com hepatite crônica associada ao cobre / Hemolytic crisis in a dog with copper-associated chronic hepatitis

Background: Copper is an essential micronutrient for the body to function properly. However, although it is a vital element,an excess of copper in the body is extremely toxic. Copper toxicity has been reported mainly in sheep. In dogs, clinicopathological signs of toxicity are characterized by chronic liver failure. This means that the hemolytic crisis so commonin sheep is a condition rarely associated with toxicity in dogs, so there are very few descriptions of this condition in theveterinary literature. The purpose of this report is to describe a case of hemolytic crisis in a dog with copper-associatedchronic hepatitis.Case: A medium-sized 6-year-old bitch was brought to the Veterinary Hospital of the Federal University of Santa Maria,with clinical presentation of apathy, anorexia and red urine. A physical examination revealed mildly jaundiced mucosaand dark brown urine. A urinalysis indicated the presence of protein, bilirubin and occult blood. The blood count revealedhypochromic macrocytic anemia, leukocytosis due to left shift neutrophilia and thrombocytopenia. Serum biochemistryshowed elevated levels of alanine aminotransferase and alkaline phosphatase. The animal was given a blood transfusiondue to the severity of her anemia, but her clinical condition worsened and she died, whereupon her body was sent for necropsy. This necropsy revealed conspicuous signs of jaundice, splenomegaly and altered liver and kidney color. The liverwas brownish, with its natural surface firm and slightly irregular. The kidneys were diffusely blackened. The urine wasdark brown. Fragments of different organs were collected, fixed in 10% buffered formalin solution, routinely processedfor histopathology and stained with hematoxylin and eosin. A histological dissection of the liver showed the hepatic lobesdissected by fibrosis, forming islands of hepatocytes and numerous lymphocytes and...(AU)