Poliartrite em cão por Leishmaniose - tratamento com miltefosina / Polyarthritis in a dog due to leishmaniasis - treatment with miltefosine

Background: Canine visceral leishmaniasis causes several clinical signs, such as lymphadenomegaly, exfoliative dermatitis, ulcerative skin lesions, and lameness. The most commonly reported locomotor changes are claudication, edema, arthralgia, joint stiffness, and muscle atrophy. Radiographic exam revealed cortical and medullary destruction, increase, or decrease in medullary opacity, proliferative periosteal reaction, osteolysis, collapse of joint spaces and soft tissue edema are observed. The aim of this report is to describe the clinical and radiographic evolution of a case of erosive polyarthritis associated with leishmaniasis in a dog before, during and after treatment with miltefosine. Case: A 7-month-old mixed-breed dog was attended due pain and limited mobility. In the orthopedic evaluation, joint swelling, stiffness, and increased pain sensitivity of the four limbs, as well as neck stiffness, were noted. Radiographic examination showed joint changes compatible with edema, with increased volume and radiopacity of the soft tissues adjacent to the joints. The segments of the patient's spine showed more severe bone alterations, the cervical spine being one of the most affected regions, with multiple bone proliferations throughout the vertebral body, especially in the ventral portion (spondylosis), compatible with polyarthritis due to leishmaniasis. Due to the suspicion, lymph node and spleen cytology was performed, confirming the diagnosis. Hematological examination revealed anemia, leukopenia due to lymphopenia and thrombocytopenia in addition to increased AST (79,4 U/L; reference: 6,2 - 13 U/L), creatine kinase (517,6 U/L; reference: 1,5 - 28,4 U/L), lactate dehydrogenase (688,4 IU/L; reference: 45 - 233 IU/L) and hyperproteinemia (7,34 g/dL; reference: 5,4 - 7,1 g/dL). Treatment with miltefosine, allopurinol, domperidone, prednisone, gabapentin and dipyrone was started. Reassessments were performed monthly for 3 consecutive months. Hematological examinations showed improvement, with resolution of anemia and thrombocytopenia, and a marked decrease in creatine kinase values. Thus, it is evident that the dog did not develop liver or kidney changes during treatment. During the treatment and monitoring in this period, the dog had a clinical improvement, which started to walk without pain. In addition, joint swellings were no longer present, however, there was no improvement in the radiographic evaluation of the joints. Discussion: Clinical signs of the locomotor system are compatible with those described in animals that had osteoarticular manifestations associated with leishmaniasis, such as arthralgia, edema, and joint stiffness. In the present report, treatment with miltefosine associated with allopurinol resulted in an improvement in the clinical picture, and this therapy is therefore promising in dogs with polyarthritis due to leishmaniasis. A case published in human medicine demonstrated the intra-articular absorption capacity of this drug. There is only one study to date that describes the radiographic evolution of a dog with arthritis due to leishmaniasis after treatment with miltefosine and allopurinol. In this case described, the dog reported remained with the osteoarticular lesions after treatment, although clinical improvement was observed, as in our report. The use of miltefosine and allopurinol are in accordance with stage II staging for leishmaniasis. In this study, although there was no improvement in the radiographic examinations, the treatment was effective in the remission of the animal's clinical condition.

Pneumocephalus and suppurative meningoencephalitis in a dog after craniofacial trauma

Background: Pneumocephalus is characterized by the presence of gas in the intracranial compartment, and it can be developed by trauma, craniofacial surgery or spontaneously. Clinical signs start within days or months after the injury and vary according to the site of involvement. Computed tomography is the ideal diagnostic tool, however skull radiography can also be used. Treatment varies according to the severity of the case, and it can be conservative or associated with surgical intervention in the most severe cases. The purpose of this report is to describe the case of a dog that developed pneumocephalus and suppurative meningoencephalitis after head trauma caused by a bite from another dog. Case: A 2-month-old bitch, mixed breed, with 3.2 kg, was referred to the Veterinary Hospital because it had been bitten on the head by another dog. Shortly after the incident, the animal showed no clinical signs. However, 2 days later, the bitch became depressed and in persistent lateral decubitus. A lesion with a crust of approximately 0.5 cm was found close to the occipital region, with bone irregularity on palpation. The animal was in lateral decubitus with muscular hypotonia, bilateral mydriasis unresponsive to light and stupor. Radiographic images showed parietal fracture and pneumocephalus. Based on the findings of physical and laboratorial exams, diagnosis of suppurative meningoencephalitis and pneumocephalus secondary to craniofacial trauma was established. Empirical broad-spectrum antimicrobial therapy was started in addition to mannitol, corticoids, and analgesics. The animal was referred for surgical debridement by trepanation, when samples were collected to bacterial culture, which was negative. Despites the care, the animal died 14 h after the surgical procedure. Histopathological examination of the frontal cortex was performed, being the histological changes compatible with suppurative meningoencephalitis. Discussion: Dog bites on the head and neck are particularly severe, and can create intracranial bleeding, disfigurement of the face, damage to peripheral structures or cranial fractures. In this report, through radiographic images, it was found that the patient had an intracerebral aerocele, since there was presence of gas in the intracranial compartment. This alteration should always be considered in animals with neurological alterations and a history of craniofacial trauma. The main neurological changes observed in the reported case were unresponsive to mydriasis and altered mental status 2 days after the trauma, and this delay in the onset of clinical signs is frequently reported in cases of pneumocephalus. Neutrophilia and leukocytosis observed can be justified by the suppurative meningoencephalitis, confirmed by the histopathological exam. Antimicrobial therapy should be started as soon as possible, and the choice must be based on their capacity to cross the blood-brain barrier and the broad spectrum. The administration of antibiotics before collecting the material for bacterial culture may explain the negative result of this test, so that it is not possible to determine whether the intracranial gas observed on the radiograph may have developed from the trauma or because of gas-producing bacteria. Head trauma can induce suppurative meningoencephalitis and pneumocephalus even in the absence of perforating wounds at the time of the consultation. The neurological signs can start days after the trauma. Besides the clinical and surgical treatments, the prognosis of any bacterial infection of the central nervous system is poor.

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.

Liver cysts in a kitten with Platynosomum sp

Background: Hepatic cysts are rarely described in association with infections by Platynosomum sp. Infected animals are most often asymptomatic, and the severity of symptoms is associated with the number of biliary tract parasites, which may lead to cholangitis and cholangiohepatitis. Although platinosomiasis is often associated with cholangitis and cholangiohepatitis, it rarely is with polycystic disease. For the parasite's life cycle to occur, the infected cat must eliminate the eggs in the feces and three intermediate hosts are needed: snails, terrestrial isopods and vertebrates like the frog or the gecko. The eggs are ingested by the snails, then the miracids are released and matured into the mother sporocyst form, which originates child sporocysts containing the cercariae, that leave the mollusks for the soil and are ingested by the terrestrial isopod in which the cercariae matures until metacercariae. Vertebrates ingest terrestrial isopods and are ingested by felines. The present study aimed to report an unusual case of platinosomiasis with the development of multiple hepatic cysts. Case: A mixed breed male kitten was admitted with a history of apathy, hyporexia, increased abdominal volume and jaundice. In the ultrasound examination, we could see hepatomegaly and several hypoecogenic rounded structures, similar to cysts. There was an increase of serum concentration of the hepatic enzymes alanine transaminase and gamma glutamyl transferase enzyme. The parasite's eggs were investigated in the patient's feces using the simple sedimentation method, with a negative result. The animal was submitted to celiotomy and it was possible to observe several cystic structures in the liver. The cysts content was sent to cytology and culture. Cytology result was compatible with liver cyst and there was no bacterial growth in the culture. Bile fluid was collected and sent for Platynosomum sp. research using the centrifugal sedimentation test in formalin-ether solution, which allowed the parasite's eggs to be observed. The cat was treated with praziquantel,silymarin, S-Adenosyl methionine, and ursodeoxycholic acid. The patient gradually improved from jaundice and there was a reduction in abdominal volume. Discussion: This report describes a case of platinossomiasis associated with polycystic liver disease in a domestic cat, which seems to be an uncommon presentation. Most infected cats are asymptomatic, but some animals may exhibit anorexia, apathy, increased abdominal volume due to hepatomegaly and/or ascitis and jaundice. Although infestation in domestic cats is relatively common, its association with liver cysts is rare or poorly reported in the literature, representing a diagnostic challenge, which makes mandatory the inclusion of this differential diagnosis in polycystic liver diseases in cats. The diagnosis of this parasitosis can be made based on the association among clinical signs, laboratory tests and ultrasound examination, but the definitive diagnosis is usually made by visualizing the parasite's eggs. In the case described, it was not possible to observe parasite's eggs in the patient's feces, but in the bile. Platynosomum sp. infection should always be considered as a differential diagnosis in cases of polycystic liver disease in cats, especially in countries with tropical or subtropical climate. Early diagnosis and appropriate treatment were fundamental for the improvement of the patient's clinical condition.