Eosinophilic Meningomyelitis Probably Associated with Toxoplasmosis in a Cat

Background: The cerebrospinal fluid (CSF) of healthy cats presents up to 5 cells/µL, with predominance of mononuclear cells and the presence of more than 1% eosinophils is rare and should always be considered an abnormal finding. There is no consensus on the term eosinophilic pleocytosis, as it is used to indicate the presence of more than 10 eosinophils/µL or more than 10% of the total neutrophils. The increase in eosinophils in the CSF may result from infectious, inflammatory, neoplastic and idiopathic diseases. The objective of this paper is to report a case of marked pleocytosis in CSF, with 84% eosinophils, probably due to toxoplasmosis, in a cat with paraparesis and diffuse spinal pain.Case: A mixed breed female cat, neutered, adult and domiciled in a rural area was presented due to gait abnormalities in the pelvic limbs that started one day before presentation. The general physical examination was unremarkable. On neurological examination it was observed asymmetric deficit of postural reactions in pelvic limbs, patellar reflex normal to increased and pain elicited on palpation of the thoracic and lumbar spine. Based on these findings, the neurological syndrome was classified as thoracolumbar, but with diffuse pain, and the main differential diagnoses were inflammatory/infectious and neoplastic diseases. The leukogram showed eosinophilia and the serum biochemistry showed no significant changes. Serological assays for feline immunodeficiency virus and feline leukemia virus were negative. Analysis of cerebrospinal fluid (CSF) identified marked pleocytosis with 84% eosinophils and increase in protein concentration. Myelography showed no compressive or expansive changes. Fungal culture for CSF cryptococcosis was negative. Serum immunofluorescence antibody titer for Toxoplasma gondii (IgG) was 1:256. There was a marked improvement after treatment with sulfametoxazole/trimethoprim and pyrimethamine and after 3 weeks of treatment, there was almost complete recovery of neurological signs and after 9 months the cat was neurologically normal.Discussion: The most common causes of acute-onset thoracolumbar spinal cord syndrome in cats, with diffuse pain on spinal palpation, are meningomyelitis of inflammatory/infectious origin, such as feline infectious peritonitis (FIP) and neoplasms such as lymphoma. Other meningomyelitis of inflammatory origin, such as infectious and immune-mediated meningomyelitis of unknown origin are considered uncommon in cats. Although the clinical, systemic and neurological signs of FIP and toxoplasmosis may have similarities, in the present case FIP was not considered responsible for the observed signs, as the evolution of the case and the analysis of the CSF tend to be different. The peripheral eosinophilia, the cytological analysis of the CSF, characterized by marked eosinophilic pleocytosis, associated with a positive titer for toxoplasmosis, good response to treatment and improvement in the neurological condition, with survival for more than 9 months after treatment, rules out the possibility of FIP. Neurological signs observed in the absence of systemic signs are more common in cases of protozoan reactivation, which probably occurred in the present case. The possibility of toxoplasmosis in the patient in this report was reinforced by the fact that the animal came from a rural area. Eosinophilia of CSF is most commonly associated with parasitic infections, although it can be caused by a variety of infectious agents, but in the cat of the present report, the marked eosinophilic pleocytosis was likely due to toxoplasmosis, which is a rare occurrence in this specie. In conclusion, toxoplasmosis should be considered in the differential diagnosis of focal spinal cord lesions in cats. The identification of laboratory findings as well as the appropriate therapy favored the good evolution of the condition.Keywords: eosinophilic pleocytosis, feline, Toxoplasma gondii, cerebrospinal fluid.Descritores: pleocitose eosinofílica, felino, Toxoplasma gondii, líquido cerebroespinhal.

Motor polyneuropathy in an adult dog, probably caused by toxoplasmosis : Case Report

Background: Nonambulatory flaccid tetraparesis can be the result of diseases of the peripheral nervous system and it is characterized by generalized lower motor neuron (LMN) signs, as weakness, tetraparesis/tetraplegia, decreased muscle tone and reflexes. The term polyneuropathy is used for dysfunction of multiple peripheral nerves. In Brazil, there are several etiologies for polyneuropathy in dogs, such as acute idiopathic polyradiculoneuritis, botulism and myasthenia gravis. Toxoplasma gondii is an uncommon cause of LMN diseases in dogs. The aim of this report was to describe a case of flaccid tetraplegia toxoplasmosis in an adult dog with a Toxoplasma gondii serology with a markedly elevated IgG titer of 1:4096. Case: A 4-year-old intact mongrel male dog, weighing 19.6 kg, was referred to the Veterinary Medical Teaching Hospital of the Universidade Estadual de Londrina (UEL) with a 5-day history of weakness that progressed to tetraparesis. Physical examination revealed no significant changes other than the dull and unkempt coat. Neurologic examination revealed severe tetraparesis that was worse in the pelvic limbs, with decreased muscle tone in all four limbs. Postural reactions and the interdigital reflex were absent in all four limbs, as was the patellar reflex, but pain perception was present. There were no clinical signs of dysfunction on examination of the cranial nerves. Laboratory tests were performed, and creatine kinase was elevated (819 U/L). Blood was drawn to look for antibodies to Toxoplasma gondii and Neospora caninum class IgG using the indirect immunofluorescence technique. The antibody titer for Toxoplasma gondii (IgG) was 1:4096. A chest radiograph was performed to look for megaesophagus, and a pulmonary pattern suggestive of mild diffuse pneumonia was observed. Treatment was performed with sulfamethoxazole and trimethoprim, and the dog's condition improved slightly. Discussion: Based on lower motor neuron findings, the neurologic lesion was localized in the nerve roots, peripheral nerves, neuromuscular junctions, and muscles. The most important diseases in the list of differential diagnoses were immune-mediated or infectious polyradiculoneuritis (toxoplasmosis, neosporosis), myasthenia gravis, toxic polyneuropathy (botulism, chronic organophosphate poisoning), and paraneoplastic polyneuropathy. Among these differential diagnoses, polyradiculoneuritis is one of the most common. It is an idiopathic inflammatory disease. Exposure to raccoon saliva (in the U.S.), vaccination, or infection have been proposed as precipitating causes, but the triggers of this disease remain unknown. Serology for neosporosis was negative, while IgG titers for toxoplasmosis were 1:4096. In a previous study, dogs with acute polyradiculoneuritis were more likely to have T. gondii IgG serum antibody titers than dogs without neurologic signs. Infection with the protozoa T. gondii and N. caninum can cause intense polyradiculoneuritis in dogs accompanied by myositis, especially in puppies. One treatment trial was based on the administration of sulfonamide-trimethoprim with pyrimethamine, whose efficacy in the treatment of toxoplasmosis in dogs has also been reported in the literature. Neurologic deficits improved slightly, and there is a possibility that certain signs may not disappear completely because of the permanent damage caused by inflammation of the nervous system, as observed in the present case. The case had the limitation that it was not possible to perform other laboratory tests to demonstrate histopathologically the presence of Toxoplasma gondii organisms in muscles or nerves. Recovery of normal function is less likely in protozoan polyradiculoneuritis than in noninfectious polyradiculoneuritis. Thus, in the present case, the main suspicion was polyradiculoneuritis secondary to toxoplasmosis. Although it is a rare condition, it is important to consider toxoplasmosis in dogs with LMN-type tetraparesis or tetraplegia. Keywords: polyneuropathy, polyradiculoneuritis, tetraparesis, dogs, peripheral nervous system. Título: Polineuropatia motora em cão adulto Descritores: polineuropatia, polirradiculoneurite, tetraparesia, cães, sistema nervoso periférico.Background: Nonambulatory flaccid tetraparesis can be the result of diseases of the peripheral nervous system and it is characterized by generalized lower motor neuron (LMN) signs, as weakness, tetraparesis/tetraplegia, decreased muscle tone and reflexes. The term polyneuropathy is used for dysfunction of multiple peripheral nerves. In Brazil, there are several etiologies for polyneuropathy in dogs, such as acute idiopathic polyradiculoneuritis, botulism and myasthenia gravis. Toxoplasma gondii is an uncommon cause of LMN diseases in dogs. The aim of this report was to describe a case of flaccid tetraplegia probably caused by toxoplasmosis in an adult dog. Case: A 4-year-old, 19.6-kg, intact mongrel male dog, was presented with a 5-day history of weakness that progressed to tetraparesis. Physical examination revealed no significant changes other than the dull and unkempt coat. Neurologic examination revealed severe tetraparesis that was worse in the pelvic limbs, with decreased muscle tone in all four limbs. Postural reactions and the interdigital reflex were absent in all four limbs, as was the patellar reflex, but pain perception was present. There were no clinical signs of dysfunction on examination of the cranial nerves. Laboratory tests were performed, and creatine kinase was elevated (819 U/L). Blood was drawn to look for antibodies to Toxoplasma gondii and Neospora caninum class IgG using the indirect immunofluorescence technique. The antibody titer for Toxoplasma gondii (IgG) was 1:4096. A chest radiograph was performed to look for megaesophagus, and a pulmonary pattern suggestive of mild diffuse pneumonia was observed. Treatment was performed with sulfamethoxazole and trimethoprim, and the dog's condition improved slightly. Discussion: Based on lower motor neuron findings, the neurologic lesion was localized to nerve roots, peripheral nerves, neuromuscular junctions, and muscles. The most important diseases in the list of differential diagnoses were immune-mediated or infectious polyradiculoneuritis (toxoplasmosis, neosporosis), myasthenia gravis, toxic polyneuropathy (botulism, chronic organophosphate poisoning), and paraneoplastic polyneuropathy. Among these differential diagnoses, polyradiculoneuritis is one of the most common. It is an idiopathic inflammatory disease. Exposure to raccoon saliva (in the U.S.), vaccination, or infection have been proposed as precipitating causes, but the triggers of this disease remain unknown. Serology for neosporosis was negative, while IgG titers for toxoplasmosis were 1:4096. In a previous study, dogs with acute polyradiculoneuritis were more likely to have T. gondii IgG serum antibody titers than dogs without neurologic signs. Infection with the protozoa T. gondii and N. caninum can cause intense polyradiculoneuritis in dogs accompanied by myositis, especially in puppies. One treatment trial was based on the administration of sulfonamide-trimethoprim with pyrimethamine, whose efficacy in the treatment of toxoplasmosis in dogs has also been reported in the literature. Neurologic deficits improved slightly, and there is a possibility that certain signs may not disappear completely because of the permanent damage caused by inflammation of the nervous system, as observed in the present case. The case had the limitation that it was not possible to perform other laboratory tests to demonstrate histopathologically the presence of T. gondii organisms in muscles or nerves. Recovery of normal function is less likely in protozoan polyradiculoneuritis than in noninfectious polyradiculoneuritis. Thus, in the present case, the main suspicion was polyradiculoneuritis secondary to toxoplasmosis. Although it is a rare condition, it is important to consider toxoplasmosis in dogs with LMN-type tetraparesis or tetraplegia

Motor polyneuropathy in an adult dog, probably caused by toxoplasmosis : Case Report

Background: Nonambulatory flaccid tetraparesis can be the result of diseases of the peripheral nervous system and it is characterized by generalized lower motor neuron (LMN) signs, as weakness, tetraparesis/tetraplegia, decreased muscle tone and reflexes. The term polyneuropathy is used for dysfunction of multiple peripheral nerves. In Brazil, there are several etiologies for polyneuropathy in dogs, such as acute idiopathic polyradiculoneuritis, botulism and myasthenia gravis. Toxoplasma gondii is an uncommon cause of LMN diseases in dogs. The aim of this report was to describe a case of flaccid tetraplegia toxoplasmosis in an adult dog with a Toxoplasma gondii serology with a markedly elevated IgG titer of 1:4096. Case: A 4-year-old intact mongrel male dog, weighing 19.6 kg, was referred to the Veterinary Medical Teaching Hospital of the Universidade Estadual de Londrina (UEL) with a 5-day history of weakness that progressed to tetraparesis. Physical examination revealed no significant changes other than the dull and unkempt coat. Neurologic examination revealed severe tetraparesis that was worse in the pelvic limbs, with decreased muscle tone in all four limbs. Postural reactions and the interdigital reflex were absent in all four limbs, as was the patellar reflex, but pain perception was present. There were no clinical signs of dysfunction on examination of the cranial nerves. Laboratory tests were performed, and creatine kinase was elevated (819 U/L). Blood was drawn to look for antibodies to Toxoplasma gondii and Neospora caninum class IgG using the indirect immunofluorescence technique. The antibody titer for Toxoplasma gondii (IgG) was 1:4096. A chest radiograph was performed to look for megaesophagus, and a pulmonary pattern suggestive of mild diffuse pneumonia was observed. Treatment was performed with sulfamethoxazole and trimethoprim, and the dog's condition improved slightly. Discussion: Based on lower motor neuron findings, the neurologic lesion was localized in the nerve roots, peripheral nerves, neuromuscular junctions, and muscles. The most important diseases in the list of differential diagnoses were immune-mediated or infectious polyradiculoneuritis (toxoplasmosis, neosporosis), myasthenia gravis, toxic polyneuropathy (botulism, chronic organophosphate poisoning), and paraneoplastic polyneuropathy. Among these differential diagnoses, polyradiculoneuritis is one of the most common. It is an idiopathic inflammatory disease. Exposure to raccoon saliva (in the U.S.), vaccination, or infection have been proposed as precipitating causes, but the triggers of this disease remain unknown. Serology for neosporosis was negative, while IgG titers for toxoplasmosis were 1:4096. In a previous study, dogs with acute polyradiculoneuritis were more likely to have T. gondii IgG serum antibody titers than dogs without neurologic signs. Infection with the protozoa T. gondii and N. caninum can cause intense polyradiculoneuritis in dogs accompanied by myositis, especially in puppies. One treatment trial was based on the administration of sulfonamide-trimethoprim with pyrimethamine, whose efficacy in the treatment of toxoplasmosis in dogs has also been reported in the literature. Neurologic deficits improved slightly, and there is a possibility that certain signs may not disappear completely because of the permanent damage caused by inflammation of the nervous system, as observed in the present case. The case had the limitation that it was not possible to perform other laboratory tests to demonstrate histopathologically the presence of Toxoplasma gondii organisms in muscles or nerves. Recovery of normal function is less likely in protozoan polyradiculoneuritis than in noninfectious polyradiculoneuritis. Thus, in the present case, the main suspicion was polyradiculoneuritis secondary to toxoplasmosis. Although it is a rare condition, it is important to consider toxoplasmosis in dogs with LMN-type tetraparesis or tetraplegia. Keywords: polyneuropathy, polyradiculoneuritis, tetraparesis, dogs, peripheral nervous system. Título: Polineuropatia motora em cão adulto Descritores: polineuropatia, polirradiculoneurite, tetraparesia, cães, sistema nervoso periférico.Background: Nonambulatory flaccid tetraparesis can be the result of diseases of the peripheral nervous system and it is characterized by generalized lower motor neuron (LMN) signs, as weakness, tetraparesis/tetraplegia, decreased muscle tone and reflexes. The term polyneuropathy is used for dysfunction of multiple peripheral nerves. In Brazil, there are several etiologies for polyneuropathy in dogs, such as acute idiopathic polyradiculoneuritis, botulism and myasthenia gravis. Toxoplasma gondii is an uncommon cause of LMN diseases in dogs. The aim of this report was to describe a case of flaccid tetraplegia probably caused by toxoplasmosis in an adult dog. Case: A 4-year-old, 19.6-kg, intact mongrel male dog, was presented with a 5-day history of weakness that progressed to tetraparesis. Physical examination revealed no significant changes other than the dull and unkempt coat. Neurologic examination revealed severe tetraparesis that was worse in the pelvic limbs, with decreased muscle tone in all four limbs. Postural reactions and the interdigital reflex were absent in all four limbs, as was the patellar reflex, but pain perception was present. There were no clinical signs of dysfunction on examination of the cranial nerves. Laboratory tests were performed, and creatine kinase was elevated (819 U/L). Blood was drawn to look for antibodies to Toxoplasma gondii and Neospora caninum class IgG using the indirect immunofluorescence technique. The antibody titer for Toxoplasma gondii (IgG) was 1:4096. A chest radiograph was performed to look for megaesophagus, and a pulmonary pattern suggestive of mild diffuse pneumonia was observed. Treatment was performed with sulfamethoxazole and trimethoprim, and the dog's condition improved slightly. Discussion: Based on lower motor neuron findings, the neurologic lesion was localized to nerve roots, peripheral nerves, neuromuscular junctions, and muscles. The most important diseases in the list of differential diagnoses were immune-mediated or infectious polyradiculoneuritis (toxoplasmosis, neosporosis), myasthenia gravis, toxic polyneuropathy (botulism, chronic organophosphate poisoning), and paraneoplastic polyneuropathy. Among these differential diagnoses, polyradiculoneuritis is one of the most common. It is an idiopathic inflammatory disease. Exposure to raccoon saliva (in the U.S.), vaccination, or infection have been proposed as precipitating causes, but the triggers of this disease remain unknown. Serology for neosporosis was negative, while IgG titers for toxoplasmosis were 1:4096. In a previous study, dogs with acute polyradiculoneuritis were more likely to have T. gondii IgG serum antibody titers than dogs without neurologic signs. Infection with the protozoa T. gondii and N. caninum can cause intense polyradiculoneuritis in dogs accompanied by myositis, especially in puppies. One treatment trial was based on the administration of sulfonamide-trimethoprim with pyrimethamine, whose efficacy in the treatment of toxoplasmosis in dogs has also been reported in the literature. Neurologic deficits improved slightly, and there is a possibility that certain signs may not disappear completely because of the permanent damage caused by inflammation of the nervous system, as observed in the present case. The case had the limitation that it was not possible to perform other laboratory tests to demonstrate histopathologically the presence of T. gondii organisms in muscles or nerves. Recovery of normal function is less likely in protozoan polyradiculoneuritis than in noninfectious polyradiculoneuritis. Thus, in the present case, the main suspicion was polyradiculoneuritis secondary to toxoplasmosis. Although it is a rare condition, it is important to consider toxoplasmosis in dogs with LMN-type tetraparesis or tetraplegia

The stress-induced soybean NAC transcription factor GmNAC81 plays a positive role in developmentally programmed leaf senescence

The onset of leaf senescence is a highly regulated developmental change that is controlled by both genetics and the environment. Senescence is triggered by massive transcriptional reprogramming, but functional information about its underlying regulatory mechanisms is limited. In the current investigation, we performed a functional analysis of the soybean (Glycine max) osmotic stress- and endoplasmic reticulum (ER) stress-induced NAC transcription factor GmNAC81 during natural leaf senescence using overexpression studies and reverse genetics. GmNAC81-overexpressing lines displayed accelerated flowering and leaf senescence but otherwise developed normally. The precocious leaf senescence of GmNAC81-overexpressing lines was associated with greater Chl loss, faster photosynthetic decay and higher expression of hydrolytic enzyme-encoding GmNAC81 target genes, including the vacuolar processing enzyme (VPE), an executioner of vacuole-triggered programmed cell death (PCD). Conversely, virus-induced gene silencing-mediated silencing of GmNAC81 delayed leaf senescence and was associated with reductions in Chl loss, lipid peroxidation and the expression of GmNAC81 direct targets. Promoter–reporter studies revealed that the expression pattern of GmNAC81 was associated with senescence in soybean leaves. Our data indicate that GmNAC81 is a positive regulator of age-dependent senescence and may integrate osmotic stress- and ER stress-induced PCD responses with natural leaf senescence through the GmNAC81/VPE regulatory circuit

AMAZONIA CAMTRAP: A data set of mammal, bird, and reptile species recorded with camera traps in the Amazon forest

The Amazon forest has the highest biodiversity on Earth. However, information on Amazonian vertebrate diversity is still deficient and scattered across the published, peer-reviewed, and gray literature and in unpublished raw data. Camera traps are an effective non-invasive method of surveying vertebrates, applicable to different scales of time and space. In this study, we organized and standardized camera trap records from different Amazon regions to compile the most extensive data set of inventories of mammal, bird, and reptile species ever assembled for the area. The complete data set comprises 154,123 records of 317 species (185 birds, 119 mammals, and 13 reptiles) gathered from surveys from the Amazonian portion of eight countries (Brazil, Bolivia, Colombia, Ecuador, French Guiana, Peru, Suriname, and Venezuela). The most frequently recorded species per taxa were: mammals: Cuniculus paca (11,907 records); birds: Pauxi tuberosa (3713 records); and reptiles: Tupinambis teguixin (716 records). The information detailed in this data paper opens up opportunities for new ecological studies at different spatial and temporal scales, allowing for a more accurate evaluation of the effects of habitat loss, fragmentation, climate change, and other human-mediated defaunation processes in one of the most important and threatened tropical environments in the world. The data set is not copyright restricted; please cite this data paper when using its data in publications and we also request that researchers and educators inform us of how they are using these data