scholarly journals Bovine congenital babesiosis

2021 ◽  
Vol 14 (1) ◽  
pp. 70-74
Author(s):  
Luan Henker ◽  
Marina Lorenzett ◽  
Saulo Pavarini

Diagnostic Exercise from The Latin Comparative Pathology Group. Clinical History: A crossbred, stillborn bovine fetus, with nine months of gestation, was submitted for postmortem examination. The dam that aborted was a 2-year-old heifer that did not have any additional clinical signs. The owner observed several late-term abortions and stillbirths in this farm during the referred calving season. Necropsy Findings: Necropsy findings included moderate accumulation of light red fluid in the abdominal and thoracic cavities, mild hemoglobin imbibition, as well as collapsed lungs. The liver was markedly enlarged, had rounded edges, and moderate, diffuse yellow discoloration. The gallbladder was filled with thick, grumous bile, and the spleen was moderately enlarged. The kidneys had moderate diffuse dark red discoloration, and the urinary bladder was distended with dark-red urine. The grey matter of the brain and the spinal cord was markedly pink-red discolored. Squashes of the spleenand brain were prepared and routinely stained with PanóticoRápido® (Laborclin, Brazil).

2002 ◽  
Vol 46 (8) ◽  
pp. 2420-2426 ◽  
Author(s):  
Karl V. Clemons ◽  
Raymond A. Sobel ◽  
Paul L. Williams ◽  
Demosthenes Pappagianis ◽  
David A. Stevens

ABSTRACT The efficacy of intravenously administered liposomal amphotericin B (AmBisome [AmBi]) for the treatment of experimental coccidioidal meningitis was compared with those of oral fluconazole (FLC) and intravenously administered conventional amphotericin B (AMB). Male New Zealand White rabbits were infected by intracisternal inoculation of arthroconidia of Coccidioides immitis. Starting 5 days postinfection, animals received one of the following: 5% dextrose water diluent; AMB given at 1 mg/kg of body weight; AmBi given at 7.5, 15, or 22.5 mg/kg intravenously three times per week for 3 weeks; or oral FLC given at 80 mg/kg for 19 days. One week after the cessation of therapy, all survivors were euthanatized, the numbers of CFU remaining in the spinal cord and brain were determined, and histological analyses were performed. All AmBi-, FLC-, or AMB-treated animals survived and had prolonged lengths of survival compared with those for the controls (P < 0.0001). Treated groups had significantly lower numbers of white blood cells and significantly lower protein concentrations in the cerebrospinal fluid compared with those for the controls (P < 0.01 to 0.0005) and had fewer clinical signs of infection (e.g., weight loss, elevated temperature, and neurological abnormalities including motor abnormalities). The mean histological scores for AmBi-treated rabbits were lower than those for FLC-treated and control rabbits (P < 0.016 and 0.0005, respectively); the scores for AMB-treated animals were lower than those for the controls (P < 0.0005) but were similar to those for FLC-treated rabbits. All regimens reduced the numbers of CFU in the brain and spinal cord compared with those for the controls (P ≤0.0005). AmBi-treated animals had 3- to 11-fold lower numbers of CFU than FLC-treated rabbits and 6- to 35-fold lower numbers of CFU than AmB-treated rabbits. Three of eight animals given 15 mg of AmBi per kg had no detectable infection in either tissue, whereas other doses of AmBi or FLC cleared either the brain or the spinal cord of infection in fewer rabbits. In addition, clearance of the infection from both tissues was achieved in none of the rabbits, and neither tissue was cleared of infection in AMB-treated animals. Overall, these data indicate that intravenously administered AmBi is superior to oral FLC or intravenous AMB and that FLC is better than AMB against experimental coccidioidal meningitis. These data indicate that AmBi may offer an improvement in the treatment of coccidioidal meningitis. Additional studies are warranted.


2008 ◽  
Vol 15 (2) ◽  
pp. 180-188 ◽  
Author(s):  
CP Gilmore ◽  
JJG Geurts ◽  
N Evangelou ◽  
JCJ Bot ◽  
RA van Schijndel ◽  
...  

Background Post-mortem studies demonstrate extensive grey matter demyelination in MS, both in the brain and in the spinal cord. However the clinical significance of these plaques is unclear, largely because they are grossly underestimated by MR imaging at conventional field strengths. Indeed post-mortem MR studies suggest the great majority of lesions in the cerebral cortex go undetected, even when performed at high field. Similar studies have not been performed using post-mortem spinal cord material. Aim To assess the sensitivity of high field post-mortem MRI for detecting grey matter lesions in the spinal cord in MS. Methods Autopsy material was obtained from 11 MS cases and 2 controls. Proton Density-weighted images of this formalin-fixed material were acquired at 4.7Tesla before the tissue was sectioned and stained for Myelin Basic Protein. Both the tissue sections and the MR images were scored for grey matter and white matter plaques, with the readers of the MR images being blinded to the histopathology results. Results Our results indicate that post-mortem imaging at 4.7Tesla is highly sensitive for cord lesions, detecting 87% of white matter lesions and 73% of grey matter lesions. The MR changes were highly specific for demyelination, with all lesions scored on MRI corresponding to areas of demyelination. Conclusion Our work suggests that spinal cord grey matter lesions may be detected on MRI more readily than GM lesions in the brain, making the cord a promising site to study the functional consequences of grey matter demyelination in MS.


2021 ◽  
Vol 31 (Supplement_2) ◽  
Author(s):  
Maiara Carolina Perussolo ◽  
Bassam Felipe Mogharbel ◽  
Lucia de Noronha ◽  
Katherine Athayde Teixeira de Carvalho

Abstract Background Multiple sclerosis (MS) is an autoimmune disease of the central nervous system, characterized as an inflammatory demyelinating disease. It presents a diversity of neurologic signs and symptoms as well the incapacities. Since the need for advances in MS treatment, many studies are for new therapeutic technologies, mainly through using preclinical models as experimental autoimmune encephalomyelitis (EAE). This study aimed to observe and analyze the development in Lewis rats-induced model of EAE. Methods It was used 23 females of Rattus norvegicus, from 6 to 8 weeks, weighing around 170 g. Of 23 rats, 19 underwent EAE induction distributed in six groups to establish the evolution of clinical signs. B. pertussis toxin (PTX) doses were 200, 250, 300, 350–400 ng, and four animals as the control group. The animals had weight and scores analyzed daily, starting seven and ending 24 days after induction. Then, all animals were euthanized, and the brain and spinal cord were collected for histopathological analyses. Results The results showed that the dose of 250 ng of PTX induced de higher score and weight reduction. All groups who received the PTX demonstrated histopathological findings. Those characterized as leukocyte infiltration, activation of microglia and astrocytes, and demyelinated plaques in the brain. In the spinal cord, the loosening of the myelinated fibers was observed by increasing the axonal space in all tested doses of PTX. Conclusions EAE was not dose-dependent. Histopathological findings do not proportionally related to clinical signs, as in human patients with MS.


Author(s):  
SC Hammond ◽  
M Almomen ◽  
A Mineyko ◽  
A Pauranik

Background: Acute flaccid myelitis (AFM) is a condition which causes acute paralysis in pediatric patients. Although awareness of AFM is increasing, the pathophysiology and full spectrum of clinical, biochemical, and radiographic features remain to be fully elucidated. Methods: We report a 5 year-old, previously healthy, male patient who presented with acute right upper extremity weakness following a two day history of fever, cough, and fatigue. The patient underwent extensive inflammatory and infectious workup in addition to MRI imaging of the brain, spinal cord, and bilateral brachial plexuses. Results: Infectious and inflammatory workup did not identify a causative agent. The patient was seen to have bilateral asymmetric (R&gt;L) thickening and enhancement of the anterior horn cells of his cervical (C3-C7) spine, consistent with the spinal grey matter lesions previously described in patients with AFM. Enhancement of the corresponding anterior nerve rootlets and bilateral brachial plexuses was also seen. Conclusions: Patients with acute flaccid myelitis may demonstrate grey matter enhancement extending beyond the spinal cord to the peripheral nerves and plexuses, a radiographic finding which has not previously been published.


2008 ◽  
Vol 45 (6) ◽  
pp. 934-938 ◽  
Author(s):  
C. J. Gibson ◽  
N. M. A. Parry ◽  
R. M. Jakowski ◽  
D. Eshar

A 2–year-old, female hedgehog presented with an 8–month history of progressive, ascending paresis/paralysis and was tentatively diagnosed with wobbly hedgehog syndrome. She died awaiting further diagnostic tests, and the owners consented to postmortem examination. Grossly, the bladder was large and flaccid and the cervical and lumbar spinal cord were regionally enlarged, light grey, and friable with multifocal hemorrhages. The thoracic spinal cord was grossly normal. Microscopically all regions of the spinal cord had similar changes, although the cervical and lumbar sections were most severely affected. These regions were completely effaced by a moderately cellular infiltration of highly pleomorphic polygonal to spindle shaped cells, mineralization, and necrosis, which were most consistent with anaplastic astrocytoma. The thoracic spinal cord white matter was similarly infiltrated by the neoplastic cells, with perivascular extension into the otherwise normal grey matter. A diagnosis of anaplastic astrocytoma was confirmed using immunohistochemical stains that were positive for glial fibrillary acidic protein and S100.


2016 ◽  
Vol 19 (1) ◽  
pp. 21-26 ◽  
Author(s):  
Frances E Taylor-Brown ◽  
Steven De Decker

Objectives The aim of the study was to describe the clinical features, diagnostic imaging findings, treatment and outcome in cats diagnosed with presumptive acute non-compressive nucleus pulposus extrusion. Methods Medical records and imaging studies of cats diagnosed with presumptive acute non-compressive nucleus pulposus extrusion were retrospectively reviewed. Information on long-term outcome was acquired from patient records and from either owners or referring veterinary surgeons via a telephone questionnaire. Results Eleven cats met the inclusion criteria. All cats had a peracute onset of clinical signs, with eight cats experiencing witnessed (n = 6) or suspected (n = 2) external trauma based on imaging findings. Neuroanatomical localisation included C1–C5 (n = 1), T3–L3 (n = 7) and L4–S3 (n = 3) spinal cord segments. MRI revealed acute non-compressive nucleus pulposus extrusions located at C3–C4 (n = 1), T12–T13 (n = 1), T13–L1 (n = 1), L1–L2 (n = 1), L3–L4 (n = 3), L4–L5 (n = 1) and L5–L6 intervertebral disc spaces (n = 3). Treatment included supportive care and 10 cats were discharged with a median hospitalisation time of 10 days (range 3–26 days). One cat was euthanased during hospitalisation owing to complications unrelated to neurological disease. All cats that presented as non-ambulatory regained an ambulatory status with the median time to ambulation of 17 days (range 6–21 days). Overall, the outcome for cats diagnosed with acute non-compressive nucleus pulposus extrusion was successful, with almost 90% returning to ambulation with urinary and faecal continence. Conclusions and relevance The majority of cats diagnosed with acute non-compressive nucleus pulposus extrusion had good outcomes. Acute non-compressive nucleus pulposus extrusion should be considered as a differential diagnosis for cats presenting with peracute onset of spinal cord dysfunction, particularly if there is a clinical history or evidence of trauma.


2018 ◽  
Vol 46 ◽  
pp. 6
Author(s):  
Julia Gabriela Wronski ◽  
Bianca Santana Cecco ◽  
Luan Cleber Henker ◽  
Marina Paula Lorenzett ◽  
Paulo Michel Roehe ◽  
...  

Background: Herpetic meningoencephalitis is an infectious contagious disease worldwide distributed, most often caused by bovine alphaherpesvirus type 5 (BoHV-5), although bovine alphaherpesvirus type 1 (BoHV-1) may occasionally be the causative agent. The disease is characterized by subacute to acute clinical onset, often affecting animals submitted to stressful situations. Clinical signs are mainly neurologic due to meningoencephalitis and cortical necrosis. The involvement of the spinal cord has also been reported, however in BoHV-1 associated disease only. The aim of this report is to describe an outbreak of bovine meningoencephalomyelitis associated to BoHV-5.Case: In August 2017, nine 1-year-old calves died in a beef cattle farm with a flock of approximately 400 bovines. The animals presented neurological clinical signs characterized by excessive salivation, nasal and ocular discharges, incoordination, apathy, head tremors, head pressing, wide-based stance, recumbency followed by convulsions and paddling. According to the owner and referring veterinarian, affected animals displayed severe clinical signs with rapid progression and often leading to death in up to seven days. Four of these calves were submitted for necropsy, and gross lesions were present in the brain, characterized by mild to moderate multifocal hemorrhagic and soft areas. On cut surface, extensive areas of dark brown discoloration and malacia were observed. Histologically, lesions were characterized by extensive areas of liquefactive necrosis in the cerebral cortex grey matter, associated with inflammatory infiltrates composed of neutrophils, lymphocytes, plasma cells and foamy macrophages, as well as multifocal to coalescing areas of hemorrhage and fibrin deposition. Intranuclear eosinophilic inclusion bodies were rarely observed in neurons and astrocytes. On leptomeninges, there was diffuse inflammatory infiltrates of lymphocytes and plasma cells. Inflammation was also seen in a milder degree in the spinal cord, characterized by infiltrate of lymphocytes at grey matter, mainly around vessels. A herpesvirus which induced typical cytopathic effect in cell cultures was recovered from tissues. The isolated virus was typed as BoHV-5 by nucleotide sequencing analysis of the gC coding region.Discussion: The diagnosis of meningoencephalomyelitis associated to BoHV-5 was based on epidemiological, clinical, macroscopical, histological, virological and genomic findings. In the outbreak here reported, the disease occurred in young animals, with low morbidity but high lethality rates. Clinical signs on this case were consistent with previous reports on the literature. Bovines affected by BoHV-5 may display no gross lesions within the CNS; however, inflammatory and degenerative changes are frequently seen, characterized by malacia, leptomeningeal vessels hyperemia, edema and hemorrhages. Histologically, non-suppurative necrotizing meningoencephalitis is seen, with perivascular inflammatory infiltrates and, occasionally, intranuclear eosinophilic inclusion bodies in astrocytes and neurons. Similar but milder lesions were seen in the spinal cords of two of the necropsied calves, a feature which has only been previously associated to BoHV-1 infections. The identification of the implicated agent was accomplished by virus isolation in cell cultures followed by genome typing. Specific treatments for this condition are not currently available, and the number of animals that recover from clinically apparent disease is extremely low. Preventive measures are based on serological testing of herds, and segregation or elimination of seropositive calves. To avoid progression of the disease in seropositive animals, control efforts must be directed to avoid stressful conditions. Vaccination with BoHV-1 and BoHV-5 vaccines is expected to confer protection to clinical disease.


1974 ◽  
Vol 11 (1) ◽  
pp. 87-96 ◽  
Author(s):  
Jill Beech ◽  
D. C. Dodd

Eight horses with progressive neurologic signs had encephalomyelitis associated with toxoplasma-like protozoan bodies. There were scattered hemorrhagic, malacic lesions in white and grey matter in the brain and spinal cord. Microscopically there was malacia, mononuclear cell infiltration, especially perivascularly, gliosis, and various degrees of necrosis and hemorrhage. Other tissues were normal, except for the lung of one horse that had focal bronchopneumonia. The cerebrospinal fluid did not contain measurable amounts of IgM, IgG, or IgA. Serum from one horse was negative at 1:64 by the hemagglutination-inhibition test for toxoplasma antibodies.


2006 ◽  
Vol 42 (3) ◽  
pp. 226-233 ◽  
Author(s):  
Jessica S. Mikszewski ◽  
Thomas J. Van Winkle ◽  
Mark T. Troxel

Five cats had clinical signs, radiographic findings, and cerebrospinal fluid analyses consistent with fibrocartilaginous embolic myelopathy. All cats had an acute onset of nonpainful, asymmetrical spinal cord signs (paresis or paralysis of one or more limbs). Magnetic resonance imaging was performed in three cats. On T2-weighted images, an intramedullary lesion was revealed that was hyperintense to normal spinal cord gray matter. On T1-weighted images, the lesion was isointense. Three of the cats were euthanized, and postmortem examination confirmed myelomalacia with intralesional fibrocartilaginous emboli. Two cats survived and were clinically improved within 3 weeks.


1968 ◽  
Vol 46 (3) ◽  
pp. 503-510 ◽  
Author(s):  
Roy C. Anderson ◽  
Uta R. Strelive

Two caribou calves (Rangifer tarandus terraenovae) were infected experimentally with Pneumostrongylus tenuis Dougherty from white-tailed deer (Odocoileus virginianus borealis). The female calf showed slight neurologic signs from the 5th to the 14th day when she died from a mycotic infection. The male calf first showed neurologic signs on the seventh day. These signs became progressively more extreme and by the 29th day, when the animal was necropsied, it showed severe locomotory ataxia with knuckling and posterior weakness. Histological study of the spinal cord of the male revealed numerous worms in all regions of the spinal cord and in the brain stem and medulla oblongata. Traumatic lesions and worms were unusually numerous in lateral and dorsal funiculi. It is suggested that the more severe neurologic signs were caused by migration of worms into funiculi from dorsal horns of grey matter. The results are discussed in relation to the management of woodland caribou in eastern North America.


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