scholarly journals Síndrome hemorrágica pulmonar em cão associada à leptospirose

2017 ◽  
Vol 45 ◽  
pp. 5
Author(s):  
Vinícius Bentivóglio Costa Silva ◽  
Simone Tostes de Oliveira Stedile ◽  
Renato Silva De Sousa ◽  
Marlos Gonçalves Sousa
Keyword(s):  
Clinical Signs ◽  
Pulmonary Hemorrhage ◽  
Pulmonary Involvement ◽  
Respiratory Arrest ◽  
Severe Form ◽  
Pulmonary Haemorrhage ◽  
Immunological Mechanisms ◽  
Filling Time ◽  
History Of ◽  
Renal Failure Fluid

Background: Leptospirosis is probably the most widespread and prevalent zoonosis in the world, being classified as an emerging infectious disease for humans and dogs. Sporadically, dogs may present with cough and dyspnea, indicative of pulmonary involvement, associated with interstitial pneumonia and pulmonary hemorrhage with alveolar consolidation. Such changes stem from pulmonary haemorrhagic syndrome, which has emerged as a fatal complication, being documented in some areas in Europe and little described in North America. In this sense, the present study aims to report pulmonary hemorrhagic syndrome in a dog with leptospirosis.Case: A dog with no defined breed, aged 45 days, weighing 2.2 kg, with a history of apathy, anorexia, jaundice, hematochezia and vocalisation with a two day evolution was seen. Physical examination revealed a rectal temperature of 37.2°C, icteric mucosa, capillary filling time of two seconds, respiratory rate of 80 movements per minute and heart rate of 140 beats per minute, dehydration rate estimated at 8%, prostration, adequate body score, normal cardiac sounds and clean lung fields, in addition to petechiae in the abdominal region, whose palpation evidenced the presence of fluid in intestinal loops. The blood sample sent to the macroscopic serum agglutination was reagent for the serovar Icterohaemorragiae, titration of 200. Blood count revealed leukocytosis due to neutrophilia, with left-sided deviation, eosinopenia, presence of rare hypersegmentated neutrophils, rare toxic neutrophils, mild cytoplasmic basophilia and rare reactive lymphocytes. Platelet estimation demonstrated thrombocytopenia. No haemoparasites were seen. Regarding the biochemical evaluation, there were changes in liver enzymes and markers of renal failure. Fluid therapy was used with 0.9% NaCl solution, 5 mg/ kg doxycycline intravenously every 12 h and nasogastric probe for administration of nutritional support. One day after the initial evaluation, hemoptysis and diffuse crackling occurred in pulmonary lobes on auscultation. In the radiograph of the chest, pulmonary fields were characterized by a diffuse interstitial bronchial pattern and a focal area, located in the left caudal lobe, with opacification tending to the alveolar pattern. Due to pulmonary alterations, the animal presented respiratory arrest and evolved to death. During necropsy, the macroscopic evaluation revealed a pinkish coloration pattern, with multifocal reddish areas with coalescent interspersed in the parenchyma and hypocrepitation. Regarding the morphology, multifocal hemorrhagic pneumonia was observed, focally extensive, moderate to severe.Discussion: Recently, pulmonary haemorrhagic syndrome has emerged as a severe form of leptospirosis in many species, including humans and dogs. Patients may develop fulminant pulmonary haemorrhage and result in a high mortality rate. Physiopathogenesis is poorly understood, however, it is believed that there is a multifactorial pathogenesis involving factors related to both pathogen and host, such as immunological mechanisms and coagulopathies. Studies in humans have shown a better evolution after the use of cyclophosphamide, but the benefits of this therapy have not yet been determined in dogs. Therefore, pulmonary haemorrhagic syndrome should be considered in patients with leptospirosis who show respiratory changes, due to the severity of the clinical signs and the high lethality associated with this clinical condition.

scholarly journals SARS-CoV-2 infection and recurrence of anti-glomerular basement disease: a case report

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Alexander Winkler ◽  
Emanuel Zitt ◽  
Hannelore Sprenger-Mähr ◽  
Afschin Soleiman ◽  
Manfred Cejna ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Plasma Cells ◽  
Rapidly Progressive Glomerulonephritis ◽  
Kidney Injury ◽  
Pulmonary Involvement ◽  
Pulmonary Haemorrhage ◽  
Basement Membranes ◽  
High Avidity ◽  
History Of

Abstract Background Anti-glomerular basement membrane disease (GBM) disease is a rare autoimmune disease causing rapidly progressive glomerulonephritis and pulmonary haemorrhage. Recently, an association between COVID-19 and anti-glomerular basement membrane (anti-GBM) disease has been proposed. We report on a patient with recurrence of anti-GBM disease after SARS-CoV-2 infection. Case presentation The 31-year-old woman had a past medical history of anti-GBM disease, first diagnosed 11 years ago, and a first relapse 5 years ago. She was admitted with severe dyspnoea, haemoptysis, pulmonary infiltrates and acute on chronic kidney injury. A SARS-CoV-2 PCR was positive with a high cycle threshold. Anti-GBM autoantibodies were undetectable. A kidney biopsy revealed necrotising crescentic glomerulonephritis with linear deposits of IgG, IgM and C3 along the glomerular basement membrane, confirming a recurrence of anti-GBM disease. She was treated with steroids, plasma exchange and two doses of rituximab. Pulmonary disease resolved, but the patient remained dialysis-dependent. We propose that pulmonary involvement of COVID-19 caused exposure of alveolar basement membranes leading to the production of high avidity autoantibodies by long-lived plasma cells, resulting in severe pulmonary renal syndrome. Conclusion Our case supports the assumption of a possible association between COVID-19 and anti-GBM disease.

scholarly journals Pulmonary haemorrhage in Weil’s disease

2020 ◽  
Vol 13 (1) ◽  
pp. e227570
Author(s):  
Emma Boertjes ◽  
Stefanie Hillebrand ◽  
Janneke Elisabeth Bins ◽  
Laurien Oswald
Keyword(s):  
Respiratory Failure ◽  
Renal Impairment ◽  
Pulmonary Involvement ◽  
Severe Form ◽  
Pulmonary Haemorrhage ◽  
Productive Cough ◽  
Classic Case ◽  
Weil’S Disease ◽  
Weil's Disease

Leptospirosisis a zoonosis caused by spirochaetes from the species Leptospira. The more severe form of leptospirosis, known as Weil’s disease, is characterised by the triad of jaundice, renal impairment and haemorrhages. Pulmonary involvement occurs in 20%–70% of the patients, with severity ranging from non-productive cough to respiratory failure mainly due to pulmonary haemorrhage. Recognition of Weil’s disease in patients presenting with pulmonary symptoms can be difficult. This case illustrates a classic case of pulmonary haemorrhagic involvement in Weil’s disease.

scholarly journals Lung Involvement in Gaucher Disease

2020 ◽  
Author(s):  
Mahnaz PejmanSani ◽  
Keivan GohariMoghadam ◽  
Mahbube Ebrahimpur
Keyword(s):  
Gaucher Disease ◽  
Autosomal Recessive ◽  
Pulmonary Involvement ◽  
Severe Form ◽  
Lysosomal Storage ◽  
Case Presentation ◽  
Progressive Dyspnea ◽  
History Of ◽  
Chest Ct Scan ◽  
Restrictive Pattern

Introduction: Gaucher Disease is an autosomal recessive lysosomal storage disease. Pulmonary involvement in Gaucher Disease is rare and often seen in the severe form of the disease with the worst outcome. Case Presentation: A 30-year-old man and known case of Gaucher Disease presented to our clinic with history of progressive dyspnea since 8 months ago. Pulmonary function test showed restrictive pattern. Chest CT scan revealed diffuse bilateral interlobular septal thickening and small interstitial nodules with ground glass opacities in lower lobes. Conclusion: Patients with Gaucher Disease that present with progressive dyspnea may have a manifestation of interstitial or alveolar lung disease.

Intraocular tuberculosis, a challenge in diagnosis and treatment

2020 ◽  
Vol 3 ◽  
pp. 4
Author(s):  
Martina Larroude ◽  
Gustavo Ariel Budmann
Keyword(s):  
Developing Countries ◽  
Clinical Signs ◽  
Steady Increase ◽  
Ocular Tuberculosis ◽  
Industrial Countries ◽  
Choroidal Granuloma ◽  
History Of ◽  
And Migration ◽  
Ocular Tb

Ocular tuberculosis (TB) is an extrapulmonary tuberculous condition and has variable manifestations. The incidence of TB is still high in developing countries, and a steady increase in new cases has been observed in industrial countries as a result of the growing number of immunodeficient patients and migration from developing countries. Choroidal granuloma is a rare and atypical location of TB. We present a case of a presumptive choroidal granuloma. This case exposes that diagnosis can be remarkably challenging when there is no history of pulmonary TB. The recognition of clinical signs of ocular TB is extremely important since it provides a clinical pathway toward tailored investigations and decision making for initiating anti-TB therapy and to ensure a close follow-up to detect the development of any complication.

Surgical management of choke through oesophagotomy in a buffalo: A case report

2017 ◽  
Vol 12 (3) ◽  
Author(s):  
Devasee Borakhatariya ◽  
A. B. Gadara
Keyword(s):  
Case Report ◽  
Surgical Management ◽  
Clinical Presentation ◽  
Clinical Signs ◽  
Thoracic Inlet ◽  
Cervical Oesophagus ◽  
Foreign Objects ◽  
History Of ◽  
Oesophageal Obstruction ◽  
Large Animals

Oesophageal disorders are relatively uncommon in large animals. Oesophageal obstruction is the most frequently encountered clinical presentation in bovine and it may be intraluminal or extra luminal (Haven, 1990). Intraluminal obstruction or “choke” is the most common abnormality that usually occurs when foreign objects, large feedstuff, medicated boluses, trichobezoars, or oesophageal granuloma lodge in the lumen of the oesophagus. Oesophageal obstructions in bovine commonly occur at the pharynx, the cranial aspect of the cervical oesophagus, the thoracic inlet, or the base of the heart (Choudhary et al., 2010). Diagnosis of such problem depends on the history of eating particular foodstuff and clinical signs as bloat, tenesmus, retching, and salivation

scholarly journals L2HGDH Missense Variant in a Cat with L-2-Hydroxyglutaric Aciduria

Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 682
Author(s):  
Matthias Christen ◽  
Nils Janzen ◽  
Anne Fraser ◽  
Adrian C. Sewell ◽  
Vidhya Jagannathan ◽  
...  
Keyword(s):  
Current Knowledge ◽  
Genetic Defect ◽  
Clinical Signs ◽  
Missense Variant ◽  
Microcytic Anemia ◽  
Abnormal Behavior ◽  
Functional Candidate Gene ◽  
History Of ◽  
The Brain ◽  
Hydroxyglutaric Acid

A 7-month-old, spayed female, domestic longhair cat with L-2-hydroxyglutaric aciduria (L-2-HGA) was investigated. The aim of this study was to investigate the clinical signs, metabolic changes and underlying genetic defect. The owner of the cat reported a 4-month history of multiple paroxysmal seizure-like episodes, characterized by running around the house, often in circles, with abnormal behavior, bumping into obstacles, salivating and often urinating. The episodes were followed by a period of disorientation and inappetence. Neurological examination revealed an absent bilateral menace response. Routine blood work revealed mild microcytic anemia but biochemistry, ammonia, lactate and pre- and post-prandial bile acids were unremarkable. MRI of the brain identified multifocal, bilaterally symmetrical and T2-weighted hyperintensities within the prosencephalon, mesencephalon and metencephalon, primarily affecting the grey matter. Urinary organic acids identified highly increased levels of L-2-hydroxyglutaric acid. The cat was treated with the anticonvulsants levetiracetam and phenobarbitone and has been seizure-free for 16 months. We sequenced the genome of the affected cat and compared the data to 48 control genomes. L2HGDH, coding for L-2-hydroxyglutarate dehydrogenase, was investigated as the top functional candidate gene. This search revealed a single private protein-changing variant in the affected cat. The identified homozygous variant, XM_023255678.1:c.1301A>G, is predicted to result in an amino acid change in the L2HGDH protein, XP_023111446.1:p.His434Arg. The available clinical and biochemical data together with current knowledge about L2HGDH variants and their functional impact in humans and dogs allow us to classify the p.His434Arg variant as a causative variant for the observed neurological signs in this cat.

scholarly journals The application of a new laminitis scoring method to model the rate and pattern of improvement from equine endocrinopathic laminitis in a clinical setting

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
A. Meier ◽  
J. McGree ◽  
R. Klee ◽  
J. Preuß ◽  
D. Reiche ◽  
...  
Keyword(s):  
Best Practice ◽  
Clinical Status ◽  
Clinical Signs ◽  
Scoring Method ◽  
Pain Medications ◽  
Exponential Decay Model ◽  
History Of ◽  
Consistent Method ◽  
Foot Disease ◽  
New Treatments

Abstract Background Endocrinopathic, or hyperinsulinaemia-associated laminitis (HAL) is a common and debilitating equine foot disease, and although no pharmacological treatments are registered, several are under development. To evaluate the effect of such treatments, an accurate and consistent method is needed to track the clinical signs of laminitis over time, and the natural history of the disease, in terms of a ‘normal’ pattern of improvement, needs to be understood. This study examined the improvement pattern in clinical cases of naturally-occurring HAL subjected to a range of best-practice interventions, using two different scoring methods. Eighty horses and ponies with suspected HAL were enrolled in a study conducted at 16 veterinary practices across Germany. The severity of laminitis was assessed by independent veterinarians using both the traditional Obel method and a modified Obel method developed by Meier and colleagues. Assessments were made on the day of diagnosis (d 0), then on days 4, 9, 14, 25 and 42 during the intervention period. Pain medications were withheld for 24 h prior to clinical examination in all cases. Results Time to marked improvement from laminitis varied between individuals, but was difficult to monitor accurately using the Obel method, with the median grade being 2/4 on days 0 and 4, then 0/4 from d 9 onwards. More subtle changes could be identified using the Meier method, however, and the median scores were seen to follow the form of an exponential decay model in most horses, improving from 8/12 on d 0, to 0/12 on d 25. Within this composite scoring method, considerable variation was observed in the rate of improvement of individual clinical signs, with the average time taken for each sign to reach a median score of 0 ranging from 4 days (foot lift and weight shifting) to 25 days (gait when turned in a circle) across all 80 horses. Conclusions The Meier method provides a reliable and consistent method for monitoring the clinical status of horses with HAL, and despite the variability, the pattern of improvement described here should provide a useful benchmark against which individual cases and new treatments can be assessed.

scholarly journals EP20 Hypercalcaemia in sarcoidosis

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Tanya Chopra ◽  
Gordon MacDonald
Keyword(s):  
Case Report ◽  
Pulmonary Involvement ◽  
Urinary Calcium ◽  
Porta Hepatis ◽  
Mri Scan ◽  
Pet Ct ◽  
Pulmonary Macrophages ◽  
History Of ◽  
Granulomatous Tissue ◽  
Extra Pulmonary

Abstract Case report - Introduction Sarcoidosis often classically presents as Lofgren’s syndrome in up to 30% of cases, a triad of erythema nodosum, bilateral hilar lymphadenopathy and polyarthritis. However, the lack of identification and awareness of extrapulmonary manifestations of sarcoidosis can often lead to delayed diagnosis and treatment. In sarcoidosis, hypercalcaemia is a feature in only 10-20% of all cases. However, the manifestation of hypercalcaemia may be the first presentation of sarcoidosis in patients who do not show the classical features of acute sarcoidosis. Case report - Case description A 38-year-old man presented with a 5-month history of profound fatigue, poor concentration, and non-specific joint pains. He reported earlier swelling of his ankles and feet. He had lost 1 stone in weight over the last month. There was no history of fever or night sweats. He smoked 10 cigarettes per day but was otherwise fit and well. On examination urine dipstick testing was negative. There was no evidence of lymphadenopathy. Cardio-respiratory and abdominal examinations were unremarkable. Examination of his skin and joints was also unremarkable. There was mild non-tender ankle oedema. His first blood tests showed a raised adjusted calcium of 3.25 and a raised white cell count of 11.8, with an eosinophilia of 0.75. Other preliminary blood results were unremarkable (normal Hb, U+Es, LFTs, CRP, ESR, RF, anti-CCP, ANA and TFTS). His chest X-ray was reported as clear. His PTH was appropriately suppressed and vitamin D level was adequate with normal urinary calcium and normal serum protein electrophoresis. Serum ACE level was raised at 114 (normal 8-52). PTH related peptide test was not available. A CT chest abdomen and pelvis scan carried out to rule out malignancy was normal with no notable lymphadenopathy. A subsequent PET CT scan was normal. Acutely, his hypercalcaemia was treated with IV fluids and IV pamidronate. Although his calcium rapidly normalised, he reported feeling only 10% better. He complained of ongoing ankle pain. An MRI scan of both ankles with contrast showed mild synovitis of ankle, subtalar and talonavicular joints. There was also evidence of tenosynovitis. Given the constellation of hypercalcaemia, raised serum ACE level and ankle synovitis on MRI scan, he was treated for sarcoidosis with prednisolone 20mg. This led to a rapid improvement in his symptoms and normalisation of serum ACE. He was started on azathioprine as a steroid-sparing agent. Case report - Discussion In cases series, hypercalcaemia due to sarcoidosis accounts for only 6% of all hypercalcaemic patients. The mechanism of hypercalcaemia in sarcoidosis is thought to be via activated pulmonary macrophages and sarcoid lymph node granulomas which upregulate the enzyme 1-alpha hydroxylase, resulting in the increased formation of calcitriol (1,25(OH)2D3). This increases calcium absorption from the gastrointestinal tract, stimulates renal calcium reabsorption and promotes calcium release from skeletal stores, causing hypercalcaemia. This case was particularly unusual as earlier literature suggests that sarcoidosis-associated hypercalcaemia is a result of activated pulmonary macrophages and sarcoid granulomas. However, this patient had significant hypercalcaemia without any radiological lung involvement or granulomata, posing the question whether there are other pathways causing hypercalcaemia in sarcoidosis. Hypercalcaemia without pulmonary involvement may be due to the presence of small amounts of sarcoid granulomata in extra-pulmonary locations such as the porta hepatis. These may not be as easily detectable on radiological investigations but may contribute to the upregulation of 1-alpha hydroxylase and subsequent hypercalcaemia. Another explanation for the significant hypercalcaemia in this patient may be due to the production of parathyroid hormone-related peptide (PTHrP) from sarcoid granulomas and bone marrow, which upregulates renal 1-alpha hydroxylase enzymes and increases the formation of calcitriol. There was no area to obtain a tissue biopsy given the normal CT and PET CT scans, resulting in a greater reliance on history, examination, and serological investigations. In addition, 30-50% of all patients with sarcoidosis have hypercalciuria, yet this patient interestingly had only an isolated hypercalcaemia with a normal urinary calcium. Case report - Key learning points  Hypercalcaemia is rare in the absence of pulmonary involvement with only 10 cases reported in literature.Although non-specific, an elevated serum ACE level may be a useful pointer to the diagnosis of sarcoidosis in the absence of other classical signs.In this case, granulomatous tissue responsible to produce 1,25(OH)2D3 might be below the limits of radiological detection. Production may originate from extra-pulmonary sarcoid granulomatous tissue such as in the porta hepatis. Another possible mechanism for hypercalcaemia may be the production of PTHrP which has been reported in sarcoid tissue specimens and in the bone marrow.

Phlegmonous gastritis in 2 yearling horses

2022 ◽  
pp. 104063872110650
Author(s):  
Julie B. Engiles ◽  
Francisco A. Uzal ◽  
Mauricio A. Navarro ◽  
Virginia B. Reef ◽  
Susan J. Bender
Keyword(s):  
Clinical Signs ◽  
Poor Response ◽  
Abdominal Ultrasound ◽  
Mucosal Injury ◽  
Response To Treatment ◽  
Bacterial Populations ◽  
Proliferative Enteropathy ◽  
Mucosal Involvement ◽  
Phlegmonous Gastritis ◽  
History Of

Phlegmonous gastritis was diagnosed in 2 yearling fillies that were presented with a 1-wk history of fever, lethargy, and hypoproteinemia, associated with a previous diagnosis of equine proliferative enteropathy based on clinical signs and PCR assay detection of Lawsonia intracellularis in fecal samples. Abdominal ultrasound revealed enlargement of the stomach and expansion of its submucosal layer with hypoechoic fluid, as well as thickened hypomotile small intestinal segments. Given the poor prognosis and poor response to treatment, both horses were euthanized, one on the day of presentation and the other after 3 wk of intensive medical management including a combination of antimicrobials, analgesics, and intravenous colloids. At autopsy, acute mural gastritis characterized by severe submucosal edema with suppurative inflammation (i.e., phlegmonous gastritis) and necroulcerative enteritis compatible with the necrotizing form of equine proliferative enteropathy were identified in both horses. The gastric inflammation was associated with thrombosis and mixed bacterial populations, including Clostridium perfringens, that were confined to the submucosa without evidence of mucosal involvement; toxin genes compatible with C. perfringens type C were identified in one case. Human phlegmonous gastritis is an uncommon, often-fatal pyogenic infection that is often associated with mucosal injury, bacteremia, or immunocompromise. Our finding of this unusual gastric lesion in 2 horses with similar signalment, clinical disease, and spectrum of postmortem lesions suggests a similar etiopathogenesis that possibly involves local, regional, or distant hematogenous origin, and should be considered a potential complication of gastrointestinal mucosal compromise in horses.

Immune-Mediated Neutropenia in a Miniature Poodle

2019 ◽  
Vol 55 (1) ◽  
Author(s):  
Benjamin Brunson
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Aspirate ◽  
Clinical Signs ◽  
Response To Therapy ◽  
Tertiary Referral Center ◽  
Immune Mediated ◽  
Specialized Equipment ◽  
History Of ◽  
Light Sedation ◽  
The Right

ABSTRACT A 10 yr old spayed female toy poodle was presented to a tertiary referral center for a 10 day history of waxing and waning lethargy, vomiting, diarrhea, and anorexia. An immune-mediated neutropenia (IMN) was suspected to be the underlying cause of her clinical signs. A bone marrow aspirate was obtained from the chostochondral junction of the 11th and 12th ribs on the right side and provided a definitive diagnosis of IMN. A positive response to therapy and repeat blood work further confirmed the diagnosis. Obtaining bone marrow aspirates from the chostochondral junction is a safe, cheap, and reliable method of diagnosing IMN and can be performed in the private practice setting with light sedation and minimal need for specialized equipment.

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