scholarly journals Clinical, pathological, and immunohistochemistry characterization of toxoplasmosis in dogs with distemper in the semiarid region of Paraíba, Brazil

2015 ◽  
Vol 36 (6Supl2) ◽  
pp. 4251
Author(s):  
Maria Talita Soares Frade ◽  
Lisanka Ângelo Maia ◽  
Rachel Livingstone Felizola Soares Andrade ◽  
Rodrigo Cruz Alves ◽  
Elise Miyuki Yamasaki ◽  
...  
Keyword(s):  
Canine Distemper Virus ◽  
Histopathological Examination ◽  
Clinical Signs ◽  
Neurological Involvement ◽  
Semiarid Region ◽  
Histopathological Analysis ◽  
Thin Wall ◽  
Canine Distemper ◽  
Eosinophilic Inclusion ◽  
The Brain

The objective of this study was to describe the clinical, pathological, and immunohistochemistry characteristics of five cases of toxoplasmosis, an infection often associated with distemper in dogs. From January 2000 to December 2012, a retrospective study was performed analyzed dogs with distemper in the semiarid region of Paraíba. We evaluated this sample to focus on individuals who presented with concomitant structures in protozoa characteristics, and performed immunohistochemistry (IHC) tests using polyclonal anti-Toxoplasma gondii antibody. In all cases, the clinical signs were similar including digestive changes, as well as respiratory, neurological, and ocular lesions, suggesting an infection of canine distemper virus. The diagnosis of distemper was confirmed on histopathological analysis depending on the presence of intranuclear and intracytoplasmic eosinophilic inclusion bodies in different tissues. Histopathological examination also revealed the characteristic presence of parasitic cysts T. gondii in the brain in four cases, and in the lung in one case. The brain cysts were associated with multifocal areas of malacia and lung there was alveolar septa thickening due to infiltration of macrophages, lymphocytes, and plasma cells, with moderate proliferation of type II pneumocytes and coalescing multifocal areas of necrosis. These cysts are characterized by round and strongly basophilic structures, measuring approximately 5 to 70 ?m, delimited by thin wall, stained by hematoxylin and eosin, and immunomarked as brown by immunohistochemistry (IHC) using the chromogen DAB. The diagnosis of toxoplasmosis associated with infection by canine distemper virus in the five case studied was based on microscopic findings and confirmed by immunohistochemistry. Toxoplasmosis should be included in the differential diagnosis of dogs with severe progressive systemic signs, especially when respiratory and neurological involvement is suspected.

scholarly journals Clinical, pathological, and immunohistochemistry characterization of toxoplasmosis in dogs with distemper in the semiarid region of Paraíba, Brazil

2015 ◽  
Vol 36 (6Supl2) ◽  
pp. 4251 ◽  
Author(s):  
Maria Talita Soares Frade ◽  
Lisanka Ângelo Maia ◽  
Rachel Livingstone Felizola Soares Andrade ◽  
Rodrigo Cruz Alves ◽  
Elise Miyuki Yamasaki ◽  
...  
Keyword(s):  
Canine Distemper Virus ◽  
Histopathological Examination ◽  
Clinical Signs ◽  
Neurological Involvement ◽  
Semiarid Region ◽  
Histopathological Analysis ◽  
Thin Wall ◽  
Canine Distemper ◽  
Eosinophilic Inclusion ◽  
The Brain

<p>The objective of this study was to describe the clinical, pathological, and immunohistochemistry characteristics of five cases of toxoplasmosis, an infection often associated with distemper in dogs. From January 2000 to December 2012, a retrospective study was performed analyzed dogs with distemper in the semiarid region of Paraíba. We evaluated this sample to focus on individuals who presented with concomitant structures in protozoa characteristics, and performed immunohistochemistry (IHC) tests using polyclonal anti-<em>Toxoplasma gondii </em>antibody. In all cases, the clinical signs were similar including digestive changes, as well as respiratory, neurological, and ocular lesions, suggesting an infection of canine distemper virus. The diagnosis of distemper was confirmed on histopathological analysis depending on the presence of intranuclear and intracytoplasmic eosinophilic inclusion bodies in different tissues. Histopathological examination also revealed the characteristic presence of parasitic cysts <em>T. gondii </em>in the brain in four cases, and in the lung in one case. The brain cysts were associated with multifocal areas of malacia and lung there was alveolar septa thickening due to infiltration of macrophages, lymphocytes, and plasma cells, with moderate proliferation of type II pneumocytes and coalescing multifocal areas of necrosis. These cysts are characterized by round and strongly basophilic structures, measuring approximately 5 to 70 ?m, delimited by thin wall, stained by hematoxylin and eosin, and immunomarked as brown by immunohistochemistry (IHC) using the chromogen DAB. The diagnosis of toxoplasmosis associated with infection by canine distemper virus in the five case studied was based on microscopic findings and confirmed by immunohistochemistry. Toxoplasmosis should be included in the differential diagnosis of dogs with severe progressive systemic signs, especially when respiratory and neurological involvement is suspected.</p>

scholarly journals Molecular evidence for vaccine-induced canine distemper virus and canine adenovirus 2 coinfection in a fennec fox

2020 ◽  
Vol 32 (4) ◽  
pp. 598-603
Author(s):  
Kenichi Tamukai ◽  
Shohei Minami ◽  
Rio Kurihara ◽  
Hiroshi Shimoda ◽  
Ikki Mitsui ◽  
...  
Keyword(s):  
Inclusion Bodies ◽  
Canine Distemper Virus ◽  
Neuronal Degeneration ◽  
Molecular Evidence ◽  
Intranuclear Inclusions ◽  
Canine Distemper ◽  
Live Virus ◽  
Bronchial Epithelial ◽  
Eosinophilic Inclusion ◽  
The Brain

A 61-d-old fennec fox ( Vulpes zerda), 11 d after receiving a multivalent, modified-live virus vaccine containing canine distemper virus (CDV), canine adenovirus 2 (CAdV-2), parainfluenza virus, parvovirus, and canine coronavirus, developed oculonasal discharge, and subsequently convulsions, and hemoptysis, and died. Microscopic changes in the cerebrum were evident, including neuronal degeneration and necrosis; intracytoplasmic eosinophilic inclusion bodies were observed in astrocytes. CDV was detected in the brain tissue by immunohistochemistry. Pulmonary lesions of multifocal necrotizing bronchopneumonia had Cowdry type A intranuclear inclusions in the bronchial epithelial cells. Electron microscopy revealed crystalline arrays of adenovirus-like particles within the intranuclear inclusions. Additionally, the hemagglutinin gene of CDV and the CAdV-2 DNA polymerase gene were detected in the fennec fox; sequence analysis showed 100% identity with those of the vaccine strain viruses. To our knowledge, vaccine-induced CDV and CAdV-2 coinfections using molecular analysis have not been reported previously. Therefore, vaccine strains should be considered prior to CDV vaccination in nondomestic carnivores.

scholarly journals Vaccination against Canine Distemper Virus Infection in Infant Ferrets with and without Maternal Antibody Protection, Using Recombinant Attenuated Poxvirus Vaccines

2000 ◽  
Vol 74 (14) ◽  
pp. 6358-6367 ◽  
Author(s):  
Janet Welter ◽  
Jill Taylor ◽  
James Tartaglia ◽  
Enzo Paoletti ◽  
Charles B. Stephensen
Keyword(s):  
Canine Distemper Virus ◽  
Clinical Signs ◽  
Neutralizing Antibody ◽  
Maternal Antibody ◽  
Canine Distemper ◽  
Parenteral Immunization ◽  
Multiple Routes ◽  
Antibody Titers ◽  
Group 3 ◽  
Rabies Glycoprotein

ABSTRACT Canine distemper virus (CDV) infection of ferrets is clinically and immunologically similar to measles, making this a useful model for the human disease. The model was used to determine if parenteral or mucosal immunization of infant ferrets at 3 and 6 weeks of age with attenuated vaccinia virus (NYVAC) or canarypox virus (ALVAC) vaccine strains expressing the CDV hemagglutinin (H) and fusion (F) protein genes (NYVAC-HF and ALVAC-HF) would induce serum neutralizing antibody and protect against challenge infection at 12 weeks of age. Ferrets without maternal antibody that were vaccinated parenterally with NYVAC-HF (n = 5) or ALVAC-HF (n = 4) developed significant neutralizing titers (log10 inverse mean titer ± standard deviation of 2.30 ± 0.12 and 2.20 ± 0.34, respectively) by the day of challenge, and all survived with no clinical or virologic evidence of infection. Ferrets without maternal antibody that were vaccinated intranasally (i.n.) developed lower neutralizing titers, with NYVAC-HF producing higher titers at challenge (1.11 ± 0.57 versus 0.40 ± 0.37, P = 0.02) and a better survival rate (6/7 versus 0/5, P = 0.008) than ALVAC-HF. Ferrets with maternal antibody that were vaccinated parenterally with NYVAC-HF (n = 7) and ALVAC-HF (n = 7) developed significantly higher antibody titers (1.64 ± 0.54 and 1.28 ± 0.40, respectively) than did ferrets immunized with an attenuated CDV vaccine (0.46 ± 0.59;n = 7) or the recombinant vectors expressing rabies glycoprotein (RG) (0.19 ± 0.32; n = 8,P = 7 × 10−6). The NYVAC vaccine also protected against weight loss, and both the NYVAC and attenuated CDV vaccines protected against the development of some clinical signs of infection, although survival in each of the three vaccine groups was low (one of seven) and not significantly different from the RG controls (none of eight). Combined i.n.-parenteral immunization of ferrets with maternal antibody using NYVAC-HF (n = 9) produced higher titers (1.63 ± 0.25) than did i.n. immunization with NYVAC-HF (0.88 ± 0.36; n = 9) and ALVAC-HF (0.61 ± 0.43; n = 9, P = 3 × 10−7), and survival was also significantly better in the i.n.-parenteral group (3 of 9) than in the other HF-vaccinated animals (none of 18) or in controls immunized with RG (none of 5) (P = 0.0374). Multiple routes were not tested with the ALVAC vaccine. The results suggest that infant ferrets are less responsive to i.n. vaccination than are older ferrets and raises questions about the appropriateness of this route of immunization in infant ferrets or infants of other species.

scholarly journals Bullous Pemphigoid in a Dog

2021 ◽  
Vol 49 ◽  
Author(s):  
Suélen Dalegrave ◽  
Denner Francisco Tomadon Fiorin ◽  
Eduarda Gabriela Mansour ◽  
Monica Regina De Matos ◽  
Renato Herdina Erdmann ◽  
...  
Keyword(s):  
Bullous Pemphigoid ◽  
Plasma Cells ◽  
Histopathological Examination ◽  
Clinical Signs ◽  
Clinical Manifestations ◽  
Punch Biopsy ◽  
Mucous Membrane Pemphigoid ◽  
Histopathological Analysis ◽  
Biopsy Material ◽  
Clinicopathological Findings

Background: In dogs, bullous pemphigoid (BP) is a subepithelial autoimmune disease, a rare dermatopathy in the clinical routine. BP is characterized by formation of vesicles and subepidermal blisters that result from dissolution of the dermal-epithelial junction. Clinical signs of BP usually include severe dermatological alterations with a variable prognosis. The aim of this work is to report a case of BP in a dog to contribute information for diagnosis, and to present clinical and pathological aspects that emerge during development of BP.Case: An adult male mongrel dog exhibited hyperemic, exudative, crusty lesions on the lip commissure and periocular areas. Results from laboratory tests were normal. Results from parasitological and mycological tests on skin scrapings were negative. Imprint cytology of the crusts revealed presence of gram-positive cocci bacteria. In the histopathological analysis of punch biopsy material, the epidermis was detached from the dermis, leading to formation of vesicles. There were inflammatory infiltrates containing neutrophils, eosinophils, and high amounts of fibrin, and areas of multifocal orthokeratotic hyperkeratosis. Multifocal infiltrates containing lymphocytes, histiocytes, and plasma cells were observed on the superficial portions of the dermis, which indicated a diagnosis of BP. After the definitive clinical diagnosis, the animal was treated with enrofloxacin (Baytril Flavour®; 5 mg/kg once a day for 10 days), and prednisolone (Prediderm®; 2 mg/kg once a day until further instructions). On the follow-up visit, 15 days later, the clinical picture had improved, and the lesions had decreased. Continuity of the treatment was prescribed, along with a gradual decrease in the corticoid dose. The dose of prednisolone was initially reduced to 1 mg/kg once a day, and later to 0.5 mg/kg until improvement of the clinical status of the patient. Remission of the lesions was observed 13 weeks later.Discussion: The diagnosis of BP was established after identification of the clinical cutaneous lesions and observation of microscopic findings on punch biopsy material obtained from the ocular and lip regions. BP does not exhibit breed or sex predisposition, and affects adult dogs. The clinical signs of BP are characteristic of autoimmune diseases that affect the dermoepidermal junction, and consist of erythematous, ulcerated, crusty, and painful lesions on the nose, dorsal area of the muzzle, and periorbital region. However, these lesions must be differentiated, by histological analysis, from several other conditions with a similar clinical presentation. Diseases that must be considered in the differential diagnosis comprise other variants of the pemphigus complex, lupus erythematosus, drug eruption, erythema multiforme, toxic epidermal necrolysis, epitheliotropic lymphoma, inherited bullous epidermolysis, mucous membrane pemphigoid, and lymphoreticular neoplasia. The clinicopathological findings indicated that the lesions were compatible with BP. The occurrence of necrotic and erythematous lesions is due to production of antibodies accompanied by a strong response of neutrophils, which results in loss of cell adhesion and epidermal necrosis. The presence of detachment of the epidermis from the dermis, inflammation in the superficial portion of the dermis, and infiltrates containing lymphocytes, histiocytes and plasma cells observed at the histopathological examination indicated the occurrence of BP. The skin histopathological examination warranted establishment of a diagnosis and therapeutic success. The lack of recurrence of clinical manifestations 43 weeks after the end of the glucocorticoid treatment demonstrated that the therapeutic approach and the cooperation of the owner are essential for success of the treatment.

scholarly journals Disease Duration Determines Canine Distemper Virus Neurovirulence

2007 ◽  
Vol 81 (21) ◽  
pp. 12066-12070 ◽  
Author(s):  
François Bonami ◽  
Penny A. Rudd ◽  
Veronika von Messling
Keyword(s):  
Canine Distemper Virus ◽  
Disease Duration ◽  
Subsequent Development ◽  
Neurological Involvement ◽  
Disease Course ◽  
Canine Distemper ◽  
Wild Type ◽  
Neurological Signs ◽  
H Protein ◽  
Type Strains

ABSTRACT The Morbillivirus hemagglutinin (H) protein mediates attachment to the target cell. To evaluate its contribution to canine distemper virus neurovirulence, we exchanged the H proteins of the wild-type strains 5804P and A75 and assessed the pathogenesis of the chimeric viruses in ferrets. Both strains are lethal to ferrets; however, 5804P causes a 2-week disease without neurological signs, whereas A75 is associated with a longer disease course and neurological involvement. We observed that both H proteins supported neuroinvasion and the subsequent development of clinical neurological signs if given enough time, demonstrating that disease duration is the main neurovirulence determinant.

scholarly journals Natural Canine Distemper Virus Infection in Linnaeus’s 2-Toed Sloths (Choloepus didactylus)

2020 ◽  
Vol 57 (2) ◽  
pp. 311-315 ◽  
Author(s):  
Allison M. Watson ◽  
Andrew C. Cushing ◽  
Julie D. Sheldon ◽  
Eman Anis ◽  
Rebecca P. Wilkes ◽  
...  
Keyword(s):  
Virus Infection ◽  
Canine Distemper Virus ◽  
Clinical Signs ◽  
Hepatic Necrosis ◽  
Nasal Discharge ◽  
The Novel ◽  
Canine Distemper ◽  
The Central Nervous System ◽  
Lymphoid Depletion ◽  
Viral Sequencing

An outbreak of canine distemper virus in a private zoo in eastern Tennessee in July 2016 led to fatal clinical disease in 5 adult, wild-caught Linnaeus’s 2-toed sloths ( Choloepus didactylus). Clinical signs included hyporexia, lethargy, mucopurulent nasal discharge, and oral and facial ulcers. At necropsy, affected animals had crusts and ulcers on the lips, nose, tongue, and oral cavity. Microscopically, all sloths had widespread, random, hepatic necrosis; lymphoid depletion; and bronchointerstitial pneumonia. The central nervous system did not contain gross or histopathologic lesions in any of the 5 sloths, although immunoreactivity for viral antigen was present within vessel walls. Epithelial cells and histiocytes within numerous organs contained intranuclear and intracytoplasmic inclusions and occasional syncytial cells. Canine distemper virus was confirmed with immunohistochemistry and virus isolation. Viral sequencing identified the novel American-4 strain prevalent in eastern Tennessee wildlife. This is the first pathologic characterization of canine distemper virus infection in sloths (family Choloepodidae, order Pilosa) and emphasizes the significant morbidity and mortality in this species.

scholarly journals Canine Distemper Virus Antigen Detection in External Epithelia of Recently Vaccinated, Sick Dogs by Fluorescence Microscopy Is a Valuable Prognostic Indicator: TABLE 1

2014 ◽  
Vol 53 (2) ◽  
pp. 687-691 ◽  
Author(s):  
Sanjay Kapil ◽  
Tina Neel
Keyword(s):  
Clinical Outcomes ◽  
Respiratory Disease ◽  
Canine Distemper Virus ◽  
Fluorescent Antibody ◽  
Clinical Signs ◽  
Antibody Test ◽  
Prognostic Indicator ◽  
Symptomatic Therapy ◽  
Canine Distemper ◽  
Clinical Recovery

Currently, there are no reliable predictors of the clinical outcomes of domesticated dogs that have been recently vaccinated against canine distemper virus (CDV) and develop respiratory disease. In this study, vaccinated dogs from Oklahoma City that were showing clinical signs of respiratory disease were evaluated for CDV antigen using a direct fluorescent antibody test (FAT). Clinical outcomes after standard symptomatic therapy for respiratory disease were recorded, and a statistical analysis of the results was performed. We present our study showing that CDV FAT results were predictive of clinical recovery (prognostic indicator, prospects of clinical recovery) among vaccinated dogs showing clinical signs of respiratory disease. Negative CDV FAT results equated to 80% chances of recovery after symptomatic therapy, compared to 55% chances of recovery when the CDV FAT results were positive. Based on the results of this study, we show that veterinarians can make better informed decisions about the clinical outcomes of suspected CDV cases, with 2-h turnaround times, by using the CDV FAT. Thus, antemortem examination with the CDV FAT on external epithelia of recently vaccinated, sick dogs is a clinically useful diagnostic test and valuable prognostic indicator for veterinarians. Application of the CDV FAT to these samples avoids unnecessary euthanasia of dogs with suspected CDV.

scholarly journals SLAM- and Nectin-4-Independent Noncytolytic Spread of Canine Distemper Virus in Astrocytes

2015 ◽  
Vol 89 (10) ◽  
pp. 5724-5733 ◽  
Author(s):  
Lisa Alves ◽  
Mojtaba Khosravi ◽  
Mislay Avila ◽  
Nadine Ader-Ebert ◽  
Fanny Bringolf ◽  
...  
Keyword(s):  
Glial Cells ◽  
Measles Virus ◽  
Canine Distemper Virus ◽  
Morphological Evidence ◽  
Target Cells ◽  
Viral Fusion ◽  
Canine Distemper ◽  
Persistent Infections ◽  
Demyelinating Lesions ◽  
The Brain

ABSTRACTMeasles and canine distemper viruses (MeV and CDV, respectively) first replicate in lymphatic and epithelial tissues by using SLAM and nectin-4 as entry receptors, respectively. The viruses may also invade the brain to establish persistent infections, triggering fatal complications, such as subacute sclerosis pan-encephalitis (SSPE) in MeV infection or chronic, multiple sclerosis-like, multifocal demyelinating lesions in the case of CDV infection. In both diseases, persistence is mediated by viral nucleocapsids that do not require packaging into particles for infectivity but are directly transmitted from cell to cell (neurons in SSPE or astrocytes in distemper encephalitis), presumably by relying on restricted microfusion events. Indeed, although morphological evidence of fusion remained undetectable, viral fusion machineries and, thus, a putative cellular receptor, were shown to contribute to persistent infections. Here, we first showed that nectin-4-dependent cell-cell fusion in Vero cells, triggered by a demyelinating CDV strain, remained extremely limited, thereby supporting a potential role of nectin-4 in mediating persistent infections in astrocytes. However, nectin-4 could not be detected in either primary cultured astrocytes or the white matter of tissue sections. In addition, a bioengineered “nectin-4-blind” recombinant CDV retained full cell-to-cell transmission efficacy in primary astrocytes. Combined with our previous report demonstrating the absence of SLAM expression in astrocytes, these findings are suggestive for the existence of a hitherto unrecognized third CDV receptor expressed by glial cells that contributes to the induction of noncytolytic cell-to-cell viral transmission in astrocytes.IMPORTANCEWhile persistent measles virus (MeV) infection induces SSPE in humans, persistent canine distemper virus (CDV) infection causes chronic progressive or relapsing demyelination in carnivores. Common to both central nervous system (CNS) infections is that persistence is based on noncytolytic cell-to-cell spread, which, in the case of CDV, was demonstrated to rely on functional membrane fusion machinery complexes. This inferred a mechanism where nucleocapsids are transmitted through macroscopically invisible microfusion events between infected and target cells. Here, we provide evidence that CDV induces such microfusions in a SLAM- and nectin-4-independent manner, thereby strongly suggesting the existence of a third receptor expressed in glial cells (referred to as GliaR). We propose that GliaR governs intercellular transfer of nucleocapsids and hence contributes to viral persistence in the brain and ensuing demyelinating lesions.

scholarly journals Alteration of the Leptin Network in Late Morbid Obesity Induced in Mice by Brain Infection with Canine Distemper Virus

1999 ◽  
Vol 73 (9) ◽  
pp. 7317-7327 ◽  
Author(s):  
Arlette Bernard ◽  
Richard Cohen ◽  
Seng-Thuon Khuth ◽  
Bruno Vedrine ◽  
Olivier Verlaeten ◽  
...  
Keyword(s):  
Canine Distemper Virus ◽  
Leptin Receptor ◽  
Motor Impairment ◽  
Brain Structures ◽  
Receptor Expression ◽  
Leptin Resistance ◽  
Obese Mice ◽  
Canine Distemper ◽  
New Paradigm ◽  
The Brain

ABSTRACT Viruses can induce progressive neurologic disorders associated with diverse pathological manifestations, and therefore, viral infection of the brain can impair differentiated neural functions, depending on the initial viral tropism. We have previously reported that canine distemper virus (CDV) targets certain mouse brain structures, including the hypothalamus, early and selectively. Infected mice exhibit acute encephalitis, with late disease, characterized by motor impairment or obesity syndrome, appearing in some of the surviving mice several months after the initial viral replication. In the present study, we show viral persistence in the hypothalami of obese mice, as demonstrated by low, but still significant, levels of CDV nucleoprotein transcripts, associated with a dramatic decrease in F gene mRNAs. Given the pivotal role of the hypothalamus in obesity (eating behavior, energy consumption, and neuroendocrine function) and that of leptin, the adipose tissue-derived satiety factor acting through hypothalamic receptors, we analyzed the leptin networks in both obese and nonobese mice. The discrepancy found between the chronic and dramatic increase in blood leptin levels and the occurrence of obesity may be due to leptin resistance in the brain. In fact, expression of the long leptin receptor isoform, representing the functional leptin receptor, was specifically downregulated in the hypothalami of obese mice, explaining their inability to generate an adequate response to leptin in the brain. Intriguingly, during the acute phase of infection, its expression was increased in CDV-targeted structures in all infected mice and remained high in obese mice in all CDV-targeted structures, except for the hypothalamus. The biphasic change in hypothalamic leptin receptor expression seen during the progression of CDV-induced obesity provides a new paradigm for understanding mechanisms of neuroendocrinological, virus-induced abnormalities.

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