Neurological disease in human and canine leishmaniasis – clinical features and immunopathogenesis

Maia, Cristiane do Socorro Ferraz; Monteiro, Marta Chagas; Gavioli, Elaine C.; Oliveira, Fátima de Cássia Evangelista de; Oliveira, Gislaine B.; Romão, Pedro Roosevelt Torres

doi:10.1111/pim.12203

Cited by 19 publications

(10 citation statements)

References 65 publications

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“…However, the sensitivity and specificity of the DPP ® assay were lower than those observed for serum samples of naturally infected dogs (83% and 73%, respectively) [37]. The detection of antibodies in CSF indicates disruption of the blood-brain barrier or blood-CSF barrier [38]. …”

Section: Discussionmentioning

confidence: 99%

Occurrence of Leishmania infantum in the central nervous system of naturally infected dogs: Parasite load, viability, co-infections and histological alterations

et al. 2017

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Zoonotic visceral leishmaniasis is caused by the protozoan Leishmania infantum and little is known about the occurrence and pathogenesis of this parasite in the CNS. The aims of this study were to evaluate the occurrence, viability and load of L. infantum in the CNS, and to identify the neurological histological alterations associated with this protozoan and its co-infections in naturally infected dogs. Forty-eight Leishmania-seropositive dogs from which L. infantum was isolated after necropsy were examined. Cerebrospinal fluid (CSF) samples were analyzed by parasitological culture, quantitative real-time PCR (qPCR) and the rapid immunochromatographic Dual Path Platform test. Brain, spinal cord and spleen samples were submitted to parasitological culture, qPCR, and histological techniques. Additionally, anti-Toxoplasma gondii and anti-Ehrlichia canis antibodies in serum and distemper virus antigens in CSF were investigated. None of the dogs showed neurological signs. All dogs tested positive for L. infantum in the CNS. Viable forms of L. infantum were isolated from CSF, brain and spinal cord in 25% of the dogs. Anti-L. infantum antibodies were detected in CSF in 61% of 36 dogs. Inflammatory histological alterations were observed in the CNS of 31% of the animals; of these, 66% were seropositive for E. canis and/or T. gondii. Amastigote forms were associated with granulomatous non-suppurative encephalomyelitis in a dog without evidence of co-infections. The highest frequency of L. infantum DNA was observed in the brain (98%), followed by the spinal cord (96%), spleen (95%), and CSF (50%). The highest L. infantum load in CNS was found in the spinal cord. These results demonstrate that L. infantum can cross the blood-brain barrier, spread through CSF, and cause active infection in the entire CNS of dogs. Additionally, L. infantum can cause inflammation in the CNS that can lead to neurological signs with progression of the disease.

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Section: Discussionmentioning

confidence: 99%

Occurrence of Leishmania infantum in the central nervous system of naturally infected dogs: Parasite load, viability, co-infections and histological alterations

et al. 2017

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“…NS involvement during Leishmania infections is rare both in humans and dogs (Solano‐Gallego et al , Maia et al ) (Table ). In a recent report, neurological manifestations during leishmaniasis were considered “poorly documented, possibly underestimated and almost unknown by physicians and veterinarians” (Maia et al ). Data concerning the prevalence of neurological signs in infected dogs are scarce.…”

Section: Discussionmentioning

confidence: 99%

Neurological manifestations in dogs naturally infected by Leishmania infantum: descriptions of 10 cases and a review of the literature

Giannuzzi¹,

Ricciardi²,

Simone³

et al. 2017

J of Small Animal Practice

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In order to evaluate possible nervous system involvement in canine leishmaniasis, retrospective evaluation of all medical records of leishmaniotic dogs exhibiting neurological signs referred to our hospital over a 5-year period was performed. The records of 10 dogs were reviewed. Depending on the neuroanatomical localisation, the dogs underwent advanced diagnostic imaging, cerebrospinal fluid analysis, electrodiagnostic testing and histopathologic evaluations. The final neurological diagnosis was: meningoencephalitis (n=2), brain haemorrhagic stroke (n=1), haemorrhagic choroiditis (n=1), meningomyelitis (n=2), ischaemic myelopathy (n=1), polymyositis (n=2) and peripheral neuropathy (n=1). This study confirms that both central and peripheral nervous systems can be affected by leishmaniasis and provides an overview on the possible etiopathogenetic mechanisms. In addition, clinical and diagnostic findings, therapy and follow-up of affected dogs are described.

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“…The trypanosome Leishmania amazonensis is another parasite that can live in the brain of vertebrates (including humans) and has been associated with behavioral changes in its host (Petersen and Greenlee, 2011;Maia et al, 2015). Recently a study found that experimentally infected mice consistently had several key cytokines (IFN-y, IL-1,4,6,10) down regulated, while tumor necrosis factor alpha (TNF-α) was upregulated in the prefrontal cortex (Portes et al, 2016).…”

Section: Immunological Host Manipulation Immunological Manipulation Omentioning

confidence: 99%

Lessons in Mind Control: Trends in Research on the Molecular Mechanisms behind Parasite-Host Behavioral Manipulation

Herbison

2017

Front. Ecol. Evol.

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Scientific and public interest in host manipulation by parasites has surged over the past few decades, resulting in an exponential growth of cases where potential behavioral manipulation has been identified. However, these studies dwarf the number of genuine attempts to elucidate the mechanistic processes behind this behavioral manipulation. Ultimately, this imbalance has slowed progress in the study of the mechanisms underlying host manipulation. As it stands, research suggests that the mechanisms of host manipulation fall into three categories: immunological, genomic/proteomic and neuropharmacological, and forth potential category: symbioant-mediated manipulation. After exploration of the literature pertaining to these four pathways, four major trends become evident. First and foremost, there is a severe disconnect between the observed molecular and behavioral shifts in a parasitized host. Indeed, very rarely a study demonstrates that molecular changes observed in a host are the result of active manipulation by the resident parasite, or that these molecular changes directly result in behavioral manipulation that increases the parasite's fitness. Secondly, parasites may often employ multiple pathways in unison to achieve control over their hosts. Despite this, current scientific approaches usually focus on each manipulation pathway in isolation rather than integrating them. Thirdly, the relative amount of host-parasite systems yet to be investigated in terms of molecular manipulation is staggering. Finally, as a result of the aforementioned trends, guiding mechanisms or principles for the multiple types of behavioral manipulation are yet to be found. Researchers should look to identify the manipulative factors required to generate the molecular changes seen in hosts, while also considering the "multi-pronged" approach parasites are taking to manipulate behavior. Assessing gene expression and its products during transitional periods in parasites may be a key methodological approach for tackling these recent trends in the host manipulation literature.

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Neurological disease in human and canine leishmaniasis – clinical features and immunopathogenesis

Cited by 19 publications

References 65 publications

Occurrence of Leishmania infantum in the central nervous system of naturally infected dogs: Parasite load, viability, co-infections and histological alterations

Occurrence of Leishmania infantum in the central nervous system of naturally infected dogs: Parasite load, viability, co-infections and histological alterations

Neurological manifestations in dogs naturally infected by Leishmania infantum: descriptions of 10 cases and a review of the literature

Lessons in Mind Control: Trends in Research on the Molecular Mechanisms behind Parasite-Host Behavioral Manipulation

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