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

Abstract 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.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title plos one
Publication Year Start




PMID- 28419136
OWN - NLM
STAT- In-Process
DA  - 20170418
LR  - 20170418
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 4
DP  - 2017
TI  - Occurrence of Leishmania infantum in the central nervous system of naturally
      infected dogs: Parasite load, viability, co-infections and histological
      alterations.
PG  - e0175588
LID - 10.1371/journal.pone.0175588 [doi]
AB  - 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.
FAU - Oliveira, Valeria da Costa
AU  - Oliveira VDC
AD  - Laboratorio de Pesquisa Clinica em Dermatozoonoses em Animais Domesticos,
      Instituto Nacional de Infectologia Evandro Chagas, Fundacao Oswaldo Cruz, Rio de 
      Janeiro, Brazil.
FAU - Boechat, Viviane Cardoso
AU  - Boechat VC
AD  - Laboratorio de Pesquisa Clinica em Dermatozoonoses em Animais Domesticos,
      Instituto Nacional de Infectologia Evandro Chagas, Fundacao Oswaldo Cruz, Rio de 
      Janeiro, Brazil.
FAU - Mendes Junior, Artur Augusto Velho
AU  - Mendes Junior AAV
AD  - Laboratorio de Pesquisa Clinica em Dermatozoonoses em Animais Domesticos,
      Instituto Nacional de Infectologia Evandro Chagas, Fundacao Oswaldo Cruz, Rio de 
      Janeiro, Brazil.
FAU - Madeira, Maria de Fatima
AU  - Madeira MF
AD  - Laboratorio de Vigilancia em Leishmanioses, Instituto Nacional de Infectologia
      Evandro Chagas, Fundacao Oswaldo Cruz, Rio de Janeiro, Brazil.
FAU - Ferreira, Luiz Claudio
AU  - Ferreira LC
AD  - Servico de Anatomia Patologica, Instituto Nacional de Infectologia Evandro
      Chagas, Fundacao Oswaldo Cruz, Rio de Janeiro, Brazil.
FAU - Figueiredo, Fabiano Borges
AU  - Figueiredo FB
AD  - Laboratorio de Biologia Celular, Instituto Carlos Chagas, Fundacao Oswaldo Cruz, 
      Parana, Brazil.
FAU - Campos, Monique Paiva
AU  - Campos MP
AD  - Laboratorio de Pesquisa Clinica em Dermatozoonoses em Animais Domesticos,
      Instituto Nacional de Infectologia Evandro Chagas, Fundacao Oswaldo Cruz, Rio de 
      Janeiro, Brazil.
FAU - de Carvalho Rodrigues, Francisco das Chagas
AU  - de Carvalho Rodrigues FDC
AD  - Servico de Anatomia Patologica, Instituto Nacional de Infectologia Evandro
      Chagas, Fundacao Oswaldo Cruz, Rio de Janeiro, Brazil.
FAU - Carvalhaes de Oliveira, Raquel de Vasconcellos
AU  - Carvalhaes de Oliveira RV
AD  - Laboratorio de Epidemiologia Clinica, Instituto Nacional de Infectologia Evandro 
      Chagas, Fundacao Oswaldo Cruz, Rio de Janeiro, Brazil.
FAU - Amendoeira, Maria Regina Reis
AU  - Amendoeira MRR
AD  - Laboratorio de Toxoplasmose, Instituto Oswaldo Cruz, Fundacao Oswaldo Cruz, Rio
      de Janeiro, Brazil.
FAU - Menezes, Rodrigo Caldas
AU  - Menezes RC
AUID- ORCID: http://orcid.org/0000-0003-1853-3449
AD  - Laboratorio de Pesquisa Clinica em Dermatozoonoses em Animais Domesticos,
      Instituto Nacional de Infectologia Evandro Chagas, Fundacao Oswaldo Cruz, Rio de 
      Janeiro, Brazil.
LA  - eng
PT  - Journal Article
DEP - 20170418
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
EDAT- 2017/04/19 06:00
MHDA- 2017/04/19 06:00
CRDT- 2017/04/19 06:00
PHST- 2016/10/20 [received]
PHST- 2017/03/28 [accepted]
AID - 10.1371/journal.pone.0175588 [doi]
AID - PONE-D-16-38877 [pii]
PST - epublish
SO  - PLoS One. 2017 Apr 18;12(4):e0175588. doi: 10.1371/journal.pone.0175588.
      eCollection 2017.

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