scholarly journals Temporal Distribution and Parasite Load Kinetics in Blood and Tissues during Neospora caninum Infection in Mice

2006 ◽  
Vol 74 (4) ◽  
pp. 2491-2494 ◽  
Author(s):  
Esther Collantes-Fernández ◽  
Inmaculada López-Pérez ◽  
Gema Álvarez-García ◽  
Luis M. Ortega-Mora
Keyword(s):  
Acute Phase ◽  
Neospora Caninum ◽  
Clinical Signs ◽  
Chronic Phase ◽  
Temporal Distribution ◽  
Parasite Load ◽  
Caninum Infection ◽  
Kinetics Of ◽  
The Brain

ABSTRACT The kinetics of Neospora caninum loads in mice inoculated with NC-Liv or NC-1 isolates were studied. The acute phase was characterized by parasitemia and the detection of parasite DNA in several organs, whereas during the chronic phase, the parasite was detected mainly in the brain. Mice infected with NC-Liv developed clinical signs, showing higher brain parasite burdens than NC-1-infected mice.

Stage-specific expression of NcSAG4 as a marker of chronic Neospora caninum infection in a mouse model

Parasitology ◽  
2009 ◽  
Vol 136 (7) ◽  
pp. 757-764 ◽  
Author(s):  
A. AGUADO-MARTÍNEZ ◽  
L. M. ORTEGA-MORA ◽  
G. ÁLVAREZ-GARCÍA ◽  
S. RODRÍGUEZ-MARCO ◽  
V. RISCO-CASTILLO ◽  
...  
Keyword(s):  
Chronic Infection ◽  
Messenger Rna ◽  
Neospora Caninum ◽  
Expression Patterns ◽  
Chronic Phase ◽  
Chemotherapeutic Agents ◽  
Specific Gene ◽  
Mrna Levels ◽  
Caninum Infection ◽  
The Brain

SUMMARYNeospora caninum infection persists throughout the life of its intermediate host due to the conversion of tachyzoites to slowly dividing bradyzoites that encyst in the brain. This event results in persistent N. caninum infection in bovine herds and partially explains the poor efficacy of many chemotherapeutic agents and vaccine formulations. Thus, there is a need for greater understanding of the tachyzoite-to-bradyzoite conversion mechanisms. Here we studied for the first time the transcription kinetics of the N. caninum bradyzoite-specific gene NcSAG4 in brain samples from chronically infected mice by means of real-time RT-PCR. NcSAG4-messenger RNA (mRNA) levels increased significantly during the chronic phase but followed 2 different expression patterns depending on the isolate used for murine inoculation. NcSAG4-mRNA levels in brains from Nc-1-inoculated mice peaked during late chronic infection (on day 64 post-infection, p.i.), whereas those from Nc-Liv-inoculated mice peaked earlier during the chronic infection (on day 32 p.i.). This difference could be a reflection of the different abilities of these isolates to replicate and form cysts in parasitized brains. These results are consistent with our observations of anti-rNcSAG4 antibody production; low levels were present at seroconversion and slowly increased during the chronic phase. In contrast, NcSAG1 transcription levels, which mark the tachyzoite stage, were maintained without variation in both groups of mice. This suggests the presence of a significant amount of tachyzoites or intermediate zoites expressing NcSAG1 in the brain, even during the late chronic infection.

scholarly journals CHARACTERIZATION OF PATHOLOGY AND PARASITE LOAD IN OUTBRED AND INBRED MOUSE MODELS OF CHRONIC NEOSPORA CANINUM INFECTION

2004 ◽  
Vol 90 (3) ◽  
pp. 579-583 ◽  
Author(s):  
Esther Collantes-Fernández ◽  
Gema Álvarez-García ◽  
Valentín Pérez-Pérez ◽  
Juana Pereira-Bueno ◽  
Luis Miguel Ortega-Mora
Keyword(s):  
Mouse Models ◽  
Neospora Caninum ◽  
Inbred Mouse ◽  
Parasite Load ◽  
Caninum Infection

scholarly journals Evaluation of clinical signs, parasitemia, hematologic and biochemical changes in cattle experimentally infected with Trypanosoma vivax

2016 ◽  
Vol 25 (1) ◽  
pp. 69-81 ◽  
Author(s):  
Otavio Luiz Fidelis Junior ◽  
Paulo Henrique Sampaio ◽  
Rosangela Zacarias Machado ◽  
Marcos Rogério André ◽  
Luiz Carlos Marques ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Acute Phase ◽  
Blood Cells ◽  
White Blood Cells ◽  
Clinical Signs ◽  
Chronic Phase ◽  
Diagnostic Value ◽  
Biochemical Changes ◽  
Severe Neutropenia ◽  
Trypanosoma Vivax

Abstract Infections by Trypanosoma vivax cause great losses to livestock in Africa and Central and South Americas. Outbreaks due this parasite have been occurred with increasing frequency in Brazil. Knowledge of changes caused byT. vivax during the course of this disease can be of great diagnostic value. Thus, clinical signs, parasitemia, hematologic and biochemical changes of cattle experimentally infected by this hemoparasite were evaluated. Two distinct phases were verified during the infection – an acute phase where circulating parasites were seen and then a chronic phase where fluctuations in parasitemia were detected including aparasitemic periods. A constant reduction in erythrocytes, hemoglobin and packed cell volume (PVC) were observed. White blood cells (WBC) showed pronounced changes such as severe neutropenia and lymphopenia during the acute phase of the illness. Decreases in cholesterol, albumin, aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and increases in glucose, globulin, protein, and alkaline phosphatase (ALP) were observed. The “Lins” isolate of T. vivax showed pathogenicity for cattle, and intense parasitemia was detected in the early stages of infection. Circulating parasites were detected for about two months. The most evident laboratory abnormalities were found in WBC parameters, including thrombocytopenia.

scholarly journals Influence of Acute-Phase Parasite Load on Pathology, Parasitism, and Activation of the Immune System at the Late Chronic Phase of Chagas’ Disease

1999 ◽  
Vol 67 (1) ◽  
pp. 308-318 ◽  
Author(s):  
Claudio R. F. Marinho ◽  
Maria Regina D’Império Lima ◽  
Marcos G. Grisotto ◽  
José M. Alvarez
Keyword(s):  
Immune System ◽  
Chagas Disease ◽  
Acute Phase ◽  
Serum Antibody ◽  
Chronic Phase ◽  
Parasite Load ◽  
Interleukin 4 ◽  
High Dose ◽  
Macrophage Phenotype ◽  
High Parasite

ABSTRACT To obtain low and high parasite loads in the acute phase of Chagas’ disease, A/J mice were infected with 103 or 105 Trypanosoma cruzi trypomastigotes of the Y strain and treated on day 6 with benznidazol. One year later, chronically infected mice were screened for subpatent parasitemias, tissue pathology, and immune response. Mice infected with the high parasite inoculum showed higher levels of chronic parasitemias, heart and striated muscle inflammation, and activation of the immune system than did mice infected with the low inoculum. Concerning the activation of the immune system, the main findings for high-dose-infected mice were (i) increased numbers of splenocytes, with preferential expansion of CD8+ and B220− CD5− cells, many of them bearing a macrophage phenotype; (ii) higher frequencies of B (B220+), CD4+, and CD8+ large lymphocytes; (iii) a shift of CD4+ cells towards a CD45RBLow phenotype; (iv) increased frequencies of both CD45RBLow and CD45RBHigh large CD4+cells; (v) augmented numbers of total immunoglobulin (Ig)-secreting cells, with predominance of IgG2a-producing cells; and (vi) increased production of gamma interferon and interleukin 4. In addition, these mice presented lower IgM and higher IgG2a and IgG1 parasite-specific serum antibody levels. Our results indicate that the parasite load at the acute phase of T. cruzi infection influences the activation of the immune system and development of Chagas’ disease pathology at the late chronic phase of the disease.

RecNcMIC3-1-R is a microneme- and rhoptry-based chimeric antigen that protects against acute neosporosis and limits cerebral parasite load in the mouse model for Neospora caninum infection

Vaccine ◽  
2011 ◽  
Vol 29 (40) ◽  
pp. 6967-6975 ◽  
Author(s):  
Thierry Monney ◽  
David Rütti ◽  
Michelle Schorer ◽  
Karim Debache ◽  
Denis Grandgirard ◽  
...  
Keyword(s):  
Mouse Model ◽  
Neospora Caninum ◽  
Parasite Load ◽  
Caninum Infection

scholarly journals Microneme Protein 6 Is Involved in Invasion and Egress by Neospora caninum

Pathogens ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 201
Author(s):  
Xianmei Wang ◽  
Di Tang ◽  
Fei Wang ◽  
Gaowei Jin ◽  
Lifang Wang ◽  
...  
Keyword(s):  
Neospora Caninum ◽  
Parasite Load ◽  
Host Cells ◽  
Host Cell Invasion ◽  
Caninum Infection ◽  
Apicomplexan Parasites ◽  
Key Steps ◽  
Microneme Protein ◽  
Adhesion And Invasion ◽  
Microneme Proteins

Background: Neospora caninum, is the etiological agent of neosporosis, an infection that causes abortions in cattle and nervous system dysfunction in dogs. Invasion and egress are the key steps of the pathogenesis of N. caninum infection. Microneme proteins (MICs) play important roles in the recognition, adhesion, and invasion of host cells in other apicomplexan parasites. However, some MICs and their functions in N. caninum infection have rarely been reported. Methods: The homologous recombination strategy was used to investigate the function of MIC6 in N. caninum infection. Results: ΔNcMIC6 showed a smaller plaque size and weakened capacities of invasion and egress than Nc1. Transcription levels of the egress-related genes CDPK1, PLP1, and AMA1 of ΔNcMIC6 were downregulated. Due to the lack of NcMIC6, virulence of the pathogen in the infected mouse was weakened. The subcellular localization of NcMIC1 and NcMIC4 in ΔNcMIC6, however, did not change. Nevertheless, the transcription levels of MIC1 and MIC4 in ΔNcMIC6 were downregulated, and the expression and secretion of MIC1 and MIC4 in ΔNcMIC6 were reduced compared with that in Nc1. Furthermore, the absence of NcMIC6 weakened the virulence in mice and lower parasite load detected in mice brains. Conclusions: NcMIC6 is involved in host cell invasion and egress in N. caninum and may work synergistically with other MICs to regulate the virulence of the pathogen. These data lay a foundation for further research into the function and application of NcMIC6.

Trigeminal Neuropathy in Dogs: A Retrospective Study of 29 Cases (1991–2000)

2002 ◽  
Vol 38 (3) ◽  
pp. 262-270 ◽  
Author(s):  
Philipp D. Mayhew ◽  
William W. Bush ◽  
Eric N. Glass
Keyword(s):  
Neospora Caninum ◽  
Clinical Signs ◽  
Unknown Origin ◽  
Sensory Innervation ◽  
Caninum Infection ◽  
Trigeminal Neuropathy ◽  
Fluid Analysis ◽  
Mean Time ◽  
Muscles Of Mastication

The medical records of 29 dogs unable to close their mouths due to flaccid paralysis or paresis of the muscles innervated by the mandibular branch of the trigeminal nerve, were reviewed. Idiopathic trigeminal neuropathy was diagnosed in 26 dogs based on complete resolution of clinical signs and lack of any long-term neurological disease. Of these dogs, golden retrievers were over-represented. No age, sex, or seasonal predispositions were identified. Trigeminal sensory innervation deficits were observed in 35% (9/26), facial nerve deficits were observed in 8% (2/26), and Horner’s syndrome was observed in 8% (2/26) of dogs. Electromyographic examination of the muscles of mastication revealed abnormalities in seven of nine dogs. Results of cerebrospinal fluid analysis were abnormal in seven of eight dogs. Corticosteroid therapy did not affect the clinical course of the disease. Mean time to recovery was 22 days. Lymphosarcoma, Neospora caninum infection, and severe polyneuritis of unknown origin were diagnosed in three of 29 dogs at necropsy.

Pathological and immunological findings in placentas from pregnant BALB/c mice infected with Neospora caninum at early and late stages of gestation

2011 ◽  
Vol 56 (3) ◽  
Author(s):  
Inmaculada López-Pérez ◽  
Esther Collantes-Fernández ◽  
Silvia Rojo-Montejo ◽  
Vanesa Navarro-Lozano ◽  
Verónica Risco-Castillo ◽  
...  
Keyword(s):  
Neospora Caninum ◽  
Placental Tissue ◽  
Parasite Load ◽  
Late Gestation ◽  
Histopathological Analysis ◽  
Caninum Infection ◽  
Tnf Α ◽  
Ifn Γ ◽  
Late Stages

AbstractNeospora caninum is transmitted from a cow to its foetus by vertical transmission and the timing of infection in gestation is an important factor in determining the disease outcome. Few studies have explored the role of the placenta in the outcome of N. caninum infection during pregnancy. Here, we described the N. caninum presence, parasite load, local immune response, and histopathological lesions at the materno-foetal interface after infection of BALB/c mice at early and late stages of gestation. In mice infected at early gestation, N. caninum DNA was detected in foetoplacentary units 7 days post-infection (PI) and in the placenta, but not in viable foetuses on day 14 PI, indicating that the parasite was multiplying primarily in the placental tissues without reaching the foetus. Moreover, parasite DNA was detected in resorptions, suggesting that foetal death could be a consequence of infection. An increase in IFN-γ, TNF-α and IL-10 expression was observed in N. caninum PCR-positive placentas, which could favour N. caninum foetal transmission and be harmful to both the placenta and the foetus. Histopathological analysis revealed necrosis affecting both the maternal and foetal sides of the placenta. At late gestation, transmission occurred rapidly following infection (day 3 PI), but parasite were rarely found. In addition, an increase in cytokine expression was observed in spleen and placental tissues from infected animals, while a downregulation in IL-4 expression was only observed in the spleen. Finally, necrosis in the placenta was limited to the maternal side, suggesting that the parasite is mainly multiplying in the placental tissue at this stage. Thus, the results of the present study indicate that the placenta may be actively involved in N. caninum pathogenesis.

scholarly journals Prolonged Gray Matter Disease without Demyelination Caused by Theiler's Murine Encephalomyelitis Virus with a Mutation in VP2 Puff B

2001 ◽  
Vol 75 (16) ◽  
pp. 7494-7505 ◽  
Author(s):  
Ikuo Tsunoda ◽  
Yoshiaki Wada ◽  
Jane E. Libbey ◽  
Thomas S. Cannon ◽  
Frank G. Whitby ◽  
...  
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Virus Infection ◽  
Acute Phase ◽  
Gray Matter ◽  
Chronic Phase ◽  
Theiler's Murine Encephalomyelitis Virus ◽  
Theiler’S Murine Encephalomyelitis Virus ◽  
Encephalomyelitis Virus ◽  
The Brain

ABSTRACT Theiler's murine encephalomyelitis virus (TMEV) is divided into two subgroups based on neurovirulence. During the acute phase, DA virus infects cells in the gray matter of the central nervous system (CNS). Throughout the chronic phase, DA virus infects glial cells in the white matter, causing demyelinating disease. Although GDVII virus also infects neurons in the gray matter, infected mice developed a severe polioencephalomyelitis, and no virus is detected in the white matter or other areas in the CNS in rare survivors. Several sequence differences between the two viruses are located in VP2 puff B and VP1 loop II, which are located near each other, close to the proposed receptor binding site. We constructed a DA virus mutant, DApBL2M, which has the VP1 loop II of GDVII virus and a mutation at position 171 in VP2 puff B. While DApBL2M virus replicated less efficiently than DA virus during the acute phase, DApBL2M-induced acute polioencephalitis was comparable to that in DA virus infection. Interestingly, during the chronic phase, DApBL2M caused prolonged gray matter disease in the brain without white matter involvement in the spinal cord. This is opposite what is observed during wild-type DA virus infection. Our study is the first to demonstrate that conformational differences via interaction of VP2 puff B and VP1 loop II between GDVII and DA viruses can play an important role in making the transition of infection from the gray matter in the brain to the spinal cord white matter during TMEV infection.

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