The Experts below are selected from a list of 138 Experts worldwide ranked by ideXlab platform
Lela K. Riley - One of the best experts on this subject based on the ideXlab platform.
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Prolonged perturbations of tumour necrosis factor-α and interferon-γ in mice inoculated with Clostridium piliforme
Journal of Medical Microbiology, 2000Co-Authors: Roger A. Van Andel, Craig L. Franklin, Hook Rr, Cynthia Besch-williford, Lela K. RileyAbstract:Clostridium piliforme is an obligate intracellular bacterium that causes enterohepatic disease in many animal species. C. piliforme infections are commonly subclinical in laboratory rats and mice, and little is known about host regulation of disease or of the effects of C. piliforme infections on investigations that use subclinically infected animals. To assess host regulation of subclinical C. piliforme infections and the effects of those infections on laboratory mice, the expression of the pro-inflammatory cytokines tumour necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) was evaluated at 0, 1, 3, 7, 14 and 28 days after inoculation with C. piliforme . Subclinical infection was induced in weanling C. piliforme -susceptible DBA/2 or -resistant C57BL/6 mice with either a toxic or a non-toxic C. piliforme strain. Hepatic lesions and bacteria were demonstrated histologically in both mouse strains for 14 days after inoculation with the toxigenic bacterial strain, but were never demonstrated histologically following inoculation with the non-toxigenic strain. Hepatic TNF-α and IFN-γ mRNA and serum protein levels were similarly elevated in both mouse strains 1 day after inoculation with both C. piliforme strains, as evaluated by reverse transcription PCR and enzyme-linked immunosorbent assays, respectively. Elevation of IFN-γ persisted for 14 days after inoculation; TNF-α remained elevated at 28 days after inoculation.
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Effects of neutrophil, natural killer cell, and macrophage depletion on murine Clostridium piliforme infection
Infection and immunity, 1997Co-Authors: R. A. Van Andel, Craig L. Franklin, Cynthia Besch-williford, N Van Rooijen, Lela K. RileyAbstract:Clostridium piliforme infection (Tyzzer’s disease) induces enterohepatic disease in many domestic and laboratory animals. Murine susceptibility to Tyzzer’s disease varies with host strain, age, and immune status. However, little is known about the role of the immune system in control of this disease. To investigate the role of host immunity in Tyzzer’s disease, mice were depleted of either neutrophils, natural killer cells, or macrophages by antibody administration or chemotherapy. After depletion, DBA/2 mice, which are naturally susceptible to C. piliforme, or naturally resistant C57BL/6 mice were inoculated intravenously with C. piliforme. Animals were euthanized 3 days postinoculation and evaluated for gross and histologic lesions and hepatic bacterial load. In juvenile DBA/2 or C57BL/6 mice, depletion of either neutrophils or natural killer cells increased severity of disease. In adult mice, depletion of natural killer cells significantly increased severity of Tyzzer’s disease in the resistant (C57BL/6) but not in the susceptible (DBA/2) strain. Macrophage depletion did not alter the course of infection in either mouse strain. These studies indicate an important role for neutrophils and natural killer cells in the pathogenesis of murine Tyzzer’s disease. The role of macrophages in murine C. piliforme infection will require further evaluation.
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A novel presentation of Clostridium piliforme infection (Tyzzer's disease) in nude mice.
Laboratory animal science, 1996Co-Authors: Robert S. Livingston, Craig L. Franklin, Cynthia Besch-williford, Lela K. RileyAbstract:Clostridium piliforme infection (Tyzzer's disease) was diagnosed in a colony of nude mice. Because spontaneous Tyzzer's disease had not been reported in nude mice, a study was undertaken to better define the clinicopathologic features of this disease outbreak. Sixty homozygous nude (nu/nu) females, 10 nu/nu males, and 10 heterozygous nude (nu/+) females were observed for signs of disease. Over a 3-month period, 43% of the nu/nu mice died or manifested clinical signs of disease and were euthanized, but nu/+ mice remained healthy. Clinical signs of disease were infrequently observed in nu/nu mice and, when evident, were followed by rapid deterioration and death. Gross and histologic lesions, including severe hepatic and intestinal necrosis associated with C. piliforme, were observed only in clinically affected animals. Clostridium piliforme isolated from diseased livers had marked cytotoxicity in in vitro assays. This outbreak is unique in that, contrary to a previous experimental report, nu/nu mice had increased susceptibility to Tyzzer's disease, suggesting that T cells may play an important role in host defenses against C. piliforme infection. In addition, this is the first report of a toxigenic isolate of C. piliforme recovered from mice. The cytotoxin produced by the isolate may have contributed to the severity of clinical disease and lesions.
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Tyzzer's infection: host specificity of Clostridium piliforme isolates.
Laboratory animal science, 1994Co-Authors: Craig L. Franklin, Cynthia Besch-williford, Lela K. RileyAbstract:Tyzzer's disease, a well-recognized syndrome in numerous laboratory animal species, is caused by the obligate intracellular bacterium, Clostridium piliforme. Distinct isolates of C. piliforme from various laboratory animal species have been identified based on protein and antigenic heterogeneity. The goal of this study was to examine the host specificity of three well-characterized isolates of C. piliforme. Groups of mice, rats, and hamsters were experimentally infected with isolates obtained from a naturally infected mouse (M1), a naturally infected rat (R1), and a naturally infected hamster (H2). To assess infection status, animals were monitored serologically for antibody to C. piliforme over a 12-week period. Evaluation of results indicated that the M1 isolate infected rats and mice but not hamsters, whereas the R1 and H2 isolates infected only the host species from which the isolates were originally obtained. These findings suggest that C. piliforme isolates can be categorized into two types: 1) cross-infective isolates, such as M1, which can infect more than one laboratory animal species, and 2) isolates, such as R1 and H2, which have a more limited host range within laboratory animal species. These results emphasize the need to consider the host specificity of C. piliforme isolates when investigating outbreaks of Tyzzer's disease.
Akira Takakura - One of the best experts on this subject based on the ideXlab platform.
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Vet Pathol 36:613–615 (1999) Enterocolitis Associated with Dual Infection by Clostridium piliforme and Feline Panleukopenia Virus in Three Kittens
2016Co-Authors: Tetsuro Ikegami, Akira Takakura, Toshio Itoh, Kazuo Goto, Kinji Shirota, S Kawamura, Yasuo Nomura, Y. Une, Kosaku FujiwaraAbstract:Abstract. Dual infection by Clostridium piliforme and feline panleukopenia virus (FPLV) was found in three kittens. In all cases, we found focal necrosis and desquamation of epithelial cells with occasional neutrophil infiltration in the large intestine. Large filamentous bacilli and spores were observed in the epithelium by using the Warthin-Starry method. Electron microscopy revealed the vegetative forms with characteristic peritrichous flagella and spore forms. Immunohistochemically, these bacilli showed a positive reaction with mouse antisera against the RT and MSK C. piliforme strains. Polymerase chain reaction (PCR) using cecum specimens dem-onstrated the 196-bp band specific to C. piliforme 16S rRNA. All three kittens were also diagnosed as FPLV-infected on the basis of the characteristic mucosal lesions, including intranuclear inclusions and PCR study for the FPLV genomic DNA. The PCR techniques are useful for confirming the C. piliforme and FPLV infection in spontaneous cases. Key words: Cats; Clostridium piliforme; colitis; feline panleukopenia virus; PCR; Tyzzer’s disease. Tyzzer’s disease has been reported in various animal spe-cies, including laboratory, domestic, and wild animals;2 the disease was recently reported in a HIV-l–infected human pa-tient.13 Histopathological lesions caused by Clostridium pil
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specific and quantitative detection of pcr products from Clostridium piliforme helicobacter bilis h hepaticus and mouse hepatitis virus infected mouse samples using a newly developed electrochemical dna chip
Journal of Microbiological Methods, 2007Co-Authors: Kazuo Goto, Toshio Itoh, Hideki Horiuchi, Haruka Shinohara, Katsumi Motegi, Koji Hashimoto, Sadato Hongo, Nobuhiro Gemma, Nobuhito Hayashimoto, Akira TakakuraAbstract:We developed a microfabricated electrochemical DNA chip for detection of polymerase chain reaction (PCR) products from 16S rRNA sequences of Clostridium piliforme (Cp), Helicobacter bilis (Hb) and Helicobacter hepaticus (Hh), and the nucleocapsid protein gene of mouse hepatitis virus (MHV). This chip does not require DNA labeling, and the hybridization signal can be detected as an anodic current. The average anodic currents of 9 (Cp), 5 (Hb), 8 (Hh) and 7 (MHV) PCR positive samples derived from feces of spontaneously infected mice (Cp, Hb and Hh) and MHV-contaminated tumor cells were 27.9+/-7.2, 31.9+/-8.1, 29.3+/-10.1, and 27.6+/-3.0 nA, respectively. On the other hand, the average anodic currents of 19 (Cp), 27 (Hb), 18 (Hh), and 13 (MHV) PCR negative samples were 0.3+/-2.9, 3.7+/-2.4, -1.0+/-1.7, and -2.3+/-2.7 nA, respectively. The anodic current increased with increasing concentrations of pathogens. For experimentally infected samples, the results of PCR/electrophoresis were in complete accord with those of this system when anodic currents of 6.1 (Cp), 8.5 (Hb), 2.4 (Hh), and 3.1 nA (MHV) were taken as the cut-off value. The results suggested that the electrochemical DNA chip system is useful for specific and quantitative detection of PCR products.
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enterocolitis associated with dual infection by Clostridium piliforme and feline panleukopenia virus in three kittens
Veterinary Pathology, 1999Co-Authors: Tetsuro Ikegami, Akira Takakura, Toshio Itoh, Kazuo Goto, Kinji Shirota, S Kawamura, Yasuo Nomura, Kosaku FujiwaraAbstract:Dual infection by Clostridium piliforme and feline panleukopenia virus (FPLV) was found in three kittens. In all cases, we found focal necrosis and desquamation of epithelial cells with occasional neutrophil infiltration in the large intestine. Large filamentous bacilli and spores were observed in the epithelium by using the Warthin-Starry method. Electron microscopy revealed the vegetative forms with characteristic peritrichous flagella and spore forms. Immunohistochemically, these bacilli showed a positive reaction with mouse antisera against the RT and MSK C. piliforme strains. Polymerase chain reaction (PCR) using cecum specimens dem- onstrated the 196-bp band specifi ct oC. piliforme 16S rRNA. All three kittens were also diagnosed as FPLV- infected on the basis of the characteristic mucosal lesions, including intranuclear inclusions and PCR study for the FPLV genomic DNA. The PCR techniques are useful for confirming the C. piliforme and FPLV infection in spontaneous cases.
Craig L. Franklin - One of the best experts on this subject based on the ideXlab platform.
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HOST RESPONSE TO INFECTION Role of interleukin-6 in determining the course of murine Tyzzer’s disease
2015Co-Authors: R. A. Van Andel, Craig L. Franklin, Cynthia Besch-williford, Reuel R. Hook, K. RileyAbstract:Clostridium piliforme is an obligately intracellular bacterium that causes enterohepatic disease in many domestic and laboratory animal species. Susceptibility to infection is known to vary with the host immune status, species and strain, but little is known about specific immune mechanisms that regulate this disease. Subclinical infection was induced in weanling C. piliforme-susceptible DBA=2 or resistant C57BL=6 mice with either a toxic or a non-toxic C. piliforme isolate. Hepatic lesions and bacteria were evident in both mouse strains for 14 days after inoculation with the toxigenic bacterial isolate, but were never demonstrated following inoculation with the non-toxigenic isolate. All mice demonstrated increased interleukin-6 (IL-6) levels that were largely independent of host strain susceptibility to infection or virulence of the bacterial isolate. The severity of C. piliforme-induced hepatic lesions was increased by polyclonal anti-IL-6 treatment in both resistant (DBA=2) and susceptible (C57BL=6) mouse strains. These data indicate that IL-6 is important in mediating the course of murine C. piliforme infections but is not involved in determining host susceptibility to acute infection, nor is it influenced by the virulence of the C. piliforme isolate
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Prolonged perturbations of tumour necrosis factor-α and interferon-γ in mice inoculated with Clostridium piliforme
Journal of Medical Microbiology, 2000Co-Authors: Roger A. Van Andel, Craig L. Franklin, Hook Rr, Cynthia Besch-williford, Lela K. RileyAbstract:Clostridium piliforme is an obligate intracellular bacterium that causes enterohepatic disease in many animal species. C. piliforme infections are commonly subclinical in laboratory rats and mice, and little is known about host regulation of disease or of the effects of C. piliforme infections on investigations that use subclinically infected animals. To assess host regulation of subclinical C. piliforme infections and the effects of those infections on laboratory mice, the expression of the pro-inflammatory cytokines tumour necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) was evaluated at 0, 1, 3, 7, 14 and 28 days after inoculation with C. piliforme . Subclinical infection was induced in weanling C. piliforme -susceptible DBA/2 or -resistant C57BL/6 mice with either a toxic or a non-toxic C. piliforme strain. Hepatic lesions and bacteria were demonstrated histologically in both mouse strains for 14 days after inoculation with the toxigenic bacterial strain, but were never demonstrated histologically following inoculation with the non-toxigenic strain. Hepatic TNF-α and IFN-γ mRNA and serum protein levels were similarly elevated in both mouse strains 1 day after inoculation with both C. piliforme strains, as evaluated by reverse transcription PCR and enzyme-linked immunosorbent assays, respectively. Elevation of IFN-γ persisted for 14 days after inoculation; TNF-α remained elevated at 28 days after inoculation.
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Effects of neutrophil, natural killer cell, and macrophage depletion on murine Clostridium piliforme infection
Infection and immunity, 1997Co-Authors: R. A. Van Andel, Craig L. Franklin, Cynthia Besch-williford, N Van Rooijen, Lela K. RileyAbstract:Clostridium piliforme infection (Tyzzer’s disease) induces enterohepatic disease in many domestic and laboratory animals. Murine susceptibility to Tyzzer’s disease varies with host strain, age, and immune status. However, little is known about the role of the immune system in control of this disease. To investigate the role of host immunity in Tyzzer’s disease, mice were depleted of either neutrophils, natural killer cells, or macrophages by antibody administration or chemotherapy. After depletion, DBA/2 mice, which are naturally susceptible to C. piliforme, or naturally resistant C57BL/6 mice were inoculated intravenously with C. piliforme. Animals were euthanized 3 days postinoculation and evaluated for gross and histologic lesions and hepatic bacterial load. In juvenile DBA/2 or C57BL/6 mice, depletion of either neutrophils or natural killer cells increased severity of disease. In adult mice, depletion of natural killer cells significantly increased severity of Tyzzer’s disease in the resistant (C57BL/6) but not in the susceptible (DBA/2) strain. Macrophage depletion did not alter the course of infection in either mouse strain. These studies indicate an important role for neutrophils and natural killer cells in the pathogenesis of murine Tyzzer’s disease. The role of macrophages in murine C. piliforme infection will require further evaluation.
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A novel presentation of Clostridium piliforme infection (Tyzzer's disease) in nude mice.
Laboratory animal science, 1996Co-Authors: Robert S. Livingston, Craig L. Franklin, Cynthia Besch-williford, Lela K. RileyAbstract:Clostridium piliforme infection (Tyzzer's disease) was diagnosed in a colony of nude mice. Because spontaneous Tyzzer's disease had not been reported in nude mice, a study was undertaken to better define the clinicopathologic features of this disease outbreak. Sixty homozygous nude (nu/nu) females, 10 nu/nu males, and 10 heterozygous nude (nu/+) females were observed for signs of disease. Over a 3-month period, 43% of the nu/nu mice died or manifested clinical signs of disease and were euthanized, but nu/+ mice remained healthy. Clinical signs of disease were infrequently observed in nu/nu mice and, when evident, were followed by rapid deterioration and death. Gross and histologic lesions, including severe hepatic and intestinal necrosis associated with C. piliforme, were observed only in clinically affected animals. Clostridium piliforme isolated from diseased livers had marked cytotoxicity in in vitro assays. This outbreak is unique in that, contrary to a previous experimental report, nu/nu mice had increased susceptibility to Tyzzer's disease, suggesting that T cells may play an important role in host defenses against C. piliforme infection. In addition, this is the first report of a toxigenic isolate of C. piliforme recovered from mice. The cytotoxin produced by the isolate may have contributed to the severity of clinical disease and lesions.
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Tyzzer's infection: host specificity of Clostridium piliforme isolates.
Laboratory animal science, 1994Co-Authors: Craig L. Franklin, Cynthia Besch-williford, Lela K. RileyAbstract:Tyzzer's disease, a well-recognized syndrome in numerous laboratory animal species, is caused by the obligate intracellular bacterium, Clostridium piliforme. Distinct isolates of C. piliforme from various laboratory animal species have been identified based on protein and antigenic heterogeneity. The goal of this study was to examine the host specificity of three well-characterized isolates of C. piliforme. Groups of mice, rats, and hamsters were experimentally infected with isolates obtained from a naturally infected mouse (M1), a naturally infected rat (R1), and a naturally infected hamster (H2). To assess infection status, animals were monitored serologically for antibody to C. piliforme over a 12-week period. Evaluation of results indicated that the M1 isolate infected rats and mice but not hamsters, whereas the R1 and H2 isolates infected only the host species from which the isolates were originally obtained. These findings suggest that C. piliforme isolates can be categorized into two types: 1) cross-infective isolates, such as M1, which can infect more than one laboratory animal species, and 2) isolates, such as R1 and H2, which have a more limited host range within laboratory animal species. These results emphasize the need to consider the host specificity of C. piliforme isolates when investigating outbreaks of Tyzzer's disease.
Cynthia Besch-williford - One of the best experts on this subject based on the ideXlab platform.
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HOST RESPONSE TO INFECTION Role of interleukin-6 in determining the course of murine Tyzzer’s disease
2015Co-Authors: R. A. Van Andel, Craig L. Franklin, Cynthia Besch-williford, Reuel R. Hook, K. RileyAbstract:Clostridium piliforme is an obligately intracellular bacterium that causes enterohepatic disease in many domestic and laboratory animal species. Susceptibility to infection is known to vary with the host immune status, species and strain, but little is known about specific immune mechanisms that regulate this disease. Subclinical infection was induced in weanling C. piliforme-susceptible DBA=2 or resistant C57BL=6 mice with either a toxic or a non-toxic C. piliforme isolate. Hepatic lesions and bacteria were evident in both mouse strains for 14 days after inoculation with the toxigenic bacterial isolate, but were never demonstrated following inoculation with the non-toxigenic isolate. All mice demonstrated increased interleukin-6 (IL-6) levels that were largely independent of host strain susceptibility to infection or virulence of the bacterial isolate. The severity of C. piliforme-induced hepatic lesions was increased by polyclonal anti-IL-6 treatment in both resistant (DBA=2) and susceptible (C57BL=6) mouse strains. These data indicate that IL-6 is important in mediating the course of murine C. piliforme infections but is not involved in determining host susceptibility to acute infection, nor is it influenced by the virulence of the C. piliforme isolate
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Prolonged perturbations of tumour necrosis factor-α and interferon-γ in mice inoculated with Clostridium piliforme
Journal of Medical Microbiology, 2000Co-Authors: Roger A. Van Andel, Craig L. Franklin, Hook Rr, Cynthia Besch-williford, Lela K. RileyAbstract:Clostridium piliforme is an obligate intracellular bacterium that causes enterohepatic disease in many animal species. C. piliforme infections are commonly subclinical in laboratory rats and mice, and little is known about host regulation of disease or of the effects of C. piliforme infections on investigations that use subclinically infected animals. To assess host regulation of subclinical C. piliforme infections and the effects of those infections on laboratory mice, the expression of the pro-inflammatory cytokines tumour necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) was evaluated at 0, 1, 3, 7, 14 and 28 days after inoculation with C. piliforme . Subclinical infection was induced in weanling C. piliforme -susceptible DBA/2 or -resistant C57BL/6 mice with either a toxic or a non-toxic C. piliforme strain. Hepatic lesions and bacteria were demonstrated histologically in both mouse strains for 14 days after inoculation with the toxigenic bacterial strain, but were never demonstrated histologically following inoculation with the non-toxigenic strain. Hepatic TNF-α and IFN-γ mRNA and serum protein levels were similarly elevated in both mouse strains 1 day after inoculation with both C. piliforme strains, as evaluated by reverse transcription PCR and enzyme-linked immunosorbent assays, respectively. Elevation of IFN-γ persisted for 14 days after inoculation; TNF-α remained elevated at 28 days after inoculation.
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Effects of neutrophil, natural killer cell, and macrophage depletion on murine Clostridium piliforme infection
Infection and immunity, 1997Co-Authors: R. A. Van Andel, Craig L. Franklin, Cynthia Besch-williford, N Van Rooijen, Lela K. RileyAbstract:Clostridium piliforme infection (Tyzzer’s disease) induces enterohepatic disease in many domestic and laboratory animals. Murine susceptibility to Tyzzer’s disease varies with host strain, age, and immune status. However, little is known about the role of the immune system in control of this disease. To investigate the role of host immunity in Tyzzer’s disease, mice were depleted of either neutrophils, natural killer cells, or macrophages by antibody administration or chemotherapy. After depletion, DBA/2 mice, which are naturally susceptible to C. piliforme, or naturally resistant C57BL/6 mice were inoculated intravenously with C. piliforme. Animals were euthanized 3 days postinoculation and evaluated for gross and histologic lesions and hepatic bacterial load. In juvenile DBA/2 or C57BL/6 mice, depletion of either neutrophils or natural killer cells increased severity of disease. In adult mice, depletion of natural killer cells significantly increased severity of Tyzzer’s disease in the resistant (C57BL/6) but not in the susceptible (DBA/2) strain. Macrophage depletion did not alter the course of infection in either mouse strain. These studies indicate an important role for neutrophils and natural killer cells in the pathogenesis of murine Tyzzer’s disease. The role of macrophages in murine C. piliforme infection will require further evaluation.
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A novel presentation of Clostridium piliforme infection (Tyzzer's disease) in nude mice.
Laboratory animal science, 1996Co-Authors: Robert S. Livingston, Craig L. Franklin, Cynthia Besch-williford, Lela K. RileyAbstract:Clostridium piliforme infection (Tyzzer's disease) was diagnosed in a colony of nude mice. Because spontaneous Tyzzer's disease had not been reported in nude mice, a study was undertaken to better define the clinicopathologic features of this disease outbreak. Sixty homozygous nude (nu/nu) females, 10 nu/nu males, and 10 heterozygous nude (nu/+) females were observed for signs of disease. Over a 3-month period, 43% of the nu/nu mice died or manifested clinical signs of disease and were euthanized, but nu/+ mice remained healthy. Clinical signs of disease were infrequently observed in nu/nu mice and, when evident, were followed by rapid deterioration and death. Gross and histologic lesions, including severe hepatic and intestinal necrosis associated with C. piliforme, were observed only in clinically affected animals. Clostridium piliforme isolated from diseased livers had marked cytotoxicity in in vitro assays. This outbreak is unique in that, contrary to a previous experimental report, nu/nu mice had increased susceptibility to Tyzzer's disease, suggesting that T cells may play an important role in host defenses against C. piliforme infection. In addition, this is the first report of a toxigenic isolate of C. piliforme recovered from mice. The cytotoxin produced by the isolate may have contributed to the severity of clinical disease and lesions.
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Tyzzer's infection: host specificity of Clostridium piliforme isolates.
Laboratory animal science, 1994Co-Authors: Craig L. Franklin, Cynthia Besch-williford, Lela K. RileyAbstract:Tyzzer's disease, a well-recognized syndrome in numerous laboratory animal species, is caused by the obligate intracellular bacterium, Clostridium piliforme. Distinct isolates of C. piliforme from various laboratory animal species have been identified based on protein and antigenic heterogeneity. The goal of this study was to examine the host specificity of three well-characterized isolates of C. piliforme. Groups of mice, rats, and hamsters were experimentally infected with isolates obtained from a naturally infected mouse (M1), a naturally infected rat (R1), and a naturally infected hamster (H2). To assess infection status, animals were monitored serologically for antibody to C. piliforme over a 12-week period. Evaluation of results indicated that the M1 isolate infected rats and mice but not hamsters, whereas the R1 and H2 isolates infected only the host species from which the isolates were originally obtained. These findings suggest that C. piliforme isolates can be categorized into two types: 1) cross-infective isolates, such as M1, which can infect more than one laboratory animal species, and 2) isolates, such as R1 and H2, which have a more limited host range within laboratory animal species. These results emphasize the need to consider the host specificity of C. piliforme isolates when investigating outbreaks of Tyzzer's disease.
Kazuo Goto - One of the best experts on this subject based on the ideXlab platform.
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Vet Pathol 36:613–615 (1999) Enterocolitis Associated with Dual Infection by Clostridium piliforme and Feline Panleukopenia Virus in Three Kittens
2016Co-Authors: Tetsuro Ikegami, Akira Takakura, Toshio Itoh, Kazuo Goto, Kinji Shirota, S Kawamura, Yasuo Nomura, Y. Une, Kosaku FujiwaraAbstract:Abstract. Dual infection by Clostridium piliforme and feline panleukopenia virus (FPLV) was found in three kittens. In all cases, we found focal necrosis and desquamation of epithelial cells with occasional neutrophil infiltration in the large intestine. Large filamentous bacilli and spores were observed in the epithelium by using the Warthin-Starry method. Electron microscopy revealed the vegetative forms with characteristic peritrichous flagella and spore forms. Immunohistochemically, these bacilli showed a positive reaction with mouse antisera against the RT and MSK C. piliforme strains. Polymerase chain reaction (PCR) using cecum specimens dem-onstrated the 196-bp band specific to C. piliforme 16S rRNA. All three kittens were also diagnosed as FPLV-infected on the basis of the characteristic mucosal lesions, including intranuclear inclusions and PCR study for the FPLV genomic DNA. The PCR techniques are useful for confirming the C. piliforme and FPLV infection in spontaneous cases. Key words: Cats; Clostridium piliforme; colitis; feline panleukopenia virus; PCR; Tyzzer’s disease. Tyzzer’s disease has been reported in various animal spe-cies, including laboratory, domestic, and wild animals;2 the disease was recently reported in a HIV-l–infected human pa-tient.13 Histopathological lesions caused by Clostridium pil
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specific and quantitative detection of pcr products from Clostridium piliforme helicobacter bilis h hepaticus and mouse hepatitis virus infected mouse samples using a newly developed electrochemical dna chip
Journal of Microbiological Methods, 2007Co-Authors: Kazuo Goto, Toshio Itoh, Hideki Horiuchi, Haruka Shinohara, Katsumi Motegi, Koji Hashimoto, Sadato Hongo, Nobuhiro Gemma, Nobuhito Hayashimoto, Akira TakakuraAbstract:We developed a microfabricated electrochemical DNA chip for detection of polymerase chain reaction (PCR) products from 16S rRNA sequences of Clostridium piliforme (Cp), Helicobacter bilis (Hb) and Helicobacter hepaticus (Hh), and the nucleocapsid protein gene of mouse hepatitis virus (MHV). This chip does not require DNA labeling, and the hybridization signal can be detected as an anodic current. The average anodic currents of 9 (Cp), 5 (Hb), 8 (Hh) and 7 (MHV) PCR positive samples derived from feces of spontaneously infected mice (Cp, Hb and Hh) and MHV-contaminated tumor cells were 27.9+/-7.2, 31.9+/-8.1, 29.3+/-10.1, and 27.6+/-3.0 nA, respectively. On the other hand, the average anodic currents of 19 (Cp), 27 (Hb), 18 (Hh), and 13 (MHV) PCR negative samples were 0.3+/-2.9, 3.7+/-2.4, -1.0+/-1.7, and -2.3+/-2.7 nA, respectively. The anodic current increased with increasing concentrations of pathogens. For experimentally infected samples, the results of PCR/electrophoresis were in complete accord with those of this system when anodic currents of 6.1 (Cp), 8.5 (Hb), 2.4 (Hh), and 3.1 nA (MHV) were taken as the cut-off value. The results suggested that the electrochemical DNA chip system is useful for specific and quantitative detection of PCR products.
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enterocolitis associated with dual infection by Clostridium piliforme and feline panleukopenia virus in three kittens
Veterinary Pathology, 1999Co-Authors: Tetsuro Ikegami, Akira Takakura, Toshio Itoh, Kazuo Goto, Kinji Shirota, S Kawamura, Yasuo Nomura, Kosaku FujiwaraAbstract:Dual infection by Clostridium piliforme and feline panleukopenia virus (FPLV) was found in three kittens. In all cases, we found focal necrosis and desquamation of epithelial cells with occasional neutrophil infiltration in the large intestine. Large filamentous bacilli and spores were observed in the epithelium by using the Warthin-Starry method. Electron microscopy revealed the vegetative forms with characteristic peritrichous flagella and spore forms. Immunohistochemically, these bacilli showed a positive reaction with mouse antisera against the RT and MSK C. piliforme strains. Polymerase chain reaction (PCR) using cecum specimens dem- onstrated the 196-bp band specifi ct oC. piliforme 16S rRNA. All three kittens were also diagnosed as FPLV- infected on the basis of the characteristic mucosal lesions, including intranuclear inclusions and PCR study for the FPLV genomic DNA. The PCR techniques are useful for confirming the C. piliforme and FPLV infection in spontaneous cases.