RESUMEN
Type D enterotoxemia, caused by Clostridium perfringens epsilon toxin (ETX), is one of the most economically important clostridial diseases of sheep. Acute type D enterotoxemia is characterized by well-documented lesions in the nervous, cardiocirculatory, and pulmonary systems. However, discrepancies and confusion exist as to whether renal lesions are part of the spectrum of lesions of this condition, which is controversial considering that for many decades it has been colloquially referred to as "pulpy kidney disease." Here, the authors assess renal changes in an experimental model of acute type D enterotoxemia in sheep and evaluate the possible role of ETX in their genesis. Four groups of 6 sheep each were intraduodenally inoculated with either a wild-type virulent C. perfringens type D strain, an etx knockout mutant unable to produce ETX, the etx mutant strain complemented with the wild-type etx gene that regains the ETX toxin production, or sterile culture medium (control group). All sheep were autopsied less than 24 hours after inoculation; none of them developed gross lesions in the kidneys. Ten predefined histologic renal changes were scored in each sheep. The proportion of sheep with microscopic changes and their severity scores did not differ significantly between groups. Mild intratubular medullary hemorrhage was observed in only 2 of the 12 sheep inoculated with the wild-type or etx-complemented bacterial strains, but not in the 12 sheep of the other 2 groups. The authors conclude that no specific gross or histologic renal lesions are observed in sheep with experimental acute type D enterotoxemia.
Asunto(s)
Infecciones por Clostridium , Enfermedades de las Ovejas , Ovinos , Animales , Clostridium perfringens/genética , Enterotoxemia/microbiología , Infecciones por Clostridium/patología , Infecciones por Clostridium/veterinaria , Riñón/patología , Enfermedades de las Ovejas/patologíaRESUMEN
Sarcina ventriculi is a gram-positive bacterium, able to survive in extreme low pH environment. It's first description dates from 1842, by John Goodsir. Since then, just a few cases have been reported. In veterinary medicine, especially in ruminants, it causes bloating, vomiting, gastric perforation and death of the animal. It is commonly associated with delayed gastric emptying or obstruction to gastric outlet, although it's pathogenicity in humans is not fully understood. We report two cases with identification of the bacteria in gastric specimens stained with hematoxylin-eosin staining, in different clinical settings. The first patient is a young female patient, presenting cardiac arrest and death after gastric perforation and the second patient an adult male presenting with gastric adenocarcinoma, treated with partial gastrectomy followed by adjuvant chemoradiation. In our literature review, we identified forty-five cases reporting Sarcina ventriculi appearance, with a sudden increase since 2010.
Asunto(s)
Humanos , Masculino , Femenino , Adolescente , Persona de Mediana Edad , Sarcina/patogenicidad , Infecciones por Clostridium/patología , Gastroparesia/complicacionesRESUMEN
One of the main challenges associated with Clostridioides difficile infection (CDI) in humans and domestic animals is the lack of an effective preventive strategy. One strategy with promising results is the oral administration of non-toxigenic strains of C. difficile (NTCD). Recently, Z31, a NTCD strain isolated from a healthy dog, showed promising results to prevent CDI in hamsters. Thus, the present study aimed to evaluate the capacity of Z31 to prevent CDI in piglets using an experimental model. Twenty neonatal piglets were randomly distributed in three groups: G1 - 106 spores of Z31 followed by 107 spores of a toxigenic C. difficile strain (nâ¯=â¯7), G2 (positive control) - 107 spores of a toxigenic C. difficile strain (nâ¯=â¯7), and G3 (negative control) - no biological inoculum (nâ¯=â¯6). All animals were kept in individual insulators and observed for 60â¯h. Data regarding clinical signs, macro and microscopic lesions, toxigenic culture of C. difficile, and detection of A/B toxins in the feces were evaluated. All evaluated parameters were significantly lower in animals that received Z31 compared to the positive control. Thus, oral administration of Z31 was able to prevent CDI in piglets in an experimental model.
Asunto(s)
Antibiosis , Terapia Biológica/métodos , Clostridiales/crecimiento & desarrollo , Infecciones por Clostridium/prevención & control , Administración Oral , Animales , Animales Recién Nacidos , Toxinas Bacterianas/análisis , Infecciones por Clostridium/microbiología , Infecciones por Clostridium/patología , Modelos Animales de Enfermedad , Heces/química , Porcinos , Resultado del TratamientoRESUMEN
AIM: To evaluate the effect on the nonsteroidal anti-inflammatory drug indomethacin on Clostridium difficile infection (CDI) severity. MATERIALS & METHODS: Indomethacin was administered in two different mouse models of antibiotic-associated CDI in two different facilities, using a low and high dose of indomethacin. RESULTS: Indomethacin administration caused weight loss, increased the signs of severe infection and worsened histopathological damage, leading to 100% mortality during CDI. Indomethacin-treated, antibiotic-exposed mice infected with C. difficile had enhanced intestinal inflammation with increased expression of KC, IL-1ß and IL-22 compared with infected mice unexposed to indomethacin. CONCLUSION: These results demonstrate a negative impact of nonsteroidal anti-inflammatory drugs on antibiotic-associated CDI in mice and suggest that targeting the synthesis or signaling of prostaglandins might be an approach to ameliorating the severity of CDI.
Asunto(s)
Antiinflamatorios no Esteroideos/efectos adversos , Clostridioides difficile , Infecciones por Clostridium/tratamiento farmacológico , Infecciones por Clostridium/patología , Indometacina/efectos adversos , Intestinos/patología , Índice de Severidad de la Enfermedad , Animales , Antibacterianos/efectos adversos , Antiinflamatorios no Esteroideos/administración & dosificación , Modelos Animales de Enfermedad , Indometacina/administración & dosificación , Interleucina-1beta/metabolismo , Interleucinas/metabolismo , Intestinos/efectos de los fármacos , Ratones , Ratones Endogámicos C57BL , Antagonistas de Prostaglandina/efectos adversos , Prostaglandinas/biosíntesis , Factores de Riesgo , Pérdida de Peso , Interleucina-22RESUMEN
Clostridium difficile infection (CDI) are the leading cause of world-wide nosocomial acquired diarrhea. The current main clinical challenge in CDI is the elevated rate of infection recurrence that may reach up to 30% of the patients, which has been associated to the formation of dormant spores during the infection. We sought to characterize the effects of oral administration of specific anti-spore IgY in mouse models of CDI and recurrent CDI. The specificity of anti-spore IgY was evaluated in vitro. In both, initiation mouse model and recurrence mouse model, we evaluated the prophylactic and therapeutic effect of anti-spore IgY, respectively. Our results demonstrate that anti-spore IgY exhibited high specificity and titers against C. difficile spores and reduced spore adherence to intestinal cells in vitro. Administration of anti-spore IgY to C57BL/6 mice prior and during CDI delayed the appearance of the diarrhea by 1.5 day, and spore adherence to the colonic mucosa by 90%. Notably, in the recurrence model, co-administration of anti-spore IgY coupled with vancomycin delayed the appearance of recurrent diarrhea by a median of 2 days. Collectively, these observations suggest that anti-spore IgY antibodies may be used as a novel prophylactic treatment for CDI, or in combination with antibiotics to treat CDI and prevent recurrence of the infection.
Asunto(s)
Pollos/inmunología , Clostridioides difficile/inmunología , Infecciones por Clostridium/tratamiento farmacológico , Infecciones por Clostridium/prevención & control , Inmunoglobulinas/administración & dosificación , Inmunoglobulinas/farmacología , Inmunoglobulinas/uso terapéutico , Esporas Bacterianas/inmunología , Adhesinas Bacterianas/efectos de los fármacos , Administración Oral , Animales , Anticuerpos Antibacterianos/inmunología , Anticuerpos Antibacterianos/farmacología , Anticuerpos Antibacterianos/uso terapéutico , Proteínas Bacterianas/inmunología , Células CACO-2 , Infecciones por Clostridium/patología , Colon/microbiología , Diarrea/tratamiento farmacológico , Modelos Animales de Enfermedad , Combinación de Medicamentos , Heces/microbiología , Humanos , Inmunización Pasiva , Inmunoglobulina G/sangre , Inmunoglobulinas/aislamiento & purificación , Inmunoterapia , Intestinos/inmunología , Intestinos/microbiología , Ratones , Ratones Endogámicos C57BL , Vancomicina/farmacologíaRESUMEN
One of the main clinical challenges of Clostridium difficile infections (CDI) is the high rate of relapse episodes. The main determinants involved in relapse of CDI include the presence of antibiotic-resistant C. difficile spores in the colonic environment and a permanent state of dysbiosis of the microbiota caused by antibiotic therapy. A possible scenario is that phenotypes related to the persistence of C. difficile spores might contribute to relapsing infections. In this study, 8 C. difficile isolates recovered from 4 cases with relapsing infection, and 9 isolates recovered from single infection cases were analyzed for PCR ribotyping and the presence of tcdA, tcdB and cdtAB genes. Factors associated to spore persistence, sporulation, spore adherence and biofilm formation and sporulation during biofilm formation were characterized. We also evaluated motility and cytotoxicity. However, we observed no significant difference in the analyzed phenotypes among the different clinical outcomes, most likely due to the high variability observed among strains within clinical backgrounds in each phenotype and the small sample size. It is noteworthy that C. difficile spores adhered to similar extents to undifferentiated and differentiated Caco-2 cells. By contrast, spores of all clinical isolates tested had increased germination efficiency in presence of taurocholate, while decreased sporulation rate during biofilm development in the presence of glucose. In conclusion, these results show that, at least in this cohort of patients, the described phenotypes are not detrimental in the clinical outcome of the disease.
Asunto(s)
Clostridioides difficile/patogenicidad , Infecciones por Clostridium/microbiología , Esporas Bacterianas/crecimiento & desarrollo , Antibacterianos/farmacología , Proteínas Bacterianas/genética , Proteínas Bacterianas/metabolismo , Biopelículas , Células CACO-2 , Clostridioides difficile/genética , Clostridioides difficile/aislamiento & purificación , Clostridioides difficile/fisiología , Infecciones por Clostridium/patología , Estudios de Cohortes , Farmacorresistencia Bacteriana , Humanos , Fenotipo , Recurrencia , Esporas Bacterianas/genética , Esporas Bacterianas/metabolismo , Esporas Bacterianas/patogenicidad , VirulenciaRESUMEN
The prevalence of Clostridium difficile infections has increased due to the emergence of epidemic variants from diverse genetic lineages. Here we describe the emergence of a novel variant during an outbreak in a Costa Rican hospital that was associated with severe clinical presentations. This C. difficile variant elicited higher white blood cell counts and caused disease in younger patients than did other strains isolated during the outbreak. Furthermore, it had a recurrence rate, a 30-day attributable disease rate, and disease severity as great as those of the epidemic strain NAP1. Pulsed-field gel electrophoresis genotyping indicated that the outbreak strains belong to a previously undescribed variant, designated NAPCR1. Whole-genome sequencing and ribotyping indicated that the NAPCR1 variant belongs to C. difficile ribotype 012 and sequence type 54, as does the reference strain 630. NAPCR1 strains are resistant to fluoroquinolones due to a mutation in gyrA, and they possess an 18-bp deletion in tcdC that is characteristic of the epidemic, evolutionarily distinct, C. difficile NAP1 variant. NAPCR1 genomes contain 10% more predicted genes than strain 630, most of which are of hypothetical function and are present on phages and other mobile genetic elements. The increased virulence of NAPCR1 was confirmed by mortality rates in the hamster model and strong inflammatory responses induced by bacteria-free supernatants in the murine ligated loop model. However, NAPCR1 strains do not synthesize toxin A and toxin B at levels comparable to those in NAP1 strains. Our results suggest that the pathogenic potential of this emerging C. difficile variant is due to the acquisition of hypothetical functions associated with laterally acquired DNA.
Asunto(s)
Clostridioides difficile/aislamiento & purificación , Clostridioides difficile/patogenicidad , Infecciones por Clostridium/epidemiología , Diarrea/epidemiología , Brotes de Enfermedades , Animales , Clostridioides difficile/clasificación , Clostridioides difficile/genética , Infecciones por Clostridium/microbiología , Infecciones por Clostridium/patología , Costa Rica/epidemiología , Infección Hospitalaria/inducido químicamente , Infección Hospitalaria/epidemiología , Infección Hospitalaria/microbiología , ADN Bacteriano/genética , Diarrea/microbiología , Diarrea/patología , Modelos Animales de Enfermedad , Electroforesis en Gel de Campo Pulsado , Femenino , Transferencia de Gen Horizontal , Genotipo , Hospitales , Humanos , Intestinos/patología , Masculino , Mesocricetus , Ratones , Datos de Secuencia Molecular , Tipificación Molecular , Estudios Retrospectivos , Ribotipificación , Análisis de Secuencia de ADN , Análisis de Supervivencia , Virulencia , Factores de Virulencia/genéticaRESUMEN
Clostridium difficile is the major cause of antibiotic-associated diarrhea and pseudomembranous colitis in healthcare settings. However, the host factors involved in the intestinal inflammatory response and pathogenesis of C. difficile infection (CDI) are largely unknown. Here we investigated the role of leukotrienes (LTs), a group of pro-inflammatory lipid mediators, in CDI. Notably, the neutrophil chemoattractant LTB4, but not cysteinyl (cys) LTs, was induced in the intestine of C57BL/6 mice infected with either C. difficile strain VPI 10463 or strain 630. Genetic or pharmacological ablation of LT production did not ameliorate C. difficile colitis or clinical signs of disease in infected mice. Histological analysis demonstrated that intestinal neutrophilic inflammation, edema and tissue damage in mice during acute and severe CDI were not modulated in the absence of LTs. In addition, CDI induced a burst of cytokines in the intestine of infected mice in a LT-independent manner. Serum levels of anti-toxin A immunoglobulin (Ig) G levels were also not modulated by endogenous LTs. Collectively, our results do not support a role for LTs in modulating host susceptibility to CDI in mice.
Asunto(s)
Clostridioides difficile/crecimiento & desarrollo , Infecciones por Clostridium/microbiología , Infecciones por Clostridium/patología , Colitis/microbiología , Colitis/patología , Leucotrienos/metabolismo , Animales , Clostridioides difficile/inmunología , Modelos Animales de Enfermedad , Femenino , Histocitoquímica , Ratones Endogámicos C57BLRESUMEN
The objective of this study was to describe the first report involving a case of equine acute myonecrosis caused by C. novyi type A with an emphasis on clinical signs, the pathological and bacteriological analysis, and molecular identification of the microorganisms as the key of the definitive diagnosis.
Asunto(s)
Infecciones por Clostridium/veterinaria , Clostridium/clasificación , Clostridium/aislamiento & purificación , Enfermedades de los Caballos/diagnóstico , Enfermedades de los Caballos/patología , Miositis/veterinaria , Necrosis/veterinaria , Animales , Infecciones por Clostridium/diagnóstico , Infecciones por Clostridium/microbiología , Infecciones por Clostridium/patología , Análisis por Conglomerados , ADN Bacteriano/química , ADN Bacteriano/genética , ADN Ribosómico/química , ADN Ribosómico/genética , Histocitoquímica , Enfermedades de los Caballos/microbiología , Caballos , Miositis/diagnóstico , Miositis/microbiología , Miositis/patología , Necrosis/diagnóstico , Necrosis/microbiología , Necrosis/patología , Filogenia , ARN Ribosómico 16S/genética , Análisis de Secuencia de ADNRESUMEN
The objective of this study was to describe the first report involving a case of equine acute myonecrosis caused by C. novyi type A with an emphasis on clinical signs, the pathological and bacteriological analysis, and molecular identification of the microorganisms as the key of the definitive diagnosis.
Asunto(s)
Animales , Infecciones por Clostridium/veterinaria , Clostridium/clasificación , Clostridium/aislamiento & purificación , Enfermedades de los Caballos/diagnóstico , Enfermedades de los Caballos/patología , Miositis/veterinaria , Necrosis/veterinaria , Análisis por Conglomerados , Infecciones por Clostridium/diagnóstico , Infecciones por Clostridium/microbiología , Infecciones por Clostridium/patología , ADN Bacteriano/química , ADN Bacteriano/genética , ADN Ribosómico/química , ADN Ribosómico/genética , Histocitoquímica , Caballos , Enfermedades de los Caballos/microbiología , Miositis/diagnóstico , Miositis/microbiología , Miositis/patología , Necrosis/diagnóstico , Necrosis/microbiología , Necrosis/patología , Filogenia , /genética , Análisis de Secuencia de ADNRESUMEN
The objective of this study was to describe the first report involving a case of equine acute myonecrosis caused by C. novyi type A with an emphasis on clinical signs, the pathological and bacteriological analysis, and molecular identification of the microorganisms as the key of the definitive diagnosis.(AU)
Asunto(s)
Animales , Infecciones por Clostridium/veterinaria , Clostridium/clasificación , Clostridium/aislamiento & purificación , Enfermedades de los Caballos/diagnóstico , Enfermedades de los Caballos/patología , Miositis/veterinaria , Necrosis/veterinaria , Análisis por Conglomerados , Infecciones por Clostridium/microbiología , Infecciones por Clostridium/patología , ADN Bacteriano/genética , ADN Ribosómico/química , ADN Ribosómico/genética , Histocitoquímica , Enfermedades de los Caballos/microbiología , Miositis/diagnóstico , Miositis/microbiología , Necrosis/diagnóstico , Necrosis/microbiología , Necrosis/patología , Filogenia , Análisis de Secuencia de ADNRESUMEN
Non-enterotoxin (CPE)-producing Clostridium perfringens type A has been associated with enteritis in calves. Recent evidence has suggested that a novel toxin, named beta2 (CPB2), is implicated in the pathogenesis of this disease, although there is little evidence supporting this. In the current study, the role of C. perfringens type A in an outbreak of enteritis in calves was studied. Two 20-day-old dairy calves exhibiting apathy and reluctance to eat, with paresis of the anterior limbs, were euthanized for postmortem examination. Gross and histological changes compatible with acute enteritis, rumenitis, meningitis, and pneumonia were seen in both calves. Clostridium perfringens type A non-CPE, non-CPB2 was isolated from the abomasum and the small intestine. Escherichia coli ONTH8 (with cdtBIII and f17 virulence genes detected by polymerase chain reaction) was also isolated from the brain, abomasum, and intestine from both calves. All the samples were negative for Salmonella spp. When the C. perfringens strain was inoculated into bovine ligated small and large intestinal loops, cell detachment, erosion, and hemorrhage of the lamina propria were observed, predominantly in the small intestine. The results suggest that non-CPE, non-CPB2 C. perfringens type A is able to induce pathologic changes in the intestine of calves, probably enhanced by other pathogens, such as some pathogenic E. coli strains.
Asunto(s)
Enfermedades de los Bovinos/microbiología , Infecciones por Clostridium/veterinaria , Clostridium perfringens/aislamiento & purificación , Enteritis/microbiología , Enteritis/veterinaria , Animales , Bovinos , Enfermedades de los Bovinos/diagnóstico , Enfermedades de los Bovinos/patología , Infecciones por Clostridium/diagnóstico , Infecciones por Clostridium/microbiología , Infecciones por Clostridium/patología , Clostridium perfringens/genética , Enteritis/diagnóstico , Enteritis/patología , Resultado Fatal , Femenino , Laparotomía/veterinariaRESUMEN
Focal symmetrical encephalomalacia (FSE) is the most prominent lesion seen in the chronic form of enterotoxemia caused by Clostridium perfringens type D in sheep. However, this lesion has not been reported in goats. The current paper reports a case of FSE in a goat from the state of Paraíba in the Brazilian semiarid region. As reported by the farmer, 30, 4-48-month-old animals from a flock of 150 goats died after showing nervous signs, including blindness and recumbence, for periods varying between 1 and 14 days. The flock was grazing native pasture supplemented with wheat and corn bran. Additionally, lactating goats were supplemented with soybeans. A 4-month-old goat with nervous signs was examined clinically and then necropsied 3 days after the onset of clinical signs. Bilateral, focal, and symmetrical areas of brown discoloration were observed in the internal capsule and thalamus. Histologic lesions in these areas consisted of multifocal, bilateral malacia with a few neutrophils; endothelial cell swelling; perivascular edema; and hemorrhages. The etiology of these lesions was not determined. However, FSE is considered pathognomonic for C. perfringens type D enterotoxemia in sheep, and it is speculated that this microorganism was the etiologic agent in the present case. The flock had been vaccinated against type D enterotoxemia only once, approximately 3 months before the beginning of the outbreak. Insufficient immunity due to the incorrect vaccination protocol, low efficacy of the vaccine used, and a diet including large amounts of highly fermentable carbohydrates were suspected to be predisposing factors for this outbreak.
Asunto(s)
Encefalomalacia/veterinaria , Enfermedades de las Cabras/patología , Enfermedad Aguda , Animales , Enfermedad Crónica , Infecciones por Clostridium/patología , Infecciones por Clostridium/veterinaria , Clostridium perfringens/aislamiento & purificación , Encefalomalacia/microbiología , Encefalomalacia/patología , Enterotoxemia/clasificación , Enterotoxemia/microbiología , Enterotoxemia/patología , Resultado Fatal , Femenino , Enfermedades de las Cabras/microbiología , Cabras , Neuroglía/patología , Neuronas/patología , Tálamo/patologíaRESUMEN
The pathological findings in sheep with peracute experimental Clostridium perfringens type D enterotoxemia are described. Of 16 animals inoculated intraduodenally with a whole culture of this microorganism and a starch solution in the abomasum, 12 developed clinical signs including increased respiratory efforts, recumbency, paddling, bleating, convulsions, blindness, and opisthotonus. Diarrhea was not observed in any of the animals. The time lapse between the beginning of intraduodenal infusion and onset of clinical signs varied between 30 minutes and 26 hours, and the clinical course varied between 1 and 9 hours. Gross postmortem changes were observed in these 12 animals and included pulmonary edema; excess pericardial, peritoneal, or pleural fluid with or without strands of fibrin; liquid small intestinal contents; leptomeningeal edema; cerebellar coning; and subcapsular petechiae on kidneys. Histological changes consisted of severe edema of pleura and interlobular septa and around blood vessels and airways and acidophilic, homogeneous, proteinaceous perivascular edema in the brain. Five of 12 animals (42%) with clinical signs consistent with enterotoxemia lacked specific histological lesions in the brain. None of the intoxicated or control animals developed nephrosis. Glucose was detected in the urine of 3 of 6 animals that were tested for this analyte. These results stress the importance of the use of histological examination of the brain, coupled with epsilon toxin detection, for a definitive diagnosis of C. perfringens type D enterotoxemia in sheep.
Asunto(s)
Infecciones por Clostridium/patología , Infecciones por Clostridium/veterinaria , Clostridium perfringens/crecimiento & desarrollo , Enterotoxemia/microbiología , Enterotoxemia/patología , Enfermedades de las Ovejas/microbiología , Enfermedades de las Ovejas/patología , Animales , Toxinas Bacterianas/sangre , Encéfalo/microbiología , Encéfalo/patología , Infecciones por Clostridium/microbiología , Infecciones por Clostridium/orina , Enterotoxemia/orina , Ensayo de Inmunoadsorción Enzimática/veterinaria , Femenino , Tracto Gastrointestinal/microbiología , Tracto Gastrointestinal/patología , Glucosuria/veterinaria , Histocitoquímica/veterinaria , Riñón/microbiología , Riñón/patología , Pulmón/microbiología , Pulmón/patología , Masculino , Ratones , Pruebas de Neutralización , Distribución Aleatoria , OvinosAsunto(s)
Infecciones por Clostridium , Clostridium perfringens , Gastroenteritis/microbiología , Niño , Infecciones por Clostridium/tratamiento farmacológico , Infecciones por Clostridium/metabolismo , Infecciones por Clostridium/patología , Gastroenteritis/tratamiento farmacológico , Gastroenteritis/metabolismo , Gastroenteritis/patología , Humanos , Inmunohistoquímica , MasculinoRESUMEN
In cattle, a neurological lesion similar to that produced in sheep and goats by Clostridium perfringens type D enterotoxaemia has been reported. However, no causal relationship has been established between this disease and the lesion in cattle. The effects of single and multiple intravenous injections of epsilon toxin in three calves aged 6 months were studied. A further calf was inoculated intravenously with saline solution and used as a control. Epsilon toxin invariably produced neurological signs within 2-60 min of the end of the injection process. Clinical signs consisted of loss of consciousness, recumbency, convulsions, paddling, opisthotonus, hyperaesthesia and dyspnoea. Gross changes consisted of severe acute pulmonary oedema, which was particularly marked in the interlobular septa. The histological lesions consisted of intra-alveolar and interstitial oedema of the lung and variable degrees of perivascular proteinaceous oedema in the internal capsule, thalamus and cerebellar white matter. No clinical or post-mortem changes were observed in the control calf. These results show that calves are susceptible to the intravenous injection of epsilon toxin, and that they can show at least some of the histological lesions produced in sheep and goats by this toxin.
Asunto(s)
Toxinas Bacterianas/toxicidad , Enfermedades de los Bovinos/patología , Enfermedades de los Bovinos/fisiopatología , Infecciones por Clostridium/veterinaria , Clostridium perfringens , Enfermedad Aguda , Animales , Toxinas Bacterianas/administración & dosificación , Edema Encefálico/inducido químicamente , Edema Encefálico/patología , Edema Encefálico/fisiopatología , Edema Encefálico/veterinaria , Bovinos , Enfermedades de los Bovinos/microbiología , Infecciones por Clostridium/microbiología , Infecciones por Clostridium/patología , Infecciones por Clostridium/fisiopatología , Inyecciones Intravenosas , Masculino , Edema Pulmonar/inducido químicamente , Edema Pulmonar/patología , Edema Pulmonar/veterinariaRESUMEN
On smears of marrow-bone death bovines, presumptively diagnostic of black-leg, we have carried out the direct immunofluorescence test (IF). We used two labelled immunosera with fluorescein isothiocyanate. The immunosera wer prepared with the reference strain 5078 of Clostridium chauvoei as following: a) a cellular extract obtained with veronal buffer 0.045 M pH = 8.6, and b) a flagellar suspension obtained by agitation with glass beads, centrifuged at 3,500 x g, and centrifuged again at 16,000 x g during 20 min at 4 degrees C. Both antigenic preparations were injected into rabbits, five doses (0.2, 0.4, 0.8, 1.6 and 3.2 ml) each by i.v. route. Control positive strain of C. chauvoei were used, and control negative strains of C. septicum and C. perfringens were used too. Of all 56 examined samples, 26 (47.5%) gave positive IF test. These results had a 100% of correlation by culture and biochemical identification.
Asunto(s)
Examen de la Médula Ósea/métodos , Enfermedades de los Bovinos/diagnóstico , Infecciones por Clostridium/veterinaria , Técnica del Anticuerpo Fluorescente , Animales , Antígenos Bacterianos/aislamiento & purificación , Médula Ósea/microbiología , Bovinos , Enfermedades de los Bovinos/patología , Clostridium/clasificación , Clostridium/inmunología , Clostridium/aislamiento & purificación , Infecciones por Clostridium/diagnóstico , Infecciones por Clostridium/patología , Conejos , Especificidad de la EspecieRESUMEN
1. The influence of some components of the normal human intestinal flora on the acute phase of experimental infection with strain CL of Trypanosoma cruzi was studied in 30-day-old germ-free or gnotobiotic CFW (LOB) mice monoassociated with Bacteroides fragilis, Peptostreptococcus sp or Clostridium sp by intragastric inoculation of 10(6) bacteria 10 days before the intraperitoneal infection with 5 x 10(3) trypomastigotes/g body weight. 2. Significantly earlier parasitemia peak and mortality were observed in Bacteroides fragilis- and Clostridium-associated mice (16.75 +/- 0.96 and 15.00 +/- 1.15 days, respectively) when compared with germfree animals (18.83 +/- 1.17 days). More precocious mortality (10.40 +/- 2.06 days) and, curiously, much lower blood parasitemia were observed in Peptostreptococcus-associated mice than in other gnotobiotic mice. 3. The extent of cardiac tissue parasitism decreased in the following order: germfree, B. fragilis-associated, Clostridium-associated, and Peptostreptococcus-associated animals. The levels of inflammatory reaction decreased in the following order: germfree, Peptostreptococcus-associated, Clostridium-associated, and B. fragilis-associated mice. 4. These results show that the acute phase of experimental infection with T. cruzi was more severe in mice associated with strict anaerobic bacteria when compared with germfree animals. This suggests that a normal intestinal flora may be another factor, in addition to nutritional and genetic factors, responsible for the different susceptibility of organisms of the same species infected with T. cruzi.