Browsing by Subject "Clostridium perfringens"

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    A 64-Year-Old Man with Low Back Pain Due to Clostridium perfringens Lumbar Discitis
    (International Scientific Information, 2021-01-22) Bhatt, Harshil; Singh, Sandeep; Medicine, School of Medicine
    Lumbar discitis caused by Clostridium perfringens is extremely rare. There have only been 7 published cases of confirmed discitis caused by Clostridium perfringens. We write this report to underscore this unusual relationship by discussing an additional case and providing a review of the previously published cases so clinicians can adequately evaluate and treat patients presenting with discitis. CASE REPORT A 64-year-old morbidly obese man presented with an acute onset of worsening back pain and generalized weakness after incurring physical trauma related to falling. Additionally, he also developed fever and chills before the presentation. Based on the clinical presentation and elevated serum levels of inflammatory markers, magnetic resonance imaging was ordered, which showed L5-S1 discitis with extension of infection into the epidural space. Fluoroscopy-guided aspiration of the L5-S1 epidural space facilitated the detection of Clostridium perfringens as the involved pathogen. Based on the antibiotic susceptibility report, the patient was treated with intravenous ampicillin for 8 weeks, after which his symptoms resolved. CONCLUSIONS Diagnosis of discitis can be very challenging due to its ambiguous clinical presentation, especially in the elderly population due to the presence of underlying degenerative changes. Even though Clostridium perfringens remains a rare cause of lumbar discitis, it should be considered as a pathogen capable of causing infection of the vertebrae and intervertebral discs, thus allowing clinicians to make necessary diagnostic evaluations to provide appropriate targeted treatment to patients presenting with discitis.
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    Enterocolitis with fulminate sepsis in a newborn with tricho-hepato-enteric syndrome: A case report
    (OA Text, 2021-03) Lorant, Diane E.; Kua, Kok Lim; Pediatrics, School of Medicine
    Tricho-hepato-enteric syndrome is a rare autosomal recessive enteropathy that first presents as intractable diarrhea in neonates. Diarrhea persists throughout life and patients are dependent on parenteral nutrition for growth. Additional features include facial dysmorphism, trichorrhexis nodosa (woolly hair), intra-uterine growth restriction, hepatic disease, skin anomalies and a depressed immune system. Tricho-hepato-enteric syndrome is a life limiting disease with variability in its manifestations and severity. Mutations in two different genes, TTC37 or SKIV2L, cause the disorder. In this case report we present a neonate with a novel mutation in TTC37 that resulted in a severe phenotype associated with fulminate sepsis. The infant presented at one week of age with sudden onset of diarrhea and dehydration. Tricho-hepato-enteric syndrome was diagnosed by whole exome sequencing but was not initially considered because the infant lacked many of the diagnostic clinical features. Soon after presentation, the infant developed pneumoperitoneum and necrosis of entire bowel. The blood culture was positive for Clostridium perfringens. Autopsy showed bacteria in the parenchyma and vasculature of all major internal organs as well as within the bone marrow, connective tissue and skeletal muscle but there was minimal inflammatory response. The lack of migration of white blood cells to the sites of infection is likely due to the combined immunodeficiency reported in patients with tricho-hepato-enteric syndrome. This case expands our knowledge on the clinical features of tricho-hepato-enteric syndrome. Whole-exome sequencing was instrumental in making the diagnosis in an infant with an atypical presentation and should be considered early in neonates with congenital diarrhea.
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    A STUDY OF THE BETA-2 TOXIN GENE AND THE BETA-2 TOXIN IN CLOSTRIDIUM PERFRINGENS STRAINS ISOLATED FROM HUMAN SOURCES
    (2008-10-09T17:36:13Z) Roskens Dalzell, Heidi M.; Allen, Stephen D.
    Clostridium perfringens is an important human pathogen known to cause a range of diseases including diarrhea, necrotizing bowel disease and gas gangrene. Though potentially pathogenic, this microorganism is commonly identified in the fecal microbiota of healthy individuals. The major clinical findings associated with C. perfringens diseases are linked to production of potent toxins. In 1997, Gibert et al. identified a new toxin, the beta2 toxin, from a C. perfringens strain from a piglet with necrotic enteritis. Subsequently, this new beta2 toxin gene (cpb2) has been identified in C. perfringens from dogs, horses, and other animals. The principal objective of this investigation was to study cpb2 and the beta2 toxin in C. perfringens isolates from human sources. The C. perfringens isolates were grouped into three different populations: 1) fecal samples from patients suspected of having C. perfringens gastrointestinal illnesses (e.g. antibiotic-associated diarrhea or colitis), 2) extraintestinal specimen sources (e.g. wounds, abscesses, blood cultures), 3) a control group of isolates from healthy volunteers. Results of studies using different PCR methods and nucleotide sequencing revealed that cpb2 was present in the genome of isolates from all populations, and that the genetic variation between cpb2 from the different C. perfringens isolates was greater then expected. Using western blotting techniques, it was found that the beta2 protein was not expressed by all cpb2 positive C. perfringens isolates. Finally, different variants of cpb2 were cloned into E. coli, and the recombinant beta2 protein used in cell cytotoxicity assays. Results from these assays demonstrated that recombinant beta2 proteins caused a range of cellular damage at different levels of protein concentration and different lengths of time. Our results from these experiments provided new information regarding cpb2 in C. perfringens isolates from human sources; as well as on the range of variation of cpb2 genes, differences in beta2 toxin expression, and differences in the effects of recombinant beta2 toxin on enterocytes. This information could help to explain differences in virulence between C. perfringens isolates, differences in diseases and disease severity.