Biomedical subjects

Christine K Fox

Publications and source records attributed to Christine K Fox.

3 recordsLinked to original sources

PubMed2005

Infant botulism, type F, presenting at 54 hours of life.

We report a case of botulism in a 54-hour-old infant with rapidly progressive fulminant paralysis and rapid spontaneous recovery atypical for infant botulism. Clostridium baratii and type F botulinum neurotoxin were isolated from the patient's stool. This unique presentation with rapid recovery is consistent with pharmacokinetics of type F botulinum neurotoxin. Interestingly, a muscle biopsy also revealed pathologic changes early in the disease course. This article reports the youngest known case of infant botulism and only the third reported case of this disease caused by type F neurotoxin. Botulism should be considered in patients of any age with subacute or acute neuromuscular weakness.

Acute Disease↗

PubMed2005

Recent advances in infant botulism.

Since infant botulism was first identified three decades ago, our understanding of botulinum toxins and the organisms that produce them has grown. A newer classification system now recognizes Clostridium baratii and Clostridium butyricum along with Clostridium botulinum as causative agents. Recently, increasing therapeutic use of botulinum toxins has sparked substantial new research into their mechanisms of action. This research, and some case reports from infants sickened by unusual botulinum toxins suggest that disease caused by different toxin types may result in varying clinical presentations. Perhaps most significantly for pediatricians and child neurologists, a specific treatment for infant botulism has just been approved. This article reviews the clinical presentation, diagnosis, and treatment of infant botulism, including human botulism immune globulin, and discusses the various organisms and toxins that cause this disease.

Bacterial Proteins↗

PubMed2003

Regulation of hypoxia-inducible factor 1alpha and induction of vascular endothelial growth factor in a rat neonatal stroke model.

Stroke is a devastating condition occurring in at least 1 in 4000 live births in the neonatal period. Since hypoxia-inducible factor (HIF)-1alpha can modulate ischemic injury via induction of target genes that may protect cells against ischemia, and is induced after preconditioning by hypoxia in the neonatal rat brain hypoxia-ischemia model, we evaluated whether HIF-1alpha is induced after focal ischemia-reperfusion, a model for neonatal stroke. We developed an ischemia-reperfusion model in postnatal day 10 (P10) rats by transiently occluding the middle cerebral artery (MCA) for 1.5 h. The MCA territory was reperfused for 0, 4, 8, or 24 h and the expression of HIF-1alpha and its target gene, vascular endothelial growth factor (VEGF), were delineated. HIF-1alpha protein and VEGF protein peaked at 8 h, and declined subsequently at 24 h in injured cortex following 1.5 h of MCA occlusion. Double-immunolabeling indicated that both HIF-1alpha and VEGF are expressed together in neurons with a similar time course of expression. The presence of HIF-1alpha and VEGF after moderate ischemia-reperfusion injury suggests potential avenues to exploit for neuroprotection.

Animals↗