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PubMed1998

In vitro biological activity and toxicity of tetanus and botulinum neurotoxins.

Tetanus and botulinum neurotoxins are the most potent toxins known and cause tetanus and botulism, respectively. They are zinc-endopeptidases acting in the cytosol, where they cleave SNARE proteins. Here, we report on the assay of their metalloproteolytic activity in vitro on recombinant SNARE proteins. We also describe the assay of their activity in nerve cells in culture using antibodies specific for the SNARE proteins. Together with recent reports from other laboratories, these results show that the toxicity of these powerful neurotoxins can be appropriately assayed in vitro, thus reducing considerably the number of animals currently used in the evaluation of the toxicity of tetanus toxoid vaccine and of the botulinum neurotoxins to be used for human therapy.

Animals↗
PubMed1985

Are some crib deaths sudden cardiac deaths?

Research performed during the past two decades suggests that crib deaths are biphasic phenomena: the infant victims are preconditioned in subtle ways before birth so that some of their most critical physiologic functions are subtly deficient. Then, at 2 to 4 months of age, when confronted by some challenge, such as a head cold, they are unable to overcome or adapt to the stress and die, seemingly without cause. It is likely that these deaths represent a heterogeneous group of pathogenetic phenomena rather than a single entity. Spontaneous idiopathic pathologic apnea, for example, may be responsible for 5 to 7% of crib deaths. Infant botulism may account for another 5%. A recent report on a prospective study of more than 5,000 babies showed that all 3 infants who ultimately succumbed to crib death had had abnormally prolonged corrected QT intervals on day 4 of life; the report contends that that irregularity leads to ventricular fibrillation, which is then the immediate cause of death. Although this work has not been confirmed and some take issue with the method, it now seems the most valid available body of data on the subject and suggests that some crib deaths, probably less than 10%, may be sudden cardiac deaths.

Apnea↗
PubMed1987

Localized diseases of the bovine brain and spinal cord.

Localized lesions of the central nervous system do occur in cattle. Those affecting the cranial nerves and focal lesions of the spinal cord are most easily recognized by careful neurologic examination. Once the lesion has been anatomically localized, likely etiologic causes can be pursued. Probably the most common cause of cranial nerve deficits in cattle is listeriosis. Important differential diagnoses include brain and pituitary abscesses and extensions of ear infections. Other possible causes include PEM, TEME, hypovitaminosis A, and several rare, sporadic causes. In young cattle, spinal trauma and vertebral body abscesses are the most common causes of progressive paresis resulting from spinal cord lesions. Congenital abnormalities must be considered in the differential diagnoses for very young calves. Non-neurologic conditions, including fractures of the limbs and especially nutritional muscular dystrophy, must be ruled out. In older cattle, compressive neoplasms, most notably lymphosarcoma, are primarily responsible for progressive paresis. Differential diagnosis should include other neurologic conditions such as delayed organophosphate neurotoxicity; early progressive diffuse neurologic diseases such as rabies, pseudorabies, and botulism; plant toxicities; and non-neurologic conditions resulting in recumbency, such as hypocalcemia and musculoskeletal trauma.

Animals↗
PubMed1999

Therapeutics of musculoskeletal disease in the horse.

Therapeutic medications play a crucial role in the successful therapy of many musculoskeletal diseases that occur in horses. For example, appropriate antibiotic therapy is extremely important in the treatment of diseases caused by infections with microorganisms such as botulism, tetanus, osteomyelitis, and muscle abscesses. In addition, numerous prescription medications and nutritional supplements are available for the treatment of osteoarthritis in horses. Many of these agents currently on the market fall into a new class of drugs called SADMO agents. Unfortunately, the efficacy and mechanism(s) of action for many of these agents have not been well defined. There does exist a fair amount of data indicating that the parenterally administered compounds HA and PSGAGs, commonly used to treat osteoarthritis, can decrease the severity of clinical signs and perhaps slow the progression of disease. Although there are fewer data available to support the efficacy of orally administered SADMO agents, these compounds are used commonly by lay people as osteoarthritis therapies. Finally, pharmaceutical agents such as acetozolamide can play an important role in the management of the inherited HYPP condition in horses.

Adrenal Cortex Hormones↗
PubMed2002

Central nervous system infections in injection drug users.

Central nervous system infections in injection drug users are often devastating in terms of excess morbidity and mortality. In injection drug users with infective endocarditis, embolization from infected valvular vegetations may cause cerebral infarction, intracranial hemorrhage, and the formation of brain abscess. Focal intracranial infections (i.e., brain abscess and spinal epidural abscess) may occur in the absence of infective endocarditis, resulting from bacteremia that seeds the brain or epidural space. Antimicrobial therapy, combined with surgical intervention, may be essential to improve outcome from these neurologic complications. Toxin-mediated diseases (especially tetanus and wound botulism) are also seen in injection drug users. Inoculation of Clostridium spp at injection sites may lead to toxin generation and disease. Clinicians must maintain a high level of suspicion for these diagnoses in injection drug users.

Brain Abscess↗
PubMed2003

The journey of tetanus and botulinum neurotoxins in neurons.

Anaerobic bacteria of the genus Clostridia are a major threat to human and animal health, being responsible for pathologies ranging from food poisoning to gas gangrene. In each of these, the production of sophisticated exotoxins is the main cause of disease. The most powerful clostridial toxins are tetanus and botulinum neurotoxins, the causative agents of tetanus and botulism. They are structurally organized into three domains endowed with distinct functions: high affinity binding to neurons, membrane translocation and specific cleavage of proteins controlling neuroexocytosis. Recent discoveries regarding the mechanism of membrane recruitment and sorting of these neurotoxins within neurons make them ideal tools to uncover essential aspects of neuronal physiology in health and disease.

Animals↗
PubMed2002

Botulinum and tetanus neurotoxins: structure, function and therapeutic utility.

The toxic products of the anaerobic bacteria Clostridium botulinum, Clostridium butyricum, Clostridium barati and Clostridium tetani are the causative agents of botulism and tetanus. The ability of botulinum neurotoxins to disrupt neurotransmission, often for prolonged periods, has been exploited for use in several medical applications and the toxins, as licensed pharmaceutical products, now represent the therapeutics of choice for the treatment for several neuromuscular conditions. Research into the structures and activities of botulinum and tetanus toxins has revealed features of these proteins that might be useful in the design of improved vaccines, effective inhibitors and novel biopharmaceuticals. Here, we discuss the relationships between structure, mechanism of action and therapeutic use.

Animals↗
PubMed2003

Repetitive nerve stimulation and exercise testing.

Repetitive nerve stimulation and exercise testing are useful in the evaluation of patients with suspected disorders of the NMJ and muscle membrane excitability when performed with close attention to technical factors. They can be very helpful in the diagnosis of myasthenia gravis. Lambert-Eaton myasthenic syndrome, and botulism, as well as rare disorders of skeletal muscle membrane excitability, including paramyotonia congenita, myotonia congenita, myotonic dystrophy, and the periodic paralyses.

Electric Stimulation↗
PubMed2001

Neuropathogenic properties of Argas (Persicargas) walkerae larval homogenates.

Several tick species have been demonstrated, described, or suspected to cause paralysis in their host during the repletion process, presumably by impairing neurotransmission. The resulting polyneuropathy gradually spreads to the upper limbs causing incoordination and ends in respiratory failure. This form of paralysis is commonly confused with Guillain-Barrè syndrome, botulism and myasthenia gravis and although the clinical symptoms of these diseases are similar, it is not clear whether the pathogenesis is also the same. During this study we investigated the mechanism of paralysis by the tick Argas (Persicargas) walkerae by determining the effect of larval homogenates on both potassium-stimulated (calcium-dependent) and veratridine-stimulated (external calcium-independent) release of [3H]glycine from crude rat brain synaptosomes. The results indicated that larval homogenates inhibited both processes. These findings are reconcilable with the results obtained for two other paralysis-causing tick species, Ixodes holocyclus and Dermacentor andersoni, which were indicated to cause paralysis by decreasing the synthesis or release of acetylcholine at the neuromuscular junction.

Animals↗
PubMed2002

Anaerobic infections in children.

Anaerobic bacteria can cause a variety of endogenous infections in children. Because of their fastidious nature, they are difficult to isolate from infectious sites, and are often overlooked. Anaerobic infections can occur in all body sites, including the central nervous system, oral cavity, head and neck, chest, abdomen, pelvis, skin, and soft tissues. They colonize the newborn after delivery and have been recovered from several types of neonatal infections. These include cellulitis of the site of fetal monitoring, neonatal aspiration pneumonia, bacteremia, conjunctivitis, omphalitis, and infant botulism. The lack of adequate therapy may lead to clinical failures. Their isolation requires appropriate methods of collection, transportation and cultivation of specimens. Treatment is complicated by their slow growth, their polymicrobial nature and their growing resistance to antimicrobials. Antimicrobial therapy is often the only form of therapy required, whereas in others it is an important adjunct to a surgical approach. Because anaerobes are generally recovered mixed with aerobic organisms, the choice of antimicrobial agents should provide coverage of both types of pathogens.

Anti-Bacterial Agents↗
PubMed2002

[Prevention of bioterrorism by vaccines].

Prevention against the weapons of bioterrorists is limited by the multiplicity of agents that could be used. Against smallpox, stocks of the classical vaccine must be prepared, but this vaccine is dangerous and we must look for a new and safer vaccine. A vaccine against anthrax is probably possible relatively soon. One may be less optimistic concerning plague, since it is not sure that we could protect against the pulmonary plague, but research in this field is an emergency. The large number of viruses capable of inducing haemorrhagic fevers makes especially difficult the preparation of vaccines against these infections. We must also make available monoclonal antibodies that could be used as therapies against toxin, notably botulism, or against antibiotic-resistant bacteria.

Anthrax↗
PubMed2001

Texture analysis of X-ray radiographs is a more reliable descriptor of bone loss than mineral content in a rat model of localized disuse induced by the Clostridium botulinum toxin.

Botulism is a generalized paralyzing disease caused by the toxin of Clostridium botulinum (BTX). The toxin acts 3-4 days after injection by blocking the release of acetylcholine to the muscle. Six Wistar rats received a 2-U injection of BTX in the right quadriceps. Six rats were similarly injected with saline and were used as control. Paralysis of the quadriceps was obtained 4-5 days after the injection. Animals were killed 4 weeks after the BTX injection. The bone mineral content (BMC) was measured by dual-energy X-ray absorptiometry (DXA) on the femur and tibia. No side-to-side difference was observed for BMC on the whole tibia and femur in the BTX group. When subregions were selected in the bones, a significant decrease in BMC was obtained on the proximal tibia (-17.4 +/- 2.5%, p < 0.02). No significant difference could be observed on the proximal or distal femur, nor on the diaphyseal shafts. Numeric X-rays were done and a region of interest was transferred to an image analyzer. The texture of the trabecular bone was analyzed by the run length and fractal methods (skyscrapers and blanket). Significant differences were obtained on the proximal tibia for all methods except with fractal skyscrapers. On the distal femur, significant differences were obtained with the run length method, and the skyscrapers and the blanket method in the vertical direction. No differences were obtained with any method on the tibia and femur from control animals. Bone is a highly anisotropic material and its architecture at the microscopic level is conditioned by strains. The trabecular pattern differs in the proximal tibia than in the distal femural. Depending on the trabecular anisotropy, the algorithms can be more or less pertinent. BTX induced a significant bone loss on the bony subparts that are directly influenced by disuse. Texture analysis of X-ray images can reveal differences that were not evidenced by naked eyes. However, a combination of several methods appears necessary to appreciate the bone loss.

Absorptiometry, Photon↗
PubMed1987

Acetylcholine receptor antibodies in myasthenia gravis: use of a qualitative assay for diagnostic purposes.

We have modified the techniques of Lindstrom and of Tindall to measure serum acetylcholine receptor antibody using human antigen bound to 125I-alpha Bungarotoxin. By using 10 microliters of serum and precipitating antigen-antibody complexes with an excess of staph A, we found that only one out of 43 patients with clinically diagnosed active generalized Myasthenia Gravis had no antibodies. In pooling these results with the results of tests done for diagnostic purposes we found positive results in 54/55 generalized active MG, 8/21 MG in remission, 16/37 ocular MG and 0/55 healthy controls. Two out of 38 non MG were also positive and their clinical diagnosis of botulism and penicillamine treated rheumatoid arthritis have been confirmed by a one year follow-up. Most of these sera were also tested for reactivity with fetal calf AchR. Six out of 49 samples positive with the human receptor were negative with calf receptor. We conclude that our technique is extremely useful for the diagnosis of Myasthenia Gravis and that fetal calf antigen cannot replace human antigen in the assay.

Animals↗
PubMed1998

Methods of testing neuromuscular transmission in the intensive care unit.

All disorders of neuromuscular transmission (NMT) may cause ventilatory failure, albeit rarely. Respiratory muscle weakness is occasionally the presenting feature of myasthenia gravis (MG), the Lambert-Eaton myasthenic syndrome (LEMS), hypermagnesemia and botulism. Chronic MG, congenital myasthenic syndromes and LEMS may be acutely exacerbated by various intercurrent conditions and by drugs which interfere with NMT. Finally, in the ICU, difficulty in weaning from the ventilator may be caused by prolonged use of neuromuscular blocking agents. Electrophysiological studies of NMT disorders in the intensive care unit have rarely been reported. Nevertheless, the available data indicates that the electrodiagnosis of severe NMT disorders can be misleading. With severe NMT defects, the electrophysiological distinction between post-synaptic and pre-synaptic disorders is blurred and the differential diagnosis with myopathies may be difficult. A clinically suspected NMT disorder should therefore not be ruled out when electrodiagnosis fails to demonstrate the expected abnormalities.

Electric Stimulation↗
PubMed1987

Factors affecting the toxicity of rotting carcasses containing Clostridium botulinum type C.

Mice killed shortly after receiving 1300-3000 spores of Clostridium botulinum type C per os were incubated at one of four chosen temperatures together with bottles of cooked meat medium seeded with a similar inoculum. After incubation the rotting carcasses were homogenized. Sterile membrane filtrates of the homogenates (10-20.8%, w/v) and pure cultures were then titrated for toxicity. A temperature of 37 degrees C produced less toxicity in most carcasses than in cultures. At 30 degrees C, however, toxicity (often 2 X 10(5) to 2 X 10(6) mouse intraperitoneal LD/g or ml) was roughly similar in both systems, and some carcasses and cultures were still toxic (2 X 10(4) to 2 X 10(5) LD/g or ml) after 349 days. Surprisingly, at 23 degrees C, through greatly reduced in the cultures, toxicity was high in many carcasses for at least 28 days. Little or no toxin was produced in either system at 16 degrees C. Unfiltered homogenates (17.8-22.5%, w/v; dose 0.25 ml per os) of toxic carcasses incubated at 30 degrees C for 7 days invariably produced death from botulism, often within as little as 4 h, but a 1 in 10 dilution produced less than 100% mortality.

Animals↗
PubMed2005

Soft tissue infections caused by spore-forming bacteria in injecting drug users in the United Kingdom.

From 2000 to May 2004 there has been a marked increase in illness resulting from spore-forming bacteria in injecting heroin users in the United Kingdom. Clostridium novyi caused 63 cases of severe illness in 2000 and seven further cases from 2001. Wound botulism first occurred in 2000 (six cases) with 51 further cases to March 2004. Tetanus occurred in 20 cases between late 2003 and March 2004. Infections with C. histolyticum (nine cases), C. sordellii (one case) and Bacillus cereus (one case) were also reported. The reasons for the increase in illness are unclear. The major risk factor was skin- or muscle-popping. The problem appears to be here to stay. This review describes the causative organisms, pathogenesis, clinical presentation, epidemiology and treatment of cases. Clinical vigilance and a high standard of anaerobic microbiology are essential. Clinicians and laboratories must report such cases (or likely cases) rapidly so that clusters can be rapidly identified, in order to control disease. Prevention relies on tetanus immunization.

Age Distribution↗
PubMed2005

Detection of botulinum neurotoxin A in a spiked milk sample with subtype identification through toxin proteomics.

Botulinum neurotoxin (BoNT) causes the disease botulism, which can be lethal if untreated. Rapid determination of exposure to BoNT is an important public health goal. Previous work in our laboratory focused on the development of Endopep-MS, a mass spectrometry-based endopeptidase method for detecting and differentiating BoNT in buffer. This method can rapidly determine the presence of BoNT in a sample and differentiate the toxin type of BoNT present but does not yield additional information about the subtype. We now describe here the application of Endopep-MS to detect BoNT A in a spiked milk sample. This work also describes subtype identification achieved through mass spectrometric analysis of the protein toxin itself and does not require the presence of DNA from the toxin-producing bacteria. Tryptic digests of A1 and A2 subtypes of BoNT were analyzed by mass spectrometry, and peptides unique to either the A1 or A2 subtype were subjected to tandem mass spectrometry analysis to confirm their identities. Finally, subtype identification through mass spectrometric analysis was performed on BoNT A isolated from spiked milk. In its entirety, this method would allow for analysis of BoNT with toxin type identification in a few hours and subtype identification within 24 h.

Amino Acid Sequence↗
PubMed2004

Enhancement of the endopeptidase activity of purified botulinum neurotoxins A and E by an isolated component of the native neurotoxin associated proteins.

In botulism disease, neurotransmitter release is blocked by a group of structurally related neurotoxin proteins produced by Clostridium botulinum. Botulinum neurotoxins (BoNT, A-G) enter nerve terminals and irreversibly inhibit exocytosis via their endopeptidase activities against synaptic proteins SNAP-25, VAMP, and Syntaxin. Type A C. botulinum secretes the neurotoxin along with 5 other proteins called neurotoxin associated proteins (NAPs). Here, we report that hemagglutinin-33 (Hn-33), one of the NAP components, enhances the endopeptidase activity of not only BoNT/A but also that of BoNT/E, both under in vitro conditions and in rat synaptosomes. BoNT/A endopeptidase activity in vitro is about twice as high as that of BoNT/E under disulfide-reduced conditions. Addition of Hn-33 separately to nonreduced BoNT/A and BoNT/E (which otherwise have only residual endopeptidase activity) enhanced their in vitro endopeptidase activity by 21- and 25-fold, respectively. Cleavage of rat-brain synaptosome SNAP-25 by BoNTs was used to assay endopeptidase activity under nerve-cell conditions. Reduced BoNT/A and BoNT/E cleaved synaptosomal SNAP-25 by 20% and 15%, respectively. Addition of Hn-33 separately to nonreduced BoNT/A and BoNT/E enhanced their endopeptidase activities by 13-fold for the cleavage of SNAP-25 in synaptosomes, suggesting a possible functional role of Hn-33 in association with BoNTs. We believe that Hn-33 could be used as an activator in the formulation of the neurotoxin for therapeutic use.

Animals↗