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Primer on food-borne pathogens for subsistence food handlers.

Subsistence food preparations may lead to human illnesses caused by pathogenic bacteria and viruses. Little is known about the incidence of food-borne illnesses other than botulism in circumpolar indigenous populations. Lack of documentation for other pathogens may be related to the sparsely populated communities involved, limited laboratory analysis, and non-lethality to healthy individuals. This overview covers the major food-borne pathogens, their sources, transmission, growth parameters, and prevention. Examples of indigenous peoples' food preparations that may be susceptible to pathogenic bacterial growth and toxin formation are described.

Alaska↗

[Totally paralyzed or brain dead?].

In two patients, men aged 23 and 42 years, a condition that mimicked brain death was observed as a consequence of rapidly progressive complete peripheral paralyses, which included the intrinsic and extrinsic eye muscles. However, the EEG revealed a waking pattern. Maximal supportive therapy was provided, which included haemodialysis for the first patient and artificial ventilation for both patients. A slow recovery was seen after four weeks. The first patient was paralyzed following the ingestion of a large quantity of ethylene glycol and the second by botulism due to the consumption of injudiciously canned food. In patients with catastrophic brain injury, the diagnosis of brain death can be confirmed by a clinical neurological examination. In considering the diagnosis 'brain death', the most important criterion is that the cause of the brain damage is established. If the cause is insufficiently, the presence of brain death should be seriously doubted, unless an isoelectric EEG is observed.

Adult↗

Investigation of repeated vaccination as a possible cause of glomerular disease in mink.

The search for antigens capable of causing immune-complex-mediated glomerulonephritis continues. Modified live-virus vaccines commercially available for veterinary use are a possible source. In this study, repeated vaccination of mink with live-virus vaccines was investigated as a model for vaccine-induced glomerular injury. Three groups of 10-wk-old mink, 15 per group, were vaccinated once with 4-way vaccine against distemper, Pseudomonas aeruginosa infection, botulism and mink viral enteritis. Subsequently, all mink in each group each were vaccinated either with the 4-way vaccine, a monovalent canine distemper vaccine, or saline. Glomerular function was assessed at 2-wk intervals by determining the urinary protein:creatinine (P:C) ratio. Kidney sections taken at necropsy, 20 wk after the 1st vaccination, were examined by light and immunofluorescent microscopy for deposition of immunoglobulin and complement. There was no statistically significant difference between the treated and control groups based on average urinary P:C ratio medians. Light microscopic changes were detected in glomeruli, but Fisher's exact test showed no significant differences between any of the treatment groups. Deposition of immunoglobulin but not complement was significantly more frequent (P < 0.05) in the glomeruli of animals that received multiple injections of the 4-way vaccine than in the glomeruli of those given only the monovalent canine distemper vaccine or saline. These findings suggest that repeated vaccination may increase the glomerular deposition of immunoglobulin. Further studies are required to determine if the increased deposition of immunoglobulin contributes to the development of glomerular damage and to identify the antigens driving production of the deposited immunoglobulin.

Animals↗

Recognition and management of bioterrorism infections.

Recent events have demonstrated that bioterrorists have the ability to disseminate biologic agents in the United States and cause widespread social panic. Family physicians would play a key role in the initial recognition of a potential bioterrorism attack. Familiarity with the infectious agents of highest priority can expedite diagnosis and initial management, and lead to a successful public health response to such an attack. High-priority infectious agents include anthrax, smallpox, plague, tularemia, botulism, and viral hemorrhagic fever. Anthrax and smallpox must be distinguished from such common infections as influenza and varicella. Anthrax treatment is stratified into postexposure prophylaxis and treatment of confirmed cutaneous, intestinal, or inhalation anthrax. Disease prevention by vaccination and isolation of affected persons is key in preventing widespread smallpox infection. Many resources are available to physicians when a bioterrorism attack is suspected, including local public health agencies and the Centers for Disease Control and Prevention.

Anthrax↗

Laboratory diagnosis of foodborne diseases.

Many bacterial species are responsible for sporadic cases and outbreaks of foodborne intoxication and infection. The foodborne diseases are classified on the basis of the pathogenetic mechanisms involved into four categories: performed toxin, enterotoxin formed in the colonized small intestine, mucosal invasion (enterocolitis) and mucosal invasion with bacteremia. Invasive and toxigenic strains of enteropathogenic Escherichia coli are discussed. In vivo test systems for the identification of enterotoxigenic organisms and tissue culture assays for the heat-labile enterotoxin of E. coli are described. Current laboratory methods for the diagnosis of foodborne diseases of major public health interest are reviewed - botulism, staphylococcal intoxication, Clostridium perfringens enteritis, salmonellosis, enteropathogenic E. coli infection, Vibrio parahaemolyticus infection and Bacillus cereus enteritis. The role of the laboratory in the epidemiologic surveillance and investigation of foodborne diseases is emphasized.

Animals↗

Clostridium botulinum type-C intoxication associated with consumption of processed alfalfa hay cubes in horses.

An episode of nervous system dysfunction was observed in horses on 17 premises in 4 counties of southern California. Thirty-eight horses were affected, and 31 of those died. The common clinical signs of disease in the affected horses were: increased appetite; anxious attitude; rythmic, intermittent muscle tremors in the area of the tricep muscles; decreased palpebral tone; mydriasis; small hard fecal balls; and tendency to become sternally recumbent with the neck extended. The temporal distribution of cases on all 17 premises suggested a relationship between exposure to a common batch of alfalfa hay cubes and manifestations of similar clinical signs of disease in affected horses. Fifteen horses were submitted for necropsy. Diagnosis of botulism was established on the basis of detection of type-C1 toxin in the feed, in intestinal contents of 1 horse, and in the liver of the aforementioned horse and another horse. Toxigenic strains of Clostridium botulinum type-C were isolated from intestinal contents of 5 affected horses, one of which also contained type-C1 and type-C2 toxins. Seven of 10 horses treated with type-C antitoxin and plasma obtained from horses hyperimmunized with C botulinum type-C toxoids survived.

Animal Feed↗

[Suppurative meningitis in a patient with severe botulinum toxin type B poisoning].

A case of botulism with severe course is described. The patient was a woman aged 42 years treated in a gynaecology hospital department with erroneous diagnosis of peritonitis and paralytic ileus. The development of signs of meningitis caused that the patient was transferred to a hospital for infectious diseases where the correct diagnosis was established. After 63 days of treatment the patient was discharged home without any clinically detectable sequelae of the disease.

Adult↗

[Type D and A Clostridium botulinum in necropsy samples from bovines with "mal de Aguapey"].

Bacteriological studies were carried out on several necropsy samples from five animals whose deaths had been attributed to bovine botulism. This disease, regionally called Mal de Aguapey, enzootically affects animals from a wide area of the north-east of Argentina (Province of Corrientes) with a bovine population estimated at near to 2,500,000. Either C. botulinum type D, its toxin or both were identified in all animal samples, alternatively in contents of rumen, jejunum, ileum, caecum and in samples of spleen, liver and kidney (Table 1). C. botulinum type A was isolated respectively from the liver and the kidney of two animals. Cultures of 100 soil samples taken in the enzootic area were positive only for C. botulinum type A (3%). These results enlarge and confirm previous findings and lend support to the botulinic etiology of the Mal de Aguapey.

Animals↗

Electrodiagnostic evaluation of patients with myasthenia gravis and related disorders.

The technique of repetitive nerve stimulation was developed as a means of confirming a diagnosis of MG. The application of this test in the clinical evaluation of patients with muscle weakness has identified other disorders of neuromuscular transmission such as LEMS, infantile botulism, and several forms of congenital myasthenia. Repetitive nerve stimulation to several different nerves, before and after exercising the muscles, usually permits identification of disorders of neuromuscular transmission more readily than very detailed study of one muscle. There are other useful electrodiagnostic tests, but in most cases, repetitive nerve stimulation of weak muscles will permit the identification of a disorder of neuromuscular transmission.

Botulism↗

Neuromuscular disease in a dog.

Diffuse neuromuscular disease occurs sporadically in dogs. The most commonly reported diffuse neuromuscular diseases are polyradiculoneuritis (coonhound paralysis), tick paralysis, botulism, and myasthenia gravis (1,2,12). This clinical report describes an atypical presentation of a diffuse neuromuscular disease in a dog.

Animals↗

[Food-borne infections and poisonings].

A survey of the most common food borne infections (salmonellosis, tuberculosis, brucellosis, campylobacteriosis) is followed by a description of the most common food borne intoxications (botulism, staphylococcal intoxications, biogenic amines, toxic algae in mussels, i.e. "Paralytic Shellfish Poisoning").

Animals↗

[Food poisoning in cattle caused by ingestion of brewers' grains contaminated with Clostridium botulinum type B (author's transl)].

In 1977, outbreaks of disease associated with serious losses occurred on twenty cattle farms. This disease was due to the fact that the animals had been fed brewers' grains. The clinical picture was marked by anorexia, profuse salivation, regurgitation and dehydration. The course of the disease varied with the severity of the attack. Toxicological tests were negative. Cl. botulinum type B as well as toxin type B were found to be present in the brewers' grains fairly often. As a rule, Cl. botulinum was also detected in the rumen contents and faeces. The treatment of the animals is described; this resulted in recovery in a number of cases. When experimental animals were fed brewers' grains from farms on which outbreaks had occurred, this induced similar clinical pictures. The results of studies on the aetiology and pathogenesis are discussed. It is concluded that the clinical picture was an atypical form of botulism caused by Cl. botulinum type B. Possible causes of this abnormal clinical picture are discussed in greater detail.

Animal Feed↗

Fluid accumulation in the ligated intestinal loop and histopathological changes of the intestinal mucosa caused by Clostridium botulinum C2 toxin in the pheasant and chicken.

Fluid accumulation was induced in ligated intestinal loops of both pheasants and chickens injected with crude Clostridium botulinum C2 toxin. Necrosis of the epithelium and lamina propria of the duodenum and jejunum occurred in both species of bird after intraduodenal administration of crude C2 toxin. The severity of such reactions depended upon the dose and the period after administration of C2 toxin up to eight hours, and such reactions were suppressed specifically with rabbit anti-C2 toxin. These results confirm that C2 toxin is one of the causes of diarrhoea in avian botulism.

Animals↗

The action of batulinum toxin at the neuromuscular junction.

Botulism results from the action of a protein neurotoxin (mol. wt. congruent to 150,000) produced by the bacterium Clostridium botulinum, of which there are eight known strains. Botulinum neurotoxin is the most potent biological toxin known, having a median lethal dose of 5--50 ng/kg body weight. The primary site of action of botulinum toxin is the cholinergic nerve terminal, where it blocks the release of the neurotransmitter acetylcholine. Death usually results from respiratory failure. Nonlethal doses of botulinum toxin can induce sprouting of the nerve terminal and have significant postsynaptic effects, including muscle atrophy and alterations in the membrane electrical properties of the muscle fiber. There is no universally available treatment for botulinum intoxication. However, immunotherapeutic and chemotherapeutic procedures are not being developed and will be discussed.

4-Aminopyridine↗

[Morphological and histochemical reactions of an organism to the administration of Clostridium botulinum toxin. IX. Reactions of the neurons of the abducens nerve nucleus and of the Darkshevich's nucleus to the administration of C. botulinum type B toxin].

Pathomorphological and histochemical study carried out in guinea pigs at the stage of paralysis of the limbs after the oral administration of C. botulinum toxin has revealed the presence of morpho-metabolic changes pertaining to phase 2 of the development of dystrophic processes in the neurons of the nucleus of the abducent nerve and Darkshevich's nucleus. At the myasthenic stage the development of dystrophic processes in the neurons of Darkshevich's nucleus has been found to reach phase 3. The study indicates that C. botulinum toxin possesses different tropism in respect of the neurons of the oculomotor nuclei; this fact correlates with the clinical picture of botulism.

Animals↗

The role of anaerobes in human infections.

Anaerobic bacteria have been shown to play a role in infection of all types in humans. Certain infections are notable for the prominent role played by anaerobes; included are brain abscess, chronic sinusitis and otitis media, oral and dental infections, neck space infections, bite infections, lung abscess, aspiration pneumonia, empyema, intra-abdominal infections of all types (notably peritonitis, intra-abdominal abscess, and liver abscess), abdominal surgical wound infections, female genital tract infections of all types, various superficial and deep soft tissue infections, and osteomyelitis. In recent years, two new anaerobic infections have been appreciated-infant botulism and pseudomembranous colitis due to Clostridium difficile. Considerable progress has been made recently in delineating factors predisposing to anaerobic infections, virulence factors in anaerobes, and host defense mechanisms vs. these organisms. Taxonomic schemes for anaerobes have been improved and simplified considerably, as have techniques for growing and identifying anaerobic bacteria. Rapid procedures are coming into the picture. Finally, much has been learned about therapy of these infections. Although there has been some problem of increased resistance of anaerobes to antimicrobial agents, several promising new drugs are now available to offset this.

Anaerobiosis↗