1.2 BACKGROUND OF STUDY
1.3 STATEMENT OF THE PROBLEM
1.4 OBJECTIVE OF THE STUDY
1.5 SIGNIFICANCE OF THE STUDY
1.6 DEFINITION OF TERMS
CHAPTER TWO: LITERATURE REVIEW
2.1 FOOD POISON
2.2 CAUSES OF FOOD POISONING
2.3 TYPES OF FOOD POISON ORGANISM
CHAPTER THREE: RESEARCH METHODOLOGY
3.2 RESEARCH DESIGN
3.3 POPULATION OF STUDY
3.4 SAMPLING TECHNIQUE/SAMPLE SIZE
3.5 DESCRIPTION OF RESEARCH INSTRUMENT
3.6 VALIDITY/RELIABILITY OF DATA GATHERING INSTRUMENT
3.7 METHOD OF DATA COLLECTION
3.8 METHOD OF DATA ANALYSIS
CHAPTER FOUR: DATA ANALYSIS, INTERPRETATION AND DISCUSSION
4.1 DATA ANALYSIS AND RESULT
4.2 DISCUSSION OF FINDINGS
CHAPTER FIVE: SUMMARY OF FINDINGS/CONCLUSION AND RECOMMENDATION
Certain bacterial agents have been implicated in out breaks of food poisoning on the basis of presumptive and inconclusive evidence. 1 year after some of these same agent are reported in the literature without additional proof as to their etiological significance. As a result many mis-conceptions have arisen in textbooks and scientific journals regarding the role of such agents in food poisoning. It is the purpose of this paper to point out some of the problems in the field and to illustrate with a few examples some of the difficulties in assigning, significance to these organisms. Many kinds of micro-organismsm have allerged to cause food poisoning merely because they have found in large numbers in implicated foods, or in the vomitus or stools of patients. Some of these bacteria are natural inhabitants of the intestinal tract of healthy persons and there is no reason other than the circumstantial evidence cited for assigning them causative roles in food poisoning. Most food at the time of eating contains many kinds of viable bacterial and certain foods may contain millions bacteria per gram without causing illness. In the latter circumstances it should not be surprising to find the kind of organism which are isolated from heavily contaminated food also appearing in specimens of vomitus and feces.
When illness follows the eating of a specific item of food there may have been a lapse of many hours before a sample is collected for laboratory study. often the food specimen is recovered from garbage pail where it has been subject to contamination from other decaying foods and has been held at a temperature for a sufficient time to change the bacterial population from that present at the time of eating. Another error is the failure to exclude known food poisoning bacterial on their products as the cause of illness. For example, staphylococcus enterotoxin gives rise to well defined symptoms with illness appearing 1 to 5 hours (usually 2 ½ to 3 hours) after swallowing the enterotoxin. There is frequently marked prostration, and in some cases shock. Vomiting and diarrhea are prominent symptoms and blood mucus may be present in the discharges. The illness tends to be more severe when the incubation periods is short. When a large number of persons presenting these symptoms is observing, it is important to rule eat staphylococcus food poisoning before implicating another organism. Staphyloccus entrotoxin withstands boiling temperature and for this reason it is possible to have enterotoxin present in a food after the organisms have been killed.
Many bacterial other than staphylococci have assigned as causative agents in food poisoning outbreaks that were undoubtedly caused by staphylococcus enterotoxin. Although it is possible that other agents may stimulate staphylococcus food poisoning, there has never been a clearly prove example of such an exception. Aside from botulism and staphylococcus food which are caused by toxin performed in food, other outbreaks of food poisoning follow the ingestion of living organisms. The symptoms and incubation period of the latter group, which include salmonella and certain alpha-type streptococci, “may not readily be distinguished or the condition diagnosed except by finding the specific agents and excluding other types of food poisoning. Too often only media selective for the Gram negative intestinal bacteria have been used for the examination of specimens without the use of media that support growth of the alpha-type streptococcus.
Recently several species of micro-organisms such as paracolon bacilli, “ Salmonella Pulldown, (6) proteus mirabilis, (7) clostridim prefringens, 8 and hemolytic streptococci (9) have been implicated as possible causative agents of food poisoning. All of these micro-organisms when grown in suitable media produce substances which are toxic for animals by the parenteral route has frequently given rise to difficulty in the identification of enterotoxic material. In distinction to the above, a true enterotoxin is toxic when fed in adequate amounts to suitable animals. They may also be toxic by the parenterel route.
Since many of the above micro-organisms have been implicated from time to time over a period of years, it is imperative that their role in the etiology of food poisoning be established. A positive solution to the problem would involve the feeding of cultures and filtrates to human volunteers. Obviously this procedure is not to be recommended, since in the case of many members of the group of Gram-negative intestinal bacteria, their pathogenicity is unknown furthermore, in food poisoning outbreaks caused by certain well established Salmonella species (e.g S Enteritidis, S. Cholera suis), an occasional person may develop a systemic infection. Although there is little evidence that other species of Salmonella isolated in association with food poisoning produce systemic infection, the possibility of such infections is sufficient reason for condemning such as approach to the problem.
In the absence of a direct approach involving the feeding of living agents to human volunteers, proof of the etiologic significance of an agent in food poisoning outbreaks rests upon a number of observations and test. A careful epidemiological study is valuable, especially in outbreaks in which a single item of food may be established as a common denominator for all who were made ill. This becomes difficult in the presence of a prolonged incubation period. If an implicated item of food can be secured, it is important to know what has happened to it and whether or not it has been kept under refrigeration or has been heated since the time of the outbreak.
If by good fortune, the food has been refrigerated, then a quantitative study of the bacteriological flora should be made, including a search for all probable food poisoning agents. A search should be made for agents in the stools and vomitus of patients, and blood cultures may be desirable in infections resembling those caused by salmonella.
In the case of food poisoning agents such as salmonellam, which are associated with infection rather than intoxication, there may be some valuable information collected with reference to the development of agglutinins or other immune bodies in patients recovering from attacks of the disease. The interpretation of low agglutinin titers in unsatisfactory. In all cases where the agglutination test is employed the limitations of the test should be borne in mind, and the possibility of previous exposures or immunizations should be considered. It is well known that in mild attacks of gastrointestinal illness caused by salmonella, slight or no rise in agglutinin titers may be found in the sera or patients during convalescence.