TABLE OF CONTENTS

Title Page-   –         –         –         –         –         –         –         –         –         i

Certification-          –         –         –         –         –         –         –         –         ii

Dedication-  –         –         –         –         –         –         –         –         –         iii

Acknowledgments-          –         –         –         –         –         –         –         iv

Table of Contents- –         –         –         –         –         –         –         –         v-vi

CHAPTER ONE

1.0 INTRODUCTION- –         –         –         –         –         –         1-4

CHAPTER TWO

2.0 Epidemiology of Food Poisoning from Bacterial Toxin- 5-7

2.1     Types of Bacterial Toxin-          –         –         –         –         –         8

2.1.1  Endotoxins- –         –         –         –         –         –         –         –         8-9

2.1.2  Exotoxins-   –         –         –         –         –         –         –         –         9-14

2.2     Groups of Toxins- –         –         –         –         –         –         –         14-16

2.2.1  Adenglate Cyclase Affecting Bacterial Toxins-       –         –         16-19

2.2.2  Host Cell Membrane Destruction Bacterial Toxins- –         –         19-22

2.2.3  Surfactant-like toxins-     –         –         –         –         –         –         22-24

2.2.4  Protein Synthesis-Inhibiting Toxins-   –         –         –         –         24-26

2.2.5  Neurotoxins-         –         –         –         –         –         –         –         26-27

2.2.6  Superantigens-       –         –         –         –         –         –         –         27-28

CHAPTER THREE

3.0 Modes of Action of Bacterial Toxins- –         –         –         29

3.1     Plasma Membrane Permeabilization-   –         –         –         –         29-30

3.1.2  Labeling Explicit Atoms- –         –         –         –         –         –         30-32

3.1.3  Evacuating Lipids or Lipid-Tied Down Atoms-       –         –         32-33

3.1.4  Examining intracellular Courses-        –         –         –         –         33-37

CHAPTER FOUR

4.0 Summary and Conclusion- –         –         –         –         –         38

4.1     Summary-    –         –         –         –         –         –         –         –         38-39

4.2     Conclusion- –         –         –         –         –         –         –         –         39-40

References

CHAPTER ONE

1.0 INTRODUCTION

Pathogenic microscopic organisms and higher eukaryotes have hung out, prompting an exact comprehension of each other’s mechanism for infection. Through fast development, microscopic organisms have designed progressively advanced methods to hit precisely where it harms, meddling with crucial host capacities. Nonetheless, toxins are not just valuable to the microscopic organisms — they have additionally turned into fundamental resource for researchers, who would now be able to utilize them as tools to investigate cell form  (Sengupta et al., 2011).

Pathogenic microbes apply their destructive impacts in the host through a course of destructiveness factors: exotoxins, endotoxin, intrusions proteins and such. Different poisons emitted by various microorganisms subvert the host intracellular flagging pathways as well as have one of a kind partiality for explicit host cells. Nitty gritty data has been gathered throughout the years with respect to the sanitization, synthetic portrayal, chemical activity and design of different bacterial toxins. Toxins capacity to tie to the explicit target cells makes them a great contender for medication conveyance and in disease therapeutics (Michi et al., 2004)

Various immunotoxins; half breed particles of bacterial toxins and antibodies, have wide applications in malignancy and are at present under clinical preliminary. Advances in genomics and proteomics have made an abundance of data identified with the nucleotide and protein successions of various toxins and distinctive databases are accessible with expanding data therefore.

One result of the transformative race among host and microbial pathogens is the improvement of advanced and explicit harmfulness factors, which give a particularly preferred standpoint to the life form that produces them. Over the previous decade, our comprehension of the instrument of activity of bacterial poisons has expanded massively. Numerous investigations have added to the sub-atomic definition — and, some of the time, to the revelation — of imperative pathways in cell science. A striking precedent is the finding that lockjaw poison is an endopeptidase, explicit for a layer protein that is restricted on synaptic vesicles and secretory granules. This finding was essential in the meaning of the sub-atomic components that underlie managed emission. Likewise, the significance of guanine-nucleotide-official (G) proteins in flag transduction was revealed by concentrates into the activity of cholera and pertussis poisons, which adjust distinctive classes of G proteins. Since the method of action of numerous poisons has been unwound, they can be utilized as exceedingly explicit and effective apparatuses in cell science (Raghava et al., 2007).

Bacterial poisons; the solvent antigens, discharged by various pathogenic microscopic organisms have a standing notoriety of being a toxic substance emitted throughout pathogenesis. Poisons can adjust the cell capacities by specifically focusing on various flagging pathways inside the host cell so as to tilt the parity in microscopic organisms support.

A total of 66% of foodborne diseases is caused by bacteria. Major disease include botulism caused by C. botulinum, gastroenteritis caused by E. coli strains, Salmonellosis and Staphylococcal poisoning. Moreover, B cereus and V. cholera are bacteria frequently reported as causative agents of toxic infection by food in some countries, food poisoning caused by S. aureus is the most prevalent, report indicate that S. aureus can be responsible for up to 41% of food poisoning outbreaks. Although it can affect people of any age, the range with the highest incidence goes from 20 to 49 years of age where up to 58% of the cases can be concentrated. The main food products related to food poisoning caused by S. aureus are chicken and eggs, cakes, pastas, sauces, milk and its derived product.