Your Online Health Information Site

Advertisement

Gastroenteritis And Food Poisoning

Introduction

As can be seen later, both gastroenteritis and also food poisoning are diseases where the wall of the stomach or intestine gets inflamed. Formerly, up to the present time it was thought that most gastroenteritis that presented as diarrhea would be caused by various viruses. Nevertheless, lab techniques have ultimately been markedly refined. We now know indeed, that unlike viruses there are many other causes for gastroenteritis, which will be discussed in more detail below.

Common causes of vomiting and diarrhea (gastroenteritis)

_________________________________________________

Bacteria : Vibrio cholera (cholera), Salmonella typhi (salmonella or typhoid fever), Shigella sonnei (shigellosis), Staphylococcus aureus, E. coli 0157:H7 and other types, Clostridium perfringes (necrotizing enteritis), Clostridium botulinum (botulism), Campylobacter, H.pylori

Viruses (see below): rotavirus (children 3-15 months), enteric adenovirus (children less than 2 years), astrovirus, calicivirus (Norovirus, affects older children and adults), echovirus (newborns, preterm infants), rarely polio virus (in unimmunized children)

Parasites (“Traveler’s Diarrhea”) : Giardia lamblia, Cryptosporidium parvum, Entamoeba histolytica, Isospora, Cyclospora, Microsporidia, hookworm

_________________________________________________

First of all, the common denominator is that due to a chemical or bacterial toxin there is a tremendous irritation of the lining of the digestive tract, which surely leads to a loss of fluids and electrolytes. For the period of the gastroenteritis or the food poisoning there is certainly some degree of slowing of absorption of food products through the gut wall (malabsorption). Above all, on the whole children including older people and immunocompromised patients are most vulnerable to this.

 Gastroenteritis And Food Poisoning

Gastroenteritis And Food Poisoning

Reasons for developing gastroenteritis

Furthermore, what in detail do we know about why gastroenteritis occurs and how can we demonstrate in what way it affects the body? As a matter of fact, cholera notably disappeared in industrialized countries; however, as a matter of fact it is still a significant problem in development countries. Thorough scientific studies led to the success in industrialized countries. In essence these studies uniquely revealed that the bacterium, called Vibrio cholerae, produces a toxin, which by itself can cause the same symptoms as if the cholera bacterium were there. In brief, further research led to the sanitation of drinking water through water chlorination.

Mechanism of enterotoxins

Finally, we now have access to effective, improved vaccines for travellers going to cholera infested areas. This model has taught us that a specific enterotoxin, different for every pathogen, can play a major role in many gastroenteritis cases. Accordingly, examples for this can be found explicitly in many cases of traveler’s diarrhea or nursery diarrhea. In these cases we truly know that enterotoxins from Escherichia coli (E.coli) are equally important for this. In other cases such as in Salmonella, Shigella and some other E.coli strains there are local toxic factors, which the bacteria explicitly release upon contact with the mucous membrane of the gastrointestinal tract.

Blood and fluid loss from tiny ulcerations

As a result this causes tiny ulcerations and leakage of blood, fluids and electrolytes as well as protein. In the final analysis it is indeed this loss of fluids, electrolytes and proteins, which potentially can kill the affected person. The patient will survive, if he/she is attended to in the hospital setting. Specifically, the physician chiefly replaces electrolytes, fluid, protein and if necessary, blood intravenously. This restores the balance and the patient survives.

Pathogenicity different for different people

It seems like the same cause in two different persons can make the one deadly sick, while the other one will only be slightly inconvenienced. For the most part prior exposure and pre-existing antibody pool surely determines every person’s resistance. Also, it probably depends on distinctive genetic factors, on age (infants and senior citizens are most vulnerable), and on the type of toxin, bacterium, virus, parasite or chemical that particularly caused the condition. Moreover, some persons may be significantly weakened by a chronic H.pylori infection (see link for H. pylori under “gastritis” below in the “Related Topics” section) of the stomach. By the same token, a duodenal ulcer can make patients explicitly more vulnerable to other infections in the gastrointestinal system.

Transmission of pathogens

In essence, most transmissions certainly occur from person to person. This is truly the case for infections such as with Campylobacter, Shigella, Giardia and Escherichia coli 0157:H7. Meanwhile, this is explicitly the cases for Salmonella that can be transferred through animals (turtles, iguanas, diseased chickens), but also from persons such as meat handlers, particularly, if they are chronic carriers from a prior infection that never cleared. In like manner certainly eggs can also be infected with Salmonella. While a soft-boiled egg allows Salmonella, if present, to survive, conversely a hard-boiled egg cooked for 10 minutes will be free of Salmonella. At the same time meat can be contaminated from meat handlers who have open sores or boils on their hands because especially staphylococcal toxin from these pus bacteria can surely cause food poisoning.

Enteric viruses

Be this as it may, many viruses such as caliciviruses (Norwalk virus), rota viruses, adenoviruses, and astroviruses are transmitted specifically  through water/food or through the fecal-oral route. It must be remembered that one of the most well known of these, namely poliovirus, has historic significance. By all means, it is almost unknown in the Western world now, but it certainly is still a killer in development countries without child vaccination programs. Nonetheless, it also is still frequent in pockets of populations that refuse poliovirus vaccinations.

Natural course of poliomyelitis

In general, children or young adolescents with no antibody level against poliovirus will get polio. In this case there is a slight fever, throat infection and vomiting after about 4 to 5 days. Notably, it is important to realize that in about 90% of cases it is a relatively minor clinical disease. In contrast, another key point is that in the other 10% the more severe major poliomyelitis that occurs presents after an incubation time of about 1 or 2 weeks as an acute disease with a high fever, a severe headache and neck stiffness. It is important to realize that it is extremely contagious.

Result of poliomyelitis

As a result there can be swallowing and breathing problems depending on what centers in the spinal cord and brain the poliovirus affects. Consequently a progressive asymmetrical limb weakness and muscle paralysis will occur with preserved sensitivity in the skin. Another key point is that even when the person survives polio, decades later a post-poliomyelitis syndrome can produce muscle weakness and extreme fatigues, which are disabling.

Norovirus and other gastroenteritis causes

On the other hand, many outbreaks of gastoenteritis on cruise ships or in nursing homes are due to Norovirus (an older name for it is Norwalk agent). Above all. the list above gives you an idea about the common causes of gastroenteritis (vomiting and diarrhea). At the same time there are many other agents that can produce diarrhea and vomiting, which are the major symptoms of gastroenteritis. Such toxins are found in mushrooms and garden plants But not to mention seafood beyond its freshness date (clams, fish and mussels), or heavy metals such as mercury, lead, arsenic or cadmium. In like manner, use of antibiotics for various medical conditions can change the gut flora and give rise to a chronic inflammation of the colon with the bacterium Clostridium difficile, which is difficult to treat.

Signs and symptoms

First, generally speaking the patient feels sick, may vomit, then develops diarrhea and abdominal cramps. Second, dehydration sets in fast as vomiting and diarrhea continue and for this reason the affected person cannot keep fluids down by mouth. Depending on what the underlying cause for the digestive tract disease is, there maybe different symptoms, which might become apparent. Third, typhoid fever, which is caused by the bacterium Salmonella typhi, is causing constipation more often than diarrhea. However, in the light of ulcerations in the lining of the small bowel, finally there can be serious blood loss into the gut.  Equally important, 1% of cases present with bowel perforation (Ref. 28) and peritonitis.

Meanwhile, with a viral gastroenteritis the onset is usually slower over one or two days, and the diarrhea that ensues tends to be watery without any blood.

For further details and for a description of the treatments for the various causes of gastroenteritis see the links below under “Related Topics”.

References

1. M Frevel Aliment Pharmacol Ther 2000 Sep (9): 1151-1157.

2. M Candelli et al. Panminerva Med 2000 Mar 42(1): 55-59.

3. LA Thomas et al. Gastroenterology 2000 Sep 119(3): 806-815.

4. R Tritapepe et al. Panminerva Med 1999 Sep 41(3): 243-246.

5. The Merck Manual, 7th edition, by M. H. Beers et al., Whitehouse       Station, N.J., 1999. Chapters 20,23, 26.

6. EJ Simchuk et al. Am J Surg 2000 May 179(5):352-355.

7. G Uomo et al. Ann Ital Chir 2000 Jan/Feb 71(1): 17-21.

8. PG Lankisch et al. Int J Pancreatol 1999 Dec 26(3): 131-136.

9. HB Cook et al. J Gastroenterol Hepatol 2000 Sep 15(9): 1032-1036.

10. W Dickey et al. Am J Gastroenterol 2000 March 95(3): 712-714.

11. M Hummel et al. Diabetologia 2000 Aug 43(8): 1005-1011.

12. DG Bowen et al. Dig Dis Sci 2000 Sep 45(9):1810-1813.

13. The Merck Manual, 7th edition, by M. H. Beers et al., Whitehouse  Station, N.J., 1999.Chapter 31, page 311.

14. O Punyabati et al. Indian J Gastroenterol 2000 Jul/Sep 19(3):122-125.

15. S Blomhoff et al. Dig Dis Sci 2000 Jun 45(6): 1160-1165.

16. M Camilleri et al. J Am Geriatr Soc 2000 Sep 48(9):1142-1150.

More references

17. MJ Smith et al. J R Coll Physicians Lond 2000 Sep/Oct 34(5): 448-451.

18. YA Saito et al. Am J Gastroenterol 2000 Oct 95(10): 2816-2824.

19. M Camilleri Am J Med 1999 Nov 107(5A): 27S-32S.

20. CM Prather et al. Gastroenterology 2000 Mar 118(3): 463-468.

21. MJ Farthing : Baillieres Best Pract Res Clin Gastroenterol 1999 Oct 13(3): 461-471.

22. D Heresbach et al. Eur Cytokine Netw 1999 Mar 10(1): 7-15.

23. BE Sands et al. Gastroenterology 1999 Jul 117(1):58-64.

24. B Greenwood-Van Meerveld et al.Lab invest 2000 Aug 80(8):1269-1280.

25. GR Hill et al. Blood 2000 May 1;95(9): 2754-2759.

26. RB Stein et al. Drug Saf 2000 Nov 23(5):429-448.

27. JM Wagner et al. JAMA 1996 Nov 20;276 (19): 1589-1594.

28. James Chin, M.D. Control of Communicable Diseases Manual. 17th ed., American Public Health Association, 2000.

29. The Merck Manual, 7th edition, by M. H. Beers et al., Whitehouse Station, N.J., 1999. Chapter 157, page1181.

30. Textbook of Primary Care Medicine, 3rd ed., Copyright © 2001 Mosby, Inc., pages 976-983: “Chapter 107 – Acute Abdomen and Common Surgical Abdominal Problems”.

31. Marx: Rosen’s Emergency Medicine: Concepts and Clinical Practice, 5th ed., Copyright © 2002 Mosby, Inc. , p. 185:”Abdominal pain”.

32. Feldman: Sleisenger & Fordtran’s Gastrointestinal and Liver Disease, 7th ed., Copyright © 2002 Elsevier, p. 71: “Chapter 4 – Abdominal Pain, Including the Acute Abdomen”.

33. Ferri: Ferri’s Clinical Advisor: Instant Diagnosis and Treatment, 2004 ed., Copyright © 2004 Mosby, Inc.

Last modified: August 31, 2018

Disclaimer
This outline is only a teaching aid to patients and should stimulate you to ask the right questions when seeing your doctor. However, the responsibility of treatment stays in the hands of your doctor and you.