Acute infectious diarrhea (food poisoning)

Acute infectious diarrhea (food poisoning)

    * Introduction
    * Addressing the patient with infectious diarrhea
    * Epidemiology
    * Food poisoning - bacterial contamination of food
    * Diagnostic Laboratory
    * Treatment
    * Prophylaxis of acute infectious diarrhea
Diarrhea is an abnormal situation, the patient often eliminate unformed stools accompanied by incomplete digestion of food ingested. It's wrong opinion whose seats are considered to be frequent diarrhea decisive for the diagnosis of diarrhea is the presence of unformed stools containing undigested or incompletely digested food.

Digestive tract diseases in the world is second in frequency after upper respiratory tract disease. They are dangerous, because in some cases cause rapid dehydration and death of the patient's body, within a few hours of first symptoms.

Acute diarrheal diseases predominantly affecting people in developing countries under (Africa, Asia, Latin America), and especially children in these areas, being the leading cause of death.

Diarrhea prevent digestion and absorption of food from the digestive tract, causing malnutrition in this way, accompanied by scadereea body's resistance to opportunistic infections.
  Diarrhea may be due to digestive causes or extradigestive: -Digestive causes of diarrhea: infectious and parasitic diseases, pancreatopatii, malabsorption. -Causes of diarrhea extradigestive: strong emotions, endocrine or renal causes.
Diarrhea may be seen as a mechanism by which the body tries to remove as soon as a harmful factor, reached inside the digestive tract, intestinal transit is accelerated, resulting in inefficient absorption of water and incomplete digestion of food (with malnutrition) in the same time will increase the amount of intestinal secretions and in some cases digestive manifestations may accompany the elimination of the stool, blood, pus or mucus.

The existence of a diarrheic syndrome requires the development of investigations to elucidate the etiology: copro-parasitological examination of faeces, Rectoscope, colonoscopy or barium enema tests to evaluate the function of absorption in the gut and pancreas function.

 
Pathogen of acute infectious diarrhea Mecanisnemele

Diarrhea occurs when germs (bacteria, viruses or fungi), manage to overcome the body's defense mechanisms. To establish a diagnosis and correct treatment is important to understand how these factors act of aggression on the digestive tract.

Pathogen reaches the digestive tract with food intake. A pathogen cause disease when a minimum number of organisms ingested. For example, 10-100 Shigella bacteria are enough to cause diarrhea. Some bacteria are spread by direct interpersonal contact (Giardia, Shigella, Entamoeba) and multiply in other foods until they develop infectious dose (Salmonella).

To trigger the disease, microorganisms must first adhere to the intestinal mucosal epithelium. Bacteria on the surface, a series of proteins, called adezins, which have a role in attachment to intestinal cells (eg, work on cholera). If microorganisms would not be able to attach the brush at the edge of the enterocytes (epithelial cells in the gut), they could not produce toxic phenomena of infectious diarrheal disease.

 
After invasion of intestinal epithelial cells, pathogens will produce toxins: -Enterotoxins: disrupt the secretion of intestinal secretory cells, causing watery diarrhea. -Citoxine: cause cells of the intestinal mucosa. -Neurotoxins: act over the nervous system.

Cholera toxin can be given as an example of how its action, is an enterotoxin, it has the effect of chlorine to increase intestinal secretion, and decreased Na permeation, resulting in fluid loss and diarrhea. E. coli produces a toxin (thermolabile enterotoxin), which acts by a mechanism similar to that triggered by cholera toxin.

Citotoxinele act more aggressively than bacterial enterotoxins. They destroy the intestinal lining cells, and produce a dysentery syndrome, characterized by removing seats that contain blood, mucus and numerous inflammatory cells (leukocytes).

Neurotoxinele trigger symptoms shortly after eating contaminated food, they act on the central nervous system and cause vomiting.

Sometimes the agent may be particularly virulent and invade cells lining the gut, for example, Shigella or E. coli. These bacteria will invade the intestinal mucosa cells, replicate intracellularly and then will be spread to neighboring cells. Salmonella invade the intestinal mucosa but usually it does not cause destruction of enterocytes, causing dysentery syndrome, is very incomplete.

 
Host defense mechanisms

Each food ingestion is a potential danger to humans. Usually the food will not get perfectly clean. Although the digestive system to communicate directly with the external environment contaminated with microorganisms, it has developed a number of mechanisms to defend against microbial invasion.

In the digestive tract there is normally an indigenous bacterial flora, preventing colonization of intestinal pathogens enterotoxici. Consumption of antibiotics can lead to destruction of the body's own bacteria, exposing the patient to infections with enteropathogens.

Shows colon in most of the anaerobic flora that by maintaining low pH (acid pH) and the production of volatile fatty acids creates a barrier against colonization by enteropathogens.

The pH of gastric acid, is an important barrier to defend the body against external aggression. Disruption or neutralizing acid secretion by administration of drugs (antacids) enteric colonization increases risk. However, there are microorganisms that can not be destroyed by gastric acidity (rotaviruses).

All the body's defense mechanism is the normal intestinal motility and that the fact that mobilizes food in the intestine, shorten the micro-stationary, thus lowering the risk of infection. In the digestive system, immune system is well represented. Cell-mediated immunity protects against pathogens effectively. Humoral immunity is achieved by means of IgG and IgM antibodies (immunoglobulins G and M) taken from the systemic circulation, and by IgA secreted by intestinal mucosa. IgA is important in binding the bacterial antigen, favoring its processing and secretion of antibody after the onset.