AG may run an asymptomatic, typical or severe course, depending on the overall health of the patient, the pathogenicity of the causative agent, the infectious dose and degree of dehydration.

The typical course consists of a short prodromal phase with mild fever, nausea and vomiting. Diarrhea and possibly an increase in body temperature marks the subsequent phase of disease that usually doesn't last longer than three or four days. It has been suggested that high fever is generally caused by bacteria, while mild fever indicates viral gastroenteritis. Both incubation period and duration of illness are usually shorter if the causative agent is a virus. It has to be noted though, that these parameters are little specific and sensitive [9]. AG is usually self-limiting.

Melena is not characteristic for AG, but may be observed if pathogens either penetrate deep into the intestinal wall or mechanically destroy its inner layers. This condition may be provoked by certain bacterial and parasitic species, e.g., by enterohemorrhagic Escherichia coli or Shigella spp., or may result from an exacerbation of a rather harmless infection in immunocompromised patients.

Information regarding symptom onset, frequency and quantity of vomiting, diarrhea and micturition as well as possible loss of body weight should be obtained during the initial interview. Reduced ingestion of water, decrease of urine output and body weight indicate an advanced state of dehydration.

Laboratory analyses of blood samples may confirm a suspected dehydration if such diagnosis cannot be made during clinical examination. In any case, such tests are very helpful to assess water and electrolyte imbalances and to recognize acidosis. In cases of severe dehydration, kidney function should be monitored by repeated measurements of urea and creatinine.

Especially in cases of prolonged gastroenteritis, i.e., if diarrhea does persist for more than four days, detection of blood in stool samples may serve as an additional hint at bacterial or parasitic genesis. Such analysis may be followed by bacterial culture, molecular biological exams or immunoassays to identify the etiologic agent of the disease. The latter may also be carried out to specify the causative pathogen in case of viral infection, if this information is of interest due to clinical or epidemiological reasons. Serological tests may yield positive findings after more than 24 hours of illness and for up to two weeks after infection.

Treatment is supportive and mainly aims at compensating for fluid and electrolyte loss and avoiding severe dehydration. Thirst, skin turgor, mucous membranes, blood pressure and urine output are suitable parameters to continuously evaluate the current state of hydration.

Mild cases of dehydration may be treated with oral rehydration therapy. The latter may even be indicated before unequivocal symptoms of fluid loss manifest. In contrast, oral rehydration is generally not sufficient to revoke severe lack of fluids. Here, intravenous administration of saline solutions, possibly supplemented with lacking electrolytes, is required.

Antiemetics and antidiarrheal compounds are generally not applied, particularly not in young children.

Patients may, however, benefit from administration of probiotics. Both duration of diarrhea and hospitalization have been shown to be shortened if patients receive probiotics, although their precise mechanisms of action are not yet completely understood [10]. They have been suggested to suppress proliferation of pathogenic microorganisms and to modulate immune function. Of note, probiotics may have a beneficial but only limited effect in AG patients.

Prognosis is usually excellent if an appropriate state of hydration is kept. Rapid dehydration and difficult rehydration may be an issue in children, old people and those that are immunodeficient or suffer from other comorbidities. Intravenous rehydration is often required in these cases. Prognosis worsens significantly with the inability to compensate for fluid loss sustained through vomitus and diarrhea.

The vast majority of AG cases is caused by distinct species of viruses. Rotavirus, for instance, accounts for hundreds of millions of annual cases in children aged less than five years [1]. There are few children in the world who are older than three years and who have not suffered from an infection with rotavirus. Over the course of the last decades, a plethora of other viral agents has also been related to AG. The most common are:

• Caliciviridae. This family comprises the genera norovirus and sapovirus. The former includes several species sometimes referred to as Norwalk and Norwalk-like viruses.
• Enteric adenoviruses 40 and 41
• Astrovirus
• Coronavirus and torovirus, both pertaining to the family of Coronaviridae

Data regarding the relative share of each of the aforementioned species in overall viral AG prevalence vary largely [4] [5]. Also, infections with more than one pathogen are very common.

It has been estimated that one out of five cases is caused by bacteria. Most commonly, Enterobacteriaceae account for them. In detail, the following species have been related with AG:

• Escherichia coli
• Salmonella spp.
• Shigella spp.
• Yersina spp.
• Campylobacter spp.
• Vibrio cholerae

With regards to parasites, acute inflammation of the gastrointestinal tract is often mediated by protozoa. These species have to be mentioned in this context:

• Cryptosporidium spp.
• Entamoeba histolytica
• Giardia lamblia

There are significant differences between industrialized nations and developing countries regarding the likelihood of gastroenteritis being triggered by any of the above mentioned species. Bacterial and parasitic AG, for instance, are much more common in the developing world. This fact results from an overall improved sanitary status in developed countries and points out that disease incidence - at least regarding those pathogens - may be diminished by taking the appropriate hygiene measures.

It has been estimated that more than 130 million children aged less than five years are affected by viral gastroenteritis every year [1]. Although viral infection accounts for the majority of cases, the overall number of AG will surely surpass this number if bacterial and parasitic forms as well as patients pertaining to other age groups are considered, too. Annually, almost one million children die from AG. These values result in a worldwide mortality of 0.7% for pediatric AG patients. However, there are large geographical differences and mortality in industrialized countries is generally about 1 per 100,000 children. Mortality may be significantly reduced by making immunization against rotavirus part of the routine pediatric care [6] [7].

AG may affect people of all races and both genders. Most patients are children and the age peak corresponds to infants aged less than two years, but the disease may be diagnosed in patients of any age.

Seasonal dependency has been shown for AG incidence. More cases are registered during the cold season than during warm summer months.

Fecal-oral transmission and contaminated water and food are the main sources of infection, although droplet infection has been described for some agents related to AG.

With regards to viral AG, pathogens infect enterocytes, replicate inside these cells and subsequently mediate cell lysis. This process leads to epithelium atrophy. Repair mechanisms set in, but only immature cells can repopulate the damaged intestinal parts. Thus, impaired intestinal function may persist even after the causative pathogens have been eliminated. Of note, release of viruses from host cells has been described to occur without lysis. While this has consequences for potential histopathological analysis in as much as only few epithelial lesions will be visible, enterocytic function is still disturbed and AG symptoms will set in nevertheless. Similarly, release of toxins may alter intestinal function without any obvious damage to villi or crypts.

Diarrhea may result from maldigestion and reduced absorption of osmotically active compounds or from active secretion of electrolytes and water into the intestinal lumen [8]. Presumably, both processes contribute to diarrhea in most cases of AG: An inflamed intestinal wall will be restricted in function, show a decreased permeability for certain molecules that consequently draw water into the lumen, and stimulation of the enteric nervous system augments active water and electrolyte secretion. These conditions may be provoked by all kinds of pathogens by means of cell lysis as described above, release of toxins, invasion of the intestinal wall and initiation of an immune response, or mechanical damage alone.

Appropriate hygiene measures may largely contribute to reduce the risk of contracting gastroenteritis:

• Regular hand washing, especially after close contact to children and before eating
• Education of children to adopt this behavior themselves
• Avoidance of ingestion of water or food of unknown sources unless it has been boiled, cooked or peeled, respectively (water spring, unpasteurized milk, ice cream, fruits, etc.)
• The latter particularly applies while traveling

Vaccines are available for certain types of AG [7].

Acute gastroenteritis (AG) is a very common disease associated with inflammation of the stomach and intestines that can be triggered by all kinds of pathogens, i.e., by viruses, bacteria and parasites, and by consciously or unconsciously ingested toxins. By far most cases are caused by viral infection, especially with rotavirus. With regards to bacteria, those species pertaining to the family of Enterobacteriaceae are most frequently associated with AG.

Patients of all ages may present with AG, but the majority of affected individuals are children. In pediatric patients, sporadic infection with rotavirus triggers AG. Similar cases may be observed in adults, but the relevant pathogen spectrum is wider and additionally comprises enteric adenovirus, astrovirus and calicivirus [1]. The latter is actually the most frequently isolated pathogen in this regards. Calicivirus may also account for epidemics of AG. Such cases usually occur due to contamination of water or food and simultaneous ingestion of the pathogen by many people [2].

AG is characterized by a sudden onset of symptoms - typically fever, malaise, abdominal pain, nausea, vomiting and diarrhea - but severity may vary widely. In industrialized countries, self-limiting diarrhea is the most common manifestation of AG. Here, symptoms subside within a few days. However, diarrhea may provoke severe dehydration and become life-threatening in risk groups like children, old people and those suffering from comorbidities. And although morbidity is high, mortality is still rather low in these geographical regions. In contrast, AG is one of the leading causes of death in developing countries [3]. Highest mortality rates are encountered in pediatric patients. They result from the inability to compensate for severe loss of fluids and dehydration.

In case of infectious AG, pathogens are excreted with stools and may take a number of different routes towards new hosts. Direct contact and fecal-oral transmission is one of the main forms of spread of disease and particularly occurs among children in all parts of the world. Ingestion of contaminated water or food is the other way of contracting AG and does not require direct contact to an infected person. This may largely be prevented by application of appropriate hygienic measures in the food industry and, on a personal level, by avoiding consumption of unboiled water or food of unknown quality. The incubation period usually lasts a few days.

Acute gastroenteritis (AG) is the medical term for what is commonly called the "stomach but". This disease is characterized by sudden onset of symptoms that indicate an inflammation of stomach and intestines.

Although AG may be diagnosed in patients of any age, most patients are young children.

Causes

Most cases of AG are caused by viruses. Distinct species have been associated with this condition and the most frequently detected strains are rotavirus, norovirus, adenovirus and astrovirus. Bacteria, particularly those pertaining to the family of Enterobacteriaceae, and parasites may also cause infectious AG. All these pathogens may be transmitted via fecal-oral transmission or by consumption of contaminated water and food.

Less frequently, AG is triggered by conscious or unconscious ingestion of toxins.

Symptoms

After a short prodromal phase of mild fever, nausea and vomiting, diarrhea sets in. Severity of symptoms may differ according to the overall health of the patient, the pathogenicity of the causative agent and the infectious dose. The disease is usually self-limiting after a few days.

Children, old people, immunodeficient individuals and those suffering from other diseases are at higher risks of dehydration while being affected by AG. Severe dehydration may lead to death.

Diagnosis

Diagnosis of AG is based on the patient's medical history and clinical examination. Additional diagnostic measures are rarely required but may be carried out in more severe cases to assess water and electrolyte imbalances. Also, if diarrhea persists for more than four days, stool samples may be obtained for further analysis as to the cause of the disease.

Treatment

In most cases, no specific treatment is necessary.

It is of utmost importance that AG patients remain hydrated. Oral rehydration therapy is required in mild cases of dehydration while intravenous administration of saline solutions and possibly electrolytes is necessary to treat more severely dehydrated patients.

Antiemetics and antidiarrheal are not routinely administered. This particularly applies to pediatric patients.

1. Wilhelmi I, Roman E, Sanchez-Fauquier A. Viruses causing gastroenteritis. Clin Microbiol Infect. 2003; 9(4):247-262.
2. Mellou K, Sideroglou T, Potamiti-Komi M, et al. Epidemiological investigation of two parallel gastroenteritis outbreaks in school settings. BMC Public Health. 2013; 13:241.
3. Ramani S, Kang G. Viruses causing childhood diarrhoea in the developing world. Curr Opin Infect Dis. 2009; 22(5):477-482.
4. Chhabra P, Payne DC, Szilagyi PG, et al. Etiology of viral gastroenteritis in children
5. Shoja Z, Jalilvand S, Mollaei-Kandelous Y, Validi M. Epidemiology of viral gastroenteritis in Iran. Pediatr Infect Dis J. 2014; 33(2):218-220.
6. Amador JJ, Vicari A, Turcios-Ruiz RM, et al. Outbreak of rotavirus gastroenteritis with high mortality, Nicaragua, 2005. Rev Panam Salud Publica. 2008; 23(4):277-284.
7. Bayard V, DeAntonio R, Contreras R, et al. Impact of rotavirus vaccination on childhood gastroenteritis-related mortality and hospital discharges in Panama. Int J Infect Dis. 2012; 16(2):e94-98.
8. Lorrot M, Vasseur M. How do the rotavirus NSP4 and bacterial enterotoxins lead differently to diarrhea? Virol J. 2007; 4:31.
9. Chemaly RF, Yen-Lieberman B, Schindler SA, Goldfarb J, Hall GS, Procop GW. Rotaviral and bacterial gastroenteritis in children during winter: an evaluation of physician ordering patterns. J Clin Virol. 2003; 28(1):44-50.
10. Vandenplas Y, Salvatore S, Vieira M, Devreker T, Hauser B. Probiotics in infectious diarrhoea in children: are they indicated? Eur J Pediatr. 2007; 166(12):1211-1218.