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Infantile Gastroenteritis

Infantile gastroenteritis is a common illness worldwide, causing significant morbidity and mortality, especially in developing countries. Its main characteristic is the presence of diarrhea, defined as stools more than 15g/kg for infants younger than 2 years and greater than 200 g for children and beyond that age and adults.

Presentation

Infantile gastroenteritis presentation widely varies depending on its etiology and severity. In viral gastroenteritis, most often caused by rotavirus, there is low fever, vomiting, and water-like stools. Most rotavirus patients are younger than 2 years [1]. Blood is absent in the fecal matter.

Severe abdominal pain and bloody diarrhea point to a bacterial etiology.

The existence of dehydration should be thoroughly assessed. Important clinical indicators are low blood pressure, tachycardia, thready pulse, significant weight loss, dry mucous membranes, and oliguria. The consciousness state may be decreased in severely affected infants.

The physician should inquire about the types of food the patient has ingested, which may point to a specific pathogen: dairy products may contain Staphylococcus, Campylobacter, Listeria or Salmonella species. Meat can be infected by Clostridium perfringens, Aeromonas, Staphylococcus and Salmonella or Campylobacter species, while seafood intake may lead to astrovirus, Vibrio, Aeromonas or Plesiomonas species infection. If symptoms occur sooner than 6 hours after ingestion, a preformed toxin, like those produced by Bacillus or Staphylococcus should be suspected. Nosocomial infection of various types has also been documented [2].

Aeromonas induces acute watery diarrhea or a more severe, cholera-like illness, with blood present in the stool [3]. Bacillus cereus causes precocious emetic syndrome that usually resolves within 24 hours [4] and watery diarrhea accompanied by severe cramps [5]. Campylobacter infection is characterized by a pre-diarrhea period, with fever, myalgia and abdominal pain [6]. Clostridium difficile may be complicated by pseudomembranous colitis [7]. Escherichia coli leads to enteritis that may progress to hemorrhagic colitis and hemolytic uremic syndrome [8]. Diarrhea usually lasts for 1 to 3 days and is accompanied by headache, dizziness, lymphadenopathy, rash and myalgia [9]. Nontyphoidal Salmonella infection is characterized by diarrhea that usually lasts less than a week, but may lead to extraintestinal complications, such as urinary tract infections, osteomyelitis or arthritis. Salmonella typhi is the etiological agent of typhoid fever, a condition with diarrhea, vomiting, anorexia, fever, headaches and rose spots. Bloody stools may be present both in Salmonella [10] and Shigella patients [11]. Cholera is described as afebrile, watery, painless diarrhea. A more severe form, cholera gravis may give rise to an immense liquid loss which rapidly progresses to severe dehydration and death [12]. Yersinia enterocolitica can be the causative agent of terminal ileitis and mesenteric lymphadenitis and may mimic appendicitis [13]. Complaints may persist up to one year in Yersinia infection [14]. The physician should inquire about associated symptoms of parasitic infections, like anal pruritus, that may be accompanied by diarrhea.

Workup

In cases where physical examination suggests a bacterial, protozoal or parasitic infection, laboratory tests are required in order to elucidate the etiology. In all situations where dehydration signs are observed, the physician should evaluate the gravity of the condition by ordering complete blood cell count, serum electrolytes, urea, and creatinine.

Clinical judgment indicates what tests may be necessary for a specific patient. Giardia lamblia is identified by enzyme immunoassay. Rapid antigen stool testing may highlight the presence of rotavirus, while polymerase chain reaction is used in calicivirus infection. Human astrovirus genotyping is possible in selected cases [15]. The stool should be examined for parasite ova and larvae [16], as well as leukocytes, that signify enteroinvasive infection. Bacterial cultures are extremely valuable [17] and should always be performed if the patient is febrile. Cultures for Campylobacter, Salmonella, and Shigella should be obtained if white or red blood cells are identified in the stool. Escherichia coli is identified if the stool is cultured on a specific environment such as a chromogenic media [18]. This is method valuable in Yersinia [19], Salmonella [20] and Vibrio [21] species, as well. A blood agar plate is useful for the detection of Aeromonas spp., Vibrio spp. and Plesiomonas spp. Campylobacter should be cultured on blood-free charcoal-cefoperazone-deoxycholate agar or Skirrow medium [22] or it can be identified using its characteristic Gram stain morphology. Antibiotic susceptibility testing is indicated in infants younger than 6 months or immunocompromised children, as well as those with prolonged evolution.

If the diarrhea is considered to be part of an ulcerative colitis or Crohn's disease, a colonoscopy may be indicated. This procedure sometimes visualizes pseudomembranes in Clostridium difficile infection. If this microorganism is identified, the physician should keep in mind and monitor the risk of developing toxic megacolon [23], intestinal perforation [24], renal failure or septic shock.

Treatment

Prognosis

The prognosis for infantile gastroenteritis is generally good, especially with prompt treatment. Most children recover within a few days to a week. However, severe dehydration can lead to complications if not addressed quickly. Long-term effects are rare, but repeated episodes may impact growth and development.

Etiology

Infantile gastroenteritis is primarily caused by infectious agents, including:

  • Viruses: Rotavirus and norovirus are the most common culprits.
  • Bacteria: Such as Escherichia coli and Salmonella.
  • Parasites: Like Giardia lamblia.

Non-infectious causes, such as food allergies or intolerances, are less common but possible.

Epidemiology

Gastroenteritis is a leading cause of illness in infants worldwide. It is more prevalent in developing countries due to limited access to clean water and sanitation. In developed countries, outbreaks often occur in daycare settings. Vaccination against rotavirus has significantly reduced the incidence of viral gastroenteritis in infants.

Pathophysiology

The pathophysiology of infantile gastroenteritis involves the invasion of the gastrointestinal tract by pathogens. These agents disrupt the normal absorption and secretion processes in the intestines, leading to diarrhea and vomiting. The loss of fluids and electrolytes results in dehydration, which is the primary concern in infants.

Prevention

Preventing infantile gastroenteritis involves several strategies:

  • Vaccination: Rotavirus vaccines are effective in reducing the incidence and severity of viral gastroenteritis.
  • Hygiene: Regular handwashing and proper food handling can prevent the spread of infections.
  • Breastfeeding: Provides protective antibodies and reduces the risk of infections.
  • Safe Water and Sanitation: Access to clean water and proper sanitation facilities is crucial.

Summary

Infantile gastroenteritis is a common condition characterized by diarrhea, vomiting, and abdominal pain in infants. It is primarily caused by infections and can lead to dehydration. Prompt diagnosis and treatment are essential for recovery. Preventive measures, including vaccination and good hygiene practices, play a vital role in reducing the incidence of this condition.

Patient Information

For parents and caregivers, understanding infantile gastroenteritis is important for managing the condition effectively. Key points include:

  • Recognize Symptoms: Be aware of signs like diarrhea, vomiting, and dehydration.
  • Hydration is Key: Ensure your child stays hydrated with oral rehydration solutions.
  • Continue Feeding: Maintain regular breastfeeding or formula feeding.
  • Seek Medical Advice: If symptoms persist or worsen, consult a healthcare professional.

By staying informed and taking preventive measures, you can help protect your child from the effects of gastroenteritis.

References

  1. Sánchez-Fauquier A, Wilhelmi I, Colomina J, Cubero E, Roman E. Diversity of group A human rotavirus types circulating over a 4-year period in Madrid, Spain. J Clin Microbiol. 2004;42:1609-1613
  2. Calbo E, Freixas N, Xercavins M, et al. Foodborne nosocomial outbreak of SHV1 and CTX-M-15-producing Klebsiella pneumoniae: epidemiology and control. Clin Infect Dis. 2011;52(6):743-9.
  3. Janda J, Abbott L. The genus Aeromonas: taxonomy, pathogenicity, and infection. Clin Microbiol Rev. 2010;23:35–73.
  4. Ehling-Schulz M, Fricker M, Scherer S. Bacillus cereus, the causative agent of an emetic type of food-borne illness. Mol Nutr Food Res. 2004;48:479–487.
  5. Stenfors Arnesen L, Fagerlund A, Granum P. From soil to gut: Bacillus cereus and its food poisoning toxins. FEMS Microbiol Rev. 2008;32:579–606.
  6. Fernandez-Cruz A, Munoz P, Mohedano R, et al. Campylobacter bacteremia: clinical characteristics, incidence, and outcome over 23 years. Medicine. 2010;89:319–330.
  7. Dallal R, Harbrecht B, Boujoukas A, et al. Fulminant Clostridium difficile: an underappreciated and increasing cause of death and complications. Ann Surg. 2002;235:363–372.
  8. Rohde H, Qin J, Cui Y, et al. Open-source genomic analysis of Shiga-toxin-producing E. coli O104:H4. N Engl J Med. 2011;365:718–724.
  9. Tarr P, Gordon C, Chandler W. Shiga-toxin-producing Escherichia coli and haemolytic uraemic syndrome. Lancet. 2005;365:1073–1086.
  10. Parry C, Hien T, Dougan G, et al. Typhoid fever. N Engl J Med. 2002;347:1770–1782.
  11. von Seidlein L, Kim D, Ali M, et al. A multicentre study of Shigella diarrhoea in six Asian countries: disease burden, clinical manifestations, and microbiology. PLoS Med. 2006;3(9):e353.
  12. Harris J, LaRocque R, Qadri F, et al. Cholera. Lancet. 2012;379:2466–2476.
  13. Ong K, Gould L, Chen D, et al. Changing epidemiology of Yersinia enterocolitica infections: markedly decreased rates in young black children, Foodborne Diseases Active Surveillance Network (FoodNet), 1996-2009. Clin Infect Dis. 2012;54(5):S385–S390
  14. Rosner B, Werber D, Hohle M, et al. Clinical aspects and self-reported symptoms of sequelae of Yersinia enterocolitica infections in a population-based study, Germany 2009-2010. BMC Infect Dis. 2013;13:236.
  15. Cardoso D, Fiaccadori F, Souza M, et al. Detection and genotyping of astroviruses from children with acute gastroenteritis from Goiânia, Goiás, Brazil. Med Sci Monit. 2002;8: 624-628.
  16. La Via W. Parasitic gastroenteritis.Pediatr Ann. 1994;23(10):556-60.
  17. Humphries R, Linscott A. Laboratory diagnosis of bacterial gastroenteritis. Clin Microbiol Rev. 2015;28(1):3-31.
  18. Church D, Emshey D, Semeniuk H, et al. Evaluation of BBL CHROMagar O157 versus sorbitol-MacConkey medium for routine detection of Escherichia coli O157 in a centralized regional clinical microbiology laboratory. J Clin Microbiol. 2007;45:3098–3100.
  19. Renaud N, Lecci L, Courcol R, et al. CHRO Magar Yersinia, a new chromogenic agar for screening of potentially pathogenic Yersinia enterocolitica isolates in stools. J Clin Microbiol. 2013;51:1184–1187.
  20. Maddocks S, Olma T, , Chen S. Comparison of CHROMagar Salmonella medium and xylose-lysine-desoxycholate and Salmonella-Shigella agars for isolation of Salmonella strains from stool samples. J Clin Microbiol. 2002;40:2999–3003.
  21. Eddabra R, Piemont Y, Scheftel J. Evaluation of a new chromogenic medium, chromID Vibrio, for the isolation and presumptive identification of Vibrio cholerae and Vibrio parahaemolyticus from human clinical specimens. Eur J Clin Microbiol Infect Dis. 2011;30:733–737.
  22. Endtz H, Ruijs G, Zwinderman A, et al. Comparison of six media, including a semisolid agar, for the isolation of various Campylobacter species from stool specimens. J Clin Microbiol. 1991;29:1007–1010.
  23. Earhart M. The identification and treatment of toxic megacolon secondary to pseudomembranous colitis. Dimens Crit Care Nurs. 2008;27:249–254.
  24. Hall J, Berger D. Outcome of colectomy for Clostridium difficile colitis: a plea for early surgical management. Am J Surg. 2008;196:384–388.
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