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Enteritis

Enteritis is an of the , most commonly caused by ingestion of food or water contaminated with or viruses, leading to symptoms such as severe , , and . While often self-limiting in healthy individuals, it can result in and requires medical attention in severe cases, particularly among infants, the elderly, or those with underlying conditions. The primary infectious causes of enteritis include bacterial pathogens like , , and , as well as viruses such as and , and parasites like . Non-infectious forms encompass , which develops as a side effect of for cancers in the or , causing acute or intestinal . Autoimmune conditions, such as , and other factors like nonsteroidal anti-inflammatory drug (NSAID) use or celiac disease can also trigger enteritis by damaging the intestinal lining. Symptoms typically emerge within hours to days of exposure and include watery or bloody , , fever, and loss of appetite, with complications like imbalances possible if untreated. Diagnosis often involves stool cultures to identify pathogens, alongside imaging or endoscopic procedures for persistent cases. Treatment focuses on rehydration through oral or intravenous fluids, with antibiotics reserved for bacterial infections; supportive care suffices for most viral cases, which resolve in a few days. Enteritis contributes significantly to global morbidity, with infectious variants accounting for millions of cases annually, often linked to poor or travel to endemic areas. Prevention strategies emphasize hand , safe handling, and against in vulnerable populations.

Introduction and Background

Definition

Enteritis is defined as inflammation of the , which comprises the , , and . This condition primarily affects the mucosal lining but can extend to deeper layers of the intestinal wall, depending on the underlying cause and severity. The plays a critical role in nutrient absorption, processing digested food to extract essential vitamins, minerals, carbohydrates, fats, and proteins for bodily use. Its extensive surface area, facilitated by villi and microvilli, makes it particularly vulnerable to inflammatory processes that can impair this function and lead to . Enteritis is distinguished from related conditions such as , which involves inflammation of both the small and large intestines, and , which encompasses inflammation of the along with the small and large intestines. Enteritis is classified as acute or based on its onset and duration. Acute enteritis typically presents with sudden onset and is often self-limiting, resolving within a few days, while enteritis persists over time and is frequently associated with underlying systemic diseases. Common causes include infections from or viruses, though non-infectious factors can also contribute.

Etymology and History

The term "enteritis" derives from the Greek words enteron, meaning "intestine," and -itis, denoting , forming a medical Latin compound that entered English usage around as a description of acute bowel inflammation. This etymological construction reflects the classical roots of , with the suffix -itis commonly applied to inflammatory conditions since the time of physicians. The word's first documented appearance in dates to the mid-18th century, attributed to French François Boissier de Sauvages de Lacroix, who used it to classify inflammatory disorders of the intestines. Early descriptions of intestinal inflammation resembling enteritis appear in ancient medical texts, where , in the 5th century BCE, documented symptoms such as , , and seasonal patterns in children, attributing them to imbalances in bodily humors like excess . These accounts, preserved in the , marked the initial recognition of enteritis-like conditions as distinct from general digestive ailments, influencing later Greco-Roman physicians like and , who further described its acute manifestations in pediatric cases. By the , advancements in enabled the linkage of enteritis to infectious agents; pioneers such as and Pasteur's germ theory (developed in the 1870s–1880s) facilitated the identification of bacteria in intestinal tissues, shifting perceptions from humoral imbalances to microbial causes, as seen in early observations of pathogens in and cases. In the , the identification of non-infectious forms advanced the understanding of enteritis; notably, in 1932, Burrill B. Crohn, Ginzburg, and Gordon D. Oppenheimer described "regional ileitis" (later termed ) as a , granulomatous of the , distinguishing it from acute infectious variants through histopathological analysis of surgical specimens. This seminal paper, published in the Journal of the American Medical Association, highlighted transmural involvement and skip lesions, establishing enteritis as encompassing both infectious and idiopathic etiologies. Post-1950s, the advent of antibiotics like penicillin (widespread by the 1940s) and sulfonamides allowed differentiation of bacterial enteritis from persistent cases, while emerging immunological research—such as the 1950s studies on by researchers like Henry Kunkel—revealed immune-mediated mechanisms in forms, prompting a reclassification from largely idiopathic to etiology-based categories. This evolution underscored enteritis as a spectrum of conditions, with modern diagnostics building on these historical foundations.

Epidemiology

Incidence and Prevalence

Enteritis, as a key component of infectious diarrheal diseases, imposes a substantial burden, particularly among vulnerable populations. According to the (WHO), there are nearly 1.7 billion cases of childhood diarrhoeal disease annually, with enteritis accounting for a significant proportion due to its role in intestinal inflammation from pathogens like bacteria, viruses, and parasites. Broader estimates from the indicate over 6.59 billion incident cases of enteric infections worldwide in 2019, leading to approximately 1.75 million deaths, though these figures have shown a downward trend in mortality since 1990. Among these, —a major viral cause of enteritis—contributed to an estimated 1.76 million hospitalizations in children under 5 years globally in 2019, prior to widespread vaccine impacts. Regional variations highlight stark disparities, with incidence rates substantially higher in low- and middle-income countries (LMICs) due to factors such as inadequate and . In and , enteric infections like enteritis exhibit elevated prevalence, with Africa alone recording millions of cases and over 300,000 diarrheal deaths in 2020, predominantly among children. For instance, diarrheal disease incidence in these regions can reach three episodes per child under 5 per year, compared to far lower rates in high-income settings where improved has reduced occurrence. In contrast, high-income countries have seen declining enteritis rates post-introduction of and hygiene interventions, with age-standardized incidence dropping by up to 18% in low-socio-demographic index areas between 2017 and 2021. Recent trends indicate fluctuations influenced by external factors, including a temporary decline in infectious enteritis cases during the due to enhanced hygiene measures, followed by a post-2020 rebound linked to resumed international travel and climate-related events. exacerbates this through increased flooding and temperature shifts that promote pathogen survival and spread, potentially heightening diarrheal outbreaks in endemic regions. Notably, rotavirus vaccination programs have driven significant reductions, with 2024 data showing up to 50-80% decreases in hospitalizations for -associated enteritis in vaccinated populations, averting over 220,000 deaths globally since 2004.

Risk Factors

Risk factors for enteritis can be categorized as non-modifiable or modifiable, with emerging influences also contributing to susceptibility. Non-modifiable factors include age and genetic predispositions. Young children under 5 years and older adults over 65 are at heightened risk due to immature immune systems in the young and age-related immune decline, respectively, leading to more severe outcomes from infectious enteritis. Genetic factors, such as specific (HLA) alleles, predispose individuals to autoimmune forms of enteritis, as seen in inflammatory bowel diseases like , where HLA-DRB1 variants increase susceptibility to chronic inflammation. HLA associations have also been linked to severity of enteric infections in certain populations. Modifiable risk factors primarily relate to environmental, behavioral, and medical exposures that facilitate or direct . Poor and contaminated significantly elevate the risk of infectious enteritis by promoting the spread of pathogens like and viruses through fecal-oral . Travel to endemic areas with inadequate infrastructure heightens exposure to enteritis-causing agents, often manifesting as traveler's diarrhea. Immunosuppression from conditions like or treatments such as impairs mucosal defenses, increasing vulnerability to opportunistic infections and severe enteritis. Use of non-steroidal anti-inflammatory drugs (NSAIDs) is a key modifiable factor for non-infectious enteritis, as these agents damage the small intestinal mucosa, leading to ulceration and in up to 70% of chronic users. Dietary habits, including consumption of raw or undercooked foods like , , or unpasteurized , raise the risk of bacterial enteritis by introducing pathogens directly into the gut. Emerging factors are amplifying enteritis risks globally. Climate change is projected to increase vector-borne and waterborne infections, thereby elevating incidence, including enteritis, through warmer temperatures and altered patterns that expand habitats. Post-2022 data indicate rising antibiotic resistance among enteropathogenic , complicating treatment and heightening the risk of recurrent or persistent enteritis cases due to ineffective therapy and persistent .

Pathophysiology

Mechanisms of Inflammation

Enteritis involves a inflammatory cascade initiated by the activation of innate and adaptive immune cells within the intestinal mucosa. Resident macrophages and dendritic cells recognize pathogen-associated molecular patterns or damage signals, leading to the recruitment of T-cells, particularly Th1 and Th17 subsets, which amplify the response through secretion. Key proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) are released, promoting further immune cell infiltration and systemic signaling via pathways like . These cytokines disrupt the integrity of the epithelial barrier by downregulating proteins (e.g., and claudins) and inducing in enterocytes, resulting in increased permeability, mucosal , and eventual ulceration as inflammatory mediators leak into the . In acute enteritis, the inflammatory response is predominantly driven by a rapid influx of neutrophils, triggered by bacterial toxins or direct epithelial injury, which release and proteases to exacerbate tissue damage and . This phase is characterized by a short-lived, intense Th1-mediated response that resolves with clearance, often within days, minimizing long-term structural changes. In contrast, chronic enteritis features sustained activation of Th17 cells and persistent cytokine production (e.g., IL-6 and TNF-α), leading to maladaptive repair processes including mediated by transforming growth factor-beta (TGF-β) and aberrant to support inflamed tissue. Fibrotic remodeling thickens the intestinal wall, while facilitates ongoing immune cell trafficking, perpetuating a cycle of without resolution. The plays a pivotal role in enteritis through , an imbalance favoring proinflammatory taxa such as adherent-invasive , which triggers (TLR) pathways on epithelial and immune cells. communities increase (LPS) levels, activating TLR4 to initiate signaling and downstream release (e.g., IL-6, TNF-α), thereby disrupting mucosal and amplifying inflammation. Post-2023 research highlights modulation as a therapeutic target; for instance, studies on radiation-induced enteritis demonstrate that exacerbates epithelial injury via TLR-mediated responses, while interventions like restore diversity and attenuate by enhancing and reducing TLR activation.

Associated Complications

Enteritis can lead to several acute complications, primarily arising from fluid loss and systemic effects of . is a common and potentially life-threatening issue, particularly in severe cases involving profuse , as it results from significant water and depletion in the . imbalances, such as or , frequently accompany and can exacerbate cardiac and neuromuscular dysfunction if untreated. may develop in bacterial enteritis when pathogens translocate from the inflamed mucosa into the bloodstream, leading to systemic inflammatory response and multi-organ failure, especially in vulnerable populations like the elderly or immunocompromised. Additionally, due to damaged villi impairs nutrient uptake, resulting in deficiencies of vitamins (e.g., B12, ) and minerals (e.g., iron, calcium), which can manifest as or over time. In chronic forms of enteritis, such as those associated with , persistent inflammation promotes changes and structural abnormalities. Strictures, or narrowing of the intestinal due to scarring, occur in up to 50% of Crohn's patients over their disease course and can cause obstructive symptoms requiring surgical intervention. Fistulas, abnormal connections between the intestine and other organs or skin, develop in approximately 30-40% of cases, often complicating management and increasing infection risk. Long-standing chronic enteritis elevates the risk of , with patients facing a 2- to 5-fold higher incidence compared to the general population, driven by ongoing mucosal from repeated inflammatory cycles. In post-radiation enteritis, of the is a hallmark , affecting up to 20% of patients receiving pelvic radiotherapy and leading to progressive narrowing and ischemia. Rare but severe outcomes include bowel , where transmural inflammation erodes the intestinal wall, potentially causing ; this is reported in less than 1% of cases but carries high mortality, particularly in infectious or ischemic enteritis. , characterized by acute colonic dilation and systemic toxicity, can rarely complicate infectious enteritis (e.g., from ), mimicking more common associations with and necessitating emergent decompression. Recent 2024 studies highlight persistent enteritis-like symptoms in some viral cases, resembling , where antigens linger in the gut, sustaining low-grade inflammation and for months post-infection.

Etiology

Infectious Causes

Infectious enteritis is primarily caused by a variety of microbial pathogens, including viruses, , and parasites, which invade the and trigger through mechanisms such as production and epithelial cell damage. These agents are responsible for the majority of acute cases worldwide, particularly in vulnerable populations like children and travelers. Viral pathogens are the most common infectious agents, with being the leading cause of severe enteritis in children under five years old, accounting for significant morbidity in low-resource settings before widespread . spreads via the fecal-oral route, often through contaminated hands, surfaces, or objects in close-contact environments like daycare centers. , another key viral culprit, frequently causes explosive outbreaks of enteritis in semi-closed settings such as cruise ships, schools, and nursing homes, where it transmits rapidly through direct person-to-person contact, contaminated food, or water. The for is typically 12 to 48 hours, leading to sudden onset of symptoms. Bacterial causes are predominantly foodborne and include Salmonella species, *, Shigella species, and certain strains of such as enterohemorrhagic E. coli (EHEC), which are among the top contributors to enteric infections in the United States and globally. These bacteria often contaminate poultry, eggs, unpasteurized milk, and undercooked meats, with , , and Shigella leading in reported cases of bacterial . Incubation periods vary, with ranging from 6 hours to 6 days and from 2 to 5 days. Parasitic infections, though less common in developed regions, are significant in tropical and subtropical areas with poor sanitation. Giardia lamblia (also known as Giardia intestinalis) is a protozoan parasite transmitted through waterborne cysts in contaminated drinking water or recreational sources, causing prolonged watery and . Entamoeba histolytica similarly spreads via fecal-oral route in endemic regions, often through untreated water, leading to invasive enteritis that can progress to . Cryptosporidium species, another protozoan, cause self-limited watery in immunocompetent individuals but prolonged illness in immunocompromised hosts, transmitted via contaminated water or fecal-oral contact. Protozoal infections typically have longer periods of 1 to 2 weeks. Overall transmission of these pathogens occurs mainly via the fecal-oral route, facilitated by ingestion of contaminated or , poor , or direct contact with infected individuals or animals. As of 2025, emerging concerns include antibiotic-resistant strains of bacterial enteropathogens like multidrug-resistant , which complicate management in outbreaks and highlight the need for .

Non-Infectious Causes

Non-infectious causes of enteritis encompass a range of immune-mediated, vascular, iatrogenic, and other triggers that lead to inflammation of the without microbial involvement. Immune-mediated conditions are prominent among these, including , an characterized by transmural inflammation that frequently affects the , resulting in patchy, skip lesions and potential complications like strictures. Celiac disease, also known as gluten-sensitive enteropathy, is an autoimmune disorder where ingestion of triggers an that damages the small intestinal mucosa, leading to villous atrophy and . Eosinophilic enteritis involves abnormal eosinophil infiltration into the small bowel wall, often associated with allergic or idiopathic mechanisms, and can present with diverse symptoms depending on the layer of involvement, such as mucosal or muscularis layers. Vascular etiologies primarily involve ischemic enteritis, which arises from reduced blood flow to the due to mesenteric ischemia, commonly linked to in elderly patients or thromboembolic events. This hypoperfusion causes mucosal injury and , with acute forms potentially progressing to if untreated. Iatrogenic causes are significant, particularly radiation enteritis, which develops following abdominal or pelvic for malignancies; it manifests in acute phases with mucosal and shortly after exposure, while chronic phases involve and vascular sclerosis months to years later. Non-steroidal anti-inflammatory drug (NSAID)-induced enteritis results from prostaglandin inhibition, leading to increased , erosions, and ulcers in the small bowel, often underrecognized until complications like bleeding or strictures occur. Other non-infectious triggers include allergic reactions, such as (FPIES), a non-IgE-mediated primarily in infants, triggered by foods like cow's milk or soy, causing profuse and due to inflammatory mediators. Chemical toxins, including like lead or from contaminated sources, can induce enteritis through direct mucosal toxicity, resulting in erosive damage and systemic effects. Additionally, inhibitor therapies, increasingly used in since their approval, have been linked to enteritis as part of gastrointestinal immune-related adverse events, with dual therapy (e.g., anti-PD-1 and anti-CTLA-4) elevating risk through T-cell-mediated inflammation, as noted in recent reviews up to 2024.

Clinical Presentation

Signs and Symptoms

Enteritis typically presents with a range of gastrointestinal symptoms, including periumbilical abdominal cramping and pain, which arises from in the . Patients often experience watery that can be explosive in nature, particularly in infectious cases, along with and . Systemic manifestations commonly include low-grade fever, , and , reflecting the body's inflammatory response. signs, such as dry mouth, reduced urine output, and dark-colored urine, frequently develop due to fluid loss from and . In chronic forms of enteritis, persistent symptoms may lead to from and reduced appetite. Symptom variations depend on the underlying cause; for instance, invasive bacterial infections like those from can produce bloody stools. Parasitic enteritis, such as , often involves bloating and foul-smelling stools alongside cramping. In pediatric patients, particularly infants, and may accompany gastrointestinal distress, signaling discomfort and risk.

Acute versus Chronic Forms

Acute enteritis is characterized by a rapid onset, typically occurring within hours to days following exposure to a triggering agent, and is generally self-limiting, lasting 3 to 7 days in most cases. It often presents with intense gastrointestinal symptoms, such as severe , which can lead to significant fluid loss and if not managed promptly, though it resolves without long-term sequelae in healthy individuals. In contrast to more persistent forms, the acute phase allows for relatively quick restoration of intestinal function, with diversity rebounding substantially within weeks to months post-infection. Chronic enteritis, on the other hand, persists for more than 4 weeks and often follows a relapsing pattern, with symptoms waxing and waning over months or years. It is frequently associated with autoimmune conditions, such as flares in , or iatrogenic factors like , and can result in syndromes due to prolonged mucosal damage. Unlike the acute form, chronic enteritis involves insidious and ongoing low-grade , contributing to nutritional deficiencies and altered gut barrier integrity. Key differences between the two forms lie in their temporal patterns and clinical implications: acute enteritis features abrupt, high-intensity symptoms like profuse that resolve swiftly, whereas enteritis exhibits subtler, recurrent pain and leads to sustained with slower or incomplete recovery. Recent 2023 analyses indicate that while acute enteric infections show marked microbial diversity restoration approaching healthy baselines within approximately 3 months, conditions like maintain persistent , exacerbating and barrier dysfunction.

Diagnosis

Clinical Evaluation

The clinical evaluation of suspected enteritis begins with a detailed history taking to identify potential etiologies and assess severity. Clinicians inquire about the onset and duration of symptoms, such as or , to distinguish acute from forms; sudden onset within hours to days often suggests infectious causes. Recent travel history is crucial, as exposure to contaminated food or water in endemic areas increases risk for pathogens like or . Dietary history focuses on consumption of undercooked meats, unpasteurized dairy, or raw produce, while medication review includes recent antibiotics, which may predispose to difficile-associated enteritis, or nonsteroidal anti-inflammatory drugs (NSAIDs) linked to inflammatory or ischemic types. Comorbidities, such as from , , or autoimmune diseases, are evaluated for heightened susceptibility. Red flags prompting urgent assessment include bloody , indicating possible invasive infection or ischemia, and severe , which may signal complications like . The complements the history by focusing on signs of , , and systemic involvement. Abdominal assesses for diffuse or localized tenderness, particularly in the periumbilical or lower quadrants, which may indicate small bowel involvement. is evaluated through , including and , and clinical signs such as decreased skin turgor, dry mucous membranes, and reduced urine output, especially in cases of profuse . A is performed to detect occult blood, which can suggest mucosal or without overt . Fever may be present in infectious enteritis, while guarding or rigidity raises concern for . Differential considerations during evaluation aim to rule out mimics through symptom patterns and targeted maneuvers. is differentiated by migratory right lower quadrant pain, anorexia, and , often without prominent ; rebound tenderness elicited by the Blumberg sign—pain upon sudden release of deep —suggests peritoneal irritation. typically presents with left lower quadrant pain in older adults, fever, and , contrasting with the more diffuse symptoms of enteritis. Scoring tools like the Blumberg sign help identify risk, guiding the need for further investigation if positive. These assessments ensure timely recognition of enteritis while excluding surgical emergencies.

Laboratory and Imaging Tests

Laboratory tests play a crucial role in diagnosing enteritis by identifying infectious agents, assessing , and evaluating systemic effects. Stool studies are fundamental for detecting pathogens in infectious enteritis. Conventional stool culture identifies bacterial causes such as , , and by culturing fecal samples on selective media, providing speciation and antibiotic susceptibility if needed. (PCR) panels offer rapid multiplex detection of multiple pathogens, including bacteria (e.g., Clostridium difficile, enterohemorrhagic Escherichia coli), viruses (e.g., , ), and parasites, with higher sensitivity than culture alone and results available within hours. Ova and parasite examinations via microscopy detect protozoan or helminthic infections like or , often requiring multiple samples for adequate sensitivity. Fecal calprotectin testing measures levels of this protein in stool as a non-invasive marker of intestinal , particularly useful for non-infectious enteritis such as in . Elevated levels above 50 μg/g suggest active mucosal , helping differentiate inflammatory conditions like IBD from or non-inflammatory , with sensitivity around 90% for detecting IBD. Blood tests support the diagnosis by indicating or complications. A (CBC) may reveal suggestive of bacterial infection or in parasitic cases. (CRP) and (ESR) are elevated in inflammatory enteritis, such as in , helping differentiate it from non-inflammatory causes; CRP levels above 10 mg/L often correlate with active disease. Electrolyte panels assess for dehydration-induced imbalances like or , common in severe diarrheal enteritis. Imaging modalities visualize bowel wall abnormalities and complications without invasive procedures. Computed tomography (CT) enterography detects small bowel wall thickening, hyperenhancement, or complications like abscesses in inflammatory or infectious enteritis, with sensitivity exceeding 80% for active Crohn's involvement. (MRI) enterography provides similar diagnostic accuracy without , preferred for pediatric or pregnant patients to evaluate fibrosis or strictures. , particularly intestinal ultrasound, is valuable in pediatric cases for real-time assessment of bowel wall thickness and , offering a non-invasive bedside with good interobserver reliability. For chronic enteritis, upper and lower with allows direct visualization of mucosal and histological confirmation, such as granulomas in . Advanced techniques enhance evaluation of obscure or small bowel involvement. Capsule endoscopy involves swallowing a wireless camera to image the entire , identifying ulcers or erosions in Crohn's enteritis with a diagnostic yield of over 60% in suspected cases.

Management

Supportive Care

Supportive care for enteritis primarily focuses on maintaining , alleviating symptoms, and providing nutritional support to prevent complications such as , which can arise from fluid loss due to and vomiting. Oral rehydration therapy using glucose-electrolyte solutions, such as those recommended by the , is the cornerstone of treatment for mild to moderate in patients with enteritis. These solutions facilitate the of sodium and in the , effectively restoring fluid and balance without the need for intravenous intervention in most cases. For patients unable to tolerate oral intake or those with severe , intravenous fluids are administered, typically starting with a bolus of 20 mL/kg of isotonic solution like normal saline to rapidly correct . Symptom management includes the judicious use of antiemetics to control , which can otherwise hinder rehydration efforts. , a antagonist, is commonly recommended for children and adults experiencing acute associated with enteritis, as it reduces the frequency of emesis and improves oral intake. agents like may be used cautiously in adults with non-infectious or mild infectious enteritis to slow intestinal motility and reduce stool frequency, but they are contraindicated in cases of bloody or suspected invasive infection due to the risk of prolonging retention. Nutritional support emphasizes continuing a regular, age-appropriate as tolerated to avoid , rather than prolonged fasting. The —consisting of bananas, rice, applesauce, and toast—has been traditionally suggested for its bland, binding properties to ease gastrointestinal symptoms during recovery, though evidence for its superiority over a normal is limited. High-fat or dairy products should be avoided initially if develops secondary to mucosal damage. Monitoring involves assessing hydration status through clinical signs such as weight changes, skin turgor, and urine output, with home care suitable for mild cases where patients can maintain oral intake. Hospitalization is indicated for moderate to severe , particularly in children with more than 10% body , persistent , or signs of , to allow for close observation and aggressive .

Specific Treatments

Specific treatments for enteritis target the underlying , with interventions tailored to infectious, autoimmune, or other causes. For infectious enteritis, antibiotic therapy is reserved for severe or complicated cases, such as those caused by bacterial pathogens like , where is recommended at a dose of 500 mg once daily for three days in adults to reduce symptom duration and bacterial shedding. Antiviral agents are rarely used for viral enteritis, as no specific antivirals are approved for common causes like or , with management primarily supportive due to the self-limiting nature of most infections. For parasitic infections, such as caused by , antiparasitic drugs like are the mainstay, administered at 250 mg three times daily for 5-7 days in adults to achieve cure rates exceeding 80%. In autoimmune enteritis, such as that associated with , corticosteroids like are used for induction of remission in mild-to-moderate ileal involvement, with a typical regimen of 9 mg daily for 8 weeks followed by tapering, due to its targeted delivery and lower systemic side effects compared to . Biologic therapies, including inhibitors like (5 mg/kg infusions at weeks 0, 2, and 6 for induction) and integrin antagonists like (300 mg infusions at weeks 0, 2, and 6), are recommended for moderate-to-severe cases refractory to conventional therapies, achieving clinical remission in 30-50% of patients. (JAK) inhibitors, such as (45 mg daily for induction, then 15-30 mg maintenance), received FDA approval in 2023 for and are indicated for patients with inadequate response to biologics, demonstrating endoscopic response rates of approximately 40% in clinical trials. For non-infectious causes like , hyperbaric oxygen therapy, involving 90-minute sessions at 2.0-2.5 atmospheres absolute for 30-60 treatments, enhances tissue oxygenation and , leading to resolution of bleeding in 60-80% of patients with chronic -induced enteritis unresponsive to medical therapy. may be used for severe , and bile acid sequestrants like cholestyramine for symptoms. Surgical resection is indicated for complications such as strictures or ischemic enteritis, where segmental bowel removal with primary or ostomy creation is performed to address non-viable tissue, with operative mortality rates of 5-20% in cases, though 50-80% in acute non- ischemic enteritis depending on the extent of . Emerging therapies include fecal microbiota transplantation (FMT) for recurrent Clostridioides difficile-associated enteritis, recommended by the American Gastroenterological Association in 2024 guidelines for patients with multiple recurrences after antibiotic failure, using screened donor stool via or capsules to restore diversity and achieve cure rates of 85-95%. Supportive hydration remains essential alongside these targeted interventions to prevent .

Prognosis and Prevention

Prognosis

The prognosis of acute infectious enteritis is generally excellent in otherwise healthy individuals, with over 95% achieving full recovery within one week through supportive care such as rehydration. Mortality rates remain below 1% in developed countries, primarily due to access to prompt medical intervention, though rates can rise to 5-10% among malnourished children in resource-limited settings where escalates risks. For chronic forms of enteritis, outcomes vary significantly by etiology. In , a common inflammatory enteritis, biologic therapies induce clinical remission in approximately 30-50% of patients, though around 30% eventually require surgical intervention due to complications like strictures. Radiation enteritis, often a of cancer therapy, persists chronically in about 50% of affected individuals months to years post-treatment, leading to ongoing and obstructive symptoms. Influencing factors include early initiation of treatment, which markedly improves recovery trajectories, and comorbidities such as or , which worsen long-term impacts. Recent 2025 analyses highlight a 40% global decline in rotavirus-related mortality since 2010, attributable to widespread efforts that have averted over 140,000 child deaths.

Preventive Strategies

Vaccination plays a key role in preventing enteritis caused by specific pathogens. For , a leading cause of severe viral enteritis in children, two oral vaccines—RotaTeq (a ) and Rotarix (a monovalent vaccine)—are widely used and recommended for inclusion in national programs worldwide. By the end of 2024, vaccines had been introduced into routine schedules in 131 countries, achieving global coverage of approximately 59% among eligible infants, with ongoing expansions expected into 2025. These vaccines have demonstrated high efficacy in reducing severe by 85–98% in clinical trials and real-world settings. For bacterial causes like , which can lead to enteritis, the typhoid (TCV) is recommended by WHO for routine use in children in endemic areas, providing over 80% protection; for travelers, the inactivated Vi polysaccharide or live oral vaccines offer 50–80% protection. Hygiene practices are essential for preventing infectious enteritis transmitted through contaminated and water. Regular handwashing with soap and water, especially after using the , changing diapers, and before preparing or eating , significantly reduces the transmission of pathogens like , , and . Ensuring access to safe through methods such as , chlorination, or prevents waterborne enteritis, as contaminated water is a primary vector for diarrheal diseases. measures, including cooking meats to safe internal temperatures (at least 71°C or 160°F), avoiding raw or undercooked animal products, and steering clear of unwashed produce in high-risk areas, further mitigate bacterial and parasitic causes of enteritis. Additional strategies target vulnerable populations and broader . Probiotics, such as and strains, have shown efficacy in preventing antibiotic-associated —a common precursor to enteritis—in at-risk groups like hospitalized patients and those on broad-spectrum antibiotics, reducing incidence by up to 50% in meta-analyses. In immunocompromised individuals, such as those with or undergoing , enhanced control measures including vigilant screening for gastrointestinal pathogens enable early intervention to prevent severe enteritis outbreaks. At the population level, policies promoting improved sanitation infrastructure, such as sewer connections and access, have reduced incidence—including enteritis—by approximately 30–36% in targeted low-resource regions, according to global intervention studies.

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