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Infectious Colitis

Septic Colitis

Infectious colitis results in an inflammation of the colon due to various bacterial, viral, and parasitic infectious pathogens. The principal symptom is diarrhea together with other gastrointestinal and constitutional symptoms. The diagnosis is made based on clinical and microbiological findings, and treatment principles depend on the severity of the disease, including symptomatic therapy, rehydration, and pathogen-specific antimicrobial therapy.


Presentation

The clinical presentation of patients with infectious colitis is uniformly characterized by the sudden onset of diarrhea, regardless of the cause [5]. The incubation period between ingestion and development of infection is usually around several days, but it may be longer, up to a few week. Because of extensive tissue destruction and pus formation in the colon, diarrhea can contain mucus, pus, or blood (dysentery), which signalizes a more severe infection. In addition to diarrhea, GI symptoms such as abdominal pain and cramping, rectal pain, tenesmus, bloating, and nausea in some cases. Fever can be present as well, while constitutional symptoms, such as malaise, fatigue, weakness, and weight loss, appear depending on the severity of the infection. For infections that last for more than several days with persistent diarrhea, severe dehydration may occur, which can lead patients into hypotension and shock.

Abdominal Pain
  • pain and diarrhea, were suspected of having the disease.[ncbi.nlm.nih.gov]
  • A 65-year-old woman presented to the emergency department with left lower quadrant abdominal pain radiating to her left flank worsening over 2 days. She denied epigastric pain.[ncbi.nlm.nih.gov]
  • Dull or paroxysmal abdominal pains often appear before or after defecation. Stool disturbances generally appear as an alternation of constipation and diarrhea.[encyclopedia2.thefreedictionary.com]
  • It typically causes sudden lower abdominal pain/cramps and diarrhea .[healthhype.com]

Workup

The diagnostic workup of patients in whom infectious colitis is suspected comprises laboratory tests and microbiological investigations. However, one of the most important aspects of workup is patient history, which may reveal important data that may provide significant information to the physician. Recent travel to Africa and Southeast Asia or eating contaminated food may suggest possible E. coli or Salmonella infection, while intake of water from suspicious sources may suggest amoebic colitis. Recent antibiotic use and hospitalization may suggest Clostridium difficile as the causative pathogen. Data regarding similar illness of friends or coworkers may suggest an outbreak, and these elements can be really useful if obtained properly.

Initial workup should involve a full blood count (CBC), to evaluate hemoglobin and erythrocyte levels for possible anemia, and leukocytes to see the immune response (in patients with severe immunodeficiency without leukocytosis, but leukopenia, CMV colitis is a possible diagnosis). Serum electrolytes, including Na+, K+, and Cl- should be measured to assess hydration, along with serum albumin, creatinine, and blood urea nitrogen (BUN). Inflammatory parameters, including sedimentation rate, CRP and fibrinogen should be tested as well.

In all patients, the key step in microbiological investigations is obtaining stool cultures, which is the method of choice for identifying the causative agent [6]. Bacterial as well as parasitic pathogens can be detected in stool, while antigen testing may be performed in the case of Entamoeba histolytica and Clostridium difficile. In pseudomembranous colitis, Clostridium difficile toxins can be detected in stool by rapid testing, and the presumptive diagnosis can be confirmed within a day or two. CMV colitis is diagnosed using serological testing as well, while quantitative PCR techniques may be used to assess the severity of the infection. The presence of fecal leukocytes can also be investigated [7].

Other markers, such as calprotectin and lactoferrin, are proposed as markers of inflammatory processes in the bowels, but their sensitivity and specificity in infectious colitis is still controversial [8] [9].

Listeria Monocytogenes
  • Outbreaks of gastroenteritis caused by Listeria monocytogenes are most likely severely underestimated.[ncbi.nlm.nih.gov]
  • monocytogenes: Ampicillin, trimethoprim-sulfamethoxazole Enterotoxigenic Escherichia coli : Trimethoprim-sulfamethoxazole Enteropathogenic E coli : Ampicillin or trimethoprim-sulfamethoxazole Enteroinvasive E coli : None unless severe cases, then ciprofloxacin[enotes.tripod.com]
Toxoplasma Gondii
  • Cryptosporidium, a protozoan member of the family of coccidia that also includes Pneumocystis carinii and Toxoplasma gondii. Cryptosporidiosis accounts for about 10% of the cases of chronic diarrhea in patients with AIDS.[gastrointestinalatlas.com]

Treatment

Treatment of infectious colitis should be directed at the specific cause and provided along with supportive therapy.

Depending on the severity of illness, patients with infectious colitis may develop slight or severe dehydration, in which case rehydration therapy is necessary to prevent events such as electrolyte imbalance, hypotension, and hypovolemic shock. IV fluids and supplementation of deficient electrolytes should compensate fluid loss through diarrhea.

Since diarrhea is accompanied by accelerated gut motility, antimotility agents have been proposed in therapy, but more evidence is necessary to obtain clear data regarding the use of these agents [10]. Moreover, they are contraindicated in the presence of bloody stools, or suspicion of hemolytic uremic syndrome (HUS), which is why their use is still reserved in clinical practice [11]. However, in the setting of mild diarrhea, loperamide 4mg PO, with a 2mg rising dose after diarrhea, up to 16mg q24h can be used.

Targeted antimicrobial therapy is the key to resolving the infection, but until the causative agent is confirmed, empiric therapy should be initiated in patients with severe diarrhea (>6 unformed stools q24h, high fever, tenesmus, blood, or confirmation of fecal leukocytes). Fluoroquinolones, including ciprofloxacin 500mg PO q12h or levofloxacin 500mg PO q24h for 3-5 days may be given as first-line empiric therapy. Alternatives include double-strength trimethoprim-sulfamethoxazole PO q12h for 3-5 days. In patients who were recently hospitalized, or report prior antibiotic consumption, either metronidazole 500mg PO q8h for 10-14 days or vancomycin 125mg should be included because of possible Clostridium difficile infection.

Once the microbiological testing confirms the pathogen, directed therapy can be initiated. Therapy of microorganisms responsible for infectious colitis include [12]:

  • E. coli - Enterohemorrhagic and Shiga toxin-producing strains should be treated with ciprofloxacin 500 mg POq24h for 3 days. Antimotility agents are contraindicated in such cases because of increased risk of HUS, particularly in children.
  • Shigella spp. - Ciprofloxacin 500 mg PO q24h for 3 days, or Azithromycin 500 mg PO q24h for 3 days. For the pediatric population, azithromycin is the drug of choice, in doses of 10mg/kg/day for 3 days,
  • Salmonella spp. - Ciprofloxacin 500 mg PO q12h or levofloxacin 500 mg q24h for 7-10 days, while treatment may be prolonged for up to 14 days in immunocompromised patients. An alternative is azithromycin 500mg q24h for 3 days.
  • Yersinia enterocolitica - Antibiotic treatment is indicated only in severe cases, and comprises doxycycline 100 mg IV q12h combined with either tobramycin or gentamicin 5mg/kg q24h for 1 day.
  • Campylobacter spp. - Azithromycin is the drug of choice, 500 mg PO q24h for 3 days, while alternatives include erythromycin stearate 500 mg q6h for 5 days, or ciprofloxacin 500 mg PO q12h.
  • Clostridium difficile - Either metronidazole 500 mg PO q8h or 250mg q6h for 10-14 days, or vancomycin 125 mg PO q6h for 10-14 days are recommended regiments. Teicoplanin has been proposed as a more efficient drug, in doses of 400 mg PO q12h for 10 days.
  • Amoebic colitis - patients with symptomatic disease caused by Entamoeba histolytica should be treated with either metronidazole 500-750mg PO q6h for 7-10 days or tinidazole 2 gm PO q24h for 3 days. After completion of initial therapy, subsequent regimen to eradicate intestinal cysts should be eradicated by iodoquinol 650 mg PO q6h for 20 days or paromomycin PO 25-35mg/kg/day in 3 doses for 7 days.
  • Schistosomiasis - Praziquantel single dose 40mg/kg.
  • CMV colitis - Ganciclovir 5mg/kg IV q12h for 14-21 days or valganciclovir 900mg PO q12h for 14-21 days and valganciclovir is always taken with food.

Despite the fact that guidelines for treatment of infectious colitis have been made, it is imperative to obtain antimicrobial susceptibility testing in the case of bacterial colitis, because local resistance rates may significantly vary from country to country.

Prognosis

The prognosis of infectious colitis depends on several factors. The disease may range from either asymptomatic colonization and a few episodes of watery diarrhea to profound fluid and blood loss from severe infections that may be life-threatening. Diarrheal diseases are still one of the leading causes of mortality in children worldwide, which is why the diagnosis of infectious colitis in both children and adults must be made promptly

Etiology

Numerous pathogens can cause infectious colitis, and bacterial gram-negative species are most commonly responsible for this infection. Pathogens associated with infectious colitis include:

  • Escherichia coli - E. coli is a gram-negative facultative anaerobe that is normally found in the GI tract of humans, and they can either cause infection as opportunistic pathogens or acquire virulence factors and then cause virulent infection. Several E. coli species can cause colitis e.g. enterotoxigenic E. coli (ETEC), enteropathogenic (EPEC), enteroaggregative (EAEC) (usually in the small intestine), while enterohemorrhagic (EHEC) and enteroinvasive (EIEC) species of E. coli are restricted to the colon, and cause more severe infection.
  • Salmonella species - a gram-negative anaerobe, like E. coli, Salmonella is responsible for causing GI tract infections.
  • Shigella species - several types of Shigella can cause infectious colitis, most common being Shigella sonnei, but also S. flexneri and S. dysenteriae. It is often the cause of epidemic colitis because a very small number of bacteria (< 200) are sufficient to cause infection.
  • Yersinia enterocolitica - together with E. coli, Salmonella and Shigella, Y. enterocolitica belongs to the family of Enterobacteriaceae and causes infectious colitis.
  • Campylobacter species - Campylobacter jejuni and Campylobacter coli are gram negative rods that cause colitis, and are increasingly being recognized as one of the most common causes of colitis associated with bloody diarrhea [2].
  • Clostridium difficile - a gram-positive spore-forming bacterial organism that can cause potentially life-threatening pseudomembranous colitis.

It is important to distinguish pathogens that cause colitis from those that cause infection of the upper GI tract (gastroenteritis), such as Staphylococcus aureus, Bacillus cereus, and other bacterial species.

Apart from bacterial pathogens, other causes include:

  • Cytomegalovirus (CMV), which belongs to the group of human herpesviruses, can cause colitis in immunocompromised patients [3].
  • Parasitic organisms - Entamoeba histolytica is the causative agent of Amoebic colitis, an intestinal protozoan that is the most common cause of parasitic colitis. Giardia lamblia, Dientamoeba fragilis, Schistosoma mansoni, and other protozoa are causes of GI infections primarily in developing countries.

Epidemiology

Prevalence rates, mode of acquisition, as well as risk factors, vary depending on the causative agent. Key principles in the development of infectious colitis in terms of epidemiology are:

  • the ubiquitous presence of colitis throughout the world - infectious colitis is seen in patients of all ages and ethnicity throughout the world, both in developed and developing countries.
  • Risk factors for the development of infectious colitis include poor hygiene and sanitation, travel to endemic regions, such as Africa and South-east Asia, and ingestion of contaminated water and food, including eggs, dairy products, and undercooked meat.
  • Person-to-person transmission is achieved through the feco-oral route in the case of bacterial and parasitic pathogens.
  • Antibiotic consumption and a prolonged duration of hospital stay is significantly associated with pseudomembranous colitis.

Prevalence rates of colitis are related to the underlying cause and significantly vary in various regions. Some data regarding the distribution and prevalence rates in the United States and worldwide include [4]:

  • Salmonella spp. - about 20 million infections and 200,000 deaths worldwide each year, while about 350 cases occur annually in the United States.
  • E. Coli - approximately 650 million cases of enterotoxigenic E. coli infection occur worldwide each year and are observed most commonly in children and travelers, presumably through consumption of contaminated water and food. Enteropathogenic E. Coli primarily causes infection in infants, while enterohemorrhagic E. Coli is commonly seen in the developed world, with more than 70,000 infections every year in the United States.
  • Shigella spp. - About 150 million cases of shigellosis occur worldwide, and 450,000 cases are diagnosed in the United States every year.
  • Yersinia enterocolitica infection is predominantly seen in the northern hemisphere, primarily the Scandinavian countries and North America, and the majority of cases are associated with consumption of contaminated meat, dairy products, and water.
  • Amoebic colitis - Between 10-15% of people living in endemic areas (Tropical regions) for Amoebic colitis are infected with this parasite, while prevalence rates are 1-2% in the United States. Mode of acquisition is ingestion of cysts from contaminated water.
Sex distribution
Age distribution

Pathophysiology

The pathogenesis of infectious colitis includes inflammatory changes in the colon, virulence factors of the causative agent, and tissue damage. Pathophysiology depends on the causative agent:

  • Enterobacteriaceae - E. coli, Salmonella, Shigella, and Yersinia have common features in the pathogenesis of the disease, as they all possess lipopolysaccharide (LPS), which is an endotoxin. After ingestion of contaminated food products or water, they successfully evade immune defenses by invading macrophages and survive phagolysosomal destruction. As a result, they are able to establish a focal infection in the distal tract and migrate into the surrounding cells and tissues. Upon bacterial cell lysis caused by immune defenses, LPS is released and initiates numerous pro-inflammatory events, such as complement activation, cytokine release, and migration of leukocytes at the site of infection. Large concentrations of LPS can lead to thrombocytopenia, disseminated intravascular coagulation, and shock. In addition to LPS, there are other virulence factors, which aid in cell adhesion, exotoxins (such as Shiga toxin, Heat-labile toxin) which cause cell lysis, and the type III secretion system, which serves as a form of a transporter of bacterial content into cells of the GI tract.
  • Clostridium difficile - the pathogenesis of colitis caused by this bacteria involves the production of enterotoxin (toxin A), which causes lysis of cells and cell junctions, resulting in diarrhea, and cytotoxin (toxin B), which causes depolymerization of actin, destruction of the cytoskeleton, and formation of pseudomembranes in the colon. In the setting of antibiotic use, which disrupts the normal intestinal flora, this microorganism proliferates and establishes an infection.
  • CMV - Cytomegalovirus establishes a latent infection in the body, and primarily migrates into leukocytes and other cells. It is reactivated in patients with severe immunosuppression. CMV can evade immune defenses through several mechanisms, mainly by preventing antigen presentation, and disruption of natural killer cell-mediated destruction.
  • Entamoeba histolytica - After ingestion of cysts from contaminated sources, primarily water, the cysts proliferate into trophozoites, which secrete cytotoxins and cause necrosis of the large intestine, producing diarrhea.

Prevention

Prevention of infectious colitis comprises some general principles:

  • Proper hygiene and sanitation measures, including regular hand-washing, especially during travel.
  • Eating foods that are properly cooked and processed, while thorough cleaning of fruits and vegetables is recommended.
  • Intake of water should be from only safe and clean sources.

It is important to have these principles in mind, especially when traveling in developing and underdeveloped communities, since much higher rates of infection are observed in those areas.

Summary

Infectious colitis comprises a broad range of infections that result in inflammatory changes in the colon. Numerous pathogens may cause infection in the distal gastrointestinal tract, most commonly bacteria (Escherichia coli, Shigella, Salmonella, Campylobacter, Clostridium difficile, etc.) [1], but also viruses (Cytomegalovirus), parasitic (Entamoeba histolytica, Schistosoma mansoni), and fungi. In the majority of cases, pathogens are acquired through contaminated food and water, and person-to-person transmission is achieved through the feco-oral route. Cytomegalovirus (CMV) colitis and infection caused by fungi are seen in patients with severe immunosuppression, such as those with HIV infection and AIDS. Parasitic infection of the colon are more commonly observed in underdeveloped countries and are associated with poor hygiene and sanitation. Once the pathogens are inoculated into the gastrointestinal tract, they establish infection and cause a range of inflammatory changes in the colon, which impairs the permeability function of the colon, resulting in diarrhea. The prognosis varies significantly and depends on the cause, as well as the severity of the infection. Infectious colitis may range from mild watery diarrhea that can spontaneously resolve, to life-threatening infection that can progress to severe fluid loss and development of sepsis.

Depending on the features and virulence factors of the causative agent, different forms of colitis may be observed, and thus different symptoms may be encountered. In virtually all patients, however, diarrhea is the principal symptom and may be purulent and/or bloody (known as dysentery). Other symptoms include abdominal cramping, tenesmus, fever, and bloating. Constitutional symptoms, such as malaise, fatigue, and generalized weakness are almost always observed, while weight loss and anorexia are seen in severe cases.

The diagnosis of infectious colitis is aimed at identifying the causative agent, and microbiological investigation is the key. Clinical presentation may also be helpful in determining optimal therapy. Since the majority of cases are caused by bacterial species, stool cultures and the presence of fecal leukocytes should be performed. In patients with severe immunosuppression, serology or PCR for CMV, and investigation of fungal causes through serology testing should be performed from stool samples, while parasitic testing should be conducted in patients who report recent travel. Patient history, including recent food ingestion and travel, may provide vital clues that can help in determining the diagnosis.

Treatment principles of infectious colitis include symptomatic therapy, such as rehydration with either oral or IV fluids and electrolytes and pathogen-specific antimicrobial therapy. Because of growing issues of antimicrobial resistance, pathogen-specific therapy is necessary to treat infectious colitis successfully. Metronidazole, ciprofloxacin, doxycycline, azithromycin, and other drugs are used in the treatment of bacterial colitis, while ganciclovir is used for CMV colitis. Antiparasitic agents, such as praziquantel, paromomycin, or iodoquinol, are used in treating amoebic colitis.

Patient Information

Infectious colitis refers to inflammation and damage of the terminal segments of the gastrointestinal tract - the final parts of the small intestine and the colon, as a result of infection. Numerous bacterial, viral, parasitic, and fungal pathogens may be responsible for the development of infectious colitis. This infection is acquired by the feco-oral route, which means that it is either acquired from contaminated food that is not properly cooked or processed, but also from water contaminated with bacteria or parasitic cysts. Person-to-person transmission occurs due to poor hygiene. Infectious colitis is present throughout the world, and persons of all ages and ethnicity may be affected. The principal symptom of all patients is diarrhea, which may be mild and watery, or more frequent and contains pus and blood, in which case it is called dysentery. Other symptoms, such as abdominal pain, bloating, fever, malaise, weakness and fatigue are commonly encountered, and the diagnosis is obtained by examining the stool for the presence of microorganisms. Treatment is directed at the organism that is identified, but patients often need supportive therapy because of fluid loss through diarrhea, and they receive either oral or intravenous rehydration therapy. Antibiotics, such as ciprofloxacin, azithromycin, and many other, are given against bacteria, while other drugs are used in treating viral (such as ganciclovir) and parasitic (iodoquinol, metronidazole) infection. Prevention measures may significantly reduce the number of infected patients by improving daily hygiene measures, especially during travel, consuming meat which has been cooked properly and washing fruits and vegetables.

References

Article

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  3. Lin YH, Yeh CJ, Chen YJ, et al. Recurrent cytomegalovirus colitis with megacolon in an immunocompetent elderly man. J Med Virol. 2010;82:638–641.
  4. Murray PR, Rosenthal KS, Pfaller MA. Medical Microbiology 8th Edition; Mosby Elsevier. Philadelphia, 2015;
  5. DuPont HL. Approach to the patient with infectious colitis. Curr Opin Gastroenterol. 2012;28(1):39-46.
  6. Gould LH, Bopp C, Strockbine N, et al. Recommendations for diagnosis of shiga toxin-producing Escherichia coli infections by clinical laboratories. MMWR Recomm Rep. 2009;58:1–14.
  7. Harris JC, DuPont HL, Hornick RB. Fecal leukocytes in diarrheal illness. Ann Intern Med. 1972;76:697–703.
  8. Schoepfer AM, Beglinger C, Straumann A, et al. Fecal calprotectin correlates more closely with the Simple Endoscopic Score for Crohn's disease (SESCD) than CRP, blood leukocytes, and the CDAI. Am J Gastroenterol. 2010;105:162–169.
  9. Shastri YM, Bergis D, Povse N, et al. Prospective multicenter study evaluating fecal calprotectin in adult acute bacterial diarrhea. Am J Med. 2008;121:1099–1106.
  10. Koo HL, Koo DC, Musher DM, et al. Antimotility agents for the treatment of Clostridium difficile diarrhea and colitis. Clin Infect Dis. 2009;48:598–605.
  11. Nelson JM, Griffin PM, Jones TF, et al. Antimicrobial and antimotility agent use in persons with shiga toxin-producing Escherichia coli O157 infection in FoodNet Sites. Clin Infect Dis. 2011; 52:1130–1132.
  12. Gilbert DN, Chambers HF, Eliopoulos GM, Saag MS. The Sanford guide to antimicrobial therapy. 45th ed. Antimicrobial Therapy, Inc, Sperryville, VA, USA; 2015.

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Last updated: 2018-06-22 05:09