Inflammatory bowel disease–like conditions: infectious

Abbreviations

AIDS

acquired immune deficiency syndrome

CD

Crohn’s disease

CMV

Cytomegalovirus

GI

gastrointestinal

HIV

human immunodeficiency virus

IBD

inflammatory bowel disease

ICV

ileocecal valve

UC

ulcerative colitis

Introduction

Infectious bowel diseases are more common in developing countries than industrialized countries. On the other hand, the incidence and prevalence of inflammatory bowel disease (IBD) in the former are increasing . Superimposed bacterial, viral, fungal, or parasitic infection occur in patients with underlying IBD with or without concurrent use of immunosuppressive drugs. Fortunately, the majority of patients with primary infectious bowel diseases are self-limited entities. Conventional stool culture, and ova and parasites are commonly performed to identify pathogens. Multipathogen molecular panels on diarrheal stool samples and, in some cases, rectal swabs have emerged as an important diagnostic modality for the identification of various bacterial, viral, and parasitic pathogens.

Chronic infection with certain pathogens (such as tuberculosis) can lead to chronic bowel inflammation, posing a challenge in the differential diagnosis with true IBD. While upper and lower gastrointestinal (GI) endoscopies offer limited diagnostic value in acute enteritis or acute colitis, they are valuable tools for the evaluation of chronic bowel symptoms (>weeks of duration). Some of infectious enteritis or colitis have characteristic features on endoscopy. In addition, endoscopy provides access to tissue sampling. In this chapter, endoscopic features of common bacteria, virus, and parasite-associated enteritis or colitis, which mimics IBD are described ( Table 25.1 ). Superimposed infection in IBD is discussed in a separate chapter ( Chapter 23 : Superimposed infections in inflammatory bowel diseases).

Table 25.1

Common gastrointestinal pathogen-associated bowel diseases mimicking inflammatory bowel diseases.

Bacteria	Mycobacterium tuberculosis , Clostridium difficile , Salmonella , Shigella , Yersinia , Enterohemorrhagic Escherichia coli , Campylobacter , Aeromonas , Plesiomonas
Viruses	Human immunodeficiency virus, Cytomegalovirus , Epstein–Barr virus
Fungi	Candida albicans , Histoplasma , Coccidioides , Blastomyces dermatitidis
Parasites	Giardia, Cryptosporidium lamblia , Entamoeba histolytica , Strongyloides stercoralis , Schistosoma

Bacteria-associated bowel diseases

A variety of bacterial agents can cause enteritis and colitis. Some of them, particularly, intracellular bacteria can cause chronic enteritis or colitis, mimicking IBD.

Intestinal tuberculosis

The small and large bowel is a common site for extrapulmonary tuberculosis resulting from Mycobacterium tuberculosis . The causal agents can be M. tuberculosis or Mycobacterium bovis . The pathogenetic route of infection of the latter agent is through drinking contaminated dairy products. The main routes of infection of intestinal tuberculosis (ITB) are GI tract, blood flow, or adjacent tuberculous lesions. The gold standard for the diagnosis of ITB is identification of the bacteria in the stool or GI tissue specimens. However, the detection of the bacterial agent can be challenging. Skin and serological tests can only provide supportive evidence, and their use in the differential diagnosis of ITB and Crohn’s disease (CD) has been limited, especially in endemic areas of tuberculosis.

ITB and CD share many aspects of clinical, endoscopic, radiographic, and histologic examinations. Both can be presented with low-grade fever, night sweats, abdominal pain, diarrhea, or abdominal mass. Both have a predilection of involvement of the terminal ileum and ileocecal valve (ICV). Parenteral manifestations and intestinal fistula, however, appear to be more common in CD than ITB.

Endoscopy can play an important role in the differential diagnosis of ITB and CD ( Table 25.2 ). Generally, the endoscopic features of CD include aphthous ulcers, asymmetrical longitudinal ulcers, skip lesions, and the presence of strictures, fistulae, or perianal disease. The ICV often has ulcers, stricture, or deformity in patients with distal ileum ITB. In contrast, ulcers in ITB are often circumferentially distributed. While mucosal nodularity of the ileum is more common in ITB, cobblestoning of the ileal mucosa is more often seen in CD ( Figs. 25.1 and 25.2 ) . Histologic distinction between ITB and CD is discussed in a separate chapter ( Chapter 34 : Histology correlation with common endoscopic abnormalities). The overlapping features between ITB and CD can make the differential diagnosis difficult, which has mandated empiric anti-ITB therapy in some patients.

Table 25.2

Comparison of endoscopic features of intestinal tuberculosis and Crohn’s disease.

	Intestinal tuberculosis	Crohn’s disease
Orientation of ulcers	Traverse	Longitudinal
Aphthous erosions	+/−	++
Cobblestoning mucosa	+	++
Nodular mucosa	++	+
Mucosal bridge	+/−	+
Stricture	+/−	+++
Fistula	+	++
Ileocecal valve feature	Patulous	Ulcerated, strictured, or deformed
Colon and rectum involvement	+/−	+
Perianal disease	+/−	++
Skip lesion	+/−	+++

Figure 25.1, Tuberculosis in the colon: (A) Nodularity of colon mucosa; (B and C) discrete small and large superficial ulcers in the colon; (D) tissue biopsy showed granulomas.

Figure 25.2, Patterns of intestinal tuberculosis: (A) Ulcerated, patent ICV; (B) multiple ulcers in a circumferential fashion in the cecum and ICV on the background of mucosal edema; (C and D) tuberculosis in the terminal ileum in remission with pseudopolyps. ICV , Ileocecal valve.

Intracellular enteric pathogens

Invasive, intracellular bacteria, such as Salmonella enterica serotype typhi and Yersinia enterocolitica can affect GI tract, with the former causing gastroenteritis and the latter leading to enterocolitis. These foodborne illnesses normally result in acute, self-limited GI diseases. However, some of the patients may develop chronic enteritis or colitis with phenotypes overlapping with that of CD. Their chronic disease process and transmural involvement can have inflammatory, stricturing, or penetrating phenotypes, with manifestations of low-grade fever, night sweat, nausea, bloating, abdominal pain, diarrhea, hematochezia, abdominal mass, or even ascites. On endoscopy, there can be nodularity, ulcers, and strictures ( Fig. 25.3 ) . Its distinction from IBD, particularly CD, is critical, as the management of the two disease entities is different.

Figure 25.3, Sigmoid colon stricture with stool cultures positive for Salmonella Group C and Blastocystis hominis : (A) Distal proctitis with ulcerated and nodular mucosa; (B) stricture of the sigmoid colon; (C) stricture at the sigmoid colon on gastrografin enema ( green arrow ).

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