Abdominal Tuberculosis and Other Mycobacterial Infections

Vishal Sharma, Uma Debi, Harshal S Mandavdhare, and Kaushal K Prasad, Postgraduate Institute of Medical Education and Research,
Chandigarh, India
© 2018 Elsevier Inc. All rights reserved.

Gastrointestinal Tuberculosis 2
Epidemiology 2
Pathology and Pathogenesis 2
Definition and Nomenclature 2
Clinical Manifestations Including Natural History 3
Intestinal tuberculosis (ITB) 3
Other forms of luminal tuberculosis 4
Visceral tuberculosis 7
Diagnosis and Differential Diagnosis 8
Intestinal tuberculosis: diagnosis 8
Intestinal tuberculosis: differential diagnosis 9
Peritoneal tuberculosis: diagnosis 10
Peritoneal tuberculosis: differential diagnosis 10
Treatment and Follow-up 11
Prevention and Prognosis 11
Guidelines 11
Abdominal Mycobacterium avium-intracellulare (MAI) Infection 12
Definition 12
Epidemiology 12
Pathobiology 13
Clinical Manifestations Including Natural History 13
Diagnosis and Differential Diagnosis 13
Treatment 13
Prevention (Primary and Secondary and Risk Factors) 13
Prognosis 13
Guidelines 14
Summary 14
References 14
Further Reading 14

Glossary
Abdominal tuberculosis Term which describes a form of extrapulmonary tuberculosis that could involve the various organs of
the abdominal cavity like the small or large intestines, peritoneum, lymph nodes, and visceral organs, singularly or in
combination.
Adenosine deaminase It is an enzyme involved in purine metabolism and has two isoforms. ADA is produced by many cells
and also by activated lymphocytes. Elevated levels in pleural and peritoneal fluid may suggest underlying tuberculosis.
Clinically diagnosed abdominal tuberculosis It is a case of abdominal tuberculosis where the diagnosis is based on strong
clinical suspicion, with suggestive features on imaging, histology (noncaseating granulomas, chronic inflammatory changes),
cytology, and biochemistry (elevated ascitic adenosine deaminase), and with an objective response to antitubercular therapy
(mucosal healing or resolution of ascites) in the absence of microbiological evidence.
Confirmed case of abdominal tuberculosis It is a case of abdominal tuberculosis where there is objective demonstration of
presence of acid fast bacilli either on histopathology (with or without caseation necrosis), culture or polymerase chain reaction
(PCR) based assays.
Early mucosal healing The documentation of mucosal healing at the end of 2 months during the course of standard
antitubercular therapy.
Gastrointestinal tuberculosis It is the form of extrapulmonary tuberculosis that involves the esophagus and the stomach apart
from involvement of the abdominal cavity.
Intestinal tuberculosis It is the subtype of abdominal tuberculosis that involves the intestine and can present as a ulcerative
form with diarrhea, and stricturing form or hypertrophic form with abdominal pain and/or intestinal obstruction.

Encyclopedia of Gastroenterology, 2nd Edition https://doi.org/10.1016/B978-0-12-801238-3.65963-9 1

2 Abdominal Tuberculosis and Other Mycobacterial Infections

Mucosal healing Healing of ulcers in patients with intestinal tuberculosis with antitubercular therapy. It is an objective way of
documenting response to antitubercular therapy especially in clinically diagnosed cases of intestinal tuberculosis.
Peritoneal tuberculosis It is the subtype of abdominal tuberculosis that involves the peritoneum and could present as a wet
type with ascites, dry type with peritoneal and omental thickening, adhesions or as a cocoon.
Tubercular abdominal cocoon It is a special type of peritoneal tuberculosis where in matted and clumped intestinal loops are
encircled by a thickened peritoneal membrane.

Mycobacterial diseases of the abdomen broadly could be due to infection by the Mycobacterium tuberculosis (Tuberculosis) or
nontuberculous mycobacteria (NTMs). M. tuberculosis complex includes the organisms M. tuberculosis, Mycobacterium bovis, Myco-
bacterium africanum, and Mycobacterium microti. Of these M. tuberculosis is responsible for most of the cases of abdominal tuberculosis
which is an important form of extrapulmonary tuberculosis. With increase in human immunodeficiency virus (HIV) infection and
the resulting acquired immune deficiency syndrome (AIDS), clinicians also encounter infections with the NTMs more frequently
which are difficult to diagnose especially, because of existing coinfections and moreover are difficult to treat. Of the NTMs the
Mycobacterium avium complex (MAC) is a major concern and includes the species including M. avium, Mycobacterium intracellulare,
and Mycobacterium chimaera.

Gastrointestinal Tuberculosis

Abdominal tuberculosis is a common clinical condition in the tropical countries but is often difficult to diagnose as it can mimic a
number of other conditions. Intestinal involvement by tuberculosis was recognized long back and Hippocrates stated that
development of diarrhea in tubercular cases portended a fatal outcome. With the availability of effective treatment, mortality due
to abdominal tuberculosis has become uncommon. The disease is characterized by a varied clinical presentation which may be
confused with a number of other conditions. Further the low sensitivity of microbiological and histological testing adds to the
difficulty in the diagnosis. While all efforts must be made to achieve a histological or microbiological diagnosis, often the condition
has to be treated empirically. The evaluation of patients suspected to have abdominal tuberculosis should also seek to exclude the
other differential diagnosis.

Epidemiology
Tuberculosis is an important concern for clinicians across the globe and is estimated to infect around 30% of the population.
Tuberculosis accounted for around 1.7 million deaths in 2016 most of which occurred in lower and middle income countries
especially India, Indonesia, and China. The threat associated with tuberculosis has been heightened by the emergence of multidrug
resistant (MDR: resistant to rifampin and isoniazid) and extensively drug resistant strains (XDR: MDR plus resistance to at least one
fluoroquinolone and one injectable drug). While lung is the most common site of involvement, extrapulmonary tuberculosis
(EPTB) is also an important concern especially in the immunocompromised individuals (Sharma and Bhatia, 2004a). The diagnosis
of EPTB is difficult because of low sensitivity of microbiological tests and the difficulty in achieving a tissue diagnosis. Abdominal
tuberculosis is an important cause of extrapulmonary tuberculosis and accounts for 12.8% of all EPTB cases (Cherian et al., 2017).
In fact it was the third most common site of EPTB after lymphnodal and pleural effusion in a study based on Revised National
Tuberculosis Control Program in three Indian districts (Cherian et al., 2017).

Pathology and Pathogenesis

The spread of the tubercle bacilli to the abdomen could occur in multiple possible manners. These could include hematogenous
spread from the pulmonary focus, ingestion of infected sputum from active pulmonary disease, contiguous spread from infected
organs example female genital tract, and lymph nodes in the abdomen. The involvement in the abdomen may include the intestinal
tract, lymph nodes, peritoneum, or the visceral organs (Table 1).
The gross involvement of the intestinal tract could be in the form of hypertrophic or mass forming lesions, intestinal ulceration,
or intestinal strictures. The peritoneal involvement may be characterized by the presence of peritoneal fluid, peritoneal nodules and
thickening, omental or mesenteric thickening and nodularity and adhesions with the bowel wall. Abdominal cocoon may be
characterized by formation of a membraneous sac around clumped bowel loops. The histological examination may be characterized
by formation of granulomas which are usually larger than those seen in Crohn’s disease (CD). Presence of caseous necrosis or acid
fast bacilli (AFB) positivity provides some specificity to the diagnosis. The histological findings are discussed in more detail in the
section on diagnosis.
 Abdominal Tuberculosis and Other Mycobacterial Infections 3

Table 1 Patterns of involvement in gastrointestinal tuberculosis

Peritoneal
Wet-ascitic type
Dry and fibrotic type
Mixed (ascitic and fibrotic)
Tubercular abdominal cocoon (sclerosing encapsulating peritonitis)
Luminal
Intestinal
Ulcerative
Hypertrophic
Stricturing
Esophageal
Gastro-duodenal
Lymph-nodal tuberculosis
Visceral
Hepatic tuberculosis
Splenic tuberculosis
Pancreatic tuberculosis
Gall bladder and biliary tuberculosis

Definition and Nomenclature

The term abdominal tuberculosis would include the tubercular infection of any of the abdominal organs. However, the involvement
of the genitourinary systems is usually considered to be separate from abdominal tuberculosis. Gastrointestinal tuberculosis, on the
other hand, would include not just the abdominal organs but also esophagus which is extraabdominal. Gastrointestinal tubercu-
losis can be of four distinctive patterns of involvement and may involve the peritoneal cavity, the gastrointestinal tract, the visceral
organs, or the abdominal lymph nodes (Table 1). Various definitions are in vogue to define a case of abdominal tuberculosis.
Paustian’s definition of abdominal tuberculosis suggested that a confident diagnosis could be established if any of these four
features was present: caseating tubercles, acid fast bacilli (AFB) positivity in tissue, typical operative findings, and consistent
histology of mesenteric lymph nodes or growth of M. tuberculosis on culture or animal inoculation (Sharma and Bhatia, 2004a).
These criteria were modified by Logan who suggested that response to treatment should also be included as one of the criteria for the
diagnosis (Logan, 1969). Indian extrapulmonary tuberculosis (INDEX-TB) guidelines have suggested use of the term
“bacteriologically confirmed case” on the basis of positivity of microbiological tests for tuberculosis or a “clinically diagnosed
case” in cases where these tests are negative but the clinical, radiological, and histology are suggestive of tuberculosis with exclusion
of other conditions (Table 2) (Sharma et al., 2017b). However, these definitions are not specifically made for abdominal
tuberculosis and do not emphasize the presence of caseating granulomas which are considered pathognomic of tuberculosis. It is
suggested in the presence of conclusive histological or microbiological evidence (caseating granulomas or microbiological positivity
in form of positive acid fast bacilli staining, culture, or polymerase chain reaction) a diagnosis of “confirmed abdominal
tuberculosis” be made whereas in cases where the evidence is suggestive (granulomas (Fig. 1) or chronic inflammation, elevated
ascitic adenosine deaminase) the diagnosis of a “clinically diagnosed abdominal tuberculosis” be made (Sharma et al., 2017a).
When patients with clinically diagnosed abdominal tuberculosis are initiated on antitubercular therapy, it is important to exclude
other differential diagnosis and follow-up these patients for subjective and objective signs of improvement.

Clinical Manifestations Including Natural History

Intestinal tuberculosis (ITB)
Tuberculosis can involve any part of the gastrointestinal tract but most frequently involves the ileocecal region. Possible reasons
behind the predisposition of the ileocecal area are presence of physiological stasis of bowel contents, lack of digestive enzyme
activity, high resorption of fluid, and abundant lymphoid tissue in this region (Sharma Bhatia, 2004). The involvement is
characterized by three distinctive morphological patterns: ulcerative, stricturing or hypertrophic (pseudotumoral), and a combina-
tion of these (Fig. 2). The clinical symptomatology may vary with the dominant pattern of morphological involvement. While the
ulcerative form may be characterized by chronic diarrhea and malabsorption, the clinical picture of hypertrophic or stricturing form
are often dominated by abdominal pain and episodes of intestinal obstruction. Constitutional symptoms like fever, night sweats,
loss of weight, and appetite are also present in a variable number of the patients. While hematochezia is less common, it may
suggest rectal involvement. Gastrointestinal perforation may result in acute presentation and needs emergency surgery. Massive
gastrointestinal bleeding necessitating urgent surgery is uncommon but has been reported. Table 3 includes the clinical features
noted in the major series of patients with intestinal tuberculosis.
4 Abdominal Tuberculosis and Other Mycobacterial Infections

Table 2 Various criteria proposed for diagnosis of abdominal tuberculosis

Criteria Clinical situation Features

Paustian criteria (Paustian and
Bockus, 1959)
Logan’s modification (Logan, 1969)
INDEX-TB definition (Sharma et al.,
2017b)
Suggested criteria (Sharma et al.,
2017a)
Sharma, Singh and Mandavdhare
criteria (Sharma et al., 2017d)
Abdominal (i)Histology: tubercles with caseation necrosis
tuberculosis (ii)Typical surgical findings with mesenteric nodes showing evidence of tuberculosis
(iii)Animal inoculation or the culture growth of M. tuberculosis
(iv) Acid fast bacilli in the lesion
Abdominal (i)Tubercle bacilli seen on microscopy/culture
tuberculosis (ii)Caseating giant cell lesions with the clinico-radiological evidence
(iii)Probable TB: granuloma similar to “sarcoid” reaction of Crohn’s disease with the clinico-
radiological evidence of tuberculosis elsewhere, and response to ATT
Extrapulmonary Confirmed case: Microbiological positivity (positive microscopy, culture or validated PCR)
tuberculosis Clinically diagnosed case: In patients with negative microbiological tests but strong clinical
suspicion and other evidence (imaging, histology, cytology, biochemical or response to ATT)
Abdominal Confirmed case: Microbiological positivity (positive microscopy, culture or validated PCR) or
tuberculosis caseating granuloma
Clinically diagnosed case: In patients with negative microbiological tests but strong clinical
suspicion and other evidence (imaging, histology, cytology, biochemical or response to ATT)
Tubercular Confirmed TAC: Microbiological positivity or caseating granulomas
abdominal cocoon Clinically diagnosed TAC: Clinico-radiological picture with supportive biochemical, cytological,
(TAC) or histological evidence
Diagnosis of cocoon on basis of demonstration of membrane on surgery or imaging

Fig. 1 Well-defined multiple epitheloid granuloma with Langhan’s giant cell (H&E X 20).

Other forms of luminal tuberculosis

Esophageal TB
Esophagus is an uncommon site of involvement by tuberculosis (Fig. 3). Esophageal involvement is usually secondary to
mediastinal lymph nodes infiltrating or compressing the esophagus. Clinical presentation may include dysphagia and/or hema-
temesis apart from constitutional symptoms. Endoscopic features may include ulcers, submucosal bulge, sinus tracts, diverticula,
stricture, or polypoidal lesions usually in the mid-esophagus due to enlarged subcarinal lymph nodes. The disease could easily be
confused with esophageal cancer. While CT may be helpful for diagnosis, endoscopic ultrasound (EUS) aids acquisition of tissue for
cytological and microbiological work up. EUS features include thickening of the esophageal wall, adventitial disruption by
mediastinal lymphadenopathy and the lymph nodes could be heteroechoic or homogeneous with hyperechoic foci inside the
lymph nodes and lack of distinctive margins and occasionally demonstrate calcification. While ATT is effective for treatment of
esophageal tuberculosis and most of the manifestations, esophago-bronchial fistulae may require management with endoscopic
(clip application) or surgical approaches.

Gastroduodenal TB
Gastroduodenal region is another uncommon site of tuberculosis (Fig. 4) and the presence of gastric acid seems to play a protective
role. The occurrence of tuberculosis in this region may present with dyspeptic symptoms, abdominal pain, gastric outlet
 Abdominal Tuberculosis and Other Mycobacterial Infections 5

Fig. 2 Patterns of intestinal tuberculosis. (A) Showing circumferential ulceration, (B) multiple cecal ulcers and ileocecal involvement, (C) ulcer with stricture in
terminal ileum, and (D) surgical specimen of resected hypertrophic tuberculosis. Courtesy Dr Harjeet Singh M. Ch., Chandigarh.

Table 3 Clinical features of abdominal tuberculosis as reported in major series

Spalgais et al. Sharma et al. Afridi et al. Chalya et al. Chaudhary Dauda et al. Khan et al. Gilinsky et al.
(2017) (2017a) (2016) (2013) et al. (2016) (2010) (2001) (1983)
(n ¼ 200) (n ¼ 112) (n ¼ 100) (n ¼ 256) (n ¼ 756) (n ¼ 117) (n ¼ 135) (n ¼ 125)
{n(%)} {n(%)} {n(%)} {n(%)} {n(%)} {n(%)} {n(%)} {n(%)}

Pain 60(30) 110 (98.21) 72 240(93.8) 756(100) 90(77) 118(88) 85(68)

Diarrhea 94(42) 14(12.5) NA 78(30.5) 121(16) 37(32) 34(25) 35(28)
Constipation NA NA NA 165(64.5) 236(34) NA 30(22) 21(17)
Hematochezia NA 08(7.14) NA NA NA NA NA 7(6)
Intestinal NA 45(40.14) NA 127(49.6) NA NA 24(18) NA
obstruction
Fever 128(64) 70(62.5) 38 86(33.6) 496(66) 61(52) 68(50) 73(58)
LOA 45(22.5) 91(81.25) NA NA 586(78) 34(29) 36(27) NA
LOW 135(72.5) 93(83.03) 62 122(47.7) 481(64) 41(35) 58(43) 95(76)
Lump NA 11(9.82) NA 17(6.6) 77(10) 13(11) 55(41) 35(28)
abdomen
Mantoux NA 64(57.14) NA NA 546(83) 9(8) 7/9(78) 19(15)
Abnormal NA NA NA 58(22.7) 245(32) 16(14) NA 55(44)
chest X-ray
HIV All 1 NA 48(18.8) NA 9/36(26) NA NA

LOA, Loss of appetite; LOW, Loss of weight.

obstruction, failure to thrive (in pediatric age group), hematemesis and constitutional symptoms. It can closely mimic other gastric
diseases like peptic ulcer disease and malignancy. The endoscopic findings in this condition could include gastric ulcers, nodularity,
polypoidal lesions, submucosal bulge, luminal narrowing, sinus or fistulae, etc. While older reports suggest that endoscopic
diagnosis is difficult and the condition is often diagnosed after surgical resection, use of well (bite on bite biopsy) biopsies and
6 Abdominal Tuberculosis and Other Mycobacterial Infections

Fig. 3 Esophageal ulcer in a patient with HIV which turned out to be due to tuberculosis.

Fig. 4 Gastroduodenal tuberculosis. (A) Double contrast barium meal shows multiple erosions in stomach and duodenum, and (B) CT showing duodenal mural
thickening with luminal narrowing.

endoscopic mucosal resection could improve the diagnostic yield of endoscopy. Apart from the use of ATT, endoscopic dilatation
may be required in patients having gastric outlet obstruction.

Peritoneal tuberculosis
Peritoneal tuberculosis is another common pattern of involvement with abdominal tuberculosis and is usually characterized by
ascites formation. The peritoneal involvement may be related to the hematogenous spread from pulmonary lesions, spread from
local lesions in the intestine or the fallopian tubes (Sanai and Bzeizi, 2005). However, dry forms of peritoneal tuberculosis are also
recognized which may have little or no ascites and may be associated with peritoneal thickening, adhesions, omental, and
mesenteric thickening. The clinical features in a patient may be related to the pattern of underlying involvement. Although various
terms like dry-plastic and fixed-fibrotic are in vogue for the dry form of peritoneal tuberculosis, there is a considerable overlap
amongst these two patterns (Sanai and Bzeizi, 2005; Sharma and Bhatia, 2004a). Another special pattern of involvement is
abdominal cocoon (or sclerosing encapsulating peritonitis) which is characterized by presence of a membranous sac around the
intestinal loops resulting in features of pain and intestinal obstruction (Sharma et al., 2017c,d). Rarely, chylous ascites could occur
with mycobacterial infections. While the usual risk factors like poor socioeconomic status, underlying immunodeficiency or
diabetes mellitus may predispose to acquisition of tuberculosis, underlying alcoholic liver disease is also recognized as a risk factor
for peritoneal tuberculosis.
The patients with wet-ascitic pattern may have abdominal distension, pain, fever, with loss of appetite and weight as the
predominant clinical features. Abdominal examination may reveal abdominal distension and presence of ascites. The classical
 Abdominal Tuberculosis and Other Mycobacterial Infections 7

Fig. 5 CT images of peritoneal tuberculosis. (A) Showing massive ascites with displacement of bowel loops, (B) dry pattern with omental caking, (C) mixed pattern
with ascites and omental thickening, and (D) abdominal cocoon.

“doughy” feel on palpation is infrequent and represents a form of peritoneal tuberculosis where ascites formation is less dominant.
Imaging findings in these patients show ascites and may demonstrate peritoneal thickening and enhancement (Fig. 5A). Patients
with dry (or mixed dry–wet) involvement have abdominal pain and may develop intestinal obstruction (Fig. 5B,C). Imaging in
these patients may demonstrate ascites which could be loculated, omental and mesenteric thickening, peritoneal nodularity, etc.
Tubercular abdominal cocoon usually presents with abdominal pain, lump, and episodes of intestinal obstruction. The imaging
may demonstrate clumping of bowel loops, ascites, and various signs like cauliflower sign, concertina pattern of arrangement of
small bowel loops, and a bottle gourd sign demonstrating dilated duodenum up till the second or third part. The hallmark,
however, is the demonstration of a thick membrane which surrounds the small bowel loops (Fig. 5D).

Visceral tuberculosis
Hepatic tuberculosis
The involvement of liver by tubercular infection could occur in distinctive patterns: miliary or localized involvement. Miliary
involvement of the liver is part of disseminated tuberculosis and is characterized by diffuse hepatic involvement with tubercules
primarily involving the hepatic lobules and CT suggestive of multiple hypodense lesions. On the contrary, localized hepatic
involvement is usually associated with larger lesions which could be calcified and the infection is supposed to originate from the
gastrointestinal tract. Localized hepatic tuberculosis has also been labeled as tuberculoma or pseudotumoral pattern. Hepatic
abscess could also be a manifestation of the localized form of hepatic tuberculosis. The clinical manifestation could include fever,
hepatomegaly, loss of weight, abdominal pain, and deranged liver function tests. The elevation of alkaline phosphatase and
gamma-glutamyl transferase may be dominant liver function abnormality in diffuse involvement.

Pancreatic tuberculosis
Pancreatic tuberculosis could be a consequence of primary involvement of the pancreas or the peripancreatic lymph nodes and is an
uncommon entity. Even in regions endemic for tuberculosis, the commonest cause of a pancreatic mass is pancreatic cancer and
therefore, pancreatic tuberculosis is usually diagnosed after a Whipple’s procedure for a presumed pancreatic malignancy. This has
changed with the advent of advances in tissue acquisition and use of endoscopic ultrasound which can evaluate and sample
pancreatic lesions. Pancreatic tuberculosis could present with abdominal pain, fever, loss of weight or appetite, jaundice, biliary
obstruction, abdominal lump, etc. Imaging findings could reveal biliary or pancreatic ductal dilatation, pancreatic mass which
8 Abdominal Tuberculosis and Other Mycobacterial Infections

could involve any region of the pancreas, cystic or solid cystic lesions, lymphadenopathy, diffuse pancreatomegaly, calcifications,
and vascular involvement. None of the findings are distinctive for pancreatic tuberculosis and the diagnosis requires cytological and
microbiological testing. While jaundice usually responds with ATT, endoscopic retrograde cholangiography with biliary stenting
may be required in cases with associated cholangitis or lack of improvement in biliary obstruction.

Biliary and gall bladder tuberculosis

Gall bladder and the biliary tract are uncommon sites of involvement with tuberculosis. Gall bladder tuberculosis is usually a
histological surprise in patients who undergo surgery for suspected cholecystitis or gall bladder cancer. This is usually because of
nonspecific symptoms like abdominal pain, fever, loss of appetite and weight, and nonspecific imaging findings. Occasionally port
site involvement after a laparoscopic cholecystectomy may occur. Biliary involvement by tuberculosis is also uncommon and may
present as biliary stricture or lymph nodal compression of the biliary system. The diagnosis could be established by endoscopic
retrograde cholangiography using brushings or image guided FNA from the lymph nodes.

Diagnosis and Differential Diagnosis

Intestinal tuberculosis: diagnosis
Computed tomography (CT) has an important role in evaluation of patients suspected to have abdominal tuberculosis. The
findings on imaging could include mural thickening of the bowel wall, intestinal strictures which are usually short and concentric,
abdominal lymphadenopathy especially of mesenteric and retroperitoneal lymph nodes, hypodense center suggesting necrotic
lymph nodes, ascites, peritoneal and omental thickening and enhancement, etc. (Fig. 6) (Kedia et al., 2017; Limsrivilai et al., 2017).
However, none of the features are diagnostic and the findings on CT help in guiding further evaluation and targeting the involved
areas for tissue diagnosis. The use of magnetic resonance enterography (MRE) may be helpful for evaluation of intestinal
tuberculosis and detects more strictures than barium studies (Krishna, 2016). Although barium studies have been used extensively
in the past, they are limited by the inability to provide information about extraluminal features. They may still be useful in
evaluation of the length and site of intestinal strictures when planning for surgery or dilatation (Fig. 6A,B). Colonoscopy is an
important tool for evaluation of intestinal tuberculosis and helps in determination of site and pattern of involvement. Also, it
provides the tissue biopsies needed for microbiological and histological evaluation. The endoscopic findings in intestinal

Fig. 6 Radiological picture of intestinal tuberculosis. (A) Barium study showing ulceration and narrowing of the ileocecal junction, (B) multiple small bowel stricture
with proximal dilatation, (C) CT image showing thickening of distal ileum and caecum with narrowed terminal ileum, and (D) thickened ileocecal region.
 Abdominal Tuberculosis and Other Mycobacterial Infections 9

tuberculosis include intestinal ulcers (usually transverse), stricture, pseudopolyps, ileocecal region involvement. Crohn’s disease
(CD), which is an important differential diagnosis, is usually characterized by presence of linear and serpiginous ulcer, aphthous
ulcers, skip lesions, rectal involvement, etc. (Limsrivilai et al., 2017). However, there is a considerable overlap between endoscopic
findings of the two conditions and no single finding is specific for any diagnosis.
The diagnosis of intestinal tuberculosis is often based on microbiological or histological evaluation. However, both of these are
compromised by low sensitivity for the diagnosis. Therefore, response to therapy has been suggested as an important criterion for
the diagnosis of ITB (Logan’s modification of Paustian criteria). Table 2 provides different definitions used for diagnosis of
abdominal tuberculosis. The presence of caseating granulomas, confluent granuloma, or ulcer base lined by epithelioid histiocytes
are considered to be specific in discrimination of ITB from CD (Du et al., 2014). However, the sensitivity of these findings is below
50%. Acid-fast bacilli (AFB) positivity is infrequent and culture positivity from tissue samples is compromised by low sensitivity and
high turnaround times. Recent times have seen increasing focus on molecular diagnosis of ITB. In a systematic review on the use of
IS 6110 primers for the diagnosis of ITB over CD, the pooled sensitivity was 46% and specificity was 95% (Jin et al., 2017).
Therefore, while a positive polymerase chain reaction (PCR) could be supportive of the diagnosis, a negative PCR does not exclude
ITB. Xpert MTB/RIF, which has found use in pulmonary and lymphnodal TB, has a low sensitivity (8%) for the diagnosis of
intestinal TB but could suggest underlying multidrug resistant tuberculosis (MDR-TB) (Kumar et al., 2017; Sharma et al., 2018). The
overall sensitivity and specificity of microbiological and histological tools is depicted in Table 4. Table 5 provides the features used
to discriminate ITB from CD.

Intestinal tuberculosis: differential diagnosis

The most important differential diagnosis of intestinal tuberculosis is CD which mimics ITB very closely and has similar clinical
features, endoscopic findings, radiological findings, and histology. The need to discriminate the two cannot be overemphasized as a
misdiagnosis is fraught with serious consequences. The mistreatment of ITB as CD may result in flare and dissemination of
tuberculosis due to immunosuppressive drugs like steroids. On the contrary, misdiagnosis of CD as ITB results in delay of effective
therapy and exposure to ATT which may have adverse effects like drug induced liver injury.
A meta-analysis, which compared utility of clinical, endoscopic, radiological, serological, and histological characteristics for
discriminating the two entities, proposed a model to predict the diagnosis in individual patient. Amongst the clinical features male
gender, presence of diarrhea and hematochezia, perianal disease and extraintestinal lesions favor CD while shorter duration of
symptoms, presence of fever, night sweats, pulmonary or peritoneal involvement favor ITB. Amongst the endoscopic findings
ileocecal involvement, patulous IC valve, transverse ulcers favor ITB while left colonic involvement, longitudinal ulcers, skip lesions,
cobblestoning and aphthous ulcers favor the diagnosis of CD. On histology, the presence of granuloma which may be confluent,
multiple, submucosal, or large granulomas or an ulcer base lined by histiocytes favor ITB (Limsrivilai et al., 2017).
Certain CT findings may be helpful in discriminating these two entities and the presence of ascites and necrotic lymph nodes is
suggestive for the diagnosis of ITB. However, these radiological findings could occur in other diseases like malignancy (ascites,
necrotic lymph nodes) and refractory celiac sprue, Whipple’s disease, lymphoma (necrotic lymph nodes) and are not specific for
ITB. The presence of comb sign (suggestive of hypervascular mesentery), skip lesions (involvement of two or more bowel segments),
presence of asymmetric mural thickening, fibro-fatty proliferation, and distal colonic involvement seem to favor the diagnosis of
CD (Kedia et al., 2017). Serological testing for anti-Saccharomyces cerevisiae antibody (ASCA) is suggested to be of value in
discriminating CD from ITB by a meta-analysis but the data from Indian studies is not supportive for use of this antibody as the
test could be negative in patients with CD and positive in a subset of patients with ITB (Ng et al., 2014). Further, positivity of
interferon release assays can provide evidence in favor of current or past tubercular infection, however, it does not exclude the
presence of CD and the negativity does not conclusively exclude ITB.
In cases where the diagnosis is uncertain even after extensive evaluation, the clinician may need to embark on empirical therapy.
In Indian subcontinent, it is common to start empirical ATT in such cases. Recent reports suggest that documentation of ulcer

Table 4 Yield of various investigations for diagnosis of abdominal tuberculosis

Intestinal tuberculosis Peritoneal tuberculosis

Caseating granulomas 21% (15%–40%) –

Granuloma 30%–82% –
AFB positivity 6%–20% 2.9%
AFB culture 6%–54% 34.7%
TB PCR 47% (20%–87%a) 48%–75%a
GenXpert 8% 18%–19%
Ascitic ADA (>30 U/L) – 94%
Laparoscopic visualization and histology – 92% and 93%
a
High sensitivity reported with multiplex PCR (3 primers).
Modified with permission from Dawra, S., Mandavdhare, H.S., Singh, H., Sharma, V., (2017). Abdominal tuberculosis:
Diagnosis and management in 2018. Journal, Indian Academy of Clinical Medicine 18, 271–274.
10 Abdominal Tuberculosis and Other Mycobacterial Infections

Table 5 Differences between intestinal tuberculosis (ITB) and Crohn’s disease (CD)

Feature Crohn’s disease Intestinal TB

Duration of presentation Longer history Shorter

Gender predisposition
Clinical features
Location of involvement
Colonoscopic appearance
Radiologic features
Histologic features
Laboratory and serological
markers
Treatment related factors
Male Female
Chronic diarrhea Pyrexia with night sweats
Blood in stools Pulmonary involvement
Perianal disease Ascites
Extraintestinal manifestations
Oral ulcers
Left colon (rectal) Right colon (cecum)
Multiple colonic segments Lesser number of colonic segments (<4)
Longitudinal serpiginous ulcers Circumferential transverse ulcers
Cobble stoning Patulous ileocecal valve
Mucosal bridges
Aphthous ulcers
Anorectal involvement
Comb sign Ascites
Asymmetrical mural thickening Mural stratification Abdominal lymphadenopathy (>1 cm with necrotic hypodense
of intestine centre)
Skip lesions Concentric strictures
Eccentric strictures Short segment involvement
Fibrofatty proliferation Pulmonary infiltrates or fibrosis
Focally enhanced colitis Granuloma with caseation necrosis
Large, confluent granulomas
Submucosal granulomas
Lymphocyte cuffing of the granuloma
Ulcer lined by histiocytes
Positive ASCA PCR positivity of IS6110
Positive IGRA
Recurrence after surgery Response to ATT (ulcer healing or resolution of ascites)

ASCA, anti-Saccharomyces cerevisiae antibody; IGRA, interferon gamma release assay.

Modified with permission from Mandavdhare, H.S., Singh, H., Sharma, V., (2017). Recent advances in the diagnosis and management of abdominal tuberculosis. EMJ
Gastroenterology 6, 52–60.

healing with ATT in patients with a diagnostic confusion between ITB and CD suggests presence of underlying ITB (PratapMouli
et al., 2017; Sharma et al., 2018). The decline in inflammatory markers like the serum CRP levels has been shown to mimic objective
response to ATT and a lack of decline could suggest the possibility of alternative diagnosis (Sharma et al., 2017a). Use of
inflammatory markers could obviate the need for a repeat colonoscopy in subset of patients initiated on empirical ATT.

Peritoneal tuberculosis: diagnosis

The diagnosis is based on evaluation of the peritoneal fluid and the ascites usually has a high protein, low serum-ascites albumin
gradient (SAAG). The cytological examination demonstrates usually a lymphocyte predominance. Certain biomarkers especially the
measurement of ascitic adenosine deaminase (ADA) is of value in diagnosis and a level of >30 U/L has a very high specificity and
sensitivity for the diagnosis of peritoneal tuberculosis. The yield of ADA measurement could be less satisfactory in certain situations
like the chronic liver disease (CLD) where the sensitivity is lower and the picture may be confounded by presence of a high SAAG
ascites. The yield of microbiological evaluation is low, that is, testing the fluid by acid fast bacilli staining, culture or PCR like the
Xpert MTB/RIF have low sensitivity. Other markers like interferon gamma estimation could be of use. In cases where diagnostic
uncertainty persists, peritoneoscopy to visualize and sample the peritoneal tissue could be undertaken. The visual examination with
peritoneoscopy is considered to be characteristic and the findings could include ascites with thickened peritoneum which could
appear hyperemic and demonstrate yellow-whitish miliary nodules, adhesions, and cheesy material. Visual appearance alone could
provide a high sensitivity (>90%) for the diagnosis and the procedure also provides an opportunity to achieve a tissue diagnosis
(Sharma and Bhatia, 2004b).

Peritoneal tuberculosis: differential diagnosis

The differential diagnosis of peritoneal tuberculosis is broad and any condition which causes ascites could mimic including CLD
and peritoneal carcinomatosis. The imaging findings are not very useful in differentiating peritoneal tuberculosis and peritoneal
carcinomatosis, and the findings like ascites, peritoneal nodularity or masses, visceral scalloping, omental nodularity or caking,
mesenteric nodularity could be seen in both of these conditions. Cytological evaluation for malignant cells should be done at least
 Abdominal Tuberculosis and Other Mycobacterial Infections 11

thrice to exclude peritoneal carcinomatosis. Serum and/or ascitic levels of CA125 could be elevated in peritoneal tuberculosis and
should not be used to discriminate it from peritoneal carcinomatosis (Tong et al., 2017).

Treatment and Follow-up

The treatment of abdominal tuberculosis is similar to pulmonary tuberculosis and 6 months of therapy is adequate for intestinal
and peritoneal tuberculosis. For other forms of gastrointestinal tuberculosis, the exact duration of therapy is uncertain and needs to
be individualized. Apart from ATT, other interventions could be required in a subset of patients. Stricture dilatation using
endoscopic balloons could be required to treat the gastric outlet obstruction (gastroduodenal TB) or intestinal obstruction
(intestinal tuberculosis). A small subset of patients with biliary or pancreatic tuberculosis may need endoscopic retrograde
cholangiography for diagnosis or for relief of biliary obstruction. Surgery may be needed for patients who have complications
like perforation, bleeding, repeated episodes of intestinal obstruction.
6 months of antitubercular therapy (ATT) is recommended for intestinal tuberculosis and has similar clinical cure rates and
relapse rates when compared to longer duration of therapies. A Cochrane systematic review of three trials has suggested the use of
6 months of ATT for intestinal and peritoneal TB (Jullien et al., 2016). The follow-up of the patients diagnosed with intestinal TB is
of extreme importance. Many of these cases are diagnosed on basis of definition of “clinically diagnosed abdominal TB” and the
demonstration of an objective response to therapy secures the diagnosis. In patients with a diagnostic confusion between ITB and
CD and who were initiated on ATT, the endoscopic healing of the ulcers at end of ATT was 100% in ITB and was infrequent in CD
(Ng et al., 2014). Mucosal healing of ulcers occurs as early as 2 months of ATT in a majority of cases of intestinal tuberculosis and is
termed as early mucosal response (Sharma et al., 2018). Lack of ulcer healing could suggest MDR-TB or an alternative diagnosis.
Therefore, in patients who are clinically diagnosed cases (Table 2) it is important to document ulcer healing with ATT to confirm the
diagnosis. Mere resolution (or lack of resolution) of clinical symptoms should not be used to define response because a substantial
number (one-third) of the patients with CD also have symptomatic improvement with ATT and therefore documentation of
mucosal healing should be sought in such cases. Further, around half of the patients with tubercular intestinal strictures may
continue to have abdominal pain even after 6 months of ATT in spite of healing of lesions (Aggarwal et al., 2017). This is due to high
rates of persistent stricture (three-fourths) and these patients may warrant endoscopic dilatation or surgery for management of their
symptoms. Table 6 depicts outcomes in patients with tubercular intestinal strictures with ATT. The suggested approach to treatment
for abdominal tuberculosis is shown in Fig. 7.
Treatment of peritoneal tuberculosis is also similar but abdominal cocoon and some forms of dry peritoneal tuberculosis may be
complicated by episodes of intestinal obstruction which may need surgical intervention. However, conservative management of
episodes of intestinal obstruction with nil per oral, nasogastric aspiration, and intravenous fluids with initiation of ATT may help
avoid surgery in a subset of these patients.

Prevention and Prognosis

The prognosis of abdominal tuberculosis with effective treatment is usually good and mortality should be uncommon. However,
the disease may be morbid in a subset of the patients needing surgical interventions like bowel resection, adhesiolysis, and creation
of temporary ileostomy or colostomy. Abdominal tuberculosis is unlikely to be communicable unless associated with pulmonary
lesions. The prevention of EPTB pivots around the strategies to control pulmonary tuberculosis. Prevention of tuberculosis needs a
multipronged approach: early diagnosis and management of sputum positive pulmonary cases, control of HIV and other conditions
which affect immune status like diabetes mellitus, addressing the socioeconomic issues which predispose to acquisition of TB
infection like better access to sanitation and nutrition, and avoidance of overcrowding, etc. The predisposing factors for acquisition
of peritoneal tuberculosis include underlying cirrhosis, chronic kidney disease, peritoneal dialysis, use of immunosuppressive
agents (steroids, anti-TNF-alpha agents, etc.), and immunodeficiency states.

Guidelines
Indian extrapulmonary tuberculosis guidelines provide recommendations for diagnosis and management of abdominal tubercu-
losis and other forms of extrapulmonary TB (INDEX TB Guidelines).

Table 6 Outcomes in patients with tubercular intestinal strictures with ATT

Study No Clinical improvement Endoscopic/radiological stricture resolution Surgery Endoscopic dilatation

Anand et al. (1988) 34 31 (91%) 16 of 23 (70%) 3 –

Mukewar et al. (2012) 30a – 23 (76%)b 4 (13%) –
Aggarwal et al. (2017) 106 52 (50%) 25 (23%) 7 (6.6%) 12 (11%)
a
Colonic TB.
b
Lack of clarity as in text authors say all except four who underwent surgery improved.
12 Abdominal Tuberculosis and Other Mycobacterial Infections

Fig. 7 Suggested clinical approach to management of abdominal tuberculosis. Modified with permission from Mandavdhare, H.S., Singh, H., Sharma, V., (2017).
Recent advances in the diagnosis and management of abdominal tuberculosis. EMJ Gastroenterology 6, 52–60.

Abdominal Mycobacterium avium-intracellulare (MAI) Infection

Definition
It is the infection caused by atypical mycobacteria (M. avium complex or MAC) that includes three species (M. avium, Mycobacterium
intercellulare, and M. chimaera) usually acquired through environmental sources like soil and water and manifesting in immuno-
compromised host as lung disease or disseminated disease or in immunocompetent host with underlying lung disease or as cervical
lymph adenitis in children. Usually responsible for pulmonary disease in the immunocompromised, abdominal involvement
usually occurs as a component of the disseminated disease. Abdominal MAC may be related to gastrointestinal tract involvement, or
lymphnodal involvement although occasional cases of solid visceral organ or peritoneal involvement have also been reported.

Epidemiology
MAC is ubiquitously present in environment and predominantly isolated from soil and water and is the most common cause of
infection by NTM. Human disease is acquired from these environmental sources, however, human to human or animal to human
transmission is rarely seen. The portal of entry of MAC is the respiratory and the gastrointestinal tract.
 Abdominal Tuberculosis and Other Mycobacterial Infections 13

Pathobiology
As MAC infection is rare it is obvious that the body has a robust mechanism to counter this organism and when it is breached the
infection manifests. From HIV infection the role of CD4 cells as key effectors against NTM has been recognized as disseminated
disease develops as the CD4 count falls below 50 cells. TNFa is also a crucial factor in mycobacterial control. Genetic risk factors
include defect in IFNg/IL-12 synthesis and response pathways as their interaction leads to intracellular killing of the mycobacteria.

Clinical Manifestations Including Natural History

Abdominal involvement is usually part of the disseminated disease as bowel is the usual portal of entry apart from lung. As these
organisms are of low virulence they usually present over weeks to months with fever, malaise, weight loss, hepatosplenomegaly,
lymphadenopathy, and anemia. Duodenum is the commonest site of involvement presenting as yellowish nodules due to local
replication of organism and can be confused with intestinal lymphangiectasia or Whipple’s disease and in fact it can present with
intestinal lymphangiectasia with diarrhea and protein losing enteropathy and malabsorption due to chronic intraabdominal and
retroperitoneal lymphadenopathy. MAC can present with colitis, appendicitis, or terminal ileitis especially in HIV infection. MAC
infection has also been reported to result in intestinal perforation which may occur even after initiation of HAART. Lymphnodal
involvement is another important finding and MAC should be considered in the differential diagnosis of abdominal lymphade-
nopathy in immunocompromised individuals especially those with underlying HIV infection. Occurrence of MAC-bacteremia is a
late finding in these patients and certain clinical features like fever, weight loss, anemia, and elevations in lactate dehydrogenase
levels precede the development of bacteremia. Primary peritoneal involvement is uncommon with MAC infection and may occur as
a part of disseminated disease especially when the CD4 counts are particularly low. Chylous ascites has also been reported as a part
of the spectrum of gastrointestinal involvement with MAC.

Diagnosis and Differential Diagnosis

Isolation of MAC in blood is a clear evidence of the disease and isolation from biopsy specimen is a strong evidence of infection
although laboratory contamination can occur. With strong clinical suspicion and two negative blood cultures one can proceed with
biopsy and culture of bone marrow and liver. Fine needle aspiration of intraabdominal/retroperitoneal nodes can help in diagnosis.
A unique although nonspecific is markedly high levels of alkaline phosphatase reaching up to 40 times with seemingly normal
transaminases and bilirubin. Histoplasmosis and CMV can have a similar clinical presentation although histopathology can clearly
differentiate these pathogens.

Treatment
Therapy involves combination of macrolides (clarithromycin/azithromycin), ethambutol, and a rifamycin (rifampin/rifabutin)
given over a period of 12–18 months in non-HIV and till normalization of CD4 in HIV.

Prevention (Primary and Secondary and Risk Factors)

Primary prevention in HIV is usually with prophylaxis with azithromycin 1200 mg weekly, clarithromycin 1000 mg daily or
rifabutin 300 mg daily when the CD4 count is <50 cells/mL and same can be given in those with defective IFNg/IL12 pathways.

Prognosis
Untreated the disease shortens survival and death is usually due to other opportunistic infection as a results of increased HIV
replication and malnutrition. With treatment the majority have recovery although some may develop relapse at a later stage.
Other mycobacteria have also been reported to occasionally result in gastrointestinal involvement (Table 7).

Table 7 Gastrointestinal manifestations of nontuberculous mycobacteria

Nontuberculous mycobacteria Gastrointestinal manifestations

Mycobacterium avium-intracellulare complex Abdominal lymphadenopathy

Ascites including chylous ascites
Chronic diarrhea
Cholecystitis
HIV cholangiopathy
Rapid growers (Mycobacterium abscessus, Mycobacterium chelonae, Continuous ambulatory peritoneal dialysis associated peritonitis
Mycobacterium fortuitum) Surgical infections including port-site infections
Pneumonia in achalasia (M. abscessus)
Mycobacterium kansasii Continuous ambulatory peritoneal dialysis associated peritonitis
Mycobacterium gordonae Surgical infections
14 Abdominal Tuberculosis and Other Mycobacterial Infections

Guidelines
Infectious Diseases Society of America and American Thoracic Society guidelines for diagnosis, treatment and prevention of
nontuberculous mycobacterial diseases published in 2007.

Summary

Mycobacterial infections of the gastrointestinal tract include abdominal tuberculosis or the involvement by the nontuberculous
mycobacteria usually in the immunocompromised individuals. Abdominal tuberculosis remains an important concern in tropical
countries and could involve the peritoneum, gastrointestinal lumen, visceral organs, or the lymph nodes. The diagnosis is
established on basis of microbiological or histological evidence but often empirical therapy is needed. Since abdominal tuberculosis
can easily mimic other diseases like Crohn’s disease, malignancy, etc., it is important to confirm objective response in patients who
have been clinically diagnosed.

References
Afridi SP, Siddiqui RA, Rajput A, and Alam SN (2016) Spectrum of abdominal-tuberculosis in emergency surgery: 100 cases at a tertiary care centre Dow University of Health Sciences
and Civil Hospital, Karachi, Pakistan. The Journal of the Pakistan Medical Association 66: 1173–1175.
Aggarwal P, Kedia S, Sharma R, et al. (2017) Tubercular intestinal strictures show a poor response to anti-tuberculous therapy. Digestive Diseases and Sciences 62: 2847–2856.
Anand BS, Nanda R, and Sachdev GK (1988) Response of tuberculous stricture to antituberculous treatment. Gut 29: 62–69.
Chalya PL, Mchembe MD, Mshana SE, et al. (2013) Clinicopathological profile and surgical treatment of abdominal tuberculosis: A single centre experience in northwestern Tanzania.
BMC Infectious Diseases 13: 270.
Chaudhary P, Kumar R, Ahirwar N, et al. (2016) A retrospective cohort study of 756 cases of abdominal tuberculosis: Two decades single centre experience. The Indian Journal of
Tuberculosis 63: 245–250.
Cherian JJ, Lobo I, Sukhlecha A, et al. (2017) Treatment outcome of extrapulmonary tuberculosis under Revised National Tuberculosis Control Programme. The Indian Journal of
Tuberculosis 64: 104–108.
Dauda MM, Ahmed A, Okpapi JU, et al. (2010) Abdominal tuberculosis in surgical practice in northern Nigeria. Nigerian Journal of Medicine 19: 415–418.
Du J, Ma YY, Xiang H, and Li YM (2014) Confluent granulomas and ulcers lined by epithelioid histiocytes: New ideal method for differentiation of ITB and CD? A meta-analysis. PLoS
One 9: e103303.
Gilinsky NH, Marks IN, Kottler RE, and Price SK (1983) Abdominal tuberculosis. A 10-year review. South African Medical Journal 64: 849–857.
Jin T, Fei B, Zhang Y, and He X (2017) The diagnostic value of polymerase chain reaction for Mycobacterium tuberculosis to distinguish intestinal tuberculosis from Crohn’s disease:
A meta-analysis. Saudi Journal of Gastroenterology 23: 3–10.
Jullien S, Jain S, Ryan H, and Ahuja V (2016) Six-month therapy for abdominal tuberculosis. Cochrane Database of Systematic Reviews 11: CD012163.
Kedia S, Sharma R, Sreenivas V, et al. (2017) Accuracy of computed tomographic features in differentiating intestinal tuberculosis from Crohn’s disease: A systematic review with
meta-analysis. Intestinal Research 15: 149–159.
Khan MR, Khan IR, and Pal KM (2001) Diagnostic issues in abdominal tuberculosis. The Journal of the Pakistan Medical Association 51: 138–142.
Krishna S, Kalra N, Singh P, et al. (2016) Small-bowel tuberculosis: A comparative study of MR enterography and small-bowel follow-through. AJR. American Journal of Roentgenology
207: 571–577.
Kumar S, Bopanna S, Kedia S, et al. (2017) Evaluation of Xpert MTB/RIF assay performance in the diagnosis of abdominal tuberculosis. Intestinal Research 15: 187–194.
Limsrivilai J, Shreiner AB, Pongpaibul A, et al. (2017) Meta-analytic Bayesian model for differentiating intestinal tuberculosis from Crohn’s disease. The American Journal of
Gastroenterology 112: 415–427.
Logan VS (1969) Anorectal tuberculosis. Proceedings of the Royal Society of Medicine 62: 1227–1230.
Mukewar S, Mukewar S, Ravi R, et al. (2012) Colon tuberculosis: Endoscopic features and prospective endoscopic follow-up after anti-tuberculosis treatment. Clinical and Translational
Gastroenterology 3: e24.
Ng SC, Hirai HW, Tsoi KK, et al. (2014) Systematic review with meta-analysis: Accuracy of interferon-gamma releasing assay and anti-Saccharomyces cerevisiae antibody in
differentiating intestinal tuberculosis from Crohn’s disease in Asians. Journal of Gastroenterology and Hepatology 29: 1664–1670.
Paustian FF and Bockus HL (1959) So-called primary ulcerohypertrophic ileocecal tuberculosis. The American Journal of Medicine 27: 509–518.
PratapMouli V, Munot K, Ananthakrishnan A, et al. (2017) Endoscopic and clinical responses to anti-tubercular therapy can differentiate intestinal tuberculosis from Crohn’s disease.
Alimentary Pharmacology & Therapeutics 45: 27–36.
Sanai FM and Bzeizi KI (2005) Systematic review: Tuberculous peritonitis—Presenting features, diagnostic strategies and treatment. Alimentary Pharmacology & Therapeutics
22: 685–700.
Sharma MP and Bhatia V (2004a) Abdominal tuberculosis. The Indian Journal of Medical Research 120: 305–315.
Sharma MP and Bhatia V (2004b) Abdominal tuberculosis. The Indian Journal of Medical Research 120: 305–315.
Sharma V, Mandavdhare HS, Lamoria S, Singh H, and Kumar A (2017a) Serial C-reactive protein measurements in patients treated for suspected abdominal tuberculosis. Digestive and
Liver Disease. https://doi.org/10.1016/j.dld.2017.12.008.
Sharma SK, Ryan H, Khaparde S, et al. (2017b) Index-TB guidelines: Guidelines on extrapulmonary tuberculosis for India. The Indian Journal of Medical Research 145: 448–463.
Sharma V, Mandavdhare HS, Rana SS, et al. (2017c) Role of conservative management in tubercular abdominal cocoon: A case series. Infection 45: 601–606.
Sharma V, Singh H, and Mandavdhare HS (2017d) Tubercular abdominal cocoon: Systematic review of an uncommon form of tuberculosis. Surgical Infections 18: 736–741.
Sharma V, Mandavdhare HS, and Dutta U (2018) Letter: Mucosal response in discriminating intestinal tuberculosis from Crohn’s disease—When to look for it. Alimentary
Pharmacology & Therapeutics (6): 859–860.
Spalgais S, Agarwal U, Sarin R, Chauhan D, Yadav A, and Jaiswal A (2017) Role of routine abdominal ultrasonography in intensified tuberculosis case finding algorithms at HIV clinics in
high TB burden settings. BMC Infectious Diseases 17: 351.
Tong H, Tai Y, Ye C, et al. (2017) Carbohydrate antigen 125 and carcinoembryonic antigen in the differentiation of tuberculous peritonitis and peritonitis carcinomatosa. Oncotarget
8: 78068–78075.

Further Reading

Dawra S, Mandavdhare HS, Singh H, Sharma V, et al. (2017) Abdominal tuberculosis: Diagnosis and management in 2018. Journal, Indian Academy of Clinical Medicine
18: 271–274.
Debi U, Ravisankar V, Prasad KK, Sinha SK, and Sharma AK (2014) Abdominal tuberculosis of the gastrointestinal tract: Revisited. World Journal of Gastroenterology 20(40): 14831.
 Abdominal Tuberculosis and Other Mycobacterial Infections 15

Hickey AJ, Gounder L, Moosa MY, and Drain PK (2015) A systematic review of hepatic tuberculosis with considerations in human immunodeficiency virus co-infection. BMC Infectious
Diseases 15: 209.
Krishnamurthy G, Singh H, Rajendran J, et al. (2016) Gallbladder tuberculosis camouflaging as gallbladder cancer—Case series and review focussing on treatment. Therapeutic
Advances in Infectious Disease 3: 152–157.
Mandavdhare HS, Singh H, and Sharma V (2017) Recent advances in the diagnosis and management of abdominal tuberculosis. EMJ Gastroenterology 6: 52–60.
Sanai FM and Bzeizi KI (2005) Systematic review: Tuberculous peritonitis—Presenting features, diagnostic strategies and treatment. Alimentary Pharmacology & Therapeutics
22: 685–700.
Sharma V, Rana SS, Kumar A, and Bhasin DK (2016) Pancreatic tuberculosis. Journal of Gastroenterology and Hepatology 31: 310–318.
Sharma V, Singh H, and Mandavdhare HS (2017) Tubercular abdominal cocoon: Systematic review of an uncommon form of tuberculosis. Surgical Infections 18: 736–741.