Keywords
extrapulmonary tuberculosis - gallbladder tuberculosis - miliary tuberculosis
Introduction
Isolated tuberculosis (TB) of the gallbladder (GB) is extremely rare due to its intrinsic
resistance to tuberculous infections. GB is one of the uncommon sites of involvement
by TB. It might present either with features of chronic cholecystitis, cholelithiasis,
or as malignancy.[1] Because GB TB is so uncommon and has nonspecific symptoms, it can be difficult to
diagnose preoperatively.[2] Various studies have documented variable manifestations of GB. However, they do
not help in providing a precise diagnostic clue.[2] There are different symptoms that people with GB TB infection can experience, including
weight loss, vomiting, jaundice, and abdominal discomfort, the right hypochondrium
pain. However, gallstones also present with similar symptoms and are also present
in approximately 70% of GB TB cases.[3] Due to these reasons, histology is confirmatory, and preoperative predictions of
GB TB are neither specific nor verified.[4] It is believed, infection travels to GB from a local focus and travel through the
bloodstream or lymphatics.[5] It is challenging to accurately diagnose GB TB before surgery. Consequently, it
is critical to differentiate this condition from other GB disorders.[3]
Case Report
A 61-year-old female presented with pain abdomen, feeling of bloating, and indigestion
with occasional episode of vomiting. The symptoms were noted vaguely since 6 months
and aggravated 2 weeks before they decided to consult at hospital.
Upon taking detailed history, the lady was a homemaker and belonged to low socioeconomic
status. Past medical history was unremarkable and no significant findings were observed.
The past surgical history revealed minor procedures like dental interventions and
gynecological procedures during child birth. No other surgical history was present
in the patient. No clinical symptoms of TB like cough, weight loss, or altered bowel
habits was noted in the patient.
On examination, some tenderness in the right hypochondrium was noted. No other significant
findings were noted. Body mass index was not evaluated for this patient.
Laboratory investigations revealed mild microcytic hypochromic anemia with hemoglobin
of 10.5 g/dL. Differential was within normal range. Liver function test showed reversal
of A:G ratio (albumin 3.5, globulin 4.35), indicating possibility of some chronic
inflammatory process. Erythrocyte sedimentation rate was 30 mm/hour.
X-ray chest, as seen in [Fig. 1A], was unremarkable with no significant findings.
Fig. 1 (A) Anteroposterior (AP) of chest X-ray, which is normal. (B) Ultrasound (USG) abdomen, showing gallstones.
The ultrasonography of the patient was performed, which showed multiple calculi in
the GB with increased wall thickness (about 1 cm) and normal common bile duct. There
was evidence of cholecystitis and cholelithiasis. An image of the ultrasound can be
seen in [Fig. 1B].
Computed tomography (CT) was not done in this case, due to no suspicion of malignancy
and poor socioeconomic status of the patient.
Intraoperatively, very dense intraperitoneal adhesions were present between the abdominal
wall and omentum, and pericholecystic adhesions between the GB, omentum, stomach,
and duodenum. No peritoneal tubercles were present over the GB or other intra-abdominal
organs. Ascites was not present. Laparoscopic cholecystectomy with adhesionolysis
was performed and the GB specimen was sent to the laboratory for histopathological
examination. The operative time was around 2 hours with most of the time being taken
in adhesionolysis. The blood loss during surgery was at normal expected levels as
per such cases. Postoperative hospital stay was approximately 3 days and no postoperative
complications were noted. Patient was discharged in satisfactory state.
[Fig. 2A] shows gross appearance of the specimen received. Grossly, the GB measured 5 × 3 × 2 cm.
Mucosa was mostly ulcerated with few small whitish lesions in the wall of the GB.
Wall thickness ranged between 0.6 and 0.8 cm. Multiple stones were present in the
lumen. [Fig. 2B] and [C] shows the microphographs of the sections. Microscopy showed denuded lining epithelium.
There was abundant fibrosis and multiple coalescing epithelioid cell granulomas having
central caseous necrosis. These granulomata exhibited lymphoid cuffing. Langhans-type
giant cells were present. Ziehl–Neelsen stain was performed for acid-fast bacilli
(AFB), which showed magenta pink beaded bacilli. [Fig. 3] shows microphotograph of the AFB stain done in this case.
Fig. 2 (A) Gross image of gallbladder specimen, showing mildly thickened wall and mostly ulcerated
mucosa. (B,C) Microphotographs of F/E stained slides of gallbladder. The mucosa is completely
ulcerated and wall shows many well-formed epithelioid granulomas composed of epithelioid
cells with many giant cells, both Langhans and foreign body type. Peripheral cuffing
of lymphoid cells and fibrosis is also seen.
Fig. 3 Ziehl–Neelsen (ZN) stain on histopathology sections showing acid-fast bacilli.
After histopathological diagnosis, patient was called back and explained the diagnosis
and put on antituberculosis therapy (ATT). The patient was put on ATT for 6 months.
After 6 months' course, the patient is asymptomatic till date.
Discussion
D-Mycobacterium tuberculosis is the causative agent of TB. It is a difficult-to-treat
pathogen with high worldwide prevalence. It is believed that it latently infects approximately
one-quarter of the world's population.[6] Since Robert Koch's discovery of the disease in 1882, the TB epidemic appears to
be spreading throughout the world and presently TB is one of the leading causes of
death globally and a highly contagious airborne disease. Extrapulmonary (EP) TB is
a type of TB that can spread to other parts of the body, even though the disease usually
affects the lungs.[6] The majority of these cases of TB occur in middle- and low-income countries.[7] In immunocompetent hosts, EPTB causes approximately 15% of TB cases.[7]
About 1% of cases of abdominal TB are caused by hepatobiliary TB.[1] GB TB is very rare worldwide, with only few cases reported in the literature.[5] The GB's thick walls and naturally alkaline bile make it resistant to TB infection.[6] Bile's inherent essential nature prevents Mycobacterium tuberculosis from growing.[6] However, GB TB is predisposed by GB mucosal injury and low bile acid concentration
that can be caused by cystic duct obstruction.[1] The bacillus may reach GB by serosal spread from a peritoneal lesion, by canalicular
dissemination or by hematogenous or lymphatic route from nearby positive focus.[1] In our case, tubercular infection was most likely spread from focus in chest. Additionally,
approximately two-thirds of patients with GB TB have been documented to have cholelithiasis,
which serves as a nidus for the development of TB.[1] In our case also, gallstones were present. GT primarily affects women over 30 years
of age.[3] Our case was also above 30 years age (61 years old).
The pathognomonic presentation of GB TB is not well-defined. Clinical symptoms can
range from GB perforation to an unexpected histological examination.[5] Patients with GT infection may present with a combination of symptoms, such as weight
loss, vomiting, jaundice, and abdominal pain, which can be mistakenly diagnosed as
cholecystitis, biliary obstruction, or even carcinomas.[8] Right hypochondriac pain and abdominal mass may also be found.[8] Our case presented with nonspecific symptoms like pain abdomen and vomiting, which
could also be attributed to gallstones. There were no symptoms of abdominal TB or
systemic involvement of any other organ by TB was seen, indicating the unusual clinical
presentation.
There are four different ways that GB TB can present clinically: (1) as a component
of miliary TB, (2) as a component of disseminated abdominal TB, (3) as an isolated
form of TB that is frequently discovered by chance during microscopic examination
of a resected GB, and (4) as a component of an immunocompromised state like uremia,
cancer, or acquired immunodeficiency syndrome.[4] We believe our case was due to dissemination of abdominal TB, which was retrospectively
concluded by the surgeon due to unexpected extensive peritoneal adhesions and after
histopathological report, despite the patient not having any other clinical symptoms
of abdominal TB.
The ultrasound examination usually shows nonspecific or wall thickness with stones
inside.[6] In our case, the GB wall was thickened with presence of gallstones. Three different
kinds of CT findings can help in GB TB diagnosis, according to Xu et al.[12] First type is micronodular type in which there is polypoid or micronodular lesion
that exhibits a uniformly enhanced GB wall on a contrast-enhanced CT scan. Second,
thickened wall GB TB is the most prevalent variety and is often misinterpreted as
GB cancer or cholecystitis. However, in GB TB, the wall is diffuse, homogeneous, and
thicker with edema or “halo.” Third kind is the mass-forming type, which shows flecked
calcification of GB wall.[4] Our case did not get CT scan performed due to lack of suspicion of any other condition
and due to economic reasons.
Due to the lack of specific symptoms and diagnostic testing, the clinical presentation
of GB TB is ambiguous and the diagnosis is frequently delayed. A histological study
is required to provide a definitive diagnosis.[9] Langhans giant cells and caseous granulomas are characteristic histological findings
of GB TB.[6] The AFB can be detected in about 60% of cases.[6] In our case too, presence of granulomas and AFB were detected. Histopathologically,
the existence of AFB and caseous granulomas are the gold standard for TB diagnosis.[6] In our case too, the diagnosis was made after histopathological examination and
successful treatment was administered due to correct pathological diagnosis. The patient
responded well to the treatment and is presently symptom free.
GB TB remains a diagnostic challenge as clinical presentation mimics other GB diseases
such as cholecystitis and imaging features may mimic GB carcinoma. GB TB, a rare entity,
is difficult to differentiate from other GB diseases such as GB xanthogranulomatous
cholecystitis.[10]
As far as management is concerned, treatment protocols for pulmonary and extrapulmonary
diseases are identical.[11] Drug-sensitive Mycobacterium tuberculosis strains are treated using a 6-month protocol
that consists of four different medications. This must be strictly followed to prevent
resistance and recurrence.[7]
Conclusion
GB TB is a rare manifestation of abdominal TB. As there is lack of precise diagnostic
tests, preoperative diagnosis is usually not achievable. Our case report also highlights
vague and overlapping clinical and radiological features, hence histopathological
diagnosis becomes paramount for this infection in endemic areas. Thus, an increased
awareness and a high index of suspicion are necessary in endemic areas, especially
if there are any unusual surgical findings like peritoneal adhesions.
