Diagnostic and Therapeutic Strategies for Peritoneal Tuberculosis: A Review

Abstract

Peritoneal tuberculosis (PTB), although rarer than its pulmonary counterpart, is a serious health concern in regions of the world with high tuberculosis prevalence. Individuals with baseline immunocompromise condition, whether acquired or medically induced, are at greatest risk for experiencing PTB. While medical treatment of the condition is similar to that of the pulmonary disease, the generally immunocompromised state of those infected with PTB, along with a lack of highly sensitive and specific testing methods make early diagnosis difficult. This review discusses the risks factors, clinical features, diagnostic methods, and treatment options for PTB.

Keywords: Human immunodeficiency virus; Liver disease; Peritoneal tuberculosis; Tuberculosis.

Fig. 1.. Mechanisms of PTB development.

There are three main pathways through which TB infects the peritoneum. In most cases, the bacterial spread is achieved by reactivation of TB in the lungs (or other solid organs) and subsequent hematogenous or lymphatic spread to the peritoneum (depicted in 1). Though rare, peritoneal infection by the intestinal tract is possible due to the ingestion of infected milk or sputum. In this pathway, the TB infects the mucosal layer of the gastrointestinal tract, with subsequent formation of epithelioid tubercles in the lymphoid tissue of the submucosa. Caseous necrosis of the tubercles in roughly 2–4 weeks leads to mucosal ulceration and can lead to infection of deeper layers of the intestines and eventually into adjacent lymph nodes and peritoneum (depicted in 2). The third pathway of peritoneal infection involves the direct spread to the peritoneum from an infected adjacent focus, such as the fallopian tubes (pictured) or a psoas abscess (depicted in 3). The icons were adapted from flaticon.com. Abbreviations: PTB, peritoneal tuberculosis; TB, tuberculosis.

Fig. 2.. Formation of the TB granuloma in primary lung infection and subsequent spread.

Following the inhalation of contaminated aerosols, Mycobacterium tuberculosis is recognized by macrophages in the lung alveoli by surface receptors (depicted in 1). Subsequently, the bacteria are taken up by macrophages which, along with epithelial cells and neutrophils, trigger innate immune signaling pathways that allow for the production of chemokines and cytokines (depicted in 2). The release of chemokines and cytokines recruits more macrophages, lymphocytes, and dendritic cells to the infection site, where they form granulomas composed of infected macrophages in the middle, surrounded by lymphocytes (CD4+, CD8+, gamma/delta T cells). The conglomerated macrophages can also fuse to form multinucleated giant cells or differentiate into lipid rich foamy cells (depicted in 3 and 4). Within the granuloma, bacteria can survive for years, in a latent disease state. However, once triggered by external factors, such as additional immunocompromising states, the bacteria can reactivate, killing the core infected macrophages and, thereby, producing a necrotic zone at the center of the granuloma known as a caseum (depicted in 4). The granulomatous structure weakens with the caseum and eventually breaks down, releasing bacteria through the body by blood, lymph, and infectious aerosolized droplets. Abbreviation: TB, tuberculosis.

Fig. 3.. Proposed algorithm for diagnostic strategies in PTB, adapted and modified from Sinai, 2005.

Abbreviation: PTB, peritoneal tuberculosis.