Human Immunodeficiency Virus and AIDS

Transmission and pathobiology

Vertical transmission: Mother‑to‑child transmission can occur in utero, intrapartum, and via breastfeeding; HIV replicates in gut‑associated lymphoid tissue and can be shed from the gastrointestinal tract.

Acquisition determinants: Risk of transmission is influenced by maternal viral load, integrity/maturity of the infant mucosal and immune barrier, obstetric factors, and feeding practices.

Clinical features relevant to the GI tract

• Diarrhea: Common in advanced HIV/AIDS; routine bacterial stool studies are often unrevealing and multiple infectious, inflammatory, and treatment‑related causes should be considered.
• Opportunistic infections: More likely with high viral load and low CD4 counts and can involve any segment of the GI tract.
• Medication effects: Many antiretroviral and adjunctive drugs cause GI adverse effects including nausea, vomiting, abdominal pain, hepatotoxicity, and pancreatitis which can complicate evaluation.

Key opportunistic GI pathogens and syndromes

• Viral: Herpes simplex virus causes painful esophagitis and can involve small and large bowel; cytomegalovirus commonly causes esophagitis and right‑sided colitis with large linear ulcers; enteric viruses such as norovirus can cause chronic diarrhea.
• Protozoal and microparasitic: Cryptosporidium species produce small‑bowel malabsorption and may involve biliary tree leading to cholangitis; Microsporidia cause villous atrophy and malabsorption in advanced disease; Giardia causes chronic diarrheal illness.
• Bacterial: Mycobacterial infections (nontuberculous mycobacteria and Mycobacterium tuberculosis) can cause luminal ulceration, lymphadenopathy with intussusception, and Crohn‑like mucosal inflammation; invasive bacterial enteritis may occur but routine pathogens are often not found in advanced disease.
• Fungal: Candida causes oropharyngeal disease and esophagitis and can rarely involve stomach or intestine.

Diagnostic approach

• Initial evaluation: Assess HIV status and immune function (CD4 count, viral load) when relevant; perform targeted stool studies, including ova/parasites, acid‑fast stains for Cryptosporidium and mycobacteria, and antigen/PCR testing as available.
• Endoscopy and biopsy: Indicated for persistent or severe symptoms; obtain biopsies for histology, immunostains, viral PCR, and microbial cultures to identify CMV, HSV, fungi, mycobacteria, and protozoa.
• Consider medication effects: Review antiretroviral and adjunctive medications as potential contributors to GI symptoms and perform liver and pancreatic enzyme testing when indicated.

Management principles

• Antiretroviral therapy (ART): Early and effective ART reduces opportunistic infections, improves mucosal immunity, and is central to management.
• Pathogen‑directed therapy: Treat identified infections with appropriate antimicrobial or antiparasitic agents; many opportunistic infections respond poorly until immune reconstitution occurs with ART.
• Supportive care: Nutritional support, fluid/electrolyte management, and treatment of malabsorption and pancreatic or hepatic complications.
• Prophylaxis: Use prophylactic regimens for Pneumocystis and other opportunistic infections guided by CD4 count and clinical guidelines.
• Medication side effects: Manage ART‑related GI adverse effects while balancing the need for viral suppression; switch regimens only when necessary with specialist input.

Special considerations in children

• Developing immunity and microbiome: Infant and child gut immunity and microbiome maturation influence presentation and long‑term consequences of perinatal HIV infection.
• Feeding and transmission: Counseling about infant feeding must balance transmission risk with local resources and maternal viral suppression status.
• ART adherence and adverse effects: GI symptoms are a common cause of ART nonadherence; early recognition and management improve outcomes.

Clinical pearls