Pathophysiology: Sexually Transmitted Diseases

Sexually transmitted diseases (STDs) are a significant public health concern worldwide, affecting millions of individuals each year. Among these, AIDS, syphilis, and gonorrhea are particularly notable due to their prevalence, impact on health, and the complexity of their pathophysiology. Understanding the mechanisms by which these diseases develop and progress is crucial for healthcare professionals, researchers, and educators in devising effective prevention, diagnosis, and treatment strategies. This article delves into the pathophysiology of three major STDs: AIDS, syphilis, and gonorrhea.

Table of Contents

Pathophysiology of AIDS

Introduction: Acquired Immunodeficiency Syndrome (AIDS) is the final stage of infection with the Human Immunodeficiency Virus (HIV). HIV primarily targets the immune system, leading to a progressive decline in immune function.

HIV Infection and Replication:

Entry: HIV enters the body through mucous membranes or direct blood contact. The virus targets CD4+ T-helper cells, macrophages, and dendritic cells.
Binding and Fusion: HIV binds to the CD4 receptor and co-receptors (CCR5 or CXCR4) on the surface of target cells. The viral envelope fuses with the cell membrane, allowing the viral RNA to enter the host cell.
Reverse Transcription: The viral RNA is reverse-transcribed into DNA by the enzyme reverse transcriptase.
Integration: The newly formed viral DNA is integrated into the host cell’s genome by the enzyme integrase.
Replication: The host cell machinery is used to produce viral proteins and RNA.
Assembly and Budding: New viral particles are assembled and bud from the host cell, acquiring a portion of the host cell membrane as their envelope.

Immune System Impact

Acute Phase: Rapid viral replication and a significant drop in CD4+ T cells. Symptoms may resemble flu or mononucleosis.
Chronic Phase: The immune system partially controls the virus, but HIV continues to replicate at low levels. CD4+ T cell count gradually declines.
AIDS: When CD4+ T cell count falls below 200 cells/µL, the immune system is severely compromised, leading to opportunistic infections and cancers.

Pathophysiology of Syphilis

Introduction: Syphilis is a sexually transmitted infection caused by the spirochete bacterium Treponema pallidum. It progresses through distinct stages, each with unique clinical manifestations.

Stages of Syphilis

Primary Syphilis

Entry: The bacterium enters the body through minor abrasions in the skin or mucous membranes.
Chancre Formation: A painless ulcer (chancre) forms at the site of entry, typically on the genitals, anus, or mouth. The chancre is highly infectious.
Lymphatic Spread: The bacteria spread to regional lymph nodes.

Secondary Syphilis

Systemic Spread: The bacteria disseminate throughout the body, causing systemic symptoms.
Rash and Lesions: A widespread rash, often involving the palms and soles, and mucous membrane lesions (mucous patches) develop.
Other Symptoms: Fever, malaise, lymphadenopathy, and condylomata lata (wart-like lesions) may occur.

Latent Syphilis

Early Latent: Occurs within the first year after infection, with potential relapses of secondary symptoms.
Late Latent: Asymptomatic phase that can last for years. The bacteria remain dormant in the body.

Tertiary Syphilis

Gummatous Syphilis: Formation of gummas (granulomatous lesions) in various organs.
Cardiovascular Syphilis: Affects the aorta, leading to aneurysms and aortic valve insufficiency.
Neurosyphilis: Involves the central nervous system, causing symptoms like tabes dorsalis (degeneration of the spinal cord) and general paresis (neuropsychiatric symptoms).

Pathophysiology of Gonorrhea

Introduction: Gonorrhea is a common sexually transmitted infection caused by the bacterium Neisseria gonorrhoeae. It primarily affects the mucous membranes of the reproductive tract but can also infect other sites.

Infection and Spread

Adherence and Invasion

Attachment: The bacteria adhere to epithelial cells using pili and outer membrane proteins.
Invasion: The bacteria invade and multiply within epithelial cells, causing cell damage and inflammation.

Immune Response

Inflammation: The infection triggers an inflammatory response, leading to the recruitment of neutrophils and the formation of purulent exudate.
Immune Evasion: N. gonorrhoeae can evade the immune system through antigenic variation and resistance to complement-mediated killing.
Clinical Manifestations
Men: Urethritis with symptoms of dysuria and purulent discharge. Complications include epididymitis and prostatitis.
Women: Cervicitis with symptoms of vaginal discharge, intermenstrual bleeding, and dysuria. Complications include pelvic inflammatory disease (PID), which can lead to infertility and ectopic pregnancy.
Other Sites: Pharyngeal, rectal, and conjunctival infections can occur, especially in individuals engaging in oral or anal sex.

Disseminated Gonococcal Infection (DGI)

Spread: The bacteria can enter the bloodstream, leading to disseminated infection.
Symptoms: DGI can cause arthritis-dermatitis syndrome, characterized by joint pain, skin lesions, and fever.

Conclusion

Understanding the pathophysiology of these sexually transmitted diseases is crucial for developing effective prevention, diagnosis, and treatment strategies. Each disease has unique mechanisms of infection and progression, highlighting the importance of targeted medical interventions.