Chancroid pathophysiology

Jump to navigation Jump to search

Chancroid Microchapters

Home

Patient Information

Overview

Historical Perspective

Pathophysiology

Causes

Classification

Differentiating Chancroid from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Chancroid pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Chancroid pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA onChancroid pathophysiology

CDC onChancroid pathophysiology

Chancroid pathophysiologyin the news

Blogs onChancroid pathophysiology

Directions to Hospitals Treating chancroid

calculators and risk factors for Chancroid pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Nate Michalak, B.A.; Serge Korjian M.D.

Overview

Pathophysiology

Transmission

  • Chancroid may develop after transmission of class I or class II of the bacterium Haemophilus ducreyi through sexual contact.[1]
  • A class I gentically distinct subclade strain of H. ducreyi may serve as the etiologic agent of non-sexually transmitted skin ulcers.[2][3]

Pathogenesis

  • H. ducreyi class I and class II enters skin through microabrasions incurred during sexual intercourse.
  • H. ducreyi is thought to bind with epithelial cells and then colonize in the subcutaneous tissue.[4]
  • H. ducreyi is then presumed to react predominantly with B cell and some T cell markers, which may lead to development of 1 or more erythematous papules. The papule(s) may progress into pustule(s) after further bacterial growth.[4][5]
  • Ulcers develop after pustules undergo necrosis.[5] The pathogenesis of ulceration is not fully understood but may involve release of toxic products by H. ducreyi or bacterial-induced inflamation.[4]
    • Potential H. ducreyi by-products include:
Phospholipase C
Protease
Elastase
Lecithinase
Lipase
Collagenase
  • It is presumed that iron plays an essential role in chancroid pathogenesis.[4]

References

  1. Chancroid. MedlinePlus (Decemner 2, 2015). https://www.nlm.nih.gov/medlineplus/ency/article/000635.htm Accessed January 6, 2015.
  2. Marks M, Chi KH, Vahi V, Pillay A, Sokana O, Pavluck A; et al. (2014). "Haemophilus ducreyi associated with skin ulcers among children, Solomon Islands". Emerg Infect Dis. 20 (10): 1705–7. doi:10.3201/eid2010.140573. PMC 4193279. PMID 25271477.
  3. Gaston JR, Roberts SA, Humphreys TL (2015). "Molecular phylogenetic analysis of non-sexually transmitted strains of Haemophilus ducreyi". PLoS One. 10 (3): e0118613. doi:10.1371/journal.pone.0118613. PMC 4361675. PMID 25774793.
  4. 4.0 4.1 4.2 4.3 Abeck D, Johnson AP (1992). "Pathophysiological concept of Haemophilus ducreyi infection (chancroid)". Int J STD AIDS. 3 (5): 319–23. PMID 1391058.
  5. 5.0 5.1 Chancroid. Wikipedia (July 16, 2015). https://en.wikipedia.org/wiki/Chancroid Accessed on January 6, 2016.


Template:WikiDoc Sources