This species causes the sexually transmitted diseasechancroid, a major cause of genital ulceration in developing countries, often characterized by painful sores on the genitalia.[2] The first study linking this disease with the agent Hemophilus ducreyi was published in 1889 by Auguste Ducrey. Each year in the United States, there are over 2,000 cases of chancroid.[1] Chancroid starts as an erythematous papular lesion that breaks down into a painful bleeding ulcer with a necrotic base and ragged edge. It has also been found to cause chronic skin ulceration away from the genitalia, infect children and adults, and behave in a manner that mimics yaws.[3]
Haemophilus ducreyi is a Gram-negative coccobacillus, and has a shape between a spherical coccus[6] and a rod-shaped bacterium.[1] This species of bacterium has pili, fine and tangled appendages composed predominantly of protein, that allow bacteria to attach to surfaces, including those of cells.[7]H. ducreyi expresses many of the same virtulence genes with species Actinobacillus sensu stricto. Some of these genes include the genes pilA and pilC, which are responsible for pilus assembly, adherence to neighboring surfaces, and are often found in type IV pilil[8]. Presence of gene pilA codes for the structural protein found in type IV (T4) pili, and are responsible for pili adhesion and motility[8] and indicates that the pili present on H. ducreyi functionally help it adhere to surfaces and aid in the cell’s motility. The presence of gene pilC helps maintain pili longevity and structure[8]. Further shared genes include those involved with lipopolysaccharide (LOS) biosynthesis and modifications expressed in gram-negative bacteria. These LOS biosynthesis components indicate that H. ducreyi has an LOS system on its outer membrane, rather than a full lipopolysaccharide (LPS) structure. Instead, it contains lipid A and the core oligosaccharide, but is missing the outer chain[9]. The LOS structure can help mimic host structures, ultimately making it harder for the host cell to detect and fight against, contributing to immune evasion. Considered to not be a true Haemophilus species as they are a part of Pasteurellaceae, which has a distinctive lineage that will separate haemophili and clusters with the Aggregatibactor pleuropneumoniae and the Mannheimia haemolytica.[10]
Colonies
Colonies of Haemophilus ducreyi are described as yellow-grey, small, and semiopaque as well as nonmucoid. Scanning electron microscopy has been used to observe that the microbe can form a colony of many cells; the cells adhere to each other because of an intercellular matrix. The long chains bond can make it difficult to isolate a single cell of Haemophilus ducreyi, hindering the genetic studies that have been done on the microbe.[1][11]
Metabolism
Haemophilus ducreyi has been shown to have high phosphatase activity (acid phosphatase, alkaline phosphatase, and phosphoamidase).[1] The bacteria only grow at a specific temperature range of 33°-35°, any conditions above this range are suboptimal for bacterial growth.[12]
Culture
Haemophilus ducreyi is grown under micro-aerophilic conditions achieved in a sealed anaerobic jar without a catalyst, using two envelopes that generate CO2 and H2, commonly referred to as Campylobacter growth conditions.[1]
Pathogenesis
Haemophilus ducreyi is a human pathogen; and there are no known animal or environmental reservoirs.[13]H. ducreyi is an opportunistic microorganism that infects its host gaining access to the tissue that breaks in the skin or epidermis. Unlike intact skin, the damaged tissue will act as a site that bacterium can start the infection process.[10] Attachment to host cells are crucial for the early stage of establishing infection. The FLp-Tad system will be encoded by the operon known as flp-tad that is essential for the bacterial attachment to host, which will allow for H. ducreyi to finish the site of infection to form the pustular lesions.[14] Inflammation then takes place as the area of infection is inundated with lymphocytes, macrophages, and granulocytes. This pyogenic inflammation causes regional lymphadenitis in the sexually transmitted disease chancroid.[15]
Immune Evasion
H. ducreyi produces virulence factors like LspA1 & LspA2 that will assist in the bacterium to evade phagocytosis by host's immune cells. The LspA1 & LspA2 will act as an inhibitor agains the Src Family Protein Kinases that are used in the signaling pathways that will allow for phagocytosis. Resulting in neutrophils and macrophages that were recruited to the site of the infection to not be able to engulf H. ducreyi, which will cause for it to remain extracellular that will persist within the infected tissue.[16]
Toxins
Haemophilus ducreyi is able to defend itself against the immune response's T cells through two toxins: a hemolysin and the cytolethal distending toxin (CDT). CDT is characterized by its ability to arrest epithelial cells in the G2 phase of the cell cycle and combats T cells by inducing apoptosis.[17] Together, these toxins showcase the adeptness of H. ducreyi in manipulating host cell processes.
Diagnosis
Although antigen detection, serology, and genetic amplification methods are sometimes used to diagnose infections with H. ducreyi and the genetic tests have greater sensitivity, they are not widely available, so cultures are currently considered the "gold standard" test, which has about 80% sensitivity under optimal combination of media.[citation needed]
Treatment
Single-dose antibiotic treatments using macrolides, third-generation cephalosporins, or fluoroquinolone continue to be effective in treating chancroid.[citation needed] The first line treatments recommended by the U.S. Centers for Disease Control and Prevention are one of four options: azithromycin one gram orally in a single dose, ceftriaxone 250mg intramuscularly in a single dose, ciprofloxacin 500mg orally two times a day for three days, or erythromycin base 500mg orally three times a day for seven days.[18][19] Some antibodies were specific to all strains, while others targeted only certain groups of strains of H. ducreyi, indicating that the outer membrane proteins of H. ducreyi can vary in their immune recognition.[1] Infected individuals are still susceptible to reinfection due to the absence of developed protective immunity.[citation needed]
A rise in antimicrobial resistance among H. ducreyi strains result in a shift away from benzylpenicillin as the preferred treatment.[13]
↑Lewis, DA; Mitjà, O (February 2016). "Haemophilus ducreyi: from sexually transmitted infection to skin ulcer pathogen". Current Opinion in Infectious Diseases. 29 (1): 52–7. doi:10.1097/QCO.0000000000000226. PMID26658654.
↑Division of STD Prevention, National Center for HIV, Viral Hepatitis, STD, and TB Prevention, Centers for Disease Control and Prevention (22 July 2021). "Chancroid". Sexually Transmitted Infections Treatment Guidelines, 2021. U.S. Centers for Disease Control and Prevention. Retrieved 30 October 2024.
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