Virulence Factors

In human experimental models, bacteria are delivered into the skin via puncture wounds using an allergy-testing device.[3] An estimated delivered dose (EDD) of 1 colony-forming unit already results in 50% papule formation.[4]

Most bacteria localize in the dermis after 48 hr of infection. Several potential H. ducreyi virulence factors have been reported in the literature and their possible effects were studied using isogenic mutants by grafting both wild-type strains (i.e., 35000 HP) and mutant strains on each arm of volunteers.[3,4] Factors studied so far include lipooligosaccharide (LOS), pili, soluble cytolethal distending protein (sCDT), copper-zinc superoxide dis-mutase (SOD), a hemoglobin-binding outer membrane protein (OMP), a hemolysin capable of cytotoxicity, a filamentous hemagglutinin-like protein, and a zinc-binding periplasmic protein.[6]

The LOS of most H. ducreyi strains express an epitope that is also present in Neisseria strains and that is immunochemically similar to a precursor of a major blood group antigen found on human erythrocytes.[6] Pili are filamentous appendages involved in cell adhesion. The major 24-kDa pilin FtpA subunit shares no homology with other pilins present on the surface of gram-negative bacteria.[6] A gene cluster (cdt ABC) codes for the CDT proteins that were shown to block cell division in the G2 phase of the cell cycle. Superoxide dismutase are metal-loenzymes that catalyze the conversion of superoxide radicals to oxygen and hydrogen peroxide. Periplasmic Cu-Zn SODs are thought to protect against oxidative cell damage by host immune cells.[6] The hemoglobin binding OMP (108-kDa HgbA/HupA) is essential for H. ducreyi to utilize both hemoglobin and haptoglobin as a source of heme required for growth. Hemolysins encoded by the hhdA and hhdB genes are possibly responsible for release of hemoglobin from erythrocytes. Two large genes, IspA1 and IspA2, encode proteins that resemble in part the filamentous haemagglutinin (FhaB) virulence factor of Bordetella pertussis. The exact function of the Lsp-A1 and -A2 proteins remains to be determined.1-6-1 Zinc is an important trace element for maintaining structural stability and for catalytic activity of enzymes. The znuA gene of H. ducreyi encodes a periplasmic protein involved in zinc transport. The isogenic znuA mutant exhibited reduced lesions in the rabbit model.

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Fig. 1 Chancroid lesions on male thigh and penis shaft. (Courtesy of Han Fennema, M.D., Ph.D.) (View this art in color at www.dekker.com.)

frenulum (Fig. 1), whereas in women the ulcers are usually external and involve the vulva, the labia, and perianal region.[6,7] Extragenital chancroid is rare but may occur by autoinoculation of the inner thighs, breasts, and fingers.[6] A past infection does not confer protective immunity because multiple episodes of H. ducreyi infections can occur.

Clinical diagnosis of chancroid is unreliable because of similarities of the clinical presentation of different etio-logic agents of GUD, the presence of mixed infections, and atypical ulceration due to long-standing disease.[8] Next to H. ducreyi, causative pathogens of GUD are herpes simplex virus type 2 (HSV-2) and type 1 (HSV-1) and the bacteria T. pallidum (TP), which cause syphilis, and Chlamydia trachomatis, which cause lymphogranuloma venereum. In about 20-40% of GUD cases none of these pathogens are found despite use of the most sensitive assays.[9,10] Coinfection of H. ducreyi and HSV occurs commonly in the tropics.[6]

Getting Started With Dumbbells

Getting Started With Dumbbells

The use of dumbbells gives you a much more comprehensive strengthening effect because the workout engages your stabilizer muscles, in addition to the muscle you may be pin-pointing. Without all of the belts and artificial stabilizers of a machine, you also engage your core muscles, which are your body's natural stabilizers.

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