Also, treatment of sexual partners is advocated whether they develop symptoms or not as long as there was unprotected sexual intercourse with the patient within 10 days of developing the symptoms. Treatment
For the initial stages of the lesion, cleaning with soapy solution is recommended and sitz bath may be beneficial. Fluctuant nodules may require aspiration. Treatment may include more than one prescribed medication. Antibiotics
Macrolides are often used to treat chancroid. The CDC recommendation is either a single oral dose (1 gram) of azithromycin, a single IM dose (250 mg) of ceftriaxone, oral (500 mg) of erythromycin three times a day for seven days, or oral (500 mg) of ciprofloxacin twice a day for three days. Due to a paucity of reliable empirical evidence it is not clear whether macrolides are actually more effective and/or better tolerated than other antibiotics when treating chancroid. Data is limited, but there have been reports of ciprofloxacin and erythromycin resistance.Aminoglycosides such as gentamicin, streptomycin, and kanamycin has been used to successfully treat chancroid; however aminoglycoside-resistant strain of H. ducreyi have been observed in both laboratory and clinical settings. [7] Treatment with aminoglycosides should be considered as only a supplement to a primary treatment.Pregnant and lactating women, or those below 18 years of age regardless of gender, should not use ciprofloxacin as treatment for chancroid. Treatment failure is possible with HIV co-infection and extended therapy is sometimes required. Prognosis
Prognosis is excellent with proper treatment. Treating sexual contacts of affected individual helps break cycle of infection.
Mechanism of action
Pyrazinamide is a prodrug that stops the growth of M. tuberculosis. Pyrazinamide diffuses into the granuloma of M. tuberculosis, where the tuberculosis enzyme pyrazinamidase converts pyrazinamide to the active form pyrazinoic acid. Under acidic conditions of pH 5 to 6, the pyrazinoic acid that slowly leaks out converts to the protonated conjugate acid, which is thought to diffuse easily back into the bacilli and accumulate. The net effect is that more pyrazinoic acid accumulates inside the bacillus at acid pH than at neutral pH.Pyrazinoic acid was thought to inhibit the enzyme fatty acid synthase (FAS) I, which is required by the bacterium to synthesize fatty acids although this has been discounted. The accumulation of pyrazinoic acid  was also suggested to disrupt membrane potential and interfere with energy production, necessary for survival of M. tuberculosis at an acidic site of infection. However, since an acidic environment is not essential for pyrazinamide susceptibility and pyrazinamide treatment does not lead to intrabacterial acidification nor rapid disruption of membrane potential, this model has also been discounted. Pyrazinoic acid was proposed to bind to the ribosomal protein S1 (RpsA) and inhibit trans-translation, but more detailed experiments have shown that it does not have this activity.The current hypothesis is that pyrazinoic acid blocks synthesis of coenzyme A. Pyrazinoic acid binds weakly to aspartate decarboxylase (PanD), triggering its degradation. This is an unusual mechanism of action in that pyrazinamide does not directly block the action of its target, but indirectly triggers its destruction.