Final answer:
The difference between tuberculoid and lepromatous leprosy involves T-cell differentiation and effector function, where tuberculoid leprosy reflects a strong Th1 response controlling bacterial growth, and lepromatous leprosy indicates a less effective Th2 dominated immune response leading to widespread skin lesions and nerve damage.
Step-by-step explanation:
The etiological agent responsible for leprosy is Mycobacterium leprae, a bacterium that survives and replicates within the vesicular system of macrophages. The difference between tuberculoid leprosy and lepromatous leprosy is seen in the context of T-cell differentiation and effector function. Tuberculoid leprosy is characterized by a strong Th1 immune response, leading to effective containment of the bacteria with localized granulomas and few skin lesions. In contrast, lepromatous leprosy results from a Th2 dominant response, leading to an ineffective immune reaction that allows the bacteria to multiply, causing widespread skin lesions with large numbers of bacteria present.
Hansen's disease affects the peripheral nervous system (PNS), leading to damage and potential loss of extremities due to the bacteria favoring cooler temperatures in peripheral tissues. T-cell differentiation is crucial in preventing the progression from tuberculoid to lepromatous leprosy; a strong Th1 response is protective, while a Th2 response can be detrimental. Infected macrophages benefit from cytokine signals from Th1 cells, which activate metabolic pathways including the production of nitric oxide, helping kill the bacteria within macrophages.