Mycobacterium leprae Infection in Ticks and Tick-Derived Cells.

Leprosy is a zoonosis in the southern United States involving humans and wild armadillos. The majority of patients presenting with zoonotic strains of Mycobacterium leprae note extensive outdoor activity but only rarely report any history of direct contact with wild armadillos. Whether M. leprae is transmitted to new vertebrate hosts through the environment independently or with the aid of other organisms, e.g., arthropod vectors, is a fundamental question in leprosy transmission. The objectives of this study were to assess the potential for ticks to transmit M. leprae and to test if viable M. leprae can be maintained in tick-derived cells. To evaluate tick transmission, nymphal Amblyomma maculatum ticks were injected with isolated M. leprae. Infection and transmission were assessed by qPCR. Ticks infected as nymphs harbored M. leprae through vertical transmission events (nymph to adult and adult to progeny); and, horizontal transmission of M. leprae to a vertebrate host was observed. Mycobacterium leprae DNA was detected in multiple tick life cycle stages. Likewise, freshly isolated M. leprae (Thai-53) was used to infect a tick-derived cell line, and enumeration and bacterial viability were assessed at individual time points for up to 49 days. Evaluations of the viability of long-term cultured M. leprae (Thai-53 and Br4923) were also assessed in a mouse model. Tick-derived cells were able to maintain viable M. leprae over the 49-day course of infection and M. leprae remained infectious within tick cells for at least 300 days. The results of this study suggest that ticks themselves might serve as a vector for the transmission of M. leprae and that tick cells are suitable for maintenance of viable M. leprae for an extended period of time.

IL-10 treatment of macrophages bolsters intracellular survival of Mycobacterium leprae.

In these studies, metabolically active Mycobacterium leprae were maintained for as long as 8 weeks in monolayer cultures of mouse peritoneal macrophages (MPhi). Supplemental IL-10, but not TGF-beta, bolstered, directly or indirectly, M. leprae metabolism in mouse MPhi. In the cell culture system temperature setting is extremely important and 31 to 33 degrees C incubation temperature was more permissive than 37 degrees C. Acid fast staining and transmission electron microscopy (TEM) of intracellular M. leprae revealed visible elongation of bacilli cultured under the above ideal conditions.

A new model for studying the effects of Mycobacterium leprae on Schwann cell and neuron interactions.

Millions of patients with leprosy suffer from nerve damage resulting in disabilities as a consequence of Mycobacterium leprae infection. However, mechanisms of nerve damage have not been elucidated because of the lack of a model that maintains M. leprae viability and mimics disease conditions. A model was developed using viable M. leprae, rat Schwann cells, and Schwann cell-neuron cocultures incubated at 33 degrees C. M. leprae retained 56% viability in Schwann cells for 3 weeks after infection at 33 degrees C, compared with 3.6% viability at 37 degrees C. Infected Schwann cells had altered morphology and expression of genes encoding cellular adhesion molecules at 33 degrees C but were capable of interacting with and myelinating neurons. Cocultures, infected after myelination occurred, showed no morphological changes in myelin architecture after 1 month of incubation at 33 degrees C, and M. leprae retained 53% viability. This article describes a new model for studying the effects of M. leprae on Schwann cells.

A new model for studying the effects of Mycobacterium leprae on Schwann cell and neuron interactions

Millions of patients with leprosy suffer from nerve damage resulting in disabilities as a consequence of Mycobacterium leprae infection. However, mechanisms of nerve damage have not been elucidated because of the lack of a model that maintains M. leprae viability and mimics disease conditions. A model was developed using viable M. leprae, rat Schwann cells, and Schwann cell-neuron cocultures incubated at 33 degrees C. M. leprae retained 56% viability in Schwann cells for 3 weeks after infection at 33 degrees C, compared with 3.6% viability at 37 degrees C. Infected Schwann cells had altered morphology and expression of genes encoding cellular adhesion molecules at 33 degrees C but were capable of interacting with and myelinating neurons. Cocultures, infected after myelination occurred, showed no morphological changes in myelin architecture after 1 month of incubation at 33 degrees C, and M. leprae retained 53% viability. This article describes a new model for studying the effects of M. leprae on Schwann cells.

A new model for studyng the effects of Mycobacterium leprae on Schwann cell and neuron interactions

Millions of patients with leprosy suffer from nerve damage resulting in disabilities as a consequence of Mycobacterium leprae infection. However, mechanisms of nerve damage have not been elucidated because of the lack of a model that maintains M. leprae viability and mimics disease conditions. A model was developed using viable M. leprae, rat Schwann cells, and Schwann cell-neuron cocultures incubated at 33 degrees C. M. leprae retained 56 per cente viability in Schwann cells for 3 weeks after infection at 33 degrees C, compared with 3.6 per cente viability at 37 degrees C. Infected Schwann cells had altered morphology and expression of genes encoding cellular adhesion molecules at 33 degrees C but were capable of interacting with and myelinating neurons. Cocultures, infected after myelination occurred, showed no morphological changes in myelin architecture after 1 month of incubation at 33 degrees C, and M. leprae retained 53 per cente viability. This article describes a new model for studying the effects of M. leprae on Schwann cells.

Intracellular parasitism of parenchymal cells by Mycobacterium leprae

The liver, skeletal muscle, and adrenal gland obtained from two nine-banded armadillos infected with Mycobacterium leprae were studied using an electron microscope. M. leprae were found in varying numbers inside hepatocytes, Kupffer's cells, striated muscle cells, adrenal cortical and adrenal medullary cells, endothelial cells, and macrophages. There was evidence to suggest that M. leprae were actively phagocytosed by the liver and skeletal muscle cells. The inert nature of M. leprae and its behavior as an almost ideal parasite of parenchymal cells are emphasized. The question of whether this unique parasitism of parenchymal cells and the possible processing and presentation of M. leprae antigens by these cells could be responsible for aberrant immune responses is raised