Research Article: Aquatic Insects and Mycobacterium ulcerans: An Association Relevant to Buruli Ulcer Control?

Date Published: February 27, 2007

Publisher: Public Library of Science

Author(s): Manuel T Silva, Françoise Portaels, Jorge Pedrosa

Abstract: Texeira and colleagues discuss the association between arthropods and M. ulcerans in the light of a new study in PLoS Medicine.

Partial Text: Mycobacterium ulcerans infection, which can cause Buruli ulcer, is the third most common human mycobacteriosis worldwide, after tuberculosis and leprosy. Buruli ulcer occurs predominantly in humid tropical areas of Asia, Latin America, and, mainly, Africa, where the incidence has been increasing, surpassing tuberculosis and leprosy in some regions [1].

There is evidence that M. ulcerans is not transmitted person-to-person but is an environmental pathogen transmitted to humans from its aquatic niches [6,7]. However, it is not clear how this transmission occurs [6,7].

Examples of arthropod-borne diseases are leishmaniasis and Lyme disease, transmitted by sand flies and by ticks, respectively. These haematophagous vectors bite the host’s skin to take a blood meal. The bite introduces the pathogen along with saliva that profoundly alters the skin by molecules with antihemostatic activity (which enable the vector to take an effective meal) and immunosuppressive activity (which enhances the infectivity of the injected pathogen by counteracting the host immune response) [11–14]. Pre-exposure of mice to these salivary antigens induces protective immunity against pathogen transmission by neutralizing the immunosuppressive activity [11,12,14]. Furthermore, salivary molecules can adsorb to the pathogen [13,15]), a binding that can cause the microorganism to become an innocent bystander of the host’s antisalivary immunity—again leading to protection against pathogen transmission [12].

Marsollier and colleagues’ new study in PLoS Medicine [16] extends the authors’ previous observations [10] and shows that repeated biting by M. ulcerans-free N. cimicoides renders mice more resistant to the infection obtained through biting by the insects carrying M. ulcerans. The researchers also found that subcutaneous immunization of mice with salivary extracts of M. ulcerans-free N. cimicoides protected against infection following injection of M. ulcerans, but only when the bacilli were first coated with salivary proteins. This suggests that the protection conferred to mice by previous N. cimicoides biting is associated with antibodies (detected in the blood of repeatedly bitten mice) reacting with proteins of N. cimicoides saliva that would bind to M. ulcerans during its stay in the insect’s salivary glands, and would coat the bacilli when they are transmitted by biting.

There are three major limitations to the new study. The first is that the study did not analyse whether the antibodies against insect salivary proteins in mice protected by prior biting by uninfected N. cimicoides are effectors of protection or only biomarkers of the protective status. Additional studies are, thus, necessary to clarify the roles of humoral and cell-mediated immunity in such protection.

If future work supports the notion that aquatic insects are important in the transmission of the causative organism in Buruli ulcer, as some data suggest [9,10,16], the results now published in PLoS Medicine could have important public health implications.



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