Fig 1.
Multiple feeding episodes provide arboviruses opportunities to navigate anatomical barriers within mosquitoes.
(Center) Cross section of Ae. aegypti mosquito infected with Zika virus under single-feed (top) and double-feed (bottom) scenarios. A dense network of proteoglycans, termed the “basal lamina,” provides support and protection to internal tissues such as the mosquito midgut (right inserts) and ovaries (left inserts). Due to pore size limitations, arboviruses cannot easily traverse these structures. However, additional blood feeding results in distention of the midgut tissue inducing micro-perforations in the underlying basal lamina facilitating virus passage to the hemolymph and access to secondary tissues such as the salivary glands. Similarly, blood meal acquisition induces oogenesis and expansion of the ovarian tissue. It is hypothesized that such disruptions in the ovarian basal lamina could provide viruses access to the developing eggs and infection of the progeny via vertical transmission.
Fig 2.
Additional blood meals increase the transmission potential of malaria-infected mosquitoes.
(A) Cross section of an An. gambiae mosquito with the developmental stages of the human malaria parasite P. falciparum under single-feed (top) and double-feed (bottom) scenarios. Compared to a single blood meal (B), P. falciparum–infected mosquitoes provided with an additional blood meal increase oocyst growth rates and sporogony, resulting in faster rates of sporozoite salivary gland invasion and reducing the time required for malaria parasite transmission (C).
Fig 3.
Multiple feeding by infected sandflies promotes Leishmania parasite differentiation, increasing the efficiency of transmission.
(A) Depiction of Leishmania parasite development in a sandfly following a single blood meal under laboratory conditions. Immotile amastigotes (1) emerge from ingested macrophages and transform into the replicative procyclic promastigote form (2). Subsequently, replication slows, and the procyclic promastigotes transform into highly motile nectomonad promastigotes (3) and exit the peritrophic-encased blood bolus. Within the anterior portion of the midgut lumen, the parasites further develop into the replicative leptomonad promastigote form (4) and the (5) haptomonad promastigotes which attach the stomodeal valve. The leptomonads transform into infectious metacyclic promastigotes and migrate to the stomodeal valve where they can be regurgitated and transmitted during subsequent feeding events. (B) When sandflies with a mature infection take an additional blood meal, metacyclics undergo dedifferentiation into retroleptomonads (6), while earlier stages of parasite development (steps 1–5) have already matured. The production of retroleptomonads in response to an additional blood meal enables further parasite replication before differentiation back into metacyclic promastigotes, thus amplifying the number of infectious metacyclic (7) parasites that increase the potential for transmission.