Vectors

Parasites which reside within the blood or internal organs of the host have
logistical problems in terms of infecting a new host. In contrast to fecal-oral
transmission, where infective stages are excreted into the environment,
potential new hosts would not normally come into contact with the parasite.
(In evolutionary terms, transmission by blood transfusion would be a very
recent event.) Predator-prey transmission is one strategy used by protozoa
such as Toxoplasma and Sarcocystis to overcome these transmission
barriers. As the name implies, predator-prey transmission involves two
distinct hosts. The predator acquires the infection by eating an infected prey.
This will induce an intestinal infection in the predator and result in the
excretion of infective stages in the feces. The prey, generally a herbivore,
will become infected by eating the infective stages it encounters in the
environment. Following ingestion by an appropriate prey the parasite will
cross the intestinal epithelium and infect internal organs or tissues within the
host, where it waits for the next predator to ingest its prey. [Page contents]
Vector transmission is the other strategy used by protozoan parasites which
inhabit the blood or internal tissues within its host. This strategy involves a
hematophogous (ie, blood feeding) arthropod serving as an intermediary
between successive vertebrate hosts. Several human diseases caused by
protozoa are transmitted by a variety of arthropod vectors (Table). The
vectors are not simply 'flying syringes', but represent a second host for the
protozoan parasite. Thus the life cycle of vector transmitted diseases also
involves complex interactions protozoan-vector interaction analogous to the
complex human-protozoan interactions. Vector transmission probably
evolved multiple times.

Vector Transmitted Protozoa

Protozoa Vectors
Parasite Disease Common Genera
Name
Trypanosoma gambiense, African sleeping tse-tse Glossina
T. brucei sickness
Trypanosoma cruzi Chagas' disease kissing bugs, Triatoma, Rhodnius
etc.
Leishmania leishmaniasis sand fly Phlebotomus, Lutzomyia
Plasmodium malaria mosquito Anopheles
Babesia babesiosis tick Ixodes

Vector transmission also involves complex interactions between humans and

vectors. This includes the biology of human-arthropod interactions, as well
as ecological considerations. Thus vector transmitted parasites exhibit
complex life cycles involving interactions between humans, protozoa, and
arthropods. The biology of vectors and their interactions with humans
provide possible means for controlling the transmission of these diseases.
• Tsetse and African Trypanosomes
• Triatomines and Trypanosoma cruzi
• Sand Flys and Leishmania
• Anopheles and Plasmodium
• Ticks and Babesia
• Control Strategies

Tsetse and African Trypanosomes

The genus Glossina, common name tsetse, contains at least 30 species or

subspecies of flies found in subsaharan Africa. Adult tsetse are yellow,
brown, or black flies 6-14 mm long. A diagnostic character of the genus is
the 'hatchet cell' found in the center of the wings (Figure). Most species fall
into one of two major groups represented by G. palpalis and G. morsitans.
The palpalis group is associated with riverine ecologies and is frequently
found near streams, rivers, and lakes in west and central Africa. The
morsitans group is most frequently associated with savannah woodlands and
dry bush country in east Africa. The palpalis and morsitans groups are
associated with the transmission of Trypanosoma gambiense and T.
rhodesiense, respectively. The differences in the ecologies and interactions
with reserviors of these two types of tsetse contribute the different
manifestations of diseases caused by the two African trypanosme species
(See table in notes on African trypanosomes.)
Both the male and female tsetse are voracious feeders and the important
vector species tend to feed on large mammals. Tsetse means 'fly destructive
to cattle' in Sechuana (hence tsetse 'fly' is redundant). The bite of the tsetse
is painful, but usually of minor consequence. A welt will occasionally form
and some individuals will become sensitive to the saliva. However, tsetse are
persistent feeders and can be quite aggravating to humans and animals.
Tsetse are 'pool' feeders (ie, telmophages) which lacerate the skin with their
mouth parts and then ingest the blood and lymph which flow into the
superficial lesion. Trypanosome transmission occurs via the saliva which is
injected into the bite site. The saliva contains substances which dilate blood
vessels and prevent coagulation.
The life cycle of African trypanosomes involves alternating between the
vertebrate host and the tsetse vector. Trypomastigotes within the blood
stream of the vertebrate host are ingested by the tsetse and convert to
procyclic trypomastigotes which replicate within the gut of the tsetse. To
complete the life cycle, these procyclic forms must make their way to the
saliva glands. The exact mechanism by which the parasite migrates from the
tsetse gut to the saliva glands is not known. Two routes have been
proposed: 1) the classical route in which the parasite 'backtracks' through
the digestive system and migrates up the salivary duct, or 2) the direct
route in which the parasite penetrates the peritrophic membrane and gut
epithelium to gain access to the hemolymph. Either route presents barriers
and illustrates the complex interactions between the protozoan parasite and
vector (Figure).

Schematic representation of trypanosome-tsetse interactions. Trypomasitgotes are taken up

with the blood meal and pass through the food canal (FC) and crop (Cr). The blood meal is
encased in the peritrophic membrane (PM) by the proventricular valve (PV) as it enters the
midgut. Migration of the procyclic trypomastigotes from the midgut to the salivary glands (SG)
involves two possible routes (depicted by arrows): the 'classical' and the 'short circuit'. The
classical route invovles a migration towards the hindgut (Malpighian tubes, MT and rectum, R)
and exiting the peritrophic membrane. The procyclic then migrates forward through the
ectoperitrophic space, exits at the proventricular valve, passes up the food canal, and enters the
salivary duct (SD) to gain access to the salivary glands.The short circuit route involves a direct
penetration of the peritrophic membrane and gut epithelium (GE) to gain access to the
hemocoel. From the hemocoel the trypanosomes find and penetrate the salivary glands.

Diagram of developmental stages found in the

tsetse salivary gland. From Tetley and Vickerman
(1985) J. Cell Sci. 74:1.

The parasite converts to an epimastigote form after reaching the salivary

gland. The epimasigote attaches to the epithelial cells of the salivary glands
via its flagellum (fg) and undergoes further replication. Differentiation into
metacyclic trypomastigotes involves the appearance of the surface coat (sc)
and changes in the mitochondria (mt) to accompany the migration of the
kinetoplast (kt) to the posterior end (Figure). These developmental changes
are necessary preparations for becoming infective to the mammalian host.
The mature metacyclic trypomastigote detatches from the epithelial cells and
remains in the lumen of the salivary gland until being expelled during tsetse
feeding.
(Return to African Trypanosome Life Cycle or go to Control Strategies.)

Triatomines and Trypanosoma cruzi

 Picture modified from A.M. Rose
(http://www.arose.net/triatoma/pic
s.htm) and used with permission
(© H Knüttel & AM Rose).
Several genera and species of triatomines are capable of transmitting
Trypanosoma cruzi. The most important vectors are: Triatoma infestans,
Panstrongylus megistas, and Rhodnius prolixus. Triatomines are generally
large insects ranging in size from 5-30 mm. They are primarily New World
insects and range from Argentina through the United States. The life cycle
consists of five nymphal instars followed by sexually mature adults. Only the
adults have wings. Triatomines feed on blood through out their life and all
stages can become infected with T. cruzi. Common names include assassin
bug, kissing bug (in reference for its tendency to bite around the face) and
conenose bug (in reference to their pointed heads).
Most triatomines are not host specific and feed on a wide range of mammals
as well as birds and reptiles. Transmission of T. cruzi is often associated with
domiciliary species which have adapted to living in human dwellings. Such
dwellings are generally adobe or thatched roof huts which provide plenty of
hiding places for the bugs. The bugs come out at night to feed upon sleeping
people. They are capillary feeders and feeding times range from 3-30
minutes. Adults can can up to 0.25 ml of blood per feeding and a total of 4-
10 ml of vertebrate blood may be consumed by a triatomine bug during its
lifetime. The bites are usually painless, despite the large proboscis. It is
assumed that the saliva contains an anesthesia. Although triatomine feeding
causes little pain, their bites can cause an uncomfortable lesion at the site of
feeding and can elicit a hypersensitivity reaction.
Triatomines become infected when bloodstream trypomastigotes are
ingested with the blood meal. The trypomasigotes convert to epimastigotes
which are the replicative form found primarily in the midgut. The
epimastigotes will develop into non-dividing metacyclic trypomasitigotes.
Metacyclogenesis is almost exclusive to the rectum and correlates with
attachment to the rectal epithelium. Vector-parasite interactions are
important for the successful replication and differentiation of T. cruzi.(See
also: Kollien and Schaub, The development of Trypanosoma cruzi in
triatominea. Parasitol. Today 16:381; 2000.) Infectious metacyclic
trypomastigotes are excreted with the feces. This type of transmission is
referred to as 'hindgut station' or 'stercorarian' and is considerably less
efficient than salivarian transmission.
(Go to T. cruzi Life Cycle, Ecology of Transmission, or Control Strategies.)

Sand Flys and Leishmania

From Peter and Gilles (Color Atlas

of Tropical Medicine and
Parasitology)
Sand flies are the vectors for Leishmania as well as some bacterial
(bartonellosis) and viral (sand fly fever) diseases. Adult sand flies are about
2 mm in length and characterized by hair bodies and wings (Figure?).
Genera of sand flies fall into two groups: Phlebotomus and Sergentomyia
found in the Eastern hemisphere (Europe, Asia, Africa, Australia), and
Lutzomyia, Brumptomyia and Warileya in the Western hemisphere (ie, New
World). In general, the Old World sand fly species live in desert or semi-arid
ecosystems and the New World species are forest dwelling. Some of the Old
World species will breed in peridomestic situations and enter human
habitations, whereas disease transmission in the New World is associated
with humans living or working near the forest.
The sand flies responsible for the transmission of leishmaniasis are
Phlebotomus and Lutzomyia in the Old and New Worlds, respectively. The
spatial distribution of leishmaniasis and other sand fly transmitted diseases
tends to be patchy due to the limit flying range of the sand fly. Their flying is
often described as 'hopping', characterized by short bursts of flights
separated by a couple of seconds of rest. Sand flies have a short flight range
and are usually found within a dozen meters of a breeding site.
As a general rule only female sandflies take blood meals and they feed most
actively at twilight or night, or in low-light conditions such as shade. They
have short mouthparts and are pool feeders. The bite produces a rose-
colored papule surrounded by a erythematous area about 10-20 mm in
diameter.
Amastigote-infected macrophages are ingested with the blood meal and
transform into promastigotes (see Leishmania Life Cycle). These procyclic
promastigotes attached to the midgut epithelium of the fly and replicate.
Attachment is mediated by a lipophosphoglycan (LPG). LPG is an abundant
cell surface associated glycoconjugate composed of three major domains:
glycolipid membrane anchor, disaccharide repeats, and a small cap (Figure).
The LPG undergoes biochemical changes as the parasites mature into
metacyclic promastigotes. The disaccharide repeats approximately double in
number leading to an elongation of the LPG and the cap changes from
galactose to arabinose. Changing the cap structure is believed to be
associated with detachment from the gut epithelium in that adherence is
believed to be associated with galactose specific lectins found in the
sandfly's gut epithelium. The elongaton of LPG is associated with increased
complement resistance suggesting additional roles for LPG in terms of
infectivity to the vertebrate host. (For a review on Leishmania
glycoconjugates see: Descoteaux and Turco, Biochem. Biophys. Acta
1455:341; 1999.)
There are also factors within the sandfly saliva which
potentiate the infectivity of Leishmania for the
vertebrate host. Some of these salivary gland
compounds have immunosuppressive activities against
lymphocytes and macrophages which may explain the
potentiation.