170 American EntomologistȈFall 2011
Some of the greatest mysteries of medical entomology and
pathology center around the origins of devastating human
diseases such as malaria, leishmaniasis, and trypanosomiasis.
vectored by blood-sucking insects? While scientists have used a
plethora of methods attempting to unravel the seemingly complex
origins of these diseases, it may be some time before the pathways
are sorted out to everyone’s satisfaction.
Due to the microscopic, fragile features of pathogenic microor-
ganisms, paleontological evidence was never seriously considered
for solving these problems. However, recent discoveries in amber of
fossil vectors carrying vertebrate pathogens have provided valuable
information on the minimum ages, origins, and early hosts of ma-
laria, leishmaniasis, and trypanosomiasis. These discoveries attest
to the remarkable qualities of amber in preserving microorganisms
All three diseases discussed here are caused by members of the
ubiquitous group known as protozoa or protists. Most protozoa are
free-living, but others have formed commensal or symbiotic associa-
tions with insect vectors that cause millions of human deaths annu-
ally. Over 30 species of protozoa are known to infect humans, and
if roughly the same number infects the other approximately 5,000
mammalian species on earth, it can be estimated that 150,000 spe-
cies of parasitic protozoa reside in mammals alone (Manwell 1961).
Relationships between protozoa and insects were certainly es-
tablished quite early in the evolution of both groups, and over time,
these dual teams co-evolved various types of vector relationships
with vertebrates. Investigations in amber show that the three very
successful examples of co-evolution between insects and protozoa
presented here have existed for at least 100 million years.
In deciphering the life cycles of these fossil pathogenic protozoa,
that the lifestyle of fossil organisms will be similar to that of their
levels (Boucot 1990; Boucot and Poinar 2011). Since their origin hun-
dreds of millions of years ago, protozoa have undergone a multitude
environmental changes, the extinction and appearance of new hosts,
in response to vertebrate immune reactions.
Some issues in the etiology of vector-borne diseases are relevant
here. During epidemics, some individuals die from a disease while
others become infected but survive for a prolonged period, all the
while carrying the pathogen inside their bodies. These living germ
factories or reservoir hosts maintain the disease in the population for
extended periods. Hematophagous arthropods feeding on reservoir
hosts acquire pathogens, and under the right set of parameters, they
transmit them to different vertebrate groups. Such bloodsuckers
are known as bridge vectors, and the resulting host-switching is
referred to as a lateral or horizontal transfer. Bridge vectors can
move infections from birds to mammals, from lizards to birds, or
just from one mammalian group to another. Reservoir hosts, bridge
vectors, and lateral transfers play crucial roles in the co-speciation
of vector-borne diseases.
Malaria is a disease caused by parasitic protozoans that initiate
infection in the vertebrate host with microscopic sporozoites. There
are many types of malarial organisms with a wide range of arthropod
vectors. The more primitive malarias infect reptiles and birds and
The Origin of
Insect-Borne Human Diseases
as Revealed in
American EntomologistȈVolume 57, Number 3 171
One example of these is Haemoproteus, a group found in reptiles and
birds and mostly vectored by biting midges of the genus Culicoides.
An examination of biting midges in Burmese amber revealed a
specimen with a cleared abdomen that allowed an unobstructed view
into its body cavity (Fig. 1). Inside were a number of developing oo-
cysts (Fig. 2) and sporozoites (Fig. 3) of an archaic malarial parasite.
This 100 million-year-old malaria, described as Paleohaemoproteus
burmanicus, is an extinct species related to the extant Haemoproteus
(Poinar and Telford 2005). The infected biting midge belonged to
the extinct genus Protoculicoides, which is ancestral to the Culicoides
that bite us today. Morphological features of Protoculicoides indicated
that the vertebrate host was cold-blooded, and because this type of
malaria commonly occurs in reptiles today, it is likely that the ancient
and vector group for ancient malaria.
The ancestors of today’s malaria-causing pathogens were prob-
ably free-living, amoeba-like organisms that at some point invaded
the intestinal tract of insect larvae developing in the same habitat.
Eventually, these symbiotic organisms entered the gut cells of their
insect hosts, just as the protozoan parasite Malameba does in grass-
hoppers and crickets today (Ernst and Baker 1982). As the parasitic
lifestyle co-evolved, the pathogens entered the body cavity of their
insect hosts (Léger 1900). Somewhere along the evolutionary line,
malaria-like forms appeared. Those species in blood-sucking insects
soon became dixenous (with two hosts in their life cycle) as their ver-
tebrate hosts carried full-blown infections (Poinar and Telford 2005).
Probably the most advanced type of malaria is represented by
members of the genus Plasmodium, where development of the
oocyst occurs in the gut wall of mosquitoes and masses of sporozo-
ites emerge from the oocyst to be transmitted back to vertebrates
(Garnham 1966). The most notorious types of Plasmodium malaria
are four species vectored by anopheline mosquitoes (P. ovale, P.
malariae, P. falciparum, and P. vivax) that infect humans. Globally,
300–500 million new cases of human malaria occur each year, and
over a million deaths result in Africa alone (Foster and Walker 2002).
Before mosquito eradication procedures and antimalarial drugs, the
disease was established in many temperate areas of the United States
and was so severe in the 17th century that it hindered the coloniza-
tion of the east coast from Massachusetts to Georgia. Even as late
as 1934, outbreaks occurred in the U.S. that caused nearly 4,000
deaths that year and almost a million new cases the following year.
By 1944, the death rate had dropped to about 600 (Hermes 1953),
but because anopheline mosquitoes are widely distributed in North
America, malaria has the potential to re-appear in the United States.
In Plasmodium malaria, the cycle begins when a mosquito ac-
quires sexual stages, the gametocytes, from the victim’s blood. The
gametocytes fuse in the stomach of the mosquito, and the zygote
develops into a motile worm-like body (ookinete) that penetrates
through the insect’s midgut and forms a minute cyst (oocyst) on
the outer intestinal wall. The cyst grows and produces within it a
number of microscopic spindle-shaped bodies called sporozoites.
When the cyst bursts, the liberated sporozoites migrate through the
vector’s body cavity and collect in the salivary glands. At the next
blood meal, the sporozoites are transferred in the mosquito’s saliva
into a new victim, where they initiate a number of asexual cycles
and eventually end up in the blood, ready to be picked up by another
mosquito (Garnham 1966).
The age, origin, and subsequent dispersal of Plasmodium malaria
have been controversial topics, primarily due to the lack of fossil evi-
dence. Various ages proposed for the origin of human malaria range
from 15,000 to 8 million years (Pennisi 2001). Not all Plasmodium
Fig. 1. A
des sp. biting
with the primi-
Fig. 2. Oocysts
of P. burmacis
the body cavity
)LJ6SRUR]RLWHVRIP. burmacis developing in the body cavity of Pro-
172 American EntomologistȈFall 2011
malaria attacks humans or is carried by anopheline mosquitoes.
time in 1901, he used a type of Plasmodium malaria carried by cu-
licine mosquitoes that infected birds (Garnham 1966).
That type of Plasmodium malaria was discovered in a culicine
mosquito (Fig. 4) in Dominican amber. The vector, Culex malariager
(Poinar 2005a), contained gametes, an ookinete, oocysts (Fig. 5), and
sporozoites (Fig. 6) of a malarial pathogen described as Plasmodium
dominicana (Poinar 2005b). The large, pedunculated cysts of the
fossil aligned it with a type of present-day bird malaria known as
of Plasmodium malaria, the discovery shows that the pathogen
was established in the New World at least 15 million years ago, the
Support for such a theory is derived from molecular and labora-
tory studies that demonstrated a close relationship between bird
and human malaria. One study showed that P. falciparum infecting
humans had a recent avian progenitor and probably arose by lateral
transfer from birds (Waters et al. 1991). In addition, avian malaria
has been established in mammals (McGhee 1951) and can complete
its development (forming mature sporozoites) in anopheline mos-
quitoes (Jeffrey 1944).
There is also an ongoing debate whether one or more species of
human malaria originated in the Americas and was waiting to make
the leap into Homo sapiens when they arrived, or whether all were
introduced from the Old World (Africa, Asia, Europe) by Paleoameri-
cans migrating across the Bering Strait 40,000 years ago, Spanish
soldiers in the 16th century, or African slaves in the 17th century. Since
all four species of human malaria are present worldwide today (Hart
and Williams 1933), it is almost irresolvable when and where each
minimum age suggested for Dominican amber. Others have provided
evidence that some Dominican amber could be up 40 million years
old (Schlee 1990).
This discovery raises the possibility that ancient bird malaria
may have gradually evolved into a species that was laterally trans-
ferred to simians and eventually to humans when they entered the
New World. Infected migratory birds could have spread the disease
throughout Meso- and South America, as both culicine and anoph-
eline mosquitoes were present in the mid-Tertiary to serve as vec-
tors. The Dominican amber Anopheles dominicanus (Zavortink and
Poinar 2000) (Fig.7) possibly acted as a bridge vector, transferring P.
dominicana from birds to simians and humans. Culicine mosquitoes
(Fig. 4) also had the potential to function as bridge vectors, as they
presently transmit both bird and simian malaria (Hart and Williams
1933; Klein et al. 1988).
malaria to birds and
An oocyst of
dominicana in the
body cavity of its
)LJ6SRUR]RLWHVRIPlasmodium dominicana emerging from an oocyst
in the body cavity of its vector, Culex malariager,LQ'RPLQLFDQDPEHU
have served as a
bridge vector to
nium from birds
almost certain that some types of malaria arrived in the New World
by the routes mentioned above, it is now apparent that a species of
Plasmodium malaria was already established in the New World long
before humans appeared.
ϐ ǡ P.
dominicana (or a close relative) from birds to simians probably had
already occurred, and some of these new strains had subsequently
mutated into the now widespread South American simian parasite P.
American EntomologistȈVolume 57, Number 3 173
brasilianum. This species of simian malaria does not occur anywhere
else in the world (Garnham 1966), and it likely evolved into the
closely related human parasite P. malariae. Since either species can
infect both simians and humans, it is doubtful that these two forms
of malaria have been separate species for long (Garnham 1966).
There is historical evidence that malaria was established in the
in South America, they noticed that when Indians fell ill with fevers
and chills, they drank infusions of cinchona bark to cure themselves
(Garnham 1966). The natives had learned that some component
(quinine) in the bark had anti-malarial properties. Some (see Rocco
2003) claim that other diseases could have caused these fevers, but
Garnham (1966) pointed out that malaria is the only fever known to
be susceptible to quinine. Others have presented the argument that
the Indians did not know about Cinchona bark because malaria does
not occur at heights where these trees grow (Rocco 2003). However,
early botanical reports list Cinchona trees growing at elevations rang-
ing from 2,300 to 9,000 feet (Fawcett 1906), which overlap with the
altitudes at which malaria occurs. Herms (1953) reported malaria
in Quito at 9,000 feet, in Mexico at 7,500 feet, and persistent malaria
in California at about 5,500 feet.
Most North Americans are unfamiliar with the human disease
known as leishmaniasis, which is caused by several species of the
lated protozoan that shares its developmental cycle with two hosts
(dixenous). Part of its development is in the gut of its insect vector,
while the rest is completed in vertebrate blood cells. The malady is
widely distributed throughout the world, with foci of infections in
Asia, Southern Europe, Africa, the Middle East, and South America. It
is estimated that in South America alone, some 15-20 million people
are infected with leishmaniasis, with some 65 million at risk. Most
of the victims are infected with cutaneous leishmaniasis that causes
open sores on the skin. However, the infections can become internal
and Kala Azar is a severe visceral form of leishmaniasis that enters
the internal tissues. Kala Azar can reach epidemic proportions, and
epizootics were responsible for 100,000 deaths in southern Sudan
between 1989 and 1994 (Dedet 2002).
American military serving in Iraq and Afghanistan are well ac-
ϐǦLeishmania. They have learned
mosquito netting covering the tents. So far, over 750 U.S. military
personnel have been infected in Iraq and subsequently hospitalized
in the United States for diagnosis and treatment. Most were infected
with the cutaneous form of the disease (Fig. 9), but a few acquired the
potentially lethal visceral type (Berté 2005; Seppa 2004). Leishmania
has become an even greater health risk since scientists discovered
that it can work in concert with other diseases such as AIDS. The
combined effect of human co-infections of Leishmania and HIV
causes a serious new disease complex as the HIV virus weakens the
immune system and allows the potentially lethal Kala Azar to enter
the internal tissues (Dedet 2002).
Whether Leishmania arose in the Old World with reptiles as the
original hosts or in the New World (the Americas) in rodents is a
controversial and seemingly irresolvable topic (Kerr 1999; Noyes et
al. 2000). However, a recent fossil has helped solve this riddle. An
ancient form of LeishmaniaǦϐ
Fig. 9. Cutaneous
a U.S. soldier at
Army Institute of
)LJ7KH(DUO\&UHWDFHRXVVDQGÁ\Palaeomyia burmitis, vector of
Paleoleishmania proterus in Burmese amber.
174 American EntomologistȈFall 2011
found in Cretaceous amber from Burma (Fig. 10). The mouthparts
mitis Poinar (2004) are similar to the piercing and sucking forms
Ǧ ϐǡ ͳͲͲǦǦ
specimen had the ability to imbibe blood from vertebrates (Poinar
2004). Comparison with the process of blood digestion in extant
ϐ ȋͳͻͶʹȌPalaeomyia was in the
early stages of this process when it became entrapped in tree resin.
Even more astonishingly, Palaeomyia carried the developmental
stages of an ancient Leishmania, described as Paleoleishmania pro-
terus Poinar and Poinar (2004a), in its alimentary tract. Palaeomyia
ellated forms known as promastigotes in its gut (Figs. 11,12), and
amber. Amastigotes are formed in vertebrate blood cells, showing
vertebrate to complete its life cycle (Poinar and Poinar 2004a). The
reptilian blood cells (Fig. 14) were detected in the foregut of Pal-
aeomyia. These infected blood cells were almost identical to lizard
cells infected with Leishmania today (Poinar and Poinar 2004b).
ting leishmanial pathogens to reptiles 100 million years ago, lending
support to the Old World–reptile hypothesis for leishmanial origins.
Exactly when Leishmania appeared in the New World is unknown,
ϐLutzomyia adiketis Poinar (2008a) (Fig. 15)
was found in Dominican amber with promastigotes of Paleoleish-
mania neotropicum Poinar (2008a) in its foregut and midgut and
amastigotes, promastigotes, and paramastigotes (Fig. 16) in its
proboscis. The presence of amastigotes showed that P. neotropicum
was digenetic, because in Leishmania, amastigotes are only formed
in the vertebrate host.
It stands to reason that insect-transmitted diseases could not have
occurrence of vector groups is not always certain due to gaps in the
in Lebanese amber ~130 million years ago (Poinar and Milki 2001),
and that could be inferred as the earliest possible date for the origin
nectar from plants infected with Phytomonas, a plant-parasitic try-
their longevity.) Others (Baker 1965) suggest that vertebrates were
the original hosts and became naturally infected when free-living
from parasitized vertebrates.
It is more likely that the free-living ancestors of Leishmania oc-
curred in decaying organic matter and were ingested along with
multiplied in the larval gut and then been carried through the pupal
and into the adult stage. While many insects “void” their gut contents
before entering the pupal stage, tϐ
nia in the midgut
of the Burmese
from the Burmese amber
)LJ5HSWLOLDQEORRGFHOOVLQIHFWHGZLWKPaleoleishmania proterus in
WKHWKRUDFLFPLGJXWRIWKH%XUPHVHDPEHUVDQGÁ\ Arrows show amas-
tigote stage of the parasite developing inside the vertebrate blood cells.
American EntomologistȈVolume 57, Number 3 175
Transtadial transmission of the trypanosomatid Crithidiafasciculata
Leger was experimentally achieved in the mosquito Culiseta incidens
(Thompson) (Clark et al. 1964), and bacteria were shown to be trans-
mitted transtadially from larval to adult Phlebotomus duboscqi (Volf
2002). The trypanosomatid Leptomonas ctenocephali (Fantham) is
des canis (Curtis), and when mealworm larvae were experimentally
infected with Leptomonas pyrrhocoris ǤƬǤǡϐ-
lates though the pupal and into the adult stage (Steinhaus 1949).
There is actual evidence for this hypothesis in Early Cretaceous
associated with the fruiting bodies of a coral mushroom in Burmese
amber (Poinar and Brown 2003) had voided some of their intestinal
pupation (Lawyer and Perkins 2000) (Fig. 17). Associated with the
fecal deposit and debris surrounding the larvae were numerous
trypanosomatids. When a portion of the alimentary tract of one
(Poinar 2007) (Fig. 18). ϐ
promastigotes, as they had kinetoplasts located in the anterior end.
panosomatids would have been transferred to vertebrates during
blood feeding. It probably took a period of time before trypanoso-
matids became established in vertebrates and were re-acquired by
co-evolution seems to have occurred between the trypanosmatids
and their insect and vertebrate hosts. The association between
coptera) from which the Diptera supposedly evolved, as supported
(Podlipaev et al. 2004a).
The establishment of the parasites in the vertebrate host and
rare event and would only occur under ideal conditions. If the above
of trypanosomatids could have appeared at different localities and
times over the past ~100 million years. The 100 million-year-old
ϐP. proterus undoubtedly
arose independently from P. neotropicum, which could well be the
progenitor to one or more extant Neotropical Leishmania species.
of transmitting human diseases, and these include some assassin
bugs. Assassin bugs comprise the family Reduviidae (Hemiptera),
involving ~3,000 species of predatory insects, the great majority of
which attack other invertebrates. However, a small fraction, placed in
the subfamily Triatominae, exists on vertebrate blood (Lent and Wy-
godzinsky 1979) (Fig. 19). Within this triatomine group are vectors
of the notorious Chagas’ disease found in Central and South America.
Chagas’ disease is also known as American trypanosomiasis in order
African trypanosomiasis that causes sleeping sickness.
vector of Pa-
the rostrum of L.
to its apparent
behavior of the
in the gut of
176 American EntomologistȈFall 2011
The large triatomine assassin bugs remain hidden in cracks or
roof thatching during the day, but emerge at night to feed. They
frequently bite the face of their victim near the eyes or mouth, giving
rise to their common name, “kissing bugs.” The bites themselves can
result in severe reactions in sensitive individuals, causing nausea,
rapid breathing, high pulse rate, and heart palpitations. Even more
serious are what the bugs may be carrying in their bodies at the
cruzi, the causal agent of Chagas’ disease (Hoare 1972; Lent and
The transmission of Chagas’ disease is different from that of most
vector-borne pathogens. The infective stages occur in the insect’s
hindgut and reach the victim when they are defecated on the skin
during and just after feeding. Each fecal droplet contains thousands
of thrashing trypanosomes that are inoculated into the still-open
wound when the victim responds to the irritation by scratching or
membranes lining the nose and mouth.
If not treated, the infection enters a chronic stage and the para-
sites invade the heart muscle, which may result in myocarditis, heart
failure, and death. In his journals on the voyage of the Beagle, Charles
Darwin (1860) recorded being bitten by these bugs. The famous
Israeli parasitologist Saul Adler felt that Darwin’s health problems
later in life were the result of a chronic infection of Chagas’ disease
acquired during these insect attacks (Adler 1959).
The origin of kissing bug–trypanosome associations in the Ameri-
cas is controversial, with one school suggesting that triatomine bugs
evolved fairly recently from predatory ancestors, while others believe
that their blood-sucking habits are much more ancient. There was
little hope that fossils would solve this question, especially those in
amber, since these bugs are quite large and large insects can usually
escape from the sticky resin. While fossil triatomines do occur in
amber, they are quite rare and I know of only two specimens: one
undescribed species (Fig. 20) and Triatoma dominicana (Fig. 21),
both in Dominican amber.
The aforementioned debate was partly settled by the discovery of
Trypanosoma antiquus (Fig. 22) in a fecal droplet that was adjacent
to Triatoma dominicana in the amber (Poinar 2005c). The likely
vertebrate host of this ancient vector–trypanosome duo was deduced
from several bat hairs preserved adjacent to the bug.
Trypanosomes in the subgenus Schizotrypanum, to which both
T. antiquus and the causal agent of Chagas’ disease (T. cruzi) belong,
have been reported from diverse genera of bats (Hoare 1972). In
the Neotropics, triatomines are the suspected vectors of all bat try-
panosomes (Marinkelle 1982; Ryckman 1986). Bat trypanosomes
are morphologically indistinguishable from the human-infecting T.
cruzi, and all invade their vertebrate hosts through fecal contamina-
tion (Lent and Wygodzinsky 1979), as was probably the case with
The fossil not only shows that triatomine–trypanosome vector
associations evolved millions of years ago, but also that bats were
adult female triatomine bug
dominicana, a vector of
Trypanosoma antiquus, in
ancient hosts for both kissing bugs and Schizotrypanum trypano-
somes, including the human species that causes Chagas’ disease.
Turning to the Old World, when was an insect vector–trypano-
ϐǫTrypanosoma in Africa is
evolved. In a piece of Early Cretaceous amber from Burma, a biting
midge, Leptoconops nosopheris Poinar (2008b), had taken a blood
meal shortly before becoming entrapped in resin (Fig. 24). This
female contained stages of the digenetic trypanosome Paleotrypano-
soma burmanicus Poinar (2008b) in its gut and salivary glands. Some
of the trypanosomatids had collected in a salivary secretion that had
been released from the tip of the proboscis of the biting midge (Fig.
25). Today, females of the genus Leptoconops feed on reptiles, birds,
and mammals (Auezova et al.1990; Mullens et al. 1997; Mullen 2002).
The genus extends back ~130 million years, with species found in
Lebanese amber (Poinar and Milki 2001). There are 134 extant and
ȋ Ȍ ͳͶ ǡ ϐ
occur in Burmese amber (Szadziewski and Poinar 2005). However,
ϐLeptoconops, extant or extinct, associated
with trypanosomes. Both digenetic and monogenetic trypanosomes
have been reported from other extant biting midges (Sharp 1928;
Kremer et al. 1961; Baker 1976; Podlipaev et al. 2004b; Svobodová et
al. 2007), and a monogenetic species is known from a biting midge in
Burmese amber (Poinar and Poinar 2005). One extant trypanosome
Fig. 22. Flagellates of Trypanosoma antiquus in a fecal droplet from
American EntomologistȈVolume 57, Number 3 177
isolated from a biting midge was closely related to a strain isolated
from Egyptian rats and could have been transferred to the vertebrate
by the insect during blood feeding (Podlipaev et al. 2004a).
It is possible that biting midges were the ancestral vectors of
the Old World Trypanosoma lineage. Later, ϐ
have been acquired from infected hosts by other biting Diptera,
which acted as bridge vectors and transferred the parasites to new
The previous cases show how insect vectors in amber can supply
valuable information not only on the minimum dates when vertebrate
pathogens were being transmitted, but also in what part of the world
they occurred. Due to the fragility of microorganisms, unless they
result in some structural deformity in vertebrates that can survive
petrifaction, the actual existence of pathogenic forms is extremely
amber preservation. It takes time and patience to search through
thousands of amber pieces to detect and identify these ancient or-
ganisms, and then to establish co-evolutionary relationships with
their vectors. Nevertheless, at the end of the day, the excitement of
discovering the remains of an ancient vertebrate pathogen in amber
is the reward in itself.
I thank R. L. Jacobson for providing references and discussions
during the course of this study, Roberta Poinar for comments on
earlier versions of the manuscript, and Dr. Peter J. Weina, M.D.,
Walter Reed Army Institute of research, for the use of Fig. 9. I
also acknowledge the help of many scientists during the course
of these studies, especially parasitologists who have supplied
references on parasitic diseases.
Adler, S. 1959. Darwin’s Illness. Nature 184: 1102-1103.
Auezova, G., Z. Brushko, and R. Kubykin. 1990. Feeding of biting midges
(Leptoconopidae) on reptiles. Abst. 2nd Internat. Congress Dipterology,
Baker, J. R. 1965. ǤǤͳǦʹ
Baker, J.R. 1976. Biology of the Trypanosomes of birds. pp. 131-174. In
W.H.R. Lumsden and D.A. Evans (eds.). Biology of the Kinetoplastida,
Vol. 1, Academic Press, New York.
Berté, S.B. 2005. U. S. army Entomology support to deployed forces. Ameri-
can Entomol. 51: 208- 217.
Boucot, A. 1990. Evolutionary Paleobiology of Behavior and Coevolution.
Boucot, A. and G.O. Poinar, Jr. 2011. Fossil Behavior Compendium, CRC
Press, Boca Raton.
Clark, R.B., W.R. Kellen, J.E. Lindegren, and T.W. Smith. 1964. The trans-
mission of Crithidia fasiculata Leger 1902 in Culiseta incidens (Thomson).
Darwin, C. 1860. The Voyage of the Beagle (Natural History Library Edition,
edited by L. Engel, (1962), Doubleday & Co., Inc., Garden City, New York.
Dedet, J.-P. 2002. Current status of epidemiology of Leishmaniases. pp.
1-10. In J. P. Farrell (ed.). Leishmania. Kluver Academic Publishers,
Dolmatova, A.V. 1942. The life cycle of Phlebotomus papatasi (Scopoli).
Ernst, H.P. and G.L. Baker. 1982. Malameba locustae (King and Taylor)
J. Australian Entomol. Soc. 21: 295- 296.
Foster, W.A. and E.D. Walker. 2002. Mosquitoes (Culicidae). pp. 203-262.
In G. Mullen and L. Durden (eds.). Medical and Veterinary Entomology,
Academic Press, San Diego.
Garnham, P.C.C. 1966. Malaria parasites and other Haemosporidia. Black-
Hart, M.B. and C.L. Williams. 1933ǤǤǤͶ͵ǦͲǤIn M. J. Benton
(ed.). The Fossil Record 2, Chapman & Hall, London.
Hermes, W.B. 1953. Medical Entomology. Fourth Edition. The Macmillan
Company, New York.
Hoare, C. 1972. Ǥ ϐǡ
Jeffrey, G.M. 1944. Investigation on the mosquito transmission of Plasmo-
dium lophurae. American J. Hygiene 40: 251-263.
Kerr, S.F. 1999. Palaearctic origin of LeishmaniaǤǡ
de Janeiro 95: 75-80.
Klein, T.A., D.C. Akin, D.G. Young, and S.R.Telford, Jr. 1988. Sporogony,
development and ultrastructure of ϔ in Culex er-
raticus. Inter. J. Parasitol. 18: 711-719.
Kremer, M., C. Vermeil, and J. Callot. 1961. Sur quelques nematoceres
vulnerants des eaux salées continentals de l’est de la France. Bull. Assoc.
Philomath d’Alsace et de Lorraine 11: 1-7.
Lawyer, P.G. and P.V. Perkins 2000. Leishmaniasis and trypanosomiasis.
Fig. 25. Trypano-
burmanicus in the
(pointer) of Lepto-
in Early Cretaceous
Fig. 23. Blood-
of the extant
carrier of Try -
cei, the cause of
sickness in sub-
pheris, a vector of
178 American EntomologistȈFall 2011
pp. 231-298. In B.F. Eldridge and J.D. Edman (eds.). Medical Entomology.
Kluwer Academic Publishers, Dordrecht.
Léger, L. 1900ǤǤǤǤǤ
Sci. Paris 131: 722-724.
Lent, H and P. Wygodzinski. 1979. Revision of the Triatominae (Hemiptera,
American Mus. Natural History 163:123-520.
Manwell, R.D. 1961.ǤǤǡ
Marinkelle, C.J. 1982. Developmental stages of Trypanosoma cruzi-like
ϐCavernicola pilosa. Rev. Biologia Trop. 30:107-111.
McGhee, R. B. 1951. The adaption of the avian malarial parasite Plas-
modium lophurae to a continuous existence in infant mice. J. Infect.
Disease 88: 86-97.
Mullen, G.R. 2002. Biting midges (Ceratopogonidae). pp. 163-183. In
G. Mullen and L. Durden (eds.). Medical and Veterinary Entomology.
Academic Press, New York.
Mullens, B.A., C. Barrows, and A. Borkent. 1997ǤLep-
toconops (Brachyconops)californiensis (Diptera: Ceratopogonidae) on
desert sand dunes. J. Med. Entomol. 34: 735-737.
Noyes, H.A., D.A. Morrison, M.L. Chance, and J.T. Ellis. 2000. Evidence
for a Neotropical origin of Leishmania. Memoires do Instituto Oswaldo
Pennisi, E. 2001. Malaria’s beginnings: on the heels of hoes? Science 293:
Podlipaev, S.A., N.R. Sturm, I. Fiala, O. Fernandes, S.J.Westenberger, M.
Dollet, D.A. Campbell, and J. Lukes. 2004a. Diversity of insect trypano-
somatids assessed from the spliced leader RNA and 5S rRNA genes and
intergenic regions. J. Eukary. Microbiol. 51: 283-290.
Podlipaev, S.A., J. Votypka, M. Jirku, M. Svobodova, and J. Ljkes. 2004b.
Herpetomonas ztiplinka n. sp. (Kinetoplastida: Trypanosomatidae):
a parasite of the blood-sucking biting midge Culicoides kibunensis
Tokunaga, 1937 (Diptera: Ceratopogonidae). J. Parasitol. 90: 342-347.
Poinar, Jr., G.O. 2004.Palaeomyia burmitis gen. n., sp. n. (Phlebotomidae:
sucking habits. Pro. Entomol. Soc. Washington 106: 598-605.
Poinar, Jr., G.O. and R. Poinar. 2004a. Paleoleishmania proterus n. gen.,
n. sp., (Trypanosomatidae: Kinetoplastida) from Cretaceous Burmese
amber. Protista 155: 305-310.
Poinar, Jr., G.O. and R. Poinar. 2004b. Evidence of vector-borne disease of
early Cretaceous reptiles. Vector-Borne Zoonotic Diseases 4: 281- 284.
Poinar, Jr., G.O. 2005a.Culex malariager n. sp. (Diptera: Culicidae) from
Entomol. Soc. Washington 107: 548-553.
Poinar, Jr., G.O. 2005b. Plasmodium dominicana n. sp. (Plasmodiidae:
Haemospororida) from Tertiary Dominican amber. System. Parasitol.
Poinar, Jr., G.O. 2005c.Triatoma dominicana sp. n. (Hemiptera: Reduviidae:
Triatominae), and Trypanosoma antiquus sp. n. (Stercoraria: Trypano-
vector association. Vector-Borne Zoonotic Dis. 5: 72- 81.
Poinar, Jr., G.O. 2007. Early Cretaceous trypanosomatids associated with
Poinar, Jr., G. 2008a.Lutzomyia adiketis sp. n. (Diptera: Phlebotomidae), a
vector of Paleoleishmania neotropicum sp. n. (Kinetoplastida: Trypano-
somatidae) in Dominican amber. Parasites & Vectors 2008, 1: 1- 22
Poinar, Jr., G.O. 2008b.Leptoconops nosopheris sp. n. (Diptera: Ceratopogo-
nidae) and Paleotrypanosoma burmanicus gen. n., sp. n. (Kinetoplastida:
Trypanosomatidae), a biting midge-trypanosome vector association
Poinar, Jr., G.O. and R. Milki, 2001. Lebanese amber. Oregon State Uni-
versity Press, Corvallis.
Poinar, Jr., G.O. and A. E. Brown. 2003. A non-gilled hymenomycete in
Cretaceous amber. Mycol. Res. 107: 763-768.
Poinar, Jr., G.O., R.L. Jacobson, and C.L. Eisenburger. 2006. Early Cre-
ϐ ȋǣȌǤ Ǥ
Entomol. Soc. Washington 108: 785-792.
Poinar, Jr., G.O. and R. Poinar. 2005. Fossil evidence of insect pathogens.
J. Invertebr. Pathol. 89: 243-250.
Poinar, Jr., G.O. and S.R. Telford. 2005.Paleohaemoproteus burmacis gen.
n., sp. n. (Haemospororida: Plasmodiidae) from an Early Cretaceous
biting midge (Diptera: Ceratopogonidae). Parasitol. 131: 79-84.
Rocco, F. 2003. The Miraculous Fever-Tree. Harper Collins, New York.
Ryckman, R.E. 1986. The vertebrate hosts of the Triatominae of North
and Central America and the West Indies (Hempitera: Reduviidae:
Triatominae). Bull. Soc. Vector Ecol. 11: 221-241.
Schlee D. 1990. Das Bernstein-Kabinett. Stuttg Beitr Naturkunde (C). No.
28, 100 pp.
Seppa, N. 2004. Soldiers in Iraq coming down with parasitic disease. Sci-
ence News 166: 53.
Sharp, N.A.D. 1928. Filaria perstans: its development in Culicoides austeni.
Trans. R. Soc. Trop. Med. Hyg. 21: 371-396.
Svobodová, M., L. Zidková, I. Cepicka, M. Obornik, J. Lukes, and J. Vo-
typka. 2007.Sergia podlipaevi gen. nov., sp. nov. (Trypanosomatidae,
Kinetoplastida), a parasite of biting midges (Ceratopogonidae, Diptera).
Int. J. Syst. Evol. Microbiol. 57: 423-432.
Steinhaus, E.A. 1949. Principles of Insect Pathology, McGraw-Hill, New
Szadziewski, R. and G.O. Poinar, Jr. 2005. Additional biting midges (Dip-
tera: Ceratopogonidae) from Burmese amber. Polska Pismo. Entomol.
Volf, P., A. Kiewegova, and A. Nemec. 2002.
gut of Phlebotomus duboscqi (Diptera: Psychodidae): transtadial passage
and the role of female diet. Folia Parasitol. 49: 73-77.
Waters, A.P., D.G. Higgins, and T.F. McCutchan. 1991.Plasmodium falci-
parum appears to have arisen as a result of lateral transfer between avian
and human hosts. Proc. National Acad. Sci. 88: 3140-3144.
Zavortink, T.J. and G.O. Poinar, Jr. 2000.Anopheles (Nyssorhynchus)
dominicanus sp.n. (Diptera: Culicidae) from Dominican amber. Ann.
Entomol. Soc. America 93:1230-1235.
George Poinar, Jr. became courtesy professor of Zoology at Oregon State
University after retiring from the Department of Entomology and Parasitol-
ogy at the University of California, Berkeley.
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