TSHWANE UNIVERSITY OF TECHNOLOGY

FACULTY OF SCIENCE

DEPARTMENT OF BIOMEDICAL SCIENCES

BPVT20

LECTURER: MTSHALI K

DATE: MARCH 2025

NAME: TQ MANGANE

STUDENT NUMBER: 223161383

TABLE OF CONTENTS PAGES

INTRODUCTION …………………………………….3
BODY ………………………………………………….3&4

CONCLUSION ………………………………………..4

REFERENCES ………………………………………..5&6
TITLE: Mechanisms Trypanosoma brucei acquire to gain excess and survive Tsetse
fly immune system.

INTRODUCTION:

Trypanosoma is a protozoan known to cause sleeping sickness (Swallow, B. M. 2000).

During lifecycle of Trypanosoma it infects two hosts, the vector host (insect) and the
second host which in this case is a mammal (Sbicego et. Al., 1999). In this study we
will focus on how Trypanosoma invade the immune system of a Tsetse fly (vector host).
Trypanosoma brucei to be specific which is a protozoan carried by Glossina species
of Tsetse flies (Auty, H.K. et al, 2012), Trypanosoma is established in the gut of a
Tsetse fly it further mature in the proboscis and salivary gland of Tsetse fly respectively,
the lifecycle of Trypanosoma ends at a metacyclic form which is infective to
mammals(Van den Abbeele et al, 1999).
Temperature above 34% have negative impact on survival of both Trypanosoma and
tsetse fly species (Rued et al., 1990). Favourable conditions for the survival of the
above-mentioned species include moderate temperature, high relative humidity and
weak saturation deficit (Ndegwa et al, 1992; Courtin et al, 2010, Pagabeleguem et al,
2012). Nevertheless, high temperatures influence Tsetse flies to take more blood
which increases the chances of them contracting Trypanosoma while feeding from
infected mammals and transmitting the pathogen to healthy mammals (Terblanche et
al., 2008), we can conclude to say that high temperature have both positive and
negative impact.

Tsetse flies (Glossina morsitans) have a weak barrier against Trypanosoma brucei
strain (Aksoy, S. et al. 2003). Tsetse flies take blood meals in every two days, they
ingest long proliferative slender and short stumpy form of Trypanosoma brucei that
change to proliferative procyclic form meanwhile the long slender form die (Gibson,
W. and Bailey, M. 2003). Trypanosoma depends on several biotic and abiotic factors
in order to develop in the Tsetse fly midgut it then later migrates to mature in the
salivary glands (Dean et al, 1969). In Tsetse fly midgut Trypanosoma take advantage
of an anti-complement for survival since the midgut of Tsetse fly midgut is filled with
complement, Trypanosoma evolved in order to neutralise the function of serum
complement in the midgut of a Tsetse fly for the susceptible procyclic form
trypanosomes to survive in the midgut (Van Den Abbeele, J. et al. 1999). The survival
rates for successful midgut colonisations vary from 1% to 0.013–0.027% (Van Den
Abbeele, J. et al. 1999) Trypanosoma neutralise the serum complement by moving to
the ectoperitrophic space of the midgut although it is not definite if the complement
exists in that space (Walshe, D.P. et al 2011).

It is unclear how procyclic form trypanosomes are able to move to the ectoperitrophic
space, but it might be related to their ability to cooperate and communicate in response
to an outside signal (Subota, I. et al. 2011). procyclic form Trypanosomes multiply in
the ectoperitrophic space three to six days after infection, after which they cross the
peritrophic matrix (Ellis, D.S. and Evans, D.A. 1977). At six days, trypanosomes
migrate anteriorly to the proventriculus of Tsetse fly (Van Den Abbeele, J. et al. 1999),
changing into long trypomastigotes that divide asymmetrically to produce both long
and short epimastigotes

A group of RNA-binding proteins in T. brucei seem to regulate the fly's parasite

development (Kolev, N.G. et al. 2012, Subota, I. et al. 2011). T. brucei is believed to
re-enter the gut lumen and move via the foregut to the salivary glands after
differentiation in proventriculus (Van Den Abbeele, J. et al. 1999). Parasites can arrive
in the foregut anywhere between 6 and 28 dots per inch (Peacock, L. et al. (2012),
depending on the strain. Additionally, strains differ in how long it takes them to reach
the salivary gland; the strain reaches the quickest starts producing infectious
metacyclic trypomastigotes in mammals on day 12 (Van Den Abbeele, J. et al. 1999).
The majority of strains mature far more slowly.

According to a recent estimate based on genetically tagged trypanosomes, it may take

five trypanosomes to colonise the salivary gland indicating that salivary gland
colonisation is a small bottleneck (Oberle, M. et al. (2010). There is convincing proof
that the development of T. brucei meiotic stages take place at the infected salivary
gland (Peacock, L. et al. (2012). They are thought to be in charge of genetic exchange
(Peacock, L. et al. (2012). Nevertheless, there is no proof that metacyclogenesis
requires meiosis. If the infection is a success, parasite development in the salivary
gland causes a downregulation in the expression of tsetse salivary proteins through
an undefined mechanism, which alters eating behaviour and could potentially improve
transmission (Van Den Abbeele, J. et al. 2010).

The entire shift from the proliferative monomorphic Trypanosoma to procyclic form
takes place in Tsetse fly midgut. The parasites in the proventriculus undergo
differentiation into lengthy trypomastigotes (Peacock, L. et al. 2012) before migrating
to the proboscis via the foregut. The proboscis is where lengthy epimastigotes
formations differentiate (Peacock, L. et al. 2012), epimastigotes are produced by an
unidentified method after colonising the proboscis, epimastigotes cling to proboscis
and the cibarium, where metacyclogenesis takes place, via the flagellum (Peacock, L.
et al. 2012).

The establishment of Trypanosoma infection in tsetse fly midgut is regulated by

multiple factors, it depends in their ability to survive, transform and adapt after
transitioning from vertebrate blood to tsetse midgut (Simo et al, 2010). There are
several interesting outstanding questions regarding the tsetse-trypanosoma
relationship. Midgut survival and ectoperitrophic space colonisation are also the first
obstacles and bottlenecks to Trypanosoma. A significance of the establishment of
salivary gland infection is to spread of T. brucei; the majority of midgut infections do
not develop (Van Den Abbeele, J. et al. 2010).
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