Microbiology Essay: Plasmodium Life Cycle and Infection
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This essay provides a comprehensive overview of Plasmodium infection, a disease caused by the unicellular parasite responsible for malaria. It details the parasite's complex life cycle, involving both vertebrate and insect hosts, and explores the stages of infection from sporozoite injection to merozoite release. The essay highlights the various host factors that influence infection patterns and disease severity, including innate immunity, genetic predispositions, and socioeconomic factors. It also examines parasite factors such as microvasculature obstruction and parasite biomass, as well as environmental factors like temperature, rainfall, and urbanization, all of which contribute to the transmission and severity of the disease. The essay concludes by emphasizing the importance of prevention strategies, including mosquito control, protective measures, and prophylactic drug use, to combat this life-threatening condition.
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Running head- MICROBIOLOGY
Discussion on Plasmodium infection
Name of the Student
Name of the University
Author Note
Discussion on Plasmodium infection
Name of the Student
Name of the University
Author Note
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1MICROBIOLOGY
Plasmodium is a genus that belongs to unicellular parasites that have been identified
responsible for the incidence of malaria among host organisms. This unicellular parasite has a
life cycle that occurs inside the body of two hosts, namely, a vertebrate and a dipteran insect host
(Ariey et al., 2014). These species are found to contain several features that resemble other
eukaryotes. The genome is present in the nucleus. It doubles the genome in the insect host’s
midgut for a brief time (Bushell et al., 2017). The essay will discuss its life cycle and the various
host factors that influence its infection.
The Plasmodium life cycle involves several changes inside the insect and vertebrate
hosts. The parasites present in the salivary glands of infected mosquitoes, are called sporozoites
that are injected in the bosy of the host, along with the saliva when a mosquito bites the
vertebrate. They enter the bloodstream and are transported to the liver, following which they
undergo invasion and replication in the hepatocytes (Delves et al., 2012). Merozoites emerge
from the infected hepatocytes and form a ring-shaped structure that enlarges to form a
trophozoite. These are then found to mature to form schizonts that multiply and produce new
merozoites. This is followed by bursting of the infectred RBCs, thereby allowing the merozoites
to travel and infect new cells (Ke et al., 2015). Upon infection, sime merozoites are found to
differentiate into male and female gametocytes that are taken up by a mosquito, when it feeds on
the vertebrate host. They move to the vector’s midgut and develop into male and female
gametes, followed by fertilization and subsequent zygote formation. An ookinete is gradually
formed from the zygote that penetrates the midgut wall and develops an oocyst, which in turn
forms elongated sporozoites (Theisen et al., 2014).
Several differences exist in the physiology of the human host that directly influences the
pattern of transmission of the Plasmodium infection. These factors also affect the severity of the
Plasmodium is a genus that belongs to unicellular parasites that have been identified
responsible for the incidence of malaria among host organisms. This unicellular parasite has a
life cycle that occurs inside the body of two hosts, namely, a vertebrate and a dipteran insect host
(Ariey et al., 2014). These species are found to contain several features that resemble other
eukaryotes. The genome is present in the nucleus. It doubles the genome in the insect host’s
midgut for a brief time (Bushell et al., 2017). The essay will discuss its life cycle and the various
host factors that influence its infection.
The Plasmodium life cycle involves several changes inside the insect and vertebrate
hosts. The parasites present in the salivary glands of infected mosquitoes, are called sporozoites
that are injected in the bosy of the host, along with the saliva when a mosquito bites the
vertebrate. They enter the bloodstream and are transported to the liver, following which they
undergo invasion and replication in the hepatocytes (Delves et al., 2012). Merozoites emerge
from the infected hepatocytes and form a ring-shaped structure that enlarges to form a
trophozoite. These are then found to mature to form schizonts that multiply and produce new
merozoites. This is followed by bursting of the infectred RBCs, thereby allowing the merozoites
to travel and infect new cells (Ke et al., 2015). Upon infection, sime merozoites are found to
differentiate into male and female gametocytes that are taken up by a mosquito, when it feeds on
the vertebrate host. They move to the vector’s midgut and develop into male and female
gametes, followed by fertilization and subsequent zygote formation. An ookinete is gradually
formed from the zygote that penetrates the midgut wall and develops an oocyst, which in turn
forms elongated sporozoites (Theisen et al., 2014).
Several differences exist in the physiology of the human host that directly influences the
pattern of transmission of the Plasmodium infection. These factors also affect the severity of the

2MICROBIOLOGY
disease. Due to the fact that the stages of the lifecycle are quite complex, human beings are either
immune or non-immune to malaria, the disease caused by Plasmodium. Innate or natural
immunity to malaria is regarded as the host’s inherent refractoriness that prevents infection
establishment or inhibitory response against parasite introduction (Boyle et al., 2015). This
immunity is naturally present in human body and independent of previous infections. Alterations
in hemoglobin structure or certain enzymes confer protection against severe manifestation of the
infection. People living in areas of high malaria prevalence commonly exhibit these traits. Duffy
glycoprotein is a receptor for chemicals, secreted during inflammation of blood cells. Presence of
Duffy negativity in RBCs also protects against Plasmodium infection (Wright & Rayner,
2014). Acute infection is also found to induce non-specific, immediate immune response that
limits progression of the infection. This is primarily mediated by extrathymic, primordial T cells,
and autoantibody producing-B1 cells. Several genetic conditions, such as, thalassemia, inherited
hemoglobin disorders and Glucose-6-phosphate dehydrogenase (G6PD) polymorphism plays an
essential role in protecting against this infection (S Balgir, 2012). Children and women with
weak immunity are more susceptible to malaria infection in endemic areas. Poor socio-economic
factors and lack of adequate prevention literacy also influence transmission (Cdc.gov, 2018).
Plasmodium infection is generally caused due to several parasite factors. The
female Anopheles mosquito picks up the parasite from bloodstream of infected people while
biting them and obtains that blood to nurture their eggs. Inside the mosquito host body, the
parasites are found to develop and reproduce. Upon biting a person for another time, these
parasites present in the salivary glands of the mosquitoes get injected inside the host and are
passed into the blood of the host. Therefore, salivary glands invasion is one of the major events
that result in vector-borne disease transmission. Microvasculature obstruction and parasite
disease. Due to the fact that the stages of the lifecycle are quite complex, human beings are either
immune or non-immune to malaria, the disease caused by Plasmodium. Innate or natural
immunity to malaria is regarded as the host’s inherent refractoriness that prevents infection
establishment or inhibitory response against parasite introduction (Boyle et al., 2015). This
immunity is naturally present in human body and independent of previous infections. Alterations
in hemoglobin structure or certain enzymes confer protection against severe manifestation of the
infection. People living in areas of high malaria prevalence commonly exhibit these traits. Duffy
glycoprotein is a receptor for chemicals, secreted during inflammation of blood cells. Presence of
Duffy negativity in RBCs also protects against Plasmodium infection (Wright & Rayner,
2014). Acute infection is also found to induce non-specific, immediate immune response that
limits progression of the infection. This is primarily mediated by extrathymic, primordial T cells,
and autoantibody producing-B1 cells. Several genetic conditions, such as, thalassemia, inherited
hemoglobin disorders and Glucose-6-phosphate dehydrogenase (G6PD) polymorphism plays an
essential role in protecting against this infection (S Balgir, 2012). Children and women with
weak immunity are more susceptible to malaria infection in endemic areas. Poor socio-economic
factors and lack of adequate prevention literacy also influence transmission (Cdc.gov, 2018).
Plasmodium infection is generally caused due to several parasite factors. The
female Anopheles mosquito picks up the parasite from bloodstream of infected people while
biting them and obtains that blood to nurture their eggs. Inside the mosquito host body, the
parasites are found to develop and reproduce. Upon biting a person for another time, these
parasites present in the salivary glands of the mosquitoes get injected inside the host and are
passed into the blood of the host. Therefore, salivary glands invasion is one of the major events
that result in vector-borne disease transmission. Microvasculature obstruction and parasite

3MICROBIOLOGY
biomass have been strongly correlated with the severity of Plasmodium infection, which often
results in death. The parasites do not have any specific predilection for the stages of circulating
RBCs and are found to invade them all, regardless of the stage. This contributes to high rates of
parasitemias (Barber et al., 2015). Parasite biomass of Plasmodium is found to increase on
failure to initiate appropriate treatment strategies, or due to the presence of weak immune system
in the host. This eventually makes the infection more severe and results in death of the person
(Bernabeu et al., 2016). Thus, elevated parasite biomass is regarded as a major independent risk
factor that contributes to Plasmodium associated mortality. An increase in parasite biomass leads
to erythrocyte loss and subsequent sequestration of the infected RBCs in microvascular beds,
commonly referred to as cerebral malaria (Cunnington, Riley & Walther, 2013). This
sequestration is another major parasite factor that influences the severity of Plasmodium
infection. It refers to adherence of infected erythrocytes that contain the parasite’s late
developmental stages such as, the trophozoites and schizonts, to the endothelium of the venules
and the capillaries. This sequestration results in malfunctioning of various organs, thereby
resulting in coma or brain death (Milner Jr et al., 2015).
Climatic factors, such as, temperature, rainfall, and relative humidity are directly
responsible for the infection transmission. A decrease in temperature results in an increase in the
number of days required by Plasmodium to complete its life cycle. Maximum temperature
needed for its development is 40°C. The life cycle gets limited at temperatures lower than 18°C
(Cottrell et al., 2012). On the other hand, higher temperatures increase number of blood meals
and eggs laid by the mosquitoes. An increase in altitude also decreases temperature, thereby
affecting transmission (Mordecai et al., 2013). Appropriate amount of water is needed for
breeding of the mosquitoes. Stagnant water collection supports vector breeding and increases
biomass have been strongly correlated with the severity of Plasmodium infection, which often
results in death. The parasites do not have any specific predilection for the stages of circulating
RBCs and are found to invade them all, regardless of the stage. This contributes to high rates of
parasitemias (Barber et al., 2015). Parasite biomass of Plasmodium is found to increase on
failure to initiate appropriate treatment strategies, or due to the presence of weak immune system
in the host. This eventually makes the infection more severe and results in death of the person
(Bernabeu et al., 2016). Thus, elevated parasite biomass is regarded as a major independent risk
factor that contributes to Plasmodium associated mortality. An increase in parasite biomass leads
to erythrocyte loss and subsequent sequestration of the infected RBCs in microvascular beds,
commonly referred to as cerebral malaria (Cunnington, Riley & Walther, 2013). This
sequestration is another major parasite factor that influences the severity of Plasmodium
infection. It refers to adherence of infected erythrocytes that contain the parasite’s late
developmental stages such as, the trophozoites and schizonts, to the endothelium of the venules
and the capillaries. This sequestration results in malfunctioning of various organs, thereby
resulting in coma or brain death (Milner Jr et al., 2015).
Climatic factors, such as, temperature, rainfall, and relative humidity are directly
responsible for the infection transmission. A decrease in temperature results in an increase in the
number of days required by Plasmodium to complete its life cycle. Maximum temperature
needed for its development is 40°C. The life cycle gets limited at temperatures lower than 18°C
(Cottrell et al., 2012). On the other hand, higher temperatures increase number of blood meals
and eggs laid by the mosquitoes. An increase in altitude also decreases temperature, thereby
affecting transmission (Mordecai et al., 2013). Appropriate amount of water is needed for
breeding of the mosquitoes. Stagnant water collection supports vector breeding and increases
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4MICROBIOLOGY
infection rates. In addition, mosquitoes have been found to survive better under high humidity
(Bomblies, 2012). Non-climatic factors that influence transmission rates include urbanization,
migration, and population movement. Incidence of the infection rates are lower in urban areas
due to lack of empty spaces that act as breeding grounds and improved access to healthcare and
prevention strategies (Qi et al., 2012). Furthermore, drug resistance to the parasite also prevents
its transmission.
Prevention strategies include determining the risk or likelihood of getting affected, staying in
well-screened areas, using mosquito repellents, protective clothing and bed netting (Cullen &
Arguin, 2014). Prophylactic use of antimalarial drugs, such as, chloroquine while travelling in
endemic areas also helps in preventing infection transmission (Ouédraogo et al., 2014).
To conclude, it can be stated that the protozoan parasite, Plasmodium is responsible for
causing a deadly, yet curable disease among vertebrates. This parasite is transmitted by the bite
of mosquitoes, and creates life-threatening conditions that can cause significant morbidity, if not
treated. People living in warmer regions are at an increased likelihood of suffering from this
infection. Although, there are two hosts needed for completion of the parasite’s life cycle, the
insect acts as the definitive host because it acts as the feasible location where sexual reproduction
of the parasite always occurs. Thus, it can be concluded that a range of host and parasite factors
are responsible for transmission of the disease.
infection rates. In addition, mosquitoes have been found to survive better under high humidity
(Bomblies, 2012). Non-climatic factors that influence transmission rates include urbanization,
migration, and population movement. Incidence of the infection rates are lower in urban areas
due to lack of empty spaces that act as breeding grounds and improved access to healthcare and
prevention strategies (Qi et al., 2012). Furthermore, drug resistance to the parasite also prevents
its transmission.
Prevention strategies include determining the risk or likelihood of getting affected, staying in
well-screened areas, using mosquito repellents, protective clothing and bed netting (Cullen &
Arguin, 2014). Prophylactic use of antimalarial drugs, such as, chloroquine while travelling in
endemic areas also helps in preventing infection transmission (Ouédraogo et al., 2014).
To conclude, it can be stated that the protozoan parasite, Plasmodium is responsible for
causing a deadly, yet curable disease among vertebrates. This parasite is transmitted by the bite
of mosquitoes, and creates life-threatening conditions that can cause significant morbidity, if not
treated. People living in warmer regions are at an increased likelihood of suffering from this
infection. Although, there are two hosts needed for completion of the parasite’s life cycle, the
insect acts as the definitive host because it acts as the feasible location where sexual reproduction
of the parasite always occurs. Thus, it can be concluded that a range of host and parasite factors
are responsible for transmission of the disease.

5MICROBIOLOGY
References
Ariey, F., Witkowski, B., Amaratunga, C., Beghain, J., Langlois, A. C., Khim, N., ... & Lim, P.
(2014). A molecular marker of artemisinin-resistant Plasmodium falciparum
malaria. Nature, 505(7481), 50.
Barber, B. E., William, T., Grigg, M. J., Parameswaran, U., Piera, K. A., Price, R. N., ... &
Anstey, N. M. (2015). Parasite biomass-related inflammation, endothelial activation,
microvascular dysfunction and disease severity in vivax malaria. PLoS pathogens, 11(1),
e1004558.
Bernabeu, M., Danziger, S. A., Avril, M., Vaz, M., Babar, P. H., Brazier, A. J., ... & Gomes, E.
(2016). Severe adult malaria is associated with specific PfEMP1 adhesion types and high
parasite biomass. Proceedings of the National Academy of Sciences, 113(23), E3270-
E3279.
Bomblies, A. (2012). Modeling the role of rainfall patterns in seasonal malaria
transmission. Climatic change, 112(3-4), 673-685.
Boyle, M. J., Reiling, L., Feng, G., Langer, C., Osier, F. H., Aspeling-Jones, H., ... & McCarthy,
J. S. (2015). Human antibodies fix complement to inhibit Plasmodium falciparum
invasion of erythrocytes and are associated with protection against
malaria. Immunity, 42(3), 580-590.
Bushell, E., Gomes, A. R., Sanderson, T., Anar, B., Girling, G., Herd, C., ... & Mather, M. W.
(2017). Functional profiling of a Plasmodium genome reveals an abundance of essential
genes. Cell, 170(2), 260-272.
References
Ariey, F., Witkowski, B., Amaratunga, C., Beghain, J., Langlois, A. C., Khim, N., ... & Lim, P.
(2014). A molecular marker of artemisinin-resistant Plasmodium falciparum
malaria. Nature, 505(7481), 50.
Barber, B. E., William, T., Grigg, M. J., Parameswaran, U., Piera, K. A., Price, R. N., ... &
Anstey, N. M. (2015). Parasite biomass-related inflammation, endothelial activation,
microvascular dysfunction and disease severity in vivax malaria. PLoS pathogens, 11(1),
e1004558.
Bernabeu, M., Danziger, S. A., Avril, M., Vaz, M., Babar, P. H., Brazier, A. J., ... & Gomes, E.
(2016). Severe adult malaria is associated with specific PfEMP1 adhesion types and high
parasite biomass. Proceedings of the National Academy of Sciences, 113(23), E3270-
E3279.
Bomblies, A. (2012). Modeling the role of rainfall patterns in seasonal malaria
transmission. Climatic change, 112(3-4), 673-685.
Boyle, M. J., Reiling, L., Feng, G., Langer, C., Osier, F. H., Aspeling-Jones, H., ... & McCarthy,
J. S. (2015). Human antibodies fix complement to inhibit Plasmodium falciparum
invasion of erythrocytes and are associated with protection against
malaria. Immunity, 42(3), 580-590.
Bushell, E., Gomes, A. R., Sanderson, T., Anar, B., Girling, G., Herd, C., ... & Mather, M. W.
(2017). Functional profiling of a Plasmodium genome reveals an abundance of essential
genes. Cell, 170(2), 260-272.

6MICROBIOLOGY
Cdc.gov. (2018). CDC - Malaria - About Malaria - Biology - Human Factors and Malaria.
Retrieved 3 March 2018, from
https://www.cdc.gov/malaria/about/biology/human_factors.html
Cottrell, G., Kouwaye, B., Pierrat, C., Le Port, A., Bouraïma, A., Fonton, N., ... & Garcia, A.
(2012). Modeling the influence of local environmental factors on malaria transmission in
Benin and its implications for cohort study. PLoS One, 7(1), e28812.
Cullen, K. A., & Arguin, P. M. (2014). Malaria surveillance—United States, 2012. Morbidity
and Mortality Weekly Report: Surveillance Summaries, 63(12), 1-22.
Cunnington, A. J., Riley, E. M., & Walther, M. (2013). Stuck in a rut? Reconsidering the role of
parasite sequestration in severe malaria syndromes. Trends in parasitology, 29(12), 585-
592.
Delves, M., Plouffe, D., Scheurer, C., Meister, S., Wittlin, S., Winzeler, E. A., ... & Leroy, D.
(2012). The activities of current antimalarial drugs on the life cycle stages of
Plasmodium: a comparative study with human and rodent parasites. PLoS medicine, 9(2),
e1001169.
Ke, H., Lewis, I. A., Morrisey, J. M., McLean, K. J., Ganesan, S. M., Painter, H. J., ... & Vaidya,
A. B. (2015). Genetic investigation of tricarboxylic acid metabolism during the
Plasmodium falciparum life cycle. Cell reports, 11(1), 164-174.
Milner Jr, D. A., Lee, J. J., Frantzreb, C., Whitten, R. O., Kamiza, S., Carr, R. A., ... &
Dzamalala, C. (2015). Quantitative assessment of multiorgan sequestration of parasites in
fatal pediatric cerebral malaria. The Journal of infectious diseases, 212(8), 1317-1321.
Cdc.gov. (2018). CDC - Malaria - About Malaria - Biology - Human Factors and Malaria.
Retrieved 3 March 2018, from
https://www.cdc.gov/malaria/about/biology/human_factors.html
Cottrell, G., Kouwaye, B., Pierrat, C., Le Port, A., Bouraïma, A., Fonton, N., ... & Garcia, A.
(2012). Modeling the influence of local environmental factors on malaria transmission in
Benin and its implications for cohort study. PLoS One, 7(1), e28812.
Cullen, K. A., & Arguin, P. M. (2014). Malaria surveillance—United States, 2012. Morbidity
and Mortality Weekly Report: Surveillance Summaries, 63(12), 1-22.
Cunnington, A. J., Riley, E. M., & Walther, M. (2013). Stuck in a rut? Reconsidering the role of
parasite sequestration in severe malaria syndromes. Trends in parasitology, 29(12), 585-
592.
Delves, M., Plouffe, D., Scheurer, C., Meister, S., Wittlin, S., Winzeler, E. A., ... & Leroy, D.
(2012). The activities of current antimalarial drugs on the life cycle stages of
Plasmodium: a comparative study with human and rodent parasites. PLoS medicine, 9(2),
e1001169.
Ke, H., Lewis, I. A., Morrisey, J. M., McLean, K. J., Ganesan, S. M., Painter, H. J., ... & Vaidya,
A. B. (2015). Genetic investigation of tricarboxylic acid metabolism during the
Plasmodium falciparum life cycle. Cell reports, 11(1), 164-174.
Milner Jr, D. A., Lee, J. J., Frantzreb, C., Whitten, R. O., Kamiza, S., Carr, R. A., ... &
Dzamalala, C. (2015). Quantitative assessment of multiorgan sequestration of parasites in
fatal pediatric cerebral malaria. The Journal of infectious diseases, 212(8), 1317-1321.
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7MICROBIOLOGY
Mordecai, E. A., Paaijmans, K. P., Johnson, L. R., Balzer, C., Ben‐Horin, T., Moor, E., ... &
Lafferty, K. D. (2013). Optimal temperature for malaria transmission is dramatically
lower than previously predicted. Ecology letters, 16(1), 22-30.
Ouédraogo, A. L., Bastiaens, G. J., Tiono, A. B., Guelbéogo, W. M., Kobylinski, K. C.,
Ouédraogo, A., ... & Lanke, K. H. (2014). Efficacy and safety of the mosquitocidal drug
ivermectin to prevent malaria transmission after treatment: a double-blind, randomized,
clinical trial. Clinical infectious diseases, 60(3), 357-365.
Qi, Q., Guerra, C. A., Moyes, C. L., Elyazar, I. A. F., Gething, P. W., Hay, S. I., & Tatem, A. J.
(2012). The effects of urbanization on global Plasmodium vivax malaria
transmission. Malaria journal, 11(1), 403.
S Balgir, R. (2012). Community expansion and gene geography of sickle cell trait and G6PD
deficiency, and natural selection against malaria: experience from tribal land of
India. Cardiovascular & Hematological Agents in Medicinal Chemistry (Formerly
Current Medicinal Chemistry-Cardiovascular & Hematological Agents), 10(1), 3-13.
Theisen, M., Roeffen, W., Singh, S. K., Andersen, G., Amoah, L., van de Vegte-Bolmer, M., ...
& Adu, B. (2014). A multi-stage malaria vaccine candidate targeting both transmission
and asexual parasite life-cycle stages. Vaccine, 32(22), 2623-2630.
Wright, G. J., & Rayner, J. C. (2014). Plasmodium falciparum erythrocyte invasion: combining
function with immune evasion. PLoS pathogens, 10(3), e1003943.
Mordecai, E. A., Paaijmans, K. P., Johnson, L. R., Balzer, C., Ben‐Horin, T., Moor, E., ... &
Lafferty, K. D. (2013). Optimal temperature for malaria transmission is dramatically
lower than previously predicted. Ecology letters, 16(1), 22-30.
Ouédraogo, A. L., Bastiaens, G. J., Tiono, A. B., Guelbéogo, W. M., Kobylinski, K. C.,
Ouédraogo, A., ... & Lanke, K. H. (2014). Efficacy and safety of the mosquitocidal drug
ivermectin to prevent malaria transmission after treatment: a double-blind, randomized,
clinical trial. Clinical infectious diseases, 60(3), 357-365.
Qi, Q., Guerra, C. A., Moyes, C. L., Elyazar, I. A. F., Gething, P. W., Hay, S. I., & Tatem, A. J.
(2012). The effects of urbanization on global Plasmodium vivax malaria
transmission. Malaria journal, 11(1), 403.
S Balgir, R. (2012). Community expansion and gene geography of sickle cell trait and G6PD
deficiency, and natural selection against malaria: experience from tribal land of
India. Cardiovascular & Hematological Agents in Medicinal Chemistry (Formerly
Current Medicinal Chemistry-Cardiovascular & Hematological Agents), 10(1), 3-13.
Theisen, M., Roeffen, W., Singh, S. K., Andersen, G., Amoah, L., van de Vegte-Bolmer, M., ...
& Adu, B. (2014). A multi-stage malaria vaccine candidate targeting both transmission
and asexual parasite life-cycle stages. Vaccine, 32(22), 2623-2630.
Wright, G. J., & Rayner, J. C. (2014). Plasmodium falciparum erythrocyte invasion: combining
function with immune evasion. PLoS pathogens, 10(3), e1003943.
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