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By
Dr. Priti D.Diwan
Assistant Professor
Department of Zoology
J.D.Patil Sangludkar Mahavidyalay Daryapur.
Plasmodium vivax
( MALARIALPARASITE)
 The most interesting sporozoan genus is plasmodium
 Because of their malaria causing abilities , these species commonly
referred as malarial parasites
 All resides in the RBC
 Mosquitoes are the vectors
The Malarial parasite
 4 species are known to cause different types of malaria
 P.vivax, P.ovale, P.malariae and P.falciparium
 Geographically distributed in tropical and temperate countries
 P
. vivax is most commonly distributed and prevails in the
temperate regions of the world.
Life Cycle of P. vivax
• P. Vivax is the most common of the human infecting malaria fever
parasites.
• Causes benign tertian or vivax malaria, characterized by a 48 h
cycle b/w first fever and subsequent chills and fever.
• Hosts: diagenetic
a. Man:
asexual cycle in two phases
First in liver – liver schizogony
Second in RBC – erythrocytic schizogony and forms gametes
b. Mosquito:
Sexual cycle is completed in female anopheles
It involves gametogony and sporogony
Asexual cycle of P.vivax in man
[1]. Infection
• Anopheles bite resulting in the inoculation of thousands of sporozoites
along with saliva into the persons body (victim)
[2]. Sporozoites
• Infective form of parasite
• Small, spindle shaped measuring about 11-12 µ in length and 0.5-1µ
in width
[3]. Liver Schizogony
• After 30m of infection, sporozoites invades hepatic tissues andmultiply
by schizogony in two phases (pre and exo-erythrocytic)
a). Pre-erythrocytic phase
• Sporozoite becomes cryptozoite in hepatic cells and becomes spherical
and non-pigmented schizont.
• Undergo multiple fission (schizogony) and forms numerosuninucleate
cryptomerozoites
• At the end of phase, hepatic cell bursts and cryptomerozoites are
liberated.
b). Exo-erythrocytic phase
• Cryptomerozoites enter new liver cells and becomesmetacryptozoites
• Undergo similar schizogony and produces metacryptomerozoites.
[4]. Erythrocytic schizogony
• Micro metacryptomerozoites invades RBC and starts erythrocytic
schizogony and includes following stages:
a). Tropozoite stage
• Inside RBC, micro metacryptomerozoites becomes rounded and
modified into trophozoite.
b). Signet ring stage
• Trophozoite grows, develops vacuole and clinically referred as
signet ring stage.
c). Amoeboid stage
• Meanwhile signet stage develops into active amoeboid trophozoite
• At this stage, samle red eosinophilic granules appear in the
cytoplasm –schuffners granules
d). Schizont
• Amoeboid trophozoite after feeding becomes rounded, grows in
size and becomes schizont
• It undergoes schizogony and forms merozoites
• One erythrocytic cycle takes 48h
[5]. Post-erythrocytic schizogony
• Sometimes merozoites reach the liver and undergoes schizogonic
development in the liver cells –post-erythrocytic schizogony.
[6]. Formation of gametes
• Merozoites increases in size to become rounded gametocytes.
• Male – microgametocyte and female- magagametocyte
• Gametocytes donot devide but remain as intracellularparasite
until they either die or ingested by vector
Sexual cycle of P.vivax in man
[1]. Ingestion by mosquito
• Female anopheles gets the infection by sucking the blood of infected
person
• RBC are digested and gametocytes are liberated and lodged into the
cavity of the gut.
[2]. Gametogony
• Development of gametes (Haploids) from gametocyte – gametogony/
gametogenesis.
• Gamtes are of two types
a). Microgametes
• Male or microgamete undergoes exflagellation in the midgut of mosquito
• Each nucleus divides by mitosis and produce 6-8 haploid daughterand
assemble at periphery
• Cytoplasm outgrows into long thin flagella like projection and later these
projections break away as mature male gamete
b). Megagametes
• Female megagametocyte undergo some reorganisationa nd becomes a
female gamete, which is ready for fertilization.
[3]. Fertilization
• Megagamete gives out a cytoplasmic projection – fertilization cone.
• Microgamete attached to this cone and transfer its nucleusto
megagamete
• Fertilization or syngamy takes place
• Diploid zygote forms
[4]. Ookinete
• After sometime zygote becomes active and shows gliding moment andis
k/as ookinete
• It measures about 15-22 micron in length and 3 micron in width.
•It attaches itself to peritrophic membrane of gut.
[5]. Encystment
• Ookinete penetrates through walls of midgut, becomes sphericaland
begins enyst.
• The encysted zygote – oocyst / sporont
[6]. Sporogony
• Oocyst enters into a phase of asexual multiplication-sporogony
• Firstly divides by meosis and then by mitosis and formsenormous
haploid nuclei surrounded by cytoplasmic masses
• The daughter nuclei arrange themselves along the margin of
cytoplasmic masses and later forms slender finger likeprocesses
having single nuclei in each
• In this way about 10,000 minute slender and sickle bodiesare
formed-sporozoites .
• When sporozoite matures oocyst ruptures and liberated into
haeomocoel later penetrates into salivaryglands
• Whole sexual cycle completes into 0-12 days
• Now mosquito becomes infective
Pathogenesis of malarial parasite
Symptoms of malaria first appear several
days after the infection of the parasite.
This time – incubation period
Each attack of fever shows threestages:
1. Cold Stage
• At the onset of malaria patent suffers
from severe shaking chill.
• Cold stage lasts for 20 min
2. Hot stage
• As the chill subsides, the body temp rises
as high as 106°F. and lasts for 1-4 h.
3. Sweating stage
• As the temp lowers down, patent sweats
profusely.
• Fever comes down and temperature
becomes normal
 Malaria fever occurs when schizont in RBC bursts and set free
their merozoites and malarial pigment haemozoin in the plasma.
 Anemia is inevitable due to:
• Destruction of RBC
• Infected RBC become more fragile and rupture easily
• Parasite produce haemolysin- brings haemolysis
• In chronic case- spleen becomes enlarged
Control of Malaria
Control Measures falls into three categories:
1. Elimination or destruction of vector
2. Prophylaxis (prevention of infection)
3. Treatment of infected patents
[A]. Destruction of anopheles
Most effective and surest way of controlling malaria and can be
done through
• Destruction of adult mosquitoes: method used are killing of
hands, traps, fumigation, spraying and sterilization.
• Elimination of breeding places: swampy, marshy and water
logging areas are cleared out, bushes and shrubs are cleared
off etc.
• Destruction of larvae and pupae of mosquito through proper
drainage (Flowing water), oil screens, chemical larvicidesand
biological methods.
[B]. Prevention of infection
• Through the use of insect repellent, nets, gloves and by
screening bedroom windows.
[C]. Treatment
• Chlorquine and quinine: anti-erythrocytic stage drugs.
• Primaquine and pyrimethamine: anti-exoerythrocytic stage
drugs.
p vivax ppt.

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p vivax ppt.

  • 1. By Dr. Priti D.Diwan Assistant Professor Department of Zoology J.D.Patil Sangludkar Mahavidyalay Daryapur. Plasmodium vivax ( MALARIALPARASITE)
  • 2.  The most interesting sporozoan genus is plasmodium  Because of their malaria causing abilities , these species commonly referred as malarial parasites  All resides in the RBC  Mosquitoes are the vectors The Malarial parasite
  • 3.  4 species are known to cause different types of malaria  P.vivax, P.ovale, P.malariae and P.falciparium  Geographically distributed in tropical and temperate countries  P . vivax is most commonly distributed and prevails in the temperate regions of the world.
  • 4. Life Cycle of P. vivax • P. Vivax is the most common of the human infecting malaria fever parasites. • Causes benign tertian or vivax malaria, characterized by a 48 h cycle b/w first fever and subsequent chills and fever. • Hosts: diagenetic a. Man: asexual cycle in two phases First in liver – liver schizogony Second in RBC – erythrocytic schizogony and forms gametes b. Mosquito: Sexual cycle is completed in female anopheles It involves gametogony and sporogony
  • 5. Asexual cycle of P.vivax in man [1]. Infection • Anopheles bite resulting in the inoculation of thousands of sporozoites along with saliva into the persons body (victim) [2]. Sporozoites • Infective form of parasite • Small, spindle shaped measuring about 11-12 µ in length and 0.5-1µ in width
  • 6. [3]. Liver Schizogony • After 30m of infection, sporozoites invades hepatic tissues andmultiply by schizogony in two phases (pre and exo-erythrocytic) a). Pre-erythrocytic phase • Sporozoite becomes cryptozoite in hepatic cells and becomes spherical and non-pigmented schizont. • Undergo multiple fission (schizogony) and forms numerosuninucleate cryptomerozoites • At the end of phase, hepatic cell bursts and cryptomerozoites are liberated. b). Exo-erythrocytic phase • Cryptomerozoites enter new liver cells and becomesmetacryptozoites • Undergo similar schizogony and produces metacryptomerozoites.
  • 7. [4]. Erythrocytic schizogony • Micro metacryptomerozoites invades RBC and starts erythrocytic schizogony and includes following stages: a). Tropozoite stage • Inside RBC, micro metacryptomerozoites becomes rounded and modified into trophozoite. b). Signet ring stage • Trophozoite grows, develops vacuole and clinically referred as signet ring stage. c). Amoeboid stage • Meanwhile signet stage develops into active amoeboid trophozoite • At this stage, samle red eosinophilic granules appear in the cytoplasm –schuffners granules d). Schizont • Amoeboid trophozoite after feeding becomes rounded, grows in size and becomes schizont • It undergoes schizogony and forms merozoites • One erythrocytic cycle takes 48h
  • 8. [5]. Post-erythrocytic schizogony • Sometimes merozoites reach the liver and undergoes schizogonic development in the liver cells –post-erythrocytic schizogony. [6]. Formation of gametes • Merozoites increases in size to become rounded gametocytes. • Male – microgametocyte and female- magagametocyte • Gametocytes donot devide but remain as intracellularparasite until they either die or ingested by vector
  • 9.
  • 10. Sexual cycle of P.vivax in man [1]. Ingestion by mosquito • Female anopheles gets the infection by sucking the blood of infected person • RBC are digested and gametocytes are liberated and lodged into the cavity of the gut. [2]. Gametogony • Development of gametes (Haploids) from gametocyte – gametogony/ gametogenesis. • Gamtes are of two types a). Microgametes • Male or microgamete undergoes exflagellation in the midgut of mosquito • Each nucleus divides by mitosis and produce 6-8 haploid daughterand assemble at periphery • Cytoplasm outgrows into long thin flagella like projection and later these projections break away as mature male gamete b). Megagametes • Female megagametocyte undergo some reorganisationa nd becomes a female gamete, which is ready for fertilization.
  • 11. [3]. Fertilization • Megagamete gives out a cytoplasmic projection – fertilization cone. • Microgamete attached to this cone and transfer its nucleusto megagamete • Fertilization or syngamy takes place • Diploid zygote forms [4]. Ookinete • After sometime zygote becomes active and shows gliding moment andis k/as ookinete • It measures about 15-22 micron in length and 3 micron in width. •It attaches itself to peritrophic membrane of gut. [5]. Encystment • Ookinete penetrates through walls of midgut, becomes sphericaland begins enyst. • The encysted zygote – oocyst / sporont
  • 12. [6]. Sporogony • Oocyst enters into a phase of asexual multiplication-sporogony • Firstly divides by meosis and then by mitosis and formsenormous haploid nuclei surrounded by cytoplasmic masses • The daughter nuclei arrange themselves along the margin of cytoplasmic masses and later forms slender finger likeprocesses having single nuclei in each • In this way about 10,000 minute slender and sickle bodiesare formed-sporozoites . • When sporozoite matures oocyst ruptures and liberated into haeomocoel later penetrates into salivaryglands • Whole sexual cycle completes into 0-12 days • Now mosquito becomes infective
  • 13. Pathogenesis of malarial parasite Symptoms of malaria first appear several days after the infection of the parasite. This time – incubation period Each attack of fever shows threestages: 1. Cold Stage • At the onset of malaria patent suffers from severe shaking chill. • Cold stage lasts for 20 min 2. Hot stage • As the chill subsides, the body temp rises as high as 106°F. and lasts for 1-4 h. 3. Sweating stage • As the temp lowers down, patent sweats profusely. • Fever comes down and temperature becomes normal
  • 14.  Malaria fever occurs when schizont in RBC bursts and set free their merozoites and malarial pigment haemozoin in the plasma.  Anemia is inevitable due to: • Destruction of RBC • Infected RBC become more fragile and rupture easily • Parasite produce haemolysin- brings haemolysis • In chronic case- spleen becomes enlarged Control of Malaria Control Measures falls into three categories: 1. Elimination or destruction of vector 2. Prophylaxis (prevention of infection) 3. Treatment of infected patents
  • 15. [A]. Destruction of anopheles Most effective and surest way of controlling malaria and can be done through • Destruction of adult mosquitoes: method used are killing of hands, traps, fumigation, spraying and sterilization. • Elimination of breeding places: swampy, marshy and water logging areas are cleared out, bushes and shrubs are cleared off etc. • Destruction of larvae and pupae of mosquito through proper drainage (Flowing water), oil screens, chemical larvicidesand biological methods. [B]. Prevention of infection • Through the use of insect repellent, nets, gloves and by screening bedroom windows. [C]. Treatment • Chlorquine and quinine: anti-erythrocytic stage drugs. • Primaquine and pyrimethamine: anti-exoerythrocytic stage drugs.