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PLASMODIUM AND MALARIA Flashcards

1
Q

HOW MANY GENERA OF THE APICOMPLEXA INFECT HUMANS?

A

6 (ONE OF THEM PLASMODIUM CAUSING MALARIA, 3 CAUSE DIARRHEA, 1 HAS NEUROLOGICAL PATHOLOGY, AND 1 CAUSES RARE ZOONOTIC DISEASE)

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2
Q

WHAT ARE THE APICOMPLEXAN CELL ORGANELLES AND STRUCTURES?

A

APICOPLAST; METABOLIC ORGANELLE PRESENT IN MOST, BUT NOT ALL APICOMPLEXANS (DERIVED FROM CYANOBACTERIA ENDOSYMBIONT)

INNER MEMBRANE COMPLEX (IMC); A SERIES OF MEMBRANE SACKS UNDERLYING THE PLASMA MEMBRANE

PROTEIN COMPLEXES FOR GLIDIN MOTILITY AND INVASION (GLIDEOSOME, MOVING JUNCTION COMPLEX ETC ETC)

CYTOSKELETON:

  • MICROTUBULE CORSET (EXTENDS UNDERNEATHS THE APICAL THIRD OF THE PARASITE
  • ALVEOLIN NETWORK (INTERMEDIATE FILAMENT-LIKE PROTEINS)
  • ACTIN (REQUIRED FOR GLIDING MOTILITY)

SECRETORY ORGANELLES:

  • MICRONEMES (MOTILITY)
  • RHOPTRIES (INVASION)
  • DENSE GRANULES (INVASION)

+MITOCHONDRIA, NUCLEUS, PLASMA MEMBRANE (ALL THE OTHER FEATURES ABOVE ARE SPECIFIC TO APICOMPLEXA)

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3
Q

WHAT ARE THE SECRETORY ORGANELLES OF APICOMPLEXA CELLS SPECIFIC TO APICOMPLEXA? WHAT ARE THEIR ROLES?

A

SECRETORY ORGANELLES:

  • MICRONEMES (MOTILITY)
  • RHOPTRIES (INVASION)
  • DENSE GRANULES (INVASION)
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4
Q

THE METABOLIC ORGANELLE APICOPLAST, PRESENT IN MOST MEMBERS OF APICOMPLEXA, WAS DERIVED FROM?

A

DERIVED FROM CYANOBACTERIA ENDOSYMBIONT

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5
Q

HOW MANY PLASMODIUM SPECIES CAUSE HUMAN MALARIA?

A

4

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6
Q

WHICH PLASMODIUM SPECIES CAUSE HUMAN MALARIA?

A

PLASMODIUM:

  • FALCIPARUM
  • VIVAX
  • OVALE
  • MALARIAE
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7
Q

WHICH PLASMODIUM CAUSES MOST DEATHS AND WORLWIDE CASES OF MALARIA?

A

P. FALCIPARUM

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8
Q

WHICH PLASMODIUM IS THE MOST COMMON CAUSE OF MALARIA IN AFRICA?

A

P. FALCIPARUM (99.7% CASES)

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9
Q

% OF THE WORLDWIDE MALARIA CASES CAUSED BY PLASMODIUM FALCIPARUM?

A

97%

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10
Q

AFTER PLASMODIUM FALCIPARUM, WHAT IS THE MOST COMMON CAUSE OF MALARIA?

A

P. VIVAX (2%)

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11
Q

WHAT IS THE MOST COMMON CAUSE OF MALARIA IN AMERICAS?

A

PLASMODIUM VIVAX, 75%

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12
Q

WHICH PLASMODIUMS THAT CAN INFECT HUMAS ARE USUALLY UNCOMPLICATED (I.E. CAUSE MALARIA VERY RARELY)?

A

P. VIVAX, OVALE AND MALARIAE

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13
Q

WHER DO MOST MALARIA CASES OCCUR? %?

A

IN AFRICA, 94%

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14
Q

WHICH COUNTRIES ACCOUNT FOR MORE THAN 1/2 OF ALL MALARIA CASES WORLDWIDE?

A
  • NIGERIA (25%)
  • THE DEMOCRATIC REPUBLIC OF THE CONGO (12%)
  • UGANDA (5%)
  • THE IVORY HOST, MOZAMBIQUE AND NIGER (4% EACH)
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15
Q

% OF WORLD’S POPULATION LIVING IN AREAS WHERE MALARIA IS TRANSMITTED? (E.G. PARTS OF AFRICA, ASIA, AMERICAS…)

A

41%

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16
Q

2018: MALARIA DEATHS, INFECTIONS, WHO IS THE MOST AFFECTED?

A
  • 228 MILLION CASES
  • 405 000 DEATHS
  • 76% OF DEATHS CHILDREN UNDER 5
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17
Q

DEATHS FROM MALARIA MOST COMMONLY AFFECT WHICH AGEGROUP?

A

CHILDREN YOUNGER THAN 5

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18
Q

WHICH DISEASE IS CHARACTERISED BY ‘EVERY OTHER DAY FEVER’? WHAT IS THIS FEVER PTTERN LINKE TO?

A
  • MALARIA
  • LINKED TO TIMING OF PARASITE DIVISION AND RELEASE (LINKED INTO SYNCHRONISED RELEASE AND INVASION OF PARASITES FROM RED BLOOD CELLS)
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19
Q

WHAT ARE THE 2 TYPES OF MALARIA?

A

UNCOMPLICATED:

  • FEVER (CYCLES OF COLD, HOT AND SWEATING)
  • PARASITAEMIA (OFTEN VERY HIGH)
  • ANAEMIA

COMPLICATED (SEVERE):

  • SEVERE ANAEMIA
  • CEREBRAL MALARIA (COMA AND DEATH)
  • CAUSED BY P. FALCIPARUM
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20
Q

WHICH DISEASE AND PARASITE IS KNOWN TO MAKE ERYTHROCYTES ‘KNOB’?

A

MALARIA; ONLY PLASMODIUM FALCIPARUM!!!!!!!!!!

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21
Q

WHAT HAPPENS TO ERYHTROCYTES INFECTED BY PLASMODIUM FALCIPARUM?

A
  • UNDERGO CHANGES IN THEIR CELL SURFACE
  • CHANGE SHAPE A DEVELOP ‘KNOBS’ (EASILY VISIBLE BY ELECTRON MICROSCOPY)
  • THE KNOBS CONTAIN THE PARASITE PROTEIN pfEMP1 (PLASMODIUM FALCIPARUM ERYTHROCYTE PROTEIN 1)
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22
Q

IMPACT OF KNOBS ON ERYTHROCYTES CAUSED BY PLASMODIUM FALCIPORUM (MALARIA)?

A
  • PFemp1 (PROTEIN FROM THE PLASMODIUM) IN THE INFECTED KNOBS IS ‘STICKY’ —> IT CAN BIND TO AT LEAST 7 DIFFERENT RECEPTORS ON THE ENDOTHELIUM
  • THE KNOBS STICK TO: NON-INFECTED ERYTHROCYTES, FORMING ROSETTES & BLOOD VESSEL ENDOTHELIAL CELLS
  • INFECTED ERYTHROCYTES ARE LESS FLEXIBLE SO IT’S DIFFICULT FOR THEM TO PASS THROUGH THE MICROVASCULATURE (CAPILLARIES ETC)
  • EVEN NON INFECTED ERYTHROCYTES BECOME MORE RIGID THROUGH ABSORBING PLASMODIUM PROTEINS TO THEIR SURFACE —> CALLED SEQUESTRATION AND CAUSES ‘VASCULAR OCCLUSION’, BLOCKING BLOOD FLOW
  • SEQUESTRATION ENABLES THE PARASITE TO AVOID SPLEEN-DEPENDANT KILLING MECHANISMS
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23
Q

WHAT ARE ROSETTES?

A
  • FORM DUE TO PLASMODIUM FALCIPORUM CAUSED MALARIA
  • INFECTED ERYTHROCYTES DEVELOP ‘KNOBS’ AND HAVE PLASMODIUM PROTEIN (pfEMP1) ON THEIR SURFACE, WHICH MAKES THEM STICKY
  • KNOBS STICK TO NON-INFECTED ERYTHROCYTES AND FORM THESE ROSETTES
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24
Q

WHAT IS SEQUESTRATION?

A

the adherence of infected erythrocytes containing late developmental stages of the parasite (trophozoites and schizonts) to the endothelium of capillaries and venules, is characteristic of Plasmodium falciparum infections

  • CAUSES VASCULAR OCCLUSION, BLOCKING BLOOD FLOW
  • ENABLES THE PARASITE TO AVOID SPLEEN-DEPENDENT KILLING MECHANISMS
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25
Q

WHAT IS CEREBRAL MALARIA AND HOW IS IT CAUSED?

A
  • THE MOST SEVERE KIND OF MALARIA, OFTEN RESULTS IN DEATH

- CAUSED BY SEQESTRATION

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26
Q

WHAT IS CEREBRAL MALARIA AND HOW IS IT CAUSED?

A
  • THE MOST SEVERE KIND OF MALARIA, OFTEN RESULTS IN DEATH
  • CAUSED BY MASSIVE SEQUESTRATION (ADHERENCE OF PLASMODIUM FALCIPARUM INFECTED RED BLOOD CELLS TO BLOOD VESSELS, ULTIMATELY BLOCKING BLOOD FLOW) IN THE BRAIN
  • BLOCKED CAPILLAIRES BECOME SWOLLEN AND CONGESTED, LEADING TO HEMORRHAGE, COMA AND DEATH
  • IN THE BRAIN, DISCOLORATIONS (RED, PURPLE SPOTS) INDICATE THAT THE ABOVE PROCESS HAS TAKEN PLACE
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27
Q

PLASMODIU PARASITES ARE DIGENETIC, THEY NEED:

A

VECTOR: ANOPHELES SPP (MOSQUITO)
HOST: HUMAN

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28
Q

PLASMODIUM LIFECYCLE:

A

IN THE VECTOR (STEPS/FORMS):

  • GAMETES (FERTILISED)
  • ZYGOTES
  • OOKINETES
  • OOCYSTS
  • SPOROZOITES (DEVELOPMENT INTO SPOROZITES OCCURS IN THE MOSQUITO SALIVARY GLANDS)

—> SPOROZOITES ARE INFECTIVE, AND INJECTED INTO A HUMN HOST (‘SPORE’=BODY)

IN THE HOST (HUMANS):

  • TARGET HEPATOCYTES IN THE LIVER AND DEVELOP INTO MEROZOITES
  • COLONISE THE RED BLOOD CELLS
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29
Q

HOW TO MOSQUITOES (MALARIA TRANSMISSION) FEED?

A
  • DIRECTLY FROM BLOOD VESSELS
  • DURING FEEDING CONTINOUSLY RELEASE SALIVA WHICH CONTAINS ANTICLOTTING CHEMICALS ND MANY OTHER BIOACTIVE COMPOUNDS
  • IN MALARIA INFECTED MOSQUITOES, SALIVA CONTAINS PLASMODIUM PARASITES
30
Q

AFTER A MOSQUITO INFECTED WITH MALARIA INJECTS SPOROZOITES (INFECTIVE FORM OF THE PLASMODIUM) INTO THE SKIN, WHAT ARE THE POSSIBLE THINGS THAT COULD HAPPEN TO THEM?

A
  • CCA 50% REMAIN IN THE SKIN AND ARE KILLED BY IMMUNE CELLS (E.G. DENDRITIC CELLS)
  • CCA 15% ENTER LYMPH VESSELS TO END UP IN THE DRAINING LYMPH NODE WHERE THEY STIMULATE STRONG IMMUNE RESPONSE BEFORE BEING KILLED
  • CCA 35% ENTER BLOOD VESSELS TO BE PASSIVELY TRANSPORTED TO THE LIVER AND CONTINUE THEIR DEVELOPMENT
31
Q

% OF SPOROZOITES (INFECTIVE FORM OF PLASMODIUM CAUSING MALARIA) INJECTED INTO HOST SKIN THAT ACTUALLY SURVIVE, DEVELOP AND CAN CAUSE THE ILLNESS?

A

CCA 35%

32
Q

DO MALARIAL SPOROZOITES (INFECTIVE FORM OF THE PLASMODIUM WHICH IS INJECTED INTO THE SKIN) HAVE FLAGELLA?

A

NO

33
Q

ONCE MALARIAL SPOROZOITES ENTER THE BLOOD FLOW, HOW LONG DOES IT TAKE THEM TO REACH THE LIVER VIA PASSIVE BLOOD FLOW?

A

20 MINS

ABOUT 1 HOUR AFTER BEING INJECTED, THEY REACH THE LIVER

34
Q

1ST CELL TYPE THAT THE PLASMODIUM COLONISES?

A

HEPATOCYTES

35
Q

WHICH CELL TYPE DO SPOROZOITES USE TO CROSS INTO THE LIVER?

A

KUPFFER CELLS (LIVER MACROPHAGES)

36
Q

DESCRIBE PLASMODIUM LIVER INVASION?

A
  • SPOROZOITES REACH THE LIVER WITHIN 1 HOUR POST INFECTION, FIRS ATTACH TO KUPFFER CELL AND THEN CROOS INTO THE LIVER AND TRANSMIGRATE THROUGH SEVERAL HEPATOCYTES WITHOUT RUPTURING THEM
  • AFTER THAT, THE SPOROZOITE SWTICHES TO ‘INVASION MODE’ AND STARTS REPLICATING INSID A PARASITOPHOROUS VACUOLE (PV)
  • 1) IT DEVELOPS A MULTINUCLEATED ‘SCHIZONT’
  • 2) THE SCHIZONT MATURES AND FORMS THOUSANDS OF MEROZOITES BY MEMBRANE INVAGINATION
  • MEROZOITES RUPTURE PV MEMBRANE AND ENTER HOST CYTOPLASM
  • AS THE HOST CELL DIES, NUMEROUS MEROZOITES ARE ENCAPSULATED INSIDE VESICLES CALLED MEROSOMES THAT REACH THE BLOOD VESSELS
  • MEROSOMES FULL OF MEROZOITES ARE THEN CARRIED AWAY BY THE BLOODSTREAM TO REACH THE LUNGS
  • MEROZOITES ARE RELEASED IN THE LUNGS TO INFECT ERYTHROCYTES
  • HAPPENS CCA 7 DAYS AFTER INFECTION AND INCREASES THE NUMBER OF PARASITES BY 20-30,000 FOLD
37
Q

1 SPOROZOITE CAN TURN INTO UP TO HOW MANY MEROZOITES (MALARIA, PLASMODIUM)?

A

CCA 30 000

38
Q

HOW MANY DAYS AFTER INITIAL INFECTION ARE PLASMODIUMS ABLE TO REACH THE LUNGS AND INFECT RED BLOOD CELLS?

A

CCA 7

39
Q

NAME OF THE VESICLES THAT CARRY MEROZOITES (FORM OF PLASMODIUM CAUSING MALARIA) TO THE LUNGS TO SUBSEQUENTLY BE ABLE TO INFECTS RBCs?

A

MEROSOMES

40
Q

WHAT IS A SCHIZONT?

A

A MULTINUCLEATED PARASITE STRUCTURE

41
Q

WHICH STRUCTURE IS FORMED BY THE PLASMODIUM BETWEEN SPOROZOITES AND MEROZOITES?

A

SCHIZONT

42
Q

HOW DOES A SCHIZONT FORM THOUSANDS OF MEROZOITES?

A

IT MATURES AND FORMS THEM BY MEMBRANE INVAGINATION

43
Q

WHICH FORM DOES THEPLASMODIUM ENTER THE LIVER IN AND IN WHICH FORM DOES IT LEAVE?

A

IN: SPOROZOITES
OUT: MEROZOITES

44
Q

HOW DO MEROZOITES INVADE ERYTHROCYTES?

A
  • MEROZOITES ENTER RED BLOOD CELLS INSIDE A PARASITOPHOROUS VACUOLE USING THEIR INVASION MACHINERY
  • THEY THEN FORM A RING STAGE PARASITE AND HAVE A RING OF CYTOPLASM WITH A DOT OF DNA
  • THE MEROZOITE UNDERGOES MULTIPLE NUCLEAR DIVISIONS TO PRODUCE A SCHIZONT
  • SHIZONTS MATURE BY DIVISION (SCHIZOGENY), RELEASING MEROZOTES FROM THE PARASITOPHOROUS VACUOLE
  • 16-32 MEROZOITE EGRESS FROM RED BLOOD CELLS TO INFECT NEW ERYHTROCYTES
    (SOME MEROZOITES COMMIT TO SEXUAL DEVELOPMENT, CREATING A ‘COMMITTED SCHIZONT’ THEN HAVING A SEXUAL RING STAGE AND FINALLY TURNING INTO GAMETOCYTES)
45
Q

HOW MANY MEROZOITES EGRESS FROM ERYHTOCYTES AFTER INVADING THEM TO GO ON AND INFECT MORE ERYTHROCYTES?

A

16-32

46
Q

IN WHICH FORM DOES PLASMODIUM ENTER AND LEAVE ERYTHROCYTES?

A

IN: MEROZOITES
OUT: MEROZOITES (IF THEY ARE INFECTING OTHER ERYTHROCYTES,MAJORITY) + GAMETOCYTES (TRANSMISSIBLE FORM, PROCESS CALLED GAMETOCYTOGENESIS)

47
Q

% OF MEROZOITES WHICH COMMIT TO SEXUAL DEVELOPMENT OF PLASMODIUM INSTEAD OF FURTHER INFECTING ERYTHROCYTES?

A

<10%

48
Q

ARE MEROZOITES TRANSMISSIBLE (ABLE TO INFECT BITING MOSQUITO)?

A

NO

49
Q

WHICH FORM OF THE PLASMODIUM IS TRANSMISSIBLE (ABLE TO INFECT A BITING MOSQUITO)?

A

GAMETOCYTES

50
Q

WHERE DO MEROZOITES DIFFERENTIATE INTO TO TRANSMISSIBLE FORM OF THE PLASMODIUM, GAMETOCYTES?

A

IN ERYTHROCYTES

51
Q

WHAT ARE THE 2 FORMS OF GAMETOCYTES OF PLASMODIUM?

A

MICROGAMETOCYTES (ANALOGOUS TO THE MALE SPERM)

MACROGAMETOCYTES (ANALOGOUS TO THE FEMALE EGG)

52
Q

WHO MOSTLY DIES FROM MALARIA?

A

PREGNANT WOMEN AND CHILDREN YOUNGER THAN 5

53
Q

SUMMARY OF THE PLASMODIUM LIFECYCLE IN THE MAMMAL

A

1) SPOROZOITES ARE INOCULATED INTO THE DERMIS BY THE BITE OF AN INFECTED MOSQUITO
2) THEY THEN PASS INTO THE BLOOD VESSELS AND ARE TAKEN TO THE LIVER BY BLOOD FLOW
3) AT THE LIVER, THEY PASS THROUGH SEVERAL LIVER CELLS BEFORE THEY COLONISE A HEAPTOCYTE PARASITOPHOROUS VACUOLE
4) SPOROZOITES THEN DEVELOP INTO THOUSANDS OF MEROZOITES
5) MEROZOITES RE-ENTER THE BLOOD SYSTEM INSIDE VESICLES (MEROSOMES) AND REPLICATE INSIDE ERYTHROCYTES
6) MEROZOITES AREN’T TRANSMISSIBLE (CAN’T INFECTED A MOSQUITO)
7) THEY MUST DIFFERENTIATE TO GAMETOCYTES (WHILE IN RBCs) TO TRANSMIT TO MOSQUITOS

54
Q

DO THE MALE OR FEMALE GAMETOCYTES OF THE PLASMODIUM UNDERGO EXFLAGELLATION?

A

MALE

55
Q

DESCRIBE THE PROCESS OF EXFLAGELLATION OF MALE PLASMODIUM GAMETOCYTES

A
  • THE DNA RAPIDLY DUPLICATES TO 8N
  • 8 FLAGELLA ARE RAPIDLY FORMED
  • THE CELL DIVIDES INTO 8 FLAGELLATED MALE GAMETES
  • THE ONLY LIFECYCLE STAGE THAT IS FLAGELLATED!!!!!!!!!!!!!!!!!!
  • FLAGELLA MADE WITHIN 10 MINS CAUSE THEY ARE PREFORMED IN THE CYTOPLASM
56
Q

WHAT IS THE ONLY FLAGELLATED LIFECYCLE FORM OF THE PLASMODIUM?

A

MALE GAMETE (MALE GAMETOCYTES UNDERGO EXFLAGELLATION TO BECOME THESE FLAGELLATED GAMETES)

57
Q

DESCRIBE WHAT HAPPENS TO PLASMODIUM GAMETOCYTES WHEN THEY ARE INGESTED BY A BITING MOSQUITO?

A
  • TAKEN UP INTO THE MIDGUT
  • THE CHANGE IN TEMP, pH, EXPOSURE TO XANTHURENIC ACID.. STIMULATE THE GAMETOCYTES TO ROUND-UP, EGRESS FROM THE ERYTHROCYTE AND DIFFERENTIATE INTO GAMETES
  • DIFFERENTIATION TO GAMETES: MALE GAMETOCYTES UNDERGO EXFLAGELLATION
  • 8 FLAGELLATED MALE GAMETES CREATED
  • THE MALE ZYGOTES FERTILISE THE FEMALE ZYGOTES TO FORM A DIPLOID ZYGOTE
  • ZYGOTES DIFFERENTIATE INTO MOTILE OOKINETES (GLIDING MOTILITY)
  • OOKINETES ARE ALSO DIPLOID
  • OOKINETES DEGRADE THE PERITROPHIC MATRIX (PRODUCED BY THE INSECT AROUND THE BLOOD MEAL) BY SECRETING CHITINASES AND THEN TRANSVERSE THE MIDGUT EPITHELIUM
  • THE OOKINETE BECOMES AN OOCYST AND LODGES IN BASAL LAMINA (ECM) OF THE MIDGUT EPITHELIUM
  • PROCESS TAKES 10-15DAYS
  • OVER THE NEXT 10-14 DAYS, THE OOCYST(S) GROWS IN SIZE AND PRODUCES 1000s OF SPOROZOITES BY MEIOSIS (PARASITES CHANGE FROM DIPLOID TO HAPLOID)
  • ONCE MATURED, THE SPOROZOITES ARE RELEASED INTO THE OPEN HAEMOLYMPH CIRCULATION OF THE MOSQUITO
  • SPOROZOITES THEN FIND THE MOSQUITO SALIVARY GLANDS
  • SPOROZOITES ASSEMBLE INTO BUNDLES WITHIN THE SECRETORY CAVITY
  • A SMALL NUMBER OF PARAZITES ENTER THE SECRETORY DUCT AND ARE TRANSMITTED UPON BITING
58
Q

HOW MANY GAMETOCYTES DO MOSQUITOS INGEST FROM MALARIA AFFECTED PATIENTS AND HOW MANY MAKE IT TO THE OOKINETEPOINT AND THEN OOCYST POINT?

A
  • 10,000 GAMETOCYTES (INFCTIVE FORM OF THE PLASMOID WHICH IS TRANSFORMED THROUGH GAMETES INSIDE THE MOSQUITO) INGESTED
  • 1,000 OOKINETES (MOTILE DIPLOID STRUCTURES FORMED THROUGH ZYGOTE DIFFERENTIATION)
  • <5 OOCYSTS (A FORM OOKINETES TRANSFORM TO; LODGES IN BASAL LAMINA (ECM) OF THE MOSQUITO MIDGUT EPITHELIUM)
59
Q

WHAT HAPPENS TO PLASMODIUM OOCYSTS ONCE IT LODGES IN THE MIDGUT EPITHELIUM OF THE MOSQUITO?

A
  • OVER 10-14 DAYS, THE OOCYST(S) GROWS IN SIZE AND PRODUCES 1000s OF SPOROZOITES BY MEIOSIS (PARASITES CHANGE FROM DIPLOID TO HAPLOID)
  • ONCE MATURED, THE SPOROZOITES ARE RELEASED INTO THE OPEN HAEMOLYMPH CIRCULATION OF THE MOSQUITO
  • SPOROZOITES THEN FIND THE MOSQUITO SALIVARY GLANDS
  • SPOROZOITES ASSEMBLE INTO BUNDLES WITHIN THE SECRETORY CAVITY
  • A SMALL NUMBER OF PARAZITES ENTER THE SECRETORY DUCT AND ARE TRANSMITTED UPON BITING
60
Q

MOSQUITOS TRANSMITTING MALARIA ARE USUALLY VEGETARIAN. WHAT IS THE ONLY INSTANCE WHEN THE MOSQUITO WILL BITE HUMANS AND DRINK BLOOD?

A

A PREGNANT MOSQUITO

61
Q

WHERE IN THE MOSQUITO DOES PLASMODIUM FERTILISATION OCCUR?

A

IN THE MIDGUT

62
Q

IN WHICH FORM DOES PLASMODIUM ENTER THE MOSQUITO AND IN WHICH FORM DOES IT LEAVE?

A

IN: GAMETOCYTES
OUT: SPOROZOITES

63
Q

NAME PLASMODIUM LIFECYCLE STAGES AND PLACES THEY OCCUPY

A

MEROZOITE - HUMAN ERYTHROCYTES
GAMETOCYTES - MICRO=MALE, MACRO=FEMALE, IN THE ECM, TRANSIT TO MOSQUITO (INFECTIVE FORM TO THE MOSQUITO)
GAMETES - INSECT MIDGUT
OOKINETE - MOSQUITO MIDGUT
OOCYST - MIDGUT EPITHELIUM
SPOROZOITE - MOSQUITO SALIVARY GLANDS, THEN HUMAN SKIN, THEN LIVER VIA BLOOD SYSTEM, THEN LUNGS AND THEN THEY START INFECTING RBCs (INFECTIVE FORM FOR HUMANS)

64
Q

THE MALARIA HYPOTHESIS; ANTHONY ALLISON AND JOHN HALDANE

A
  • IN THE MID 20TH CENTURY
  • SUGGESTED THAT GEOGRAPHICAL OVERLAP BETWEEN SICKLE CELL ANAAEMIA AND MALARIA (AFRICA) MIGHT REFLECT A SELECTIVE ADVANTAGE OF SICKLE CELL HETEROZYGOTES AGAINST PLASMODIUM FALCIPARUM INFECTION
  • THEY SUGGESTED THAT IMPROVED SURVIVAL AMONG CARRIERS OF THE MUTATION (HbAS) IN THE FACE OF PLASMODIUM FALCIPORUM EXPOSURE MIGHT CONFER AN EVOLUTIONARY ADVANTAGE THAT COULD COMPENSATE FOR THE EARLY DEATH OF INDIVIDUALS AFFECTED BY SICKLE CELL ANEMIA (HbSS)
65
Q

MECHANISMS OF MALARIA PROTCTION IN PEOPLE WHO ARE SICKLE CELL CARRIERS (HbAS)?

A
  • LIKELY THAT A COMBINATION OF MECHANISMS PROTECTS AGAINST MALARIA
    1) ENHANCED REMOVAL (OR ‘SUICIDE’) OF PARASITIZED RBCs —> PARASITISED RBCs HAVE UP TO 8 TIMES HIGHER CHANCE OF SICKLING IN HbAS THAN HbAA (PEOPLE WITH NORMAL HEMOGLOBIN) (SICKLED, DAMAGED ERYTHROCYTES ARE CLEARED BY MACROPHAGES, REDUCING THE PARASITAEMIA)
    2) PARASITES ARE LESS ABLE TO GROW INSIDE SICKLED ERYTHROCYTES
    3) REDUCED CYTOADHERENCE AND SEQUESTRATION (LESS PfEMP1 IS MADE, SO THE ABILITY TO STICK TO BLOOD VESSELS AND AVOID CLEARENCE BY THE SPLEEN IS REDUCED) –> ALLOWS EFFICIENT CLEARING BY THE SPLEEN
    4) DECREASED ROSETTE FORMATION (ERYTHROCYTES LESS ABLE TO ROSETTE THAN NORMAL, WHICH IS ESPECIALLY PROTECTIVE AGAINST CEREBRAL, SEVERE FORMS OF MALARIA!!!!!!!!!)

EXAMPLE OF BALANCED POLYMORPHISM: A SYSTEM OF GENES IN WHICH 2 ALLELES ARE MAINTAINE IN STABLE EQUILIBRIUM BECAUSE HETEROZYGOTE IS MORE FIT THAN EITHER OF THE HOMOZYGOTES
- HAVE ONE SICKLE CELL ALLELE IS PROTECTIVE OF MALARIA!!!

66
Q

BALANCED POLYMORPHISM? EXAMPLE MALARIA

A

Balanced polymorphism is a situation in which two different versions of a gene are maintained in a population of organisms because individuals carrying both versions are better able to survive than those who have two copies of either version alone. .

  • THE SICKLE CELL ALLELE IS MAINTAINED IN AREAS WITH HIGH MALARIA BECAUSE HETEROZYGOTES ARE PROTECTED AGAINST MALARIA
  • THIS IS DESPITE THE REDUCED LIFE EXPECTANCY OF HOMOZYGOTES DUE TO SICKLE CELL ANEMIA
  • OTHER HEMOGLOBIN DISORDERS (E.G. THALASSEMIA!!!!!!!!!) HAVE BEEN MAINTAINED DUE TO SIMILAR PROTECTIVE FACTORS
  • OTHER DAMAGING MUTATIONS ARE MAINTAINED AS PROTECTIVE AGAINST INFECTIOUS DISEASE
67
Q

CHLOROQUINE IS FIRST LINE TREATMENT FOR WHICH TYPE OF PLASMODIUM?

A

P. VIVAX

68
Q

CHLOROQUINE AND MALARIA

A
  • CHLOROQUINE ORIGINALLY DEVELOPED BY GERMAN SCIENTISTS IN 1934 (MARKTED AS REOCHIN) BUT CONSIDEED TOO TOXIC FOR HUMAN USE
  • WIDELY USED AFTER WW2 TO TREAT MALARIA
  • RESISTANCE FIRST DEVELOPED INDEPENDENTLY IN SOUTHEAST ASIA, OCEANIA AND SOUTH AMERICA IN LATE 1950S AND EARLY 1960S
  • RESISTANCE IS NOW WIDESPREAD AND CHLOROQUINE IS RARELY USED AGAINST P. FALCIPARUM
69
Q

WHEN WAS CHLOROQUINE (ANTI MALARIAL DRUG) RESISTANCE FIRST DEVELOP?

A

IN LATE 1950S AND EARLY 1960S

70
Q

WHAT WA CHLOROQUINE MECHANISM OF ACTION AGAINST PLASMODIUM PRIOR TO RESISTANCE? HOW WAS RESISTANCE ACQUIRED?

A
  • HEMOGLOBIN IS A MAJOR NUTRIENT SOURCE FOR PARASITES; THEY METABOLIZE IT TO HEMOZOIN CRYSTALS INSIDE THEIR FOOD VACUOLE
  • METABOLISATION IS DONE VIA HEME, WHICH IS EXTREMELY TOXIC TO THE PARASITE BUT DOESN’T NORMALLY ACCUMULATE
  • CHLOROQUINE PREVENTS HEME BREKDOWN TO HEMOZOIN, WHICH LEADS TO HEME ACCUMULATION AND PARASITE IS KILLED

RESISTANCE:

  • PfCRT = PLASMODIUM FALCIPARUM CHLOROQUINE RESISTANCE TRANSPORTER; FUNCTION TO EXPORT PEPTIDES FROM DIGESTED PROTEINS FROM THE FOOD VACUOLE INTO THE PARASITE CYTOSOL
  • MUTATIONS IN THE TRANSPORTER MODIFY THE TRANSPORT SPECIFICITY OF THE TRANSPORTER, ALLOWING IT TO EXPORT CHLOROQUINE!! FROM THE FOOD VACUOLE
  • THE REDUCED CHLOROQUINE CONCENTRATION INSIDE THE VACUOLE ALOWS NORMAL BREAKDOWN OF TOXIC HEME
71
Q

WHAT IS THE MOST LETHAL PARASITE ON THE PLANET?

A

MALARIA (PLASMODIUM)

72
Q

WHICH LIFECYCLE STAGE OF THE PLASMODIUM INVADES THE ERYTHROCYTES AND CAUSES HUMAN DISEASE (MALARIA)?

A

MEROZOITES

INF (40 decks)

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