LEISHMANIA AND LEISHMANIASIS Flashcards
1
Q
SYMBIOTIC INTERACTIONS
A
SYMBIOSIS: A CLOSE BIOLOGICAL INTERACTION BETWEEN 2 DIFFERENT SPECIES
TYPES:
- MUTUALISM (A SYMBIOTIC RELATIONSHIP IN WHICH BOTH SPECIES BENEFIT)
- COMMENSALISM (ONE SPECIES BENEFITS WHILE OTHER SPECIES ISN’T AFFECTED)
- PARASITISM (ONE SPECIES, THE PARASITE, BENEFITS WHILE THE OTHER SPECIES, THE HOST, IS HARMED)
2
Q
KINETOPLASTIDS?
A
- VERY DIVERGENT GROUP OF ORGANISMS COMING FROM ‘EARLY BRANCHING’ PART OF THE EVOLUTIONARY TREE
- 1 BILLION YEARS OF EVOLUTIONARY DISTANCE WITH OTHER BRANCHES (HUMANS)
- KINETOPLASTID TRYPANOSOMATIDS CONTAINS SEVERAL IMPORTANT PARASITES: AFRICAN TRYPANOSOMES, AMERICAN TRYPANOSOMES, LEISHMANIA SPP
3
Q
HOW MANY TRYPANOSOMATID HUMAN PARASITES ARE THERE?
A
3
4
Q
WHAT ARE THE TRYPANOSOMATID HUMAN PARASITES?
A
TRYPANOSOMA BRUCEI: CAUSES HAT AND NAGANA, TRANSMITTED BY TSETSE FLIES, LIVES EXTRACELLULARLY AND HAS AN ELABORATE SYSTEM OF ANTIGENIC VARIATION
TRYPANOSOMA CRUZI: CAUSES CHAGAS DISEASE, TRANSMITTED BY BUGS (TRIATOMINE), LIVES INTRACELLULARLY IN THE CYTOPLASM OF VARIOUS CELLS
LEISHMANIA SPP: CAUSATIVE GENT OF LEISHMANIASIS, TRANSMITTED BY SANDFLIES (PHLEBOTOMINAE), LIVES IN THE PHAGOSOMES OF MACROPHAGES (IN HUMANS)
(ALL ARE ON THE WHO NTD LIST)
5
Q
LEISHMANIASIS; DISEASE BURDEN:
A
- 350 MILLION PEOPLE LIVE IN ENDEMIC AREAS: 98 ENDEMIC COUNTRIES
- 12 MILLION PEOPLE INFECTED
- 3-5 MILLION CLINICAL CASES
- 2 MILLION NEW CASES EACH YEAR (0.5 MIL ARE VISCERAL)
- 50 000 DEATHS FROM VL (VISCERAL LEISHMANIASIS) PER YEAR
(ABOVE FACTS FROM 2010, NOW 50 000 TO 90 000 NEW CASES OF VL)
—> VISCERA REFERRING TO ORGANS, ESP IN THE TORSO
6
Q
WHICH PATHOGENS CAUSE VISCERAL LEISHMANIASIS (VL)?
A
L. INFANTUM AND L. DONOVANI
7
Q
OTHER NAME FOR VISCERAL LEISHMANIASIS?
A
KALA-AZAR
8
Q
FATALITY OF UNTREATED VISCERAL LEISHMANIASIS?
A
95%
9
Q
IN WHICH COUNTRIES DOES VISCERAL LEISHMANIASIS MOSTLY OCCUR?
A
BRAZIL, EAST AFRICA AND INDIA
10
Q
SYMPTOMS OF VISCERAL LEISHMANIASIS?
A
- IRREGULAR BOUTS OF FEVER
- WEIGHT LOSS
- ENLARGEMENT OF THE SPLEEN AND LIVER, AND ANAEMIA
11
Q
CUTANEOUS LEISHMANIASIS?
A
CUTANEOUS = SKIN
- CAUSED BY > 20 DIFFERENT SPECIES OF LEISHMANIA
- USUALLY NOT FATAL
- MOST COMMON CAUSE OF LEISHMANIASIS
- CAUSES SKIN LESIONS, MAINLY ULCERS ON EXPOSED PARTS OF THE BODY
- USUALLY HEALS WITHIN A FEW MONTHS, BUT LEAVES LIFE-LONG SCARS AND SERIOUS DISABILITY OR STIGMA
- 600 000 - 1 000 000 NEW CASES ANNUALLY
- 95% OF CASE OCCUR IN THE AMERICAS, THE MEDITERRANEAN BASIN, THE MIDDLE EAST AND CENTRAL ASIA
12
Q
MOST COMMON FORM OF LEISHMANIASIS?
A
CUTANEOUS LEISHMANIASIS
13
Q
WHAT IS THE CAUSE OF MUCOCUTANEOUS LEISHMANIASIS?
A
LEISHMANIA BRAZILIENSIS
14
Q
MUCOCUTANEOUS LEISHMANIASIS?
A
- MUCOCUTANEOUS —> AFFECTS SKIN AND MUCUS MEMBRANE
- RARE FORM OF CUTANEOUS LEISHMANIASIS
- LEADS TO PARTIAL OR TOTAL DESTRUCTION OF THE MUCUS MEMBANES OF THE NOSE, MOUTH AND THROAT
- OVER 90% OF CASES OCCUR IN: BOLIVIA, BRAZIL, PERU AND ETHIOPIA
15
Q
LEISHMANIASIS BURDEN IS LIKELY TO INCREASE OR DECREASE IN THE FUTURE?
A
INCREASE
15
Q
LEISHMANIASIS BURDEN IS LIKELY TO INCREASE OR DECREASE IN THE FUTURE?
A
INCREASE
16
Q
WHY IS IT PREDICTED THAT THE LEISHMANIASIS BURDEN WILL INCREASE IN THE FUTURE?
A
DUE TO:
- POPULATION MOBILITY (LEISHMANIASIS EPIDEMICS OFTEN ASOCIATED WITH MIGRATION, THE MOVEMENT OF NON IMMUNE PEOPLE INTO AREAS WITH HIGH PREVALENCE)
- ENVIRONMENTAL CHANGES (CHANGES IN URBANIZATION, HUMAN INCURSION INTO FORESTED AREAS)
- CLIMATE CHANGE (CHANGES IN TEMP, RAINFALL, HUMIDITY, DROUGHT, FAMINE AND FLOOD) CAN HAVE STRONG EFFECTS ON VECTORS AND RESERVOIR HOSTS
17
Q
HOW MANY TYPES OF LEISHMANIASIS ARE THERE?
A
3: VISCERAL (AFFECTS THE VISCERA, DEADLY), CUTANEOUS (SKIN, MOST COMMON), MUCOCUTANEOUS (CAUSES TERRIBLE DISFIGUREMENT AND IS THE LEAST COMMON)
18
Q
WHAT ARE THE 2 LEISHMANIA FORMS THAT INVADE VERTEBRATE IMMUNE CELLS?
A
PROMASTIGOTE AND AMASTIGOTE
19
Q
PROMASTIGOTE VS AMASTIGOTE LEISHMANIA FORMS CHARACTERISTICS?
A
PROMASTIGOTE: INOCULATED INTO THE HOST BY THE SANDFLY, ELONGATED, FLAGELLATED FORM, POWERFUL SWIMMER, INVADES PHAGOCYTIC IMMUNE CELLS (MACROPHAGES ETC)
AMASTIGOTE: FORMED FROM PROMASTIGOTE AFTER ITS FIRST INVASION, SMALL AND ROUND, HAS A VERY SMALL IMMOTILE FLAGELLUM, INVADES PHAGOCYTIC IMMUNE CELLS (MACROPHAGES ETC), INFECTS SANDFLY
20
Q
DESCRIBE THE STRUCTURE OF PROMASTIGOTE FORM OF LEISHMANIA?
A
- 2 LARGE DNA CONTAINING ORGANELLS: KINETOPLAST (MITOCHONDRIAL DNA) & NUCLEUS; BOTH MUST DUPLICATE THEIR DNS, DIVIDE, AND SEGREGATE FOR DIVISION
- EXTENSIVE MICROTUBULE CYTOSKELETON: VITAL FOR CELL INTEGRITY AND MORPHOLOGY, DOESN’T DISASSEMBLE FOR DIVISION, RIGID CORSET-LIKE STRUCTURE
- FLAGELLAR POCKET: IVAGINATION OF THE CELL MEMBRANE, LOCATED AT THE CELL POSTERIOR, MAJOR SITE OF ALL ENDO- AND EXO- CYTOSIS, LINKED TO MAJOR SINGLE-COPY ORGANELLES INCLUDING BASAL BODY AND GOLGI (SITE WHERE THE FLAGELLUM EMERGES)
- THE FLAGELLUM: HIGHLY MOTILE (9+2 STRUCTURE —> 9 DOUBLET MICROTUBULES AND A CENTRAL PAIR)
- THE PFR (PARAFLAGELLAR ROD): ESSENTIAL FOR PROPER BEATING OF THE FLAGELLUM
21
Q
WHAT IS THE PARAFLAGELLAR ROD? (PFR)
A
- FOUND IN ALL TRYPANOSOMATIDS
- PARACRYSTALLINE WITH 3 DISTINCT DOMAINS (DISTAL, INTERMEDIATE, PROXIMAL; RELATIVE TO THE CELL BODY)
- ESSENTIAL FOR PROPER BEATING OF THE FLAGELLUM, MECHANISM OF ACTION NOT CLEAR, MAY ACT AS A ‘BIOMECHANICAL SPRING’, MAY ACT AS PLATFORM FOR ENZYMES THAT REGULATE THE FLAGELLAR BEAT
22
Q
STRUCTURE OF THE AMASTIGOTE FORM OF LEISHMANIA?
A
- AMASTIGOTES ARE EXCLUSIVELY FOUND IN THE MAMMALIAN BLOODSTREAM
- MUCH CHORTER AND ROUNDER THAN PROMASTIGOTES
- THEIR FLAGELLUM IS SHORTER AND IMMOTILE (KEY DIFFERENCE!) —> STAYS IN THE POCKET
- ALSO HAVE NUCLEUS, KINETOPLAST, FLAGELLAR POCKET AND EXTENSIVE MICROTUBULE CYTOSKELETON
- MANY OTHER BIOCHEMICAL AND CELLULAR DIFFERENCES (BECAUSE OF DIFFERENT FUNCTIONS)
- CCA 5microm
- NO MOTILITY STRUCTUES: NO CENTRAL PAIR OF THE FLAGELLUM AND NO PARAFLAGELR ROD!!!!!!!!!!
- MAY PLAY A SENSORY ROLE
23
Q
WHER ARE LEISHMANIA AMASTIGOTES EXCLUSIVELY FOUND IN MAMMALIAN HOSTS?
A
IIN THE BLOODSTREAM
24
COMPARISON OF LEISHMANIA CELL SHAPES WITH TRYPANOSOMES?
- DIFFERENT DEVELOPMENTAL STAGES AND SPECIES HAVE DIFFERENT SHAPES
- THESE ARE DEFINED BY THE FLAGELLUM POSITIONING WHICH IMPACTS THE WAY THAT EACH CELLS SWIMS
- TRYPANOSOMAS HAVE FLAGELLUM STARTING AT THE CELLPOSTERIOR AND IS BOUND TO CELL BODY (THE FLAGELLUM MOVES SLIGHTLY MORE CENTRAL WHEN IN THE EPIMASTIGOTE STAGE), WHILE LEISHMANIA'S FLAGELLUM ISN'T BOUND TO THE BODY SHAPE AND MOVES MORE FREELY
25
DIGENETIC PARASITE MEANING?
PARASITES THAT NEED MORE THAN ONE HOST TO COMPLETE THEIR LIFE CYCLE
26
EXPLAIN WHY LEISHMANIA IS A DIGENETIC PARASITE?
BECAUSE IT COLONISES 2 DIFFERENT SPECIES: IT NEEDS A VECTOR (PHLEBOTOMINE SPECIES; SAND FLIES) AND A HOST (MAMMAL, INCLUDING HUMAN)
27
HOW IS LEISHMANIA TRANSMITTED?
TRANSMITTED BY THE BITE OF INFECTED FEMALE SANDFLY
- UPON BITING, THEY 'REGURGITATE' LEISHMANIA PARASITES INTO THE WOUND
- THESE PARASITES ARE PROMASTIGOTE FORMS AND GO ON TO INFECT THE MAMMALIAN HOST
28
WHEN A SANDFLY INFECTED BY LEISHMANIA BITES A MAMMAL, WHICH FORM ARE THE LEISHMANIA PARASITES ENTERING THE WOUND IN?
PROMASTIGOTE FORM
29
LEISHMANIA LIFECYCLE WITHIN HOST CELLS?
- INFECTED SANDFLY BITES A HUMAN
- PROMASTIGOTES FROM THE WOUND SITE ARE TAKEN UP BY THE MACROPHAGES AND INTO A PARASITOPHOROUS VACUOLE
- FUSING OF LYSOSOMAL CONTENTS TO VACUOLE CAUSES THE pH TO DROP
- THE pH DROP STIMULATES DIFFERENTIATION TO THE AMASTIGOTE FORM (AFTER THAT, REMAINS IN THE AMASTIGOTE FORM; NOT ALTERED AGAIN WHEN REACHING NEW MACROPHAGES ETC)
- AMASTIGOTES DIVIDE
- AMASTIGOTES ESCAPE AND REINFECT OTHER MACROPHAGES
- AMASTIGOTES REPLICATE INSIDE THE PARASITOPHOROUS VACUOLE
- AMASTIGOTES THEN ESCAPE AND REINFECT AGAIN (CAN REACH OTHER MACROPHAGES OR BE INGESTED FROM THE EXTRACELLULAR SPACE IF ANOTHER SANDFLY BITES)
30
INFECTION AND ESCAPE CYCLE TARGETING MACROPHAGES IS CHARACTERISTIC OF WHICH PATHOGEN?
LEISHMANIA
31
EXPLAIN THE CLAIM THAT 'LEISHMANIA TARGET CELLS THAT ARE SUPPOSED TO EAT THEM'
- LEISHMANIA EXCLUSIVELY TARGET MACROPHAGES, WHICH ARE IMMUNE CELLS HIGHLY SPECIALISED FOR PHAGOCYTOSIS (INTERNALISTAION), OF MICROORGANISMS AND CELLULAR DETRTUS
- PHAGOCYTOSED MICROORGANISMS ARE THEN USUALLY DESTROYED IN MACROPHAGES BY A PLETHORA OF ORGANISMS
- HOWEVER, LEISHMANIA SUBVERT THE CLASSICAL PHAGOCYTOSIS PATHWAY AND HAVE EVOLVED TO LIVE INSIDE MACROPHAGES AND NEUTROPHILS
- AMASTIGOTES FILL UP AND DIVIDE IN MACROPHAGES, AND FINALLY GET RELEASED AS THE MACROPHAGE RUPTURES
32
HOW TO LEISHMANIA PARASITES GET INSIDE MACROPHAGES AND EXPLOIT THEM?
- PARASITES ARE INTERNALISED BY CONVENTIONAL PHAGOCYTOSIS (PARASITES BIND TO PHAGOCYTIC RECEPTORS ON THE MACROPHAGE CELL SURFACE WHICH STIMULATES MACROPHAGE'S PHAGOCYTOSIS PATHWAY AND THE PARASITE BECOMES INTERNALISED INSIDE A 'PARASITOPHOROUS VACUOLE', PV)
THE PARASITES THEN SUBVERT THE CLASSICAL PHAGOCYTOSIS PATHWAY:
- THE NUTRIENTS (LIPIDS, PROTEINS, IRONS ETC) DESTINED FOR OTHER PARTS OF THE CELL ARE DIVERTED TO THE PV TO FEED THE PARASITES
- VESICLES CONTAINING PARASITE DAMAGING FACTORS (SUCH AS OXIDISING CHEMICALS AND PROTEASES) ARE LESS ABLE TO FUSE WITH THE PV MEMBRANE
- THE PARASITE PREVENTS THE MACROPHAGE FROM ACTIVATING OTHER IMMUNE CELLS THAT MIGHT INHIBIT THE PARASITE INFECTION
33
WHT IS THE ROLE OF THE AMASTIGOTE (LEISHMANIA FORM) FLAGELLUM?
AMASTIGOTES AREN'T MOTILE BUT THEY HAVE A SMALL FLAGELLUM, WHY?
SEVERAL THEORIES:
- VESTIGIAL ORGANELLE (USELESS, MAYBE HAD A FUNCTION BEFORE BUT NOW IT'S EASIER TO KEEP IT THAN GET RID OF IT)?
- IMPORTANT FOR THE INTEGRITY OF THE FLAGELLAR POCKET (WHICH IS THE ESSENTIAL SITE FOR NUTRIENT EXCHANGE AND ENDO/EXOCYTOSIS)?
- TETHERS THE AMASTIGOTE TO THE PARASITOPHOROUS VACUOLE?
- ACTS AS A SENSORY/SIGNALING ORGANELLE? (FACILITATING HOST PARASITE INTERACTIONS)
- ALLOWS 'REMODELLING' OF THE PV MEMBRANE TO SUBVERT MACROPHAGE FUNCTION?
34
LIFE OF LEISHMANIA IN THE SANDLFY VECTOR?
- WHEN SANDLIES INGEST BLOOD OF A PERSON INFECTED WITH LEISHMANIA, THE AMASTIGOTES ARE TAKEN INTO THE SANDFLY MID-GUT
- ALL THE LEISHMANIA DEVELOPMENT IN THE SANDFLY HAPPENS IN THE DIGESTIVE TRACT
- ALL DEVELOPMENTAL STAGES ARE EXTRACELLULAR
- PARASITES START IN THE MIDGUT BLOOD MEAL AS AMASTIGOTES, BUT THEN TRANSFORM TO PROMASTIGOTE IN RESPONSE TO DROP IN TEMP AND pH
- PROMASTIGOTES THEN PROGRESS THROUGH 5 DISTINCT CHANGES (EACH HAS DIFFERENT PROLIFERATIVE STATE, MORPHOLOGY AND OCCUPIES A DIFFERENT NICHE WITHIN THE SANDFLY DIGESTIVE TRACT):
1) PROCYCLIC (COLONIZES THE MIDGUT)
2) NECTOMONAD (ATTACHED TO MIDGUT MICROVILLI, NO REPLICATION, COULD BE THE LIFE-CYCLE STAGE THAT UNDERGOES SEX)
3) LEPTOMONAD (COLONISE THE THORACIC MIDGUT AND STOMODEAL VALVE, PRODUCE PROMASTIGOTE SECRETORY GEL, PSG ---> FACILITATES TRANSMISSION)
4) HAPTOMONAD (ATTACH TO STOMODEAL VALVE LINING AND PSG VIA THEIR FLAGELLUM)
5) METACYCLIC (THORACIC MIDGUT, READY TO INFECT MAMMALIAN HOST UPON BITING)
35
SANDFLIES (VECTORS THAT TRANSMIT LESIHMANIA) ARE 'POOL FEEDERS', WHAT DOES THAT MEAN?
- MEANS THEY INSERT THEIR SAW-LIKE MOUSEPARTS INTO THE SKIN AND AGITATE THEM TO PRODUCE A SMALL WOUND INTO EHICH THE BLOOD FLOWS FROM SUPERFICIAL CAPILLARIES
36
5 STAGES OF LEISHMANIA PROMASTIGOTES IN THE SANDFLY DIGESTIVE SYSTEM?
1) PROCYCLIC (COLONIZES THE MIDGUT)
2) NECTOMONAD (ATTACHED TO MIDGUT MICROVILLI, NO REPLICATION, COULD BE THE LIFE-CYCLE STAGE THAT UNDERGOES SEX)
3) LEPTOMONAD (COLONISE THE THORACIC MIDGUT AND STOMODEAL VALVE, PRODUCE PROMASTIGOTE SECRETORY GEL, PSG ---> FACILITATES TRANSMISSION)
4) HAPTOMONAD (ATTACH TO STOMODEAL VALVE LINING AND PSG VIA THEIR FLAGELLUM)
5) METACYCLIC (THORACIC MIDGUT, READY TO INFECT MAMMALIAN HOST UPON BITING)
37
IN WHICH PART OF THE SANDFLY DOES ALL LEISHMANIA DEVELOPMENT OCCUR? IS IT INTRACELLULAR OR EXTRACELLULAR?
- IN THE DIGESTIVE SYSTEM
| - EXRACELLULAR
38
NAME OF THE STAGE OF LEISHMANIA CYCLE (FORM OF PROMASTIGOTE) IN THE SANDFLY THAT'S ABLE TO INFECT HUMANS?
METACYCLIC
39
HOW MANY SANDFLY SPECIES ARE THERE, AND HO MANY CAN TRANSMIT LEISHMANIA?
>900 SANDFLY SPECIES IN TOTAL, ONLY 98 CAN TRANSMIT LEISHMANIA
40
EVEN THOUGH INSECT HAVE VERY SOPHISTICATED IMMUNE DEFENSES TO FIGHT AGAINST UNWANTD 'PASSANGERS', LEISHMANIA IS STILL ABLE TO UTILISE SOME SANDFLY SPECIES? HOW IS THAT ACHIEVED?
- SEVERAL MECHANISMS
1) DURING FEEDING THE BLOODMEAL CONTAINING LEISHMANIA AMASTIGOTES GETS SURROUNDED BY THE PERITHROPIC MATRIX, A TOUGH 'SACK' COMPOSED OF A CHITIN AND PROTEIN MESH ---> PARASITE SECRETE CHITINASES TO BREAK FREE
2) THE SANDFLY DIGESTS ITS BLOODMEAL USING DIGESTIVE ENZYMES, 'PROTEASES' ---> PARASITES SECRETE INHIBITORS + HAVE SURFACE MOLECULES CALLED PHOSPHOGLYCANS TO PROTECT THEM AGAINST PROTEASES + DOWNREGULATE SANDFLY PROTEASE GENES
3) THE SANDFLY MAKES ANTIMICROBIAL PEPTIDES (AMPs) ---> PARASITES DOWNREGULATE THE GENETIC PATHWAYS THAT MAKE THE AMPs
4) THE BLOOD MEAL (AND ALL THE PATHOGENS INSIDE) IS ULTIMATELY EXPELLED BY DEFECATION ---> PARASITE INSERT THEIR FLAGELLUM BETWEEN THE INSECT GUT EPITHELIUM MICROVILLI TO PREVENT THEM FROM GETTING EXPELLED (SOME O GET EXPELLED BUT SOME REMAIN IN THE SANDFLY BODY) + PARASITES SECRETE PEPTIDES THAT INHIBIT THE INSECT GUT PERISTALTIC MOVEMENT (MYOINHIBITORY PEPTIDES)
41
WHY CAN LEISHMANIA TRANSMIT VIA ONLY SPECIFIC 98 OU OF >900 LEISHMANIA PARASITES?
SPECIFICITY APPEARS TO BE CONFERRED BY THE PARASITE'S ABILITY TO BIND TO PHOSPHOGLYCANS ON THE EPITHELIAL MICROVILLI (INSERT THEIR FLAGELLUM BETWEEN THE MICROVILLI TO AVOID GETTING EXPELLED BY DEFECATION)
42
SANDFLY SPECIES THAT CAN ONLY TRANSMIT ONE LEISHMANIA STRIN ARE CALLED?
SPECIFIC VECTORS
| VS PERMISSIVE; SANLIES THAT CAN TRANSMIT MORE THAN ONE LEISHMANIA TYPE
43
DESCRIBE THE 'BLOCKED SANDFLY' PHENTOYPE CAUSED BY LEISHMANIA?
1) THE STOMODEAL VALVE IS AT THE MOUTHPARTS OF THE SANDFLY AND ALLOWS ENTRY OF HOST BLOOD INTO THE SANDFLY GUT DURING FEEDING
2) PARASITES TRAVEL FROM THE MIDGUT AND ADHERE TO THE STOMODEAL VALVE
3) THE PARASITES SECRETE A HIGH MOLECULAR WEIGHT PROTEIN THAT 'SETS' INTO PROMASTIGOTE SECRETORY GEL (PSG)
4) PSG FORMS A 'PLUG' AT THE STOMODEAL VALVE CONTAINING MANY INFECTIVE PARASITES
5) THE PLUG FORCES THE VALVE TO REMAIN OPEN AND CAUSES A BLOCKAGE THAT REDUCES THE INFLOW OF BLOOD
6) THIS PROMOTES DELIVERY OF PARASITES TO THE HOST BY REGURGITATION (the spitting up of food from the esophagus or stomach without nausea or forceful contractions of the abdominal muscles)
- SANDFLIES WITH PSG ALSO FEED MORE OFTEN BECAUSE THEIR FEEDING IS INEFFICIENT
44
DO SANDFLIES WITH LEISHMANIA FEED MORE OR LESS OFTEN THAN NON-TRANSMITTING SANDFLIES?
MORE BECAUSE THEIR FEEDING IS INSUFFICIENT BECUSE OF THE PLUG CAUSED BY PROMASTIGOTE SECRETORY GEL LIMITING THE AMOUNT OF BLOOD THAT CAN ENTER THE FLY'S BODY
45
WHICH PARASIT IS TRANSMITTED FROM ITS VECTOR VIA THE MECHANISM OF REGURGITATION (the spitting up of food from the esophagus or stomach without nausea or forceful contractions of the abdominal muscles)?
LEISHMANIA
46
HOW MANY LEISHMANIA PARASITES ARE INCOLUATED PER SANFLY BITE?
500-1000
47
WHAT EFFECTS DOES PROMASTIGOTE SECRETORY GEL (PSG) INJECTED BY LEISHMANIA TRANSMITTING SANDFLY HAVE ON HOST MACROPHAGES?
IT ATTRACTS THEM
48
HOW DOES SANDFLY SALIVA INFLUENCE LESIHMANIA INFECTION? THERAPUTIC POTENTIAL?
- PROMOTES AND EXACERBATES IT
- THE SALIVA IS SECRETED DURING THE BITE INTO THE WOUND TO KEEP THE BLOOD LIQUID AND PROMOTE BLOOD FLOW TO THE BITE SITE, BUT THE SALIVA ALSO CONTAINS > 20 PHARMACOLOGICALLY ACTIVE COMPOUNDS THAT PROMOTE LEISHMANIA INFECTION (ANTICOAGULANTS TO STOP CLOTTING, VASODILATOR PEPTIDES TO PROMOTE BLOOD FLOW, ATTRACT MACROPHAGES TO THE BITE SITE, ACTIVATES MACROPHAGES FOR INFECTION)
- VACCINATION AGAINST SANDFLY SALIVA HAS BEEN SHOWN TO CONFER SOME PROTECTION AGAINST LEISHMANIA INFECTION
49
AFTER THE INITIAL INFECTION BY LEISHMANIA AND TRANSFORMATION FROM THE PROMASTIGOTE FORM, THE ONLY LIFECYCLE STAGE OF LEISHMANIA IN MAMMALS IS:
AMASTIGOTE
