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57176
Malaria
Description
Microbiology Mind Map on Malaria, created by maisie_oj on 25/04/2013.
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microbiology
microbiology
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maisie_oj
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maisie_oj
over 11 years ago
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Resource summary
Malaria
The problem of malaria (epidemiology)
Endemic in parts of;
Asia
Africa (malaria belt - subsaharan)
Latin america
Oceania
41% of the worlds population live in regions where malaria is transmitted
200-500 million cases each year
1-2 million deaths each year
75% of these are kids in africa
= 2,700 deaths each day (1 death every 30 seconds)
4th leading cause of death after perinatal coditions, pneumonias and diarrhoeal diseases
Causitive agent
Transmission
Causitive agent is transmitted in the saliva of the female Anopheles mosquito
During blood meal
30-40 different species of Anopheles mosquito known to transmit plasmodium (A. gambiae is the most well known)
Associated with living close to still water (mosquito breeding area)
Puddles to swamps
Life cycle
In insect salivary gland: sporozoites (transmissable form)
Enter host blood stream during blood meal
Travel to liver and invade hepatocytes (30mins after infection)
In hepatocyte: sporozoite nucleus divides rapidly and asynchronously - producing a schizont (one membrane, many nuclei)
The schizont differentiates to becomes many mononucleated merozoites
Hepatocyte ruptures - releasing merozoites into the blood
Infect other hepatocytes
Infect RBCs
Asexual cycle
In RBC merozoite differentiates to become a large mononucleated trophozoite (ring stage - seen in a thin blood slide under a microscope)
Trophozoite divides asexually to produce a second schizont (multinucleated cell)
The schizont differentiates to become many mononucleated merozoites
RBC ruptures releasing merozoites into the blood stream
Merozoites invade other RBCs
Sexual cycle
Some merozoites differentiate into male (micro-) and female (macro-) gametocytes
RBCs containing gametocytes are taken up by a new vector mosquito during a second blood meal
RBC breaks down in mosquito gut
Gametocytes become their respctive micro- (male) and macro- (female) gametes (sex cells)
The microgamete
Undergoes three nuclear divisions and develops flagella
Nucleated flagella separate and fuse with the macrogamete -> zygote (diploid)
Zygote becomes a mobile ookinete
Ookinete crosses the insect gut epithelium into the basal side
Ookinete undergoes meiosis in the insect's gut wall
This forms oocysts (haploid)
Oocysts undergo repetitive cycles of mitosis (all daughter cells still haploid)
Daughter cells = sporozoites
Oocyst ruptures releasing the sporozoites into the haemocoel
Sporozoites migrate from the gut wall to the salivary gland (start of cycle)
Apicomplexan (class of protozoan) protozoal disease caused by....
Pasmodium spp.
Four species are pathogenic to humans
P. falciparum
The most clinically important
15% of all malarial infections...
.... But 90% of malaria deaths
P. vivax
Actually the most common species
P. ovale
P. malariae
Pathology and bioscience
1) onset
6-18 days after mosquito bite parasites appear in the blood
This is the prepatent time (i.e. time to complete the liver stage)
It varies with species; falciparum (6-9 days), vivax (8-12 days), ovale (10-14 days) and malariae (15-18 days)
Incubation time is the time between RBC infection and the start of symptoms
This also varies between species (from 7 days [falciparum] up to 40 days [malariae])
Classical symptoms (last 4-8 hrs)
Chills/rigor
Feels cold (excessive shivering) despite an elevated temperature
Fever + headache, nausea, vomiting, malaise etc
Sweats and becomes tired
Exhaustion -> sleep -> wake up apparently fine
Repeated every 2/3 days (ovale and vivax = 2 days, malariae = 3 days; falciparum = almost continuous fever)
Cyclic fever coinsides with RBC infection and rupture (rupture causes fever)
Why?
RBC infection and development of parasites is synchronous (all in RBCs at the same time and all released at he same time)
Lysis of RBC -> parasite antigens in blood -> stimulates immune cells to produce TNF-alpha and other cytokines -> fever
Fever becomes less severe with age (immunity difference with age)
2) development
Symptoms intensify
Irregular high fever
Anxiety, delerium and other mental manifestations
Sweating, increased pulse rate, exhaustion
GI symptoms
Hepatoslenomegaly!!!
3) severe malaria
Occurs in 10% of P. falciparum cases
50% mortality
Several manifestation (can appear simultaneously or sequentially)
Nn specific fever with loss of conciousness
Severe headache, drowsiness, neurological abormalities
Convulsions, vomiting and coma -> death
Drop in haematocrit (infected and non-infected RNCs destroyed, with reduced RBC production (due to cytokines))
Reduction in O2 supply to tissues
Other abnormalities (renal, respiratory, glucose levels, jaundice etc.)
Sequestration/cytoadherence
Sequestration
Infections with P. falciparum - only the ring trophozoite can be seen (in RBCs) in ther peripheral blood
The schizonts cause the RBCs to become 'sticky' (cytoadherence) this causes them to attach to the endothelium of venules (= sequestration)
P. falciparum infected RBCs are sequestered in many organs; heart, lungs, kidneys, brain, adipose, intestines, liver, spleen and placenta
Cytoadherence
RBCs containing schizonts become sticky
Stick to other RBCs (and endothelial cells)
Infected cell binding to non-infected cells = rosetting (organised rosettes of healthy RBCs arranged around a central infected RBC)
Infected cells binding to other infected cells = clumping (irregular clumps of infected cells which have lost their structure [shperocytes])
Seen in 50% of cases (correlates with disease severity)
Sticky cells clog-up blood vessels and cause haemorrhage (especially seen in cerebral malaria)
Rosetting/clumping is caused by PfEMP1 (P.falciparum erythrocyte membrane protein)
Multidomain protein produced by the parasite that are transferred to the RBC cell surface
Forms structures called 'knobs' on the membrane of the RBC
Allows infected cells to bind other infected/non-infected cells and endothelial cells (which are expressing cell adhesion molecules)
Cell adhesion molecules expressed by venule endothelium due to inflammatory IFN-gamma and TNF-alpha
Cell adhesion molecules expressed (can bind PfEMPs) = CD36 and ICAM1
PfEMP1 structure
NH2-multiple cysteine-rich domains (feature duffy binding-like (DBL) and cysteine-rich interdomain regions (CIDR))-transmembrane domain-COOH
Number and arrangement of DBLs and CIDRs vary between different PfEMPs
Extremely antigenic (elicits a strong immune response)
However, PfEMPs are encoded by a large multi-gene family (VAR genes)
Parasites are able to switch between PfEMP gene expression (antigenic variation)
One one gene is expressed at any one time (like Trypanosoma antigenic variation [VSG]) - allelic exclusion
Deopends on the VAR promoter
Swithching VAR gene may result in a new adhesion phenotype
2% of the parasite population switch VAR genes per cycle
About 60 VAR egens
Acquired immunity
People living in endemic areas acquire immunity through natural exposure to the parasite
Acquired (or natural) immunity occurs only after copntinued exposure from multiple infections over time
Acquired immunity limits high-density parasitaemia; however it does not lead to sterile protection
Clinical immunity gives protection gives prtoection against severe effects of malaria but fails to provide strong protection against infection
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