Malaria: An Overview
Summary
This is a comprehensive teaching session relevant to medical professionals that will discuss malaria, how it is transmitted, the species of Plasmodium that causes it, different characteristics of each species, the whole cycle of malaria, and how Plasmodium vivax causes relapses. The session will provide an excellent diagram on how the lifecycle of malaria occurs and present a comparison between Plasmodium vivax and Plasmodium falciparum.
Learning objectives
Learning Objectives:
- Identify the five species of the Plasmodium parasite that cause malaria in humans
- Describe the transmission methods of malaria
- Explain the incubation, clinical symptoms and fever pattern associated with each species of Plasmodium
- Analyze the differences in the liver and erythrocyte stages of the Plasmodium lifecycle
- Distinguish between relapsing malaria and other forms of the disease and explain the importance of hypnozoites in relapse prevention.
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Hello. Otherwise. So I guess everyone can see uh malaria, a presentation. Yeah. Uh So let's start the session. Uh Now talking about malaria. Uh I guess I can see the slide has changed. Now. Now uh we talk about malaria. Malaria is a uh is a disease caused by a parasitic organism. Uh uh Did we talk about how this uh organism been transmitted? Let's talk about how the types of organisms in the late upcoming slides. First of all, let's talk about how this uh organism is transmitted from one person to another. A transmission is a vector bone transmission. So transmission is by a female anil mosquito. That is uh an is called Faus that it's a definitive host. This is where this organism in this organism. It is where the sexual face of this lifecycle. The parasite takes place and human is like an intermediate host where it along the pathway of the mosquitoes. When they feed on the humans, they will uh get infected by this organism. Uh As I mentioned earlier, the we talk about there are multiple species of this plasmodium which can cause this human malaria disease. So we have five species uh mostly the four species that is vo alba malaria. Uh this uh plasma no is a new uh newly formed one which uh can cause severe malaria. Now, we talk about the plasmodium uh VVA and it's kind of similar because it causes tertia malaria. So malaria is uh go. So uh this tertian malaria is uh what what it means is it causes a fever spike. It causes a spike of fever that uh severe fever, severe increase in temperature in 48 hours. So every 48 hours, we can see uh more or less 48 hours, we can see this spike of fevers. So that is why this trans V va and it's called tertian malaria. I mean specifically we talk about vivax. Now, vivax is uh the most common cause of less viral and mild mild disease. So we comparatively to compare all the types of malaria uh malaria organisms. This plasma vivax, it's a organism which causes a less viral and mild disease. It is the most common cause in that. And uh this vivax is dominant in Southeast Asia Asian areas and the incubation period is around 8 to 17 days. Now we talk about uh plasma overlay that is uh as I mentioned earlier, it's, it's also less common um uh less common, uh less commonly found and cause of my disease. The commons healthy, that is the most important organism involved here because it causes the most violent and the most severe disease when comparing to all species of malaria and it is a dominant in Africa because in Africa, as we, as we all know, there's increased high incidence of sickle cell anemia and all hemoglobinopathy. That is the, these hemophilia are not. So this uh uh these sickle cell disease or the hemoglobin, they provide a protective action against this malaria species because these defect are BS when infected, they die uh by themselves. So this uh plasma organism cannot replicate in those R BC. So sickle cell disease and other hemoglobin A is like hemophilia. They provide a protective action against uh malaria infection. So it's highly uh more frequently found there but there is a protective action by this. Uh hemoglobin is now the incubation period is falciparum is around 8 to 11 days and the fever spikes, the fever spikes of this falciparum. It is very irregular. They, it can be around 30 every 36 to 48 hours. But the fever is very regular. And the name given for the disease called F is falciparum malaria or malignant ter malaria. Then moving on when you talk about uh that uh plasmodium uh malaria. Now, this plasmodium malaria is a less common cause a less common, less common cause of malaria and causes a mild, it causes a very mild disease. The incubation period is around 18 to 40 days. And uh when especially talking about malaria, it affects old uh old age RBS because RBS life span is around 100 and 20 days. So very old in age RB is only affected by this plasma malaria and it causes a cough and malaria cough. In malaria means that every three days, 72 hours, there's a fever spike caused by the malaria. We'll talk about why there speak uh like in the upcoming slides. And then finally, the newly one is the plasma anomaly that is found mostly in Southeast Asia and it can cause severe malaria. So we should also be vigilant about this and the incubation period of this is around 9 to 12 days. Uh The disease caused by this condition, all Corine malaria which uh gives you fever spikes every 24 hours. So every other day, there will be fever spikes caused by this. Uh Now I see now moving on a small comparison with this plain viva and plas F. Now in plas, it mainly enters newly form red blood cells in the bone marrow. So this plain, it mainly infects that red blood cell. Whereas uh falciparum which causes severe disease can, it can enter this RBS at any stage from this uh ra size to mature and only RC. From this spectrum of RB. Uh spec spectrum of age of RB. It can enter any stage. And then uh talking about the number of parasites within R BC. In vivax. There is in a single R BC, there is only one per single parasite found inside this. Whereas in falciparum, multiple parasites can be found within one R BC. And the vivax infected rbcs, they're enlarged, they become increase in size. Whereas falciparum, they do not become enlarged. They are in the same size itself. And vivax, you can find hypnos. I will come to what these s are in the next slides. In falciparum, there are no hypnos founding. So there are no relapses and vivax, the gametocyte are around. Whereas in falciparum, the gatos are crescent shape. I will show you this uh size shape later. Now, moving on, this is an excellent diagram regarding how the muscular, how these uh stages occur in the the this pla life cycle. So as you can see in the first stage, one, this stage, one is where the infection stage in the mosquitoes of moso is female. Anil muscular inserts. It provides this uh pros that is this sharp, it inserts into the human skin and it uh takes up a blood mill when taking a blood mill. It injects the zide. Yeah, I spo this inject this organism into the human blood around 100 spors injected per saliva, per per bite, the saliva. Now, after 1 to 3 hours in the dermis, the spors into the bloodstream and is uh carried off through the bloodstream to the liver that is into the liver. So this stage is called exer cycle. That is the liver stage. Uh when the organisms get to the blood to the blood and uh uh penetrates the sinusoidal barrier and invades the hepatocytes to enter the liver cells. So, this liver stage is called exer cycle. Now, in these liver cells, these sites which was from the muscular, these spo sites, they mature into multiple spherical schon. So from spro sites, it then becomes Chaison in all in inside the red blood, inside the sorry uh it forms spors in the mosquito. It becomes thons inside liver cells. And there is around 62,000, about about these uh schizo. Now, these Kison also multiply uh schizo are multiply inside these schizo, we can find the Zs. So when these uh schizo, when the s schizo, as you can see here inside this schizo, we can see multiple meroz sites. Now, when this schizo ruptures these meroz that is uh these merozoite only around 42,000, they uh these merozoite are released into the blood. Now, this blood stage is only called er uh erythrocyte cycle. I mean the when these meroz are released in the blood, these meroz may infect is uh may infect red blood cells. Now, these merozoite, they feed off the hemoglobin, this hemoglobin which is found in the red blood cells. These merozoite, they feed off these erythrocytes. And this uh when they figure out this uh these parasites appears ring form, these parasites, they appear as uh forms here. It's called this stage. So with this ring form, it is called a ring stage. It is called a Hema troph stage. Often troph stage, they become uh mature stage, they mature its time and office. When this meroz mature, they multiply again to forms Chaison. Now, these Chaison again have multiple meroz within them. Uh These multiple meroz is name and this key again can rupture, releasing meroz. These meroz again can infect other s becoming a vicious cycle. So the cycle continues with more and more aggressively infected. Uh some of these immature immature trophy in this ring space, they can without becoming a mature tro they can uh undergo sporogony stage and uh sorry, they can enzyme troph mature sexual stage, gametocyte rather, they can become gametocyte. These gametocyte contain male and female ga gametocyte. Now, when another mosquito, another an an muscular comes and takes a blood meal from the same person they take in these gametocyte, male and female gametocyte and enter the mosquito itself. Now, in the mosquito, we have this sporogony stage that is the mosquito stage. So, in the gut of this uh uh in the gut of this mosquito, these male and female, the micro macrogamete size, they undergo uh sexual reproduction in the gut of this mosquito producing or more Ekins. These eins are produced in the gut of these mosquitoes and this in it then uh multiply and forms and oocyst forms and oos this oocyst then eventually rupture releasing uh So inside oos what is what we call sporozoite are what in, injected into human. So, inside the oos is we find multiple sporocyst. So when this is ruptures, it releases the sporocyst into the uh muscle says these uh release, they invade their way into this uh muscular salivary glands. So once uh it takes, once this mosquito takes another blood meal, this uh spor sites from this uh salivary glands of these uh mosquitoes, they will, they can enter another organism's bloodstream. So this is how the whole stage takes place from a spors extra cycle that is inside the liver. And once they are off the liver, it enters the bloodstream. That cycle from the enter cycle. It can under a vicious cycle that it can continue to affect more red blood cells. Or it can then convert into aga to sites and uh into uh another muscular can intake in these gametocyte and uh continue cycle. So this is a whole cycle of how the malaria uh conducing fixed people. Now, moving on, let's talk about some uh specific good points about uh malaria. We talk about this plasma va and they have hypnos. Now, hypnos are not forms in normal cycle. The other malaria, they don't have this uh hypno. These hypnos are in the found in the liver, in the liver when they undergo this extra erythrocyte cycle. Uh with this uh s schizo formation formation hyoid. Now, these hypnos are what causes relapses. That is they can uh re reinvade the blood after some time. That is following treatment of this malaria. These dormant forms, they can remain in the liver and cause relapse after treatment. After months or years after treatment, they can come out of the liver and they can reinfect these humans. So they can cause relapses. So, the hypnotics are very specific for transporting we vac o also the clinical manifestations of malaria, they occur due to the erythrocyte. So the uh clinical manifestations of uh this uh uh asthma or this malaria, it is due to the erythrocyte schizo and the host reaction is it that is uh the all the clinical manifestations that occurred in this human being that occurs due this erythro cycle when the uh red blood cells are infected and when, when the red blood cells are killed. And that is when the schizo rupture and red blood cells is broken off. This is where all the clinical manifestations occur. And the host reaction them also can also further increase these uh clinical features. And this exoerythrocytic cycle that is in the liver, the liver cycle does not produce any symptoms. So that is another point to know. And uh when uh we should understand that are in this febrile phase, that is when I men, as I mentioned earlier, there will be fever spikes in these organisms. So this fever spikes, it occurs in three stages. That is this febrile perox occurs in three stages. So first is a cold stage. That is the initial stage, around 50 to 30 or 15 to 60 minute glasses where the patient has intense cold and shivering. And then with hot stage, this hot stage after the cold uh for around 2 to 6 hours, you hot space. A patient has high fever, severe headache and nausea, vomiting. The patient is very uh toxic looking. And then with the sweating, sweating stage and the patient is heavily, heavily uh sweats with perfuse sweat. The patient is like drenched in rain water and the temperature drops, tempera, the patient drops rapidly. Now, this fever uh that uh this fever periodicity. It is due to the rupture of this. As you can see when the uh schizo ruptures and the R BC was ruptured that this is where the fever spike occurs. So that fever spike is only the fever is mentioned here that is increase rupture. That is when the uh uh schizo rupture and the me are released from the R BC and RB is ruptured. That is where this fever spike occurs. Moving on. Now, we talk about symptoms. These are, I mean uh these are symptoms of uh malaria, they have headache, sweating, tiredness, miga, anorexia, abdominal pain, cough fever with ri. Now, malaria is very, is a classic example of fever with chills and RIS. Now, other cause of uh uh moving out of this paraly, other cause of chills. And we can have, we can see acute pyrites cholangitis, abscesses. They also we can see fever with pr and chills there. The patient has high fever with chills there, patient shivering but has very high fever. So these uh malaria acute PTIs Lan class classic features, these conditions, this fever chills and I guess the classic features of the um moving on. Now, when you talk about organ specific symptom that signs. So when this blood symptom in the blood, when you talk about thrombo, uh when you talk about in blood, that can be thrombocytopenia, that is decreased amount of platelets in the blood after this infection. So I see increased risk of bleeding in the patient. And hemolytic can even know as you can see the malaria infects red blood cells. So when the red blood cell infected, the red blood cells are broken down with the rupture, they broke down. So there's hemolytic anemia, the red vessels are broken down. This is the intravascular hem intravascular anemia. Then we have weakness paleness because of the uh these features of dizziness G I features, we have nausea, vomiting, diarrhea, and abdominal pain and there is hepatosplenomegaly. Now, this uh as the liver as, as the liver stays, liver has increased uh action. So they have undergo liver enlargement. And also these infected RP CS, they are taken to the uh spleen to be uh that killed or uh released. So the spleen has to start working heavily. So there are spleen is *** enlarge, but also So that can be sp hely. And as the liver is damaged in this process, there can be jaw disorder causing jaw disorder form and the CNS there can be hallucinations, confusions, uh impair consciousness seizures. Now, moving on, uh talking about the complications of any uh malaria, we have this severe malaria. Now, severe malaria is a uh it's a it's a severe severe malaria. It is a condition when uh caused by plato falciparum. So this occurs when this infected R BC, they go and block the capillaries. So when the capillaries are blocked, they can cause micro infarctions in a, in a, in a blood vessels. So when they this in art disease, they can go and clump there. So they can obstruct the blood flow, the small small microvessels and capillaries. So when they block those vessels, they can cause micro infarctions which can then cause this uh complication, severe complications. So here in this severe malaria, we can see uh the severe malaria, as I mentioned, it is most commonly found in Plasmodium falciparum because it causes a high severe disease. So you can patient can be frustrated that is they can be severe, extreme, severe uh physical and mental weakness and they can cerebral malaria, hallucinations, confusion, coma, and the patient can have variable uh posturing, that's extensive posturing or dysconjugate gaze. They can under uh they can become metabolic acidotic, they can have metabolic acidosis hypoglycemia and the patient can undergo acute renal failure because of the clumping of the vessel. Uh blood vessels in this a arterioles of the glomerular the kidneys. So the kidney can undergo acute renal failure. So we can, we can see oliguria because of decreased blood supply to the kidneys. And uh there's intravascular hemolysis, as I mentioned earlier because the red blood cells are broken down within the vessels. Is intravascular hemolysis occurring here. So, with this due to the intravascular hems, hemoglobin is uh hemoglobin and hemo hemoglobin is released in circulation which can then lead to hemoglobinuria. This hemoglobinuria gives the urine a dark urine color, which is which is what is called black water fever. So, malaria are the name is blackwood fever and also another thing it can cause is acute tuber necrosis. The respiratory syndrome uh is malaria can cause pulmonary edema, acute distress, acute respiratory stress syndrome. And the live uh the heart, it can cause shock with hypotension and in the capillary filter, more than three circles, it can cause cardio shock, also heart failure. So severe malaria is a very extreme condition. You should be uh quickly uh identified and treated. Now, other uh the lab, the laboratory findings for the severe malaria as mentioned in the wo we can see that severe anemia uh for adults less than seven g and less than five g, hypoglycemia, less than 40 mg, acidosis with carol lactate with the base def for eight millis or bicarbonate is less than 15 when there's hyperactive and lactic acid is uh were elevated, more than five or patient has acute kidney, a serum creatinine level of more than three mg or urea more than 20 millimoles of the pain. When this increase in breakdown of R BC, we can see this in uh in indirect bilirubin levels increases. So when the bilirubin level is more than three mg and high malaria param. Yeah, we will file I check see later in diagnosis how the paras is measured. And uh these are the lab findings which should be a be in alert when checking for severe malaria. Now we talk about diagnosis. First of all, we should always check upon the recent travel history with the patient has traveled to any endemic areas of this malaria. And if and if the patient has taken any uh malaria chemoprophylaxis and uh this malaria should be suspected in a patient who has fever greater than 99 °F who has traveled to an endemic area or who lives in an endemic area without another obvious cause. This malaria should always be suspected. Now, with uh moving on from the uh step one, which goal is for the lab studies. So we always go for a complete blood count. So this complete blood count uh we can see because the patient has hemolytic anemia, there has decreased hemo hemoglobin and the decreased haptoglobin. Uh haptoglobin is when the red vessels are broken down when they release hemoglobin, they go and bind to this haptoglobin. So as there's a large amount of red blood cells are broken down here. These haptoglobin are used up. They cause they bind hemoglobin is HEPB used up. So the amount of free Hepb decreases. So, decreased hemoglobin, decreased hep Tobin and there's increased L DH. Now this L DH is uh enzyme which is found within R BC. So when the R BC are damaged, these L DHS are released out. So there's increased L DH are found in blood that increase indirect bilirubin is uh bilirubin is a breakdown product of he. So before it becomes conjugated, before it undergoes breakdown or conjugation in the liver, it's called indirect bilirubin. So as this my my large amount of arteries are broken down, that's increase in the glub. And as I mentioned earlier, this particular size, which are the premature forms of normal red blood cells. They also elevated and uh thrombocytopenia as I mentioned earlier. And uh that can be leuko leukocytosis or leukopenia, which is very rare. Oh onco in the metabolic profile, we can see in severe malaria. As I mentioned earlier, we can see hypoglycemia or the acute kidney injury features are just the increased serum creatinine and uh electro abnormalities and the urine analysis, we can see there's hemoglobinuria that's increased hemoglobin as because the intravascular hemolysis is taking place and other examination, arterial blood class, uh blood type and screen can be done if there's need of. Uh you need to give blood to the patient or blood and urine cultures can be done if there's an altering diagnosis. If the, you all think there's an altering diagnosis and a CSF uh analysis can be done. Uh There is a lumbar puncture can be done to rule out uh bacterial meningitis. Now we talk a specific bacteriological exam, uh bacteriological examination. Uh we have now we have a rapid diagnostic RD. They, they detect the malaria antigens. So we these malaria antigens examples, we have HRP two or this plas LDH aldea. So these detect the these an so they can uh one specific point here, they can detect the pla falciparum only but they cannot distinguish between other piece of pla such as malaria or they cannot the distinguish between them. They can only specifically add into FC. And then we have the blood smear test. Uh blood smear test is the gold standard and that is for identification of uh this plasia. So it allows a vi it allows a visualization of uh these parasites uh within this R BC. Uh to confirm this is now used to confirm the diagnosis of malaria. So we have two types of smears. We have thick smears and thin smears, no three, thin and thin smears. There should be totally six and three ticks should be taken to 24 hours apart, should be obtained. That is uh to make a complete diagnosis. Now we talk about the thick blood smear. This thick blood smear, it is a highly sensitive and it is the best initial test. So the high sensitivity test. So we exam here, we examine larger blood volume and it detects the malaria parasites. Then we have the, then we have the thin blood smear. This thin blood smear has low sensitivity but it has high specificity to confirm it. It it is used for species identification and calculation of paras. So this thin blood smear is used to identify the species and also calculate the amount of parasites in the blood. So what you can find is you can find in this uh smear, we can find Granules which are fine do these are fine brick dots within the RB infected with this pla. So as you can see only in pla and O we can find Granules within this s as you can see this, uh the point I mentioned these Granules we can see within S so those are Granules which are only found in uh S over in and also uh in uh pla infected uh uh plasma infected persons, gametocyte game that I will show, you know, the blood smears are different, different stages. And you can see here this is the imma site which uh which is found in blood. So you can see this thick dark red or purple is a sign the shape in like inclusions. So that is found IMA now we moving on we talk about metros in metro we can is Amobi Rings like this collection of uh collection of this that is Amobi Rings that is found in Metz. In the next stage. When we have IOS this Emerson is like a irregular rounding collection uh collection of Amoebi body within the it's al it's like see as you can see, it's like almost feeling the entire erythrocyte. So it's a collection, it's like a collection of bodies and bodies. Then we have the mature schizo. So in mature schizo, we have a collection of merozoite around a collection of meroz which is surrounding a pigment in the center. So it's surrounding the central darkening. So we can see surrounding central darkening. There's a lot of merozoite. This is a mature schone, same thing you can see in this diagram also then we have the games. So we compare the macrogamete sites of this sri vivax malaria. We can see there are these three are oval shaped eccentric and they are compact chromatin, compact chromatin and they are uh scattered brown pigments. The brown pigment is called uh hemo hemozoin. Now in plasma in falciparum, it is a crescentic shape, falciparum with a central nucleus by a so dark pigment. Another examination we can do is a PCR assay. This is uh very sensitive and specific for determining the PAS species, but this PCR assay is not found everywhere. Uh uh This plasmid species. Uh This PCRs is not found in every uh place. So it is not very uh usually done everywhere, but it is very effective in detecting the plasma species in patients with low param, there are less than 10 per. So this PCR is very good for detecting that uh it's like a malaria. Then. Now moving on to management uh management for this uh plasmodium, we can go for support care. Initially, that is if the patient has fever, we can treat M amino or tapi sponging of the patient of curing blankets. Uh This pharmacological management, uh we have chloroquine and if the patient is resistant to chloroquine, we can go for art therapy. So if the patient has plain Biba, we can give chloroquine for three days with following with prima qui for 14 days for confirmed uh vivax to destroy, that is also to destroy the in the liver also. So we give this pre qui for 14 additional days and also we should be very uh specific because we there can be G six PD deficiency, uh G six PD glucose, six phosphate dehydrogenase. This is an enzyme which breaks down this uh which is the enzyme which is found in RB membranes. So, this uh drug can exacerbate uh this deficiency. If there is a uh this glucose six phosphate deficiency, it's a disease. The patient has deficient G six PD enzyme. So this uh this G six B red blood cells. So given this chloroquine and all these uh quiNINE they can uh exacerbate this condition which increase in RB destruction. So, uh so giving pre qui can cause he, as I mentioned now. So you should be, you need to check with the patient has adequate amount of G six PD before starting this uh qui therapy and moving on talk, a mono infection caused by falciparum that is uncomplicated. The patient does not have this severe malaria. If the, if this um falciparum is susceptible for this primaquine and chloroquine, we can give that. But nowadays, as they become more and more resistant to that uh the drugs, now we have this artemis based combination therapy. This Artemi is the mo uh newly used drug for uh F that F that is arte that is a combination therapy. This is followed by the, this is followed by a single dose of primaquine only to eradicate. The primaquine is only to be used only to eradicate the gametocyte. Now, we have treatment of uh this uh severe that is complicated falciparum. So we should immediately give IV art oral or we should give IV artesunate is more effective than IV. So we give IV ART and also once the patient is better, once he's able to take oral medications or excluding Children, less five, they should be given weight, appropriate course of this uh ate combination therapy, followed by a single dose of primaquine. And now uh we're talking about other supportive managements for the CE disease. Uh We can uh treat acute seizures with diazePAM if needed or if this patient is dehydrated or anything, we should quickly give a rapid fluid replacement, treat boluses. And also we should also rule out other secondary bacterial infections. So we should do blood cultures, urine cultures if needed. And the uh the patient can have hypoglycemia, as I mentioned earlier in the, we talking about severe uh FCI. So we should check the blood sugar levels every four hours and we can give a dextrose infusion if required. And we can monitor the hemoglobin and renal function daily. And this parasitemia should be measured on 7 to 28 days to monitor, monitor the response of therapy for this patient and all severe uh uh falciparum should be monitored in the ICU. OK, guys. Um that's it for today then. Thank you for attending this session.