Plasmodium species (Malaria)

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Plasmodium species (Malaria)

NBME

NBME

Amino acid metabolism
Nitrogen and urea cycle
Citric acid cycle
Electron transport chain and oxidative phosphorylation
Gluconeogenesis
Glycogen metabolism
Glycolysis
Pentose phosphate pathway
Physiological changes during exercise
Cholesterol metabolism
Fatty acid oxidation
Fatty acid synthesis
Ketone body metabolism
Alkaptonuria
Cystinuria (NORD)
Hartnup disease
Homocystinuria
Maple syrup urine disease
Ornithine transcarbamylase deficiency
Phenylketonuria (NORD)
Essential fructosuria
Galactosemia
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Hereditary fructose intolerance
Lactose intolerance
Pyruvate dehydrogenase deficiency
Abetalipoproteinemia
Familial hypercholesterolemia
Hyperlipidemia
Hypertriglyceridemia
Glycogen storage disease type I
Glycogen storage disease type II (NORD)
Glycogen storage disease type III
Glycogen storage disease type IV
Glycogen storage disease type V
Mucopolysaccharide storage disease type 1 (Hurler syndrome) (NORD)
Mucopolysaccharide storage disease type 2 (Hunter syndrome) (NORD)
Fabry disease (NORD)
Gaucher disease (NORD)
Krabbe disease
Leukodystrophy
Metachromatic leukodystrophy (NORD)
Niemann-Pick disease type C
Niemann-Pick disease types A and B (NORD)
Tay-Sachs disease (NORD)
Cystinosis
Disorders of amino acid metabolism: Pathology review
Disorders of carbohydrate metabolism: Pathology review
Disorders of fatty acid metabolism: Pathology review
Dyslipidemias: Pathology review
Glycogen storage disorders: Pathology review
Lysosomal storage disorders: Pathology review
Carbohydrates and sugars
Fats and lipids
Proteins
Excess Vitamin A
Excess Vitamin D
Vitamin D deficiency
Vitamin K deficiency
Kwashiorkor
Marasmus
Iodine deficiency
Zinc deficiency
Beriberi
Folate (Vitamin B9) deficiency
Niacin (Vitamin B3) deficiency
Vitamin B12 deficiency
Vitamin C deficiency
Wernicke-Korsakoff syndrome
Fat-soluble vitamin deficiency and toxicity: Pathology review
Water-soluble vitamin deficiency and toxicity: B1-B7: Pathology review
Zinc deficiency and protein-energy malnutrition: Pathology review
Cell membrane
Cell signaling pathways
Cell-cell junctions
Cellular structure and function
Cytoskeleton and intracellular motility
Endocytosis and exocytosis
Extracellular matrix
Nernst equation
Osmosis
Resting membrane potential
Selective permeability of the cell membrane
Alport syndrome
Ehlers-Danlos syndrome
Marfan syndrome
Osteogenesis imperfecta
Primary ciliary dyskinesia
Adrenoleukodystrophy (NORD)
Zellweger spectrum disorders (NORD)
Cytoskeleton and elastin disorders: Pathology review
Peroxisomal disorders: Pathology review
DNA cloning
ELISA (Enzyme-linked immunosorbent assay)
Fluorescence in situ hybridization
Gel electrophoresis and genetic testing
Karyotyping
Polymerase chain reaction (PCR) and reverse-transcriptase PCR (RT-PCR)
Amino acids and protein folding
Cell cycle
DNA damage and repair
DNA mutations
DNA replication
DNA structure
Epigenetics
Gene regulation
Lac operon
Mitosis and meiosis
Nuclear structure
Nucleotide metabolism
Protein structure and synthesis
Transcription of DNA
Translation of mRNA
Adenosine deaminase deficiency
Lesch-Nyhan syndrome
Orotic aciduria
Bloom syndrome
Fanconi anemia
Li-Fraumeni syndrome
McCune-Albright syndrome
Xeroderma pigmentosum
Acute radiation syndrome
Purine and pyrimidine synthesis and metabolism disorders: Pathology review
Human development days 1-4
Human development days 4-7
Human development week 2
Human development week 3
Development of the digestive system and body cavities
Development of the fetal membranes
Development of the placenta
Development of the umbilical cord
Development of twins
Hedgehog signaling pathway
Ectoderm
Endoderm
Mesoderm
Development of the cardiovascular system
Fetal circulation
Development of the ear
Development of the eye
Development of the face and palate
Pharyngeal arches, pouches, and clefts
Development of the gastrointestinal system
Development of the teeth
Development of the tongue
Development of the axial skeleton
Development of the limbs
Development of the muscular system
Development of the nervous system
Development of the renal system
Development of the reproductive system
Development of the respiratory system
Evolution and natural selection
Hardy-Weinberg equilibrium
Independent assortment of genes and linkage
Inheritance patterns
Mendelian genetics and punnett squares
Achondroplasia
Alagille syndrome (NORD)
Familial adenomatous polyposis
Hereditary spherocytosis
Huntington disease
Multiple endocrine neoplasia
Myotonic dystrophy
Neurofibromatosis
Polycystic kidney disease
Treacher Collins syndrome
Tuberous sclerosis
von Hippel-Lindau disease
Albinism
Alpha-thalassemia
Beta-thalassemia
Cystic fibrosis
Friedreich ataxia
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Sickle cell disease (NORD)
Wilson disease
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Prader-Willi syndrome
Beckwith-Wiedemann syndrome
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Fragile X syndrome
Down syndrome (Trisomy 21)
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Hemophilia
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X-linked agammaglobulinemia
Autosomal trisomies: Pathology review
Miscellaneous genetic disorders: Pathology review
Muscular dystrophies and mitochondrial myopathies: Pathology review
Bacterial structure and functions
Bacillus anthracis (Anthrax)
Bacillus cereus (Food poisoning)
Corynebacterium diphtheriae (Diphtheria)
Listeria monocytogenes
Clostridium botulinum (Botulism)
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Clostridium perfringens
Clostridium tetani (Tetanus)
Actinomyces israelii
Nocardia
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Staphylococcus epidermidis
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Streptococcus agalactiae (Group B Strep)
Streptococcus pneumoniae
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Enterococcus
Bacteroides fragilis
Bartonella henselae (Cat-scratch disease and Bacillary angiomatosis)
Enterobacter
Escherichia coli
Klebsiella pneumoniae
Legionella pneumophila (Legionnaires disease and Pontiac fever)
Proteus mirabilis
Pseudomonas aeruginosa
Salmonella (non-typhoidal)
Salmonella typhi (typhoid fever)
Serratia marcescens
Shigella
Yersinia enterocolitica
Yersinia pestis (Plague)
Campylobacter jejuni
Helicobacter pylori
Vibrio cholerae (Cholera)
Moraxella catarrhalis
Neisseria gonorrhoeae
Neisseria meningitidis
Bordetella pertussis (Whooping cough)
Brucella
Francisella tularensis (Tularemia)
Haemophilus ducreyi (Chancroid)
Haemophilus influenzae
Pasteurella multocida
Mycobacterium tuberculosis (Tuberculosis)
Mycobacterium avium complex (NORD)
Mycobacterium leprae
Chlamydia pneumoniae
Chlamydia trachomatis
Gardnerella vaginalis (Bacterial vaginosis)
Mycoplasma pneumoniae
Coxiella burnetii (Q fever)
Ehrlichia and Anaplasma
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Borrelia burgdorferi (Lyme disease)
Borrelia species (Relapsing fever)
Leptospira
Treponema pallidum (Syphilis)
Malassezia (Tinea versicolor and Seborrhoeic dermatitis)
Aspergillus fumigatus
Candida
Cryptococcus neoformans
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Toxoplasma gondii (Toxoplasmosis)
Cryptosporidium
Entamoeba histolytica (Amebiasis)
Giardia lamblia
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Plasmodium species (Malaria)
Leishmania
Trichomonas vaginalis
Trypanosoma brucei
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Diphyllobothrium latum
Echinococcus granulosus (Hydatid disease)
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Anisakis
Ascaris lumbricoides
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Guinea worm (Dracunculiasis)
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Onchocerca volvulus (River blindness)
Strongyloides stercoralis
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Trichinella spiralis
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Paragonimus westermani
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Viral structure and functions
Adenovirus
Hepatitis B and Hepatitis D virus
Cytomegalovirus
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Human papillomavirus
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Poxvirus (Smallpox and Molluscum contagiosum)
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Norovirus
Coronaviruses
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HIV (AIDS)
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Rabies virus
Eastern and Western equine encephalitis virus
Rubella virus
Prions (Spongiform encephalopathy)
Antimetabolites: Sulfonamides and trimethoprim
Antituberculosis medications
Cell wall synthesis inhibitors: Cephalosporins
Cell wall synthesis inhibitors: Penicillins
DNA synthesis inhibitors: Fluoroquinolones
DNA synthesis inhibitors: Metronidazole
Mechanisms of antibiotic resistance
Miscellaneous cell wall synthesis inhibitors
Miscellaneous protein synthesis inhibitors
Protein synthesis inhibitors: Aminoglycosides
Protein synthesis inhibitors: Tetracyclines
Azoles
Echinocandins
Miscellaneous antifungal medications
Anthelmintic medications
Anti-mite and louse medications
Antimalarials
Hepatitis medications
Herpesvirus medications
Integrase and entry inhibitors
Neuraminidase inhibitors
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Nucleoside reverse transcriptase inhibitors (NRTIs)
Protease inhibitors
Introduction to pharmacology
Enzyme function
Drug administration and dosing regimens
Pharmacodynamics: Agonist, partial agonist and antagonist
Pharmacodynamics: Desensitization and tolerance
Pharmacodynamics: Drug-receptor interactions
Pharmacokinetics: Drug absorption and distribution
Pharmacokinetics: Drug elimination and clearance
Pharmacokinetics: Drug metabolism
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
Adrenergic antagonists: Presynaptic
Adrenergic receptors
Cholinergic receptors
Cholinomimetics: Direct agonists
Cholinomimetics: Indirect agonists (anticholinesterases)
Muscarinic antagonists
Sympatholytics: Alpha-2 agonists
Sympathomimetics: Direct agonists
Selective serotonin reuptake inhibitors
Atypical antidepressants
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Serotonin and norepinephrine reuptake inhibitors
Tricyclic antidepressants
Atypical antipsychotics
Typical antipsychotics
Anticonvulsants and anxiolytics: Barbiturates
Anticonvulsants and anxiolytics: Benzodiazepines
Lithium
Nonbenzodiazepine anticonvulsants
Psychomotor stimulants
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Lipid-lowering medications: Fibrates
Lipid-lowering medications: Statins
Miscellaneous lipid-lowering medications
Positive inotropic medications
Adrenal hormone synthesis inhibitors
Mineralocorticoids and mineralocorticoid antagonists
Hypoglycemics: Insulin secretagogues
Insulins
Miscellaneous hypoglycemics
Hyperthyroidism medications
Hypothyroidism medications

Assessments

Flashcards

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USMLE® Step 1 questions

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CME Credits

2.25 / 18.5 complete

High Yield Notes

6 pages

Flashcards

Plasmodium species (Malaria)

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Questions

USMLE® Step 1 style questions USMLE

0 of 4 complete

A group of microbiologists are investigating Plasmodium species and their ability to cause malaria. Which of the following stages of the Plasmodium life cycle is responsible for causing initial infection?  

External References

First Aid

2024

2023

2022

2021

Anemia

malaria p. 154

Artesunate

malaria p. 154, 198

Atovaquone

malaria p. 154

Chloroquine p. 198

malaria p. 154

Fever

malaria p. 154

Headache p. 532

malaria p. 154

Malaria

anemia in p. 415

artesunate for p. 198

Plasmodium p. , 154

quinidine/quinine for p. 198

Mosquitoes (disease vectors)

malaria p. 154

Splenomegaly

malaria p. 154

Transcript

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Malaria is an infection that can be caused by a few different types of Plasmodium species, which are single-celled parasites that get spread around by mosquitoes.

Once the plasmodium gets into the bloodstream, it starts to infect and destroy mainly liver cells and red blood cells, which causes a variety of symptoms and sometimes even death.

Malaria is a serious global health problem that affects millions of people, particularly young children under the age of 5, pregnant women, patients with other health conditions like HIV and AIDS, and travelers who have had no prior exposure to malaria.

Tropical and subtropical regions are hit the hardest, together the most affected regions form the malaria belt, which is a broad band around the equator that includes much of latin america, sub-saharan africa, south asia, and southeast asia.

There are hundreds of types of Plasmodium species, but only five cause malarial disease in humans, and those are Plasmodium falciparum, Plasmodium vivax, Plasmodium malariae, Plasmodium ovale, and Plasmodium knowlesi.

Plasmodium vivax uses a specific erythrocyte surface receptor called the Duffy antigen.

And some individuals, particularly those with sickle-cell anemia lack this receptor, meaning that Plasmodium vivax cannot get into their cells.

In other words, having sickle cell anemia is genetically related to having relative protection from Plasmodium vivax.

Other diseases, like thalassemia and G6PD deficiency make the parasite-infected erythrocyte more susceptible to dying from oxidative stress.

So despite the obvious downside to having any of these diseases, they do offer an upside when it comes to warding off a malaria infection.

In fact, because malaria has historically circulated in Africa, the genes underlying these diseases are thought to have conferred a natural selection advantage and therefore become more common in the genetic pool.

Now, malaria begins when a plasmodium-infected female Anopheles mosquito hunts for a blood meal in the evening and through the night.

Like a tiny flying vampire, the mosquito is drawn to carbon dioxide that get breathed out as well as bodily smells, like foot odor.

At this point, the Plasmodium is in a stage of development called a sporozoite, waiting patiently in the mosquito’s salivary gland.

When the mosquito pierces a person’s skin with its long and needle-shaped tusk, called a proboscis, the tiny, worm-like sporozoites spill out of the mosquito’s saliva and make it into the bloodstream.

Within minutes, the sporozoites reach the liver and mount an attack on hepatic parenchymal cells where they begin asexual reproduction also known as schizogony.

At this point, the plasmodium species vary a bit.

Over the next 1-2 weeks, Plasmodium falciparum, Plasmodium malariae, and Plasmodium knowlesi sporozoites multiply asexually and mature into merozoites, while host hepatic parenchymal cells die.

In contrast, over the next few months to years, Plasmodium vivax and Plasmodium ovale sporozoites enter into a dormant hepatic phase, where they are called hypnozoites.

Hypnozoites don’t divide - instead they snooze for a period of time before entering the process of schizogony, causing a long delay between the initial infection and symptoms from the disease.

This is called the exoerythrocytic phase because it happens outside of the erythrocyte or red blood cell, and it’s generally asymptomatic.

The merozoites are then released into the blood, and each one binds to a surface receptor and invades a red blood cell.

Plasmodium ovale and Plasmodium falciparum invade red blood cells of all ages, whereas Plasmodium vivax prefers to invade reticulocytes which are young, immature red blood cells, and Plasmodium malariae and Plasmodium knowlesi prefer to invade older red blood cells.

Once inside the red blood cell, the merozoite undergoes asexual reproduction and a series of transformational changes.

This phase is known as the erythrocytic phase of malaria, because it happens inside of the red blood cell and generally lasts 2 to 3 days.

In the first stage of the erythrocytic phase the merozoite looks like a tiny ring within the red blood cell and is called an early trophozoite or a ring form.

In the second stage, the ring form trophozoite grows and is referred to as a late trophozoite.

In the third and final stage, the parasite grows some more by digesting hemoglobin and leaves behind hemozoin, which under a microscope looks a little like a brown feces smudge on the red blood cell, and at this point the parasite is called a schizont.

This is the actual replicative phase in which the parasite undergoes mitosis and differentiates into lots of merozoites which can get released into the blood.

Now, instead of going into the erythrocytic phase again, some of the merozoites undergo gametogony which is where they divide and give rise to gametocytes which are little sausage-shaped sexual forms that can be either male or female.

These gametocytes remain inside of a red blood cell, and can get sucked up by another female Anopheles mosquito that might take a blood meal from the infected person.

The gametocytes can then reach the mosquito's gut where they mature a bit more and then fuse together to form a zygote.

This part of the plasmodium life cycle is called sporogony, and it’s sexual reproduction, as opposed to the schizogony or asexual reproduction that happened in the liver and red blood cells.

The zygote then goes on to develop further, it becomes an ookinete and then an oocyst that ruptures in the mosquito’s gut, releasing thousands of sporozoites which navigate their way into the mosquito's salivary gland, in order to repeat the cycle all over again.

Now, the incubation time, which is the period of time between infection and symptom onset, varies depending on the plasmodium species.

Plasmodium falciparum incubates for a few days, whereas Plasmodium malariae incubates for a few weeks.

The release of tumor necrosis factor alpha and other inflammatory cytokines, causes fevers that typically occur in paroxysms or short bursts, and correspond to the rupture of the infected red blood cells, which happens in waves of reproductive cycles unique for each plasmodium species.

For Plasmodium malariae, fevers happen every 72 hours, and is called quartan fever.

For Plasmodium vivax and Plasmodium ovale, fevers happen every 48 hours, and these are called tertian fever.

For Plasmodium knowlesi, the fever happens every 24 hours, and for Plasmodium falciparum, the pattern can vary - sometimes following the pattern of tertian fever, while other times the fevers happen daily, earning it the name malignant tertian fever.

Summary

Plasmodium is a genus of parasites that cause malaria in humans and other animals. Five species of Plasmodium primarily infect humans: P. falciparum, P. vivax, P. ovale, P. malariae, and P. knowlesi. People get infected with malaria when they are bitten by a plasmodium-infected female Anopheles mosquito. P. falciparum is known to cause the most dangerous form of malaria, resulting in most of malaria deaths worldwide. Treatment typically involves antimalarial drugs such as chloroquine, mefloquine, or artemisinin-based combination therapies.