You are viewing a free preview of this lesson.
Subscribe to unlock all 10 lessons in this course and every other course on LearningBro.
Microorganisms are organisms that are too small to be seen with the naked eye. This lesson provides a comprehensive overview of the four major groups of microorganisms — bacteria, viruses, fungi and protoctista — as required by the Edexcel A-Level Biology (9BI0) specification. Understanding the structural differences between these groups is essential for explaining how they cause disease and how they can be controlled.
Microorganisms are diverse and do not form a single taxonomic group. The key groups relevant to A-Level Biology are:
| Group | Cell type | Key features |
|---|---|---|
| Bacteria | Prokaryotic | No membrane-bound nucleus; cell wall of peptidoglycan (murein) |
| Viruses | Acellular (not cells) | No cellular structure; contain DNA or RNA within a protein coat |
| Fungi | Eukaryotic | Cell wall of chitin; heterotrophic; may be unicellular (yeast) or multicellular |
| Protoctista | Eukaryotic | Diverse group; some photosynthetic (algae), some parasitic (Plasmodium) |
Bacteria are prokaryotic organisms — they lack a membrane-bound nucleus and membrane-bound organelles.
| Structure | Description | Function |
|---|---|---|
| Cell wall | Made of peptidoglycan (murein) — a polymer of sugars cross-linked by short peptide chains | Maintains cell shape; prevents lysis due to osmotic pressure |
| Cell surface membrane | Phospholipid bilayer | Controls entry and exit of substances; site of some metabolic reactions |
| Capsule (slime layer) | Polysaccharide layer outside the cell wall (not always present) | Protection from phagocytosis; aids adhesion to surfaces |
| Cytoplasm | Gel-like matrix | Site of metabolic reactions |
| Ribosomes (70S) | Smaller than eukaryotic ribosomes (80S) | Protein synthesis |
| Nucleoid | Region containing a single, circular chromosome (DNA) — not enclosed by a membrane | Carries the main genetic information |
| Plasmids | Small, circular, extra-chromosomal DNA molecules | Carry genes for antibiotic resistance, toxin production; can be transferred between bacteria |
| Flagellum (plural: flagella) | Protein filament | Locomotion |
| Pili | Short, hair-like protein projections | Adhesion to surfaces; conjugation (transfer of plasmids between cells) |
| Mesosome | Infolding of the cell membrane (now debated as an artefact) | Historically associated with respiration and cell division |
Bacteria are classified into two major groups based on their cell wall structure, revealed by Gram staining:
| Feature | Gram-positive | Gram-negative |
|---|---|---|
| Peptidoglycan layer | Thick | Thin |
| Outer membrane | Absent | Present (contains lipopolysaccharides/endotoxin) |
| Gram stain colour | Purple/violet | Pink/red |
| Antibiotic susceptibility | Generally more susceptible to penicillin | Often more resistant (outer membrane acts as barrier) |
Exam Tip: Gram-negative bacteria are often harder to treat with antibiotics because their outer membrane provides an additional barrier. This is clinically important and may appear in exam questions about antibiotic resistance.
| Shape | Name | Example |
|---|---|---|
| Spherical | Cocci | Staphylococcus aureus |
| Rod-shaped | Bacilli | Escherichia coli, Mycobacterium tuberculosis |
| Spiral | Spirilla | Treponema pallidum |
| Comma-shaped | Vibrios | Vibrio cholerae |
Viruses are acellular — they are not cells and are not classified as living organisms by most biologists. They are obligate intracellular parasites, meaning they can only replicate inside a host cell.
| Structure | Description |
|---|---|
| Nucleic acid core | Either DNA or RNA (never both); may be single-stranded or double-stranded |
| Capsid | Protein coat surrounding the nucleic acid; composed of capsomeres |
| Envelope (some viruses) | Lipid bilayer derived from the host cell membrane; contains glycoprotein spikes |
| Glycoprotein spikes | Surface proteins used for attachment to host cell receptors |
| Virus | Nucleic acid | Target cells | Disease |
|---|---|---|---|
| HIV | RNA (retrovirus) | T helper cells (CD4⁺) | AIDS |
| Influenza | RNA | Respiratory epithelial cells | Flu |
| SARS-CoV-2 | RNA | Respiratory epithelial cells (ACE2 receptor) | COVID-19 |
| TMV (Tobacco mosaic virus) | RNA | Plant mesophyll cells | Mosaic disease in tobacco |
| Bacteriophage (phage) | DNA | Bacteria | Lysis of bacterial cells |
Exam Tip: Viruses are not killed by antibiotics. Antibiotics target bacterial structures (e.g. cell walls, ribosomes) that viruses do not possess. Antiviral drugs work by inhibiting specific stages of the viral replication cycle.
Fungi are eukaryotic organisms with cell walls made of chitin. They are heterotrophic, obtaining nutrients by saprotrophic (decomposer) or parasitic nutrition.
| Feature | Detail |
|---|---|
| Cell wall | Made of chitin (a polysaccharide of N-acetylglucosamine) |
| Cell membrane | Contains ergosterol (not cholesterol, as in animal cells) |
| Nucleus | Membrane-bound; eukaryotic |
| Organelles | Mitochondria, ER, Golgi, ribosomes (80S) |
| Body form | Unicellular (yeast) or multicellular (moulds and mushrooms) |
| Hyphae | Thread-like filaments forming the body of multicellular fungi; may be septate (divided) or coenocytic (undivided, multinucleate) |
| Mycelium | Network of hyphae |
Saprotrophic fungi secrete extracellular enzymes (exoenzymes) onto dead organic material, digesting it externally and absorbing the soluble products. This makes them crucial decomposers in ecosystems.
Protoctista (also called protists) are a diverse group of eukaryotic organisms that do not fit into the plant, animal, or fungi kingdoms. They include both autotrophic and heterotrophic forms.
| Type | Characteristics | Examples |
|---|---|---|
| Algae (plant-like) | Photosynthetic; contain chloroplasts | Chlorella, Spirogyra, diatoms |
| Protozoa (animal-like) | Heterotrophic; motile | Plasmodium (malaria), Amoeba, Trypanosoma |
Plasmodium is a protoctistan parasite that causes malaria. It has a complex life cycle involving two hosts:
| Stage | Host | Detail |
|---|---|---|
| Sexual reproduction | Female Anopheles mosquito | Gametes form in the mosquito gut; sporozoites migrate to salivary glands |
| Asexual reproduction | Human | Sporozoites infect liver cells, then merozoites infect red blood cells, causing their lysis |
The destruction of red blood cells causes the characteristic symptoms of malaria: fever, chills, anaemia, and fatigue.
| Feature | Bacteria | Viruses | Fungi | Protoctista |
|---|---|---|---|---|
| Cell type | Prokaryotic | Acellular | Eukaryotic | Eukaryotic |
| Nucleus | No (nucleoid) | No | Yes | Yes |
| Cell wall | Peptidoglycan | No (capsid) | Chitin | Varies (cellulose in algae; absent in protozoa) |
| Ribosomes | 70S | None | 80S | 80S |
| Reproduction | Binary fission | Host-dependent replication | Spores / budding | Binary fission / sexual |
| Size range | 0.2–10 µm | 20–300 nm | 2 µm – metres | 1 µm – cm |
| Metabolism | Own metabolism | No own metabolism | Own metabolism | Own metabolism |
| Term | Definition |
|---|---|
| Prokaryote | An organism whose cells lack a membrane-bound nucleus and membrane-bound organelles |
| Obligate intracellular parasite | An organism (e.g. a virus) that can only reproduce inside a living host cell |
| Peptidoglycan | The polymer that forms the bacterial cell wall; also called murein |
| Capsid | The protein coat of a virus |
| Chitin | The polysaccharide that forms the cell wall of fungi |
| Saprotrophic nutrition | Feeding by secreting enzymes onto dead organic matter and absorbing the soluble products |
The Edexcel 9BI0 specification places the four major pathogen classes within Topic 6: Immunity, Infection and Forensics, with substantial synoptic overlap into Topic 2: Cells, Viruses and Reproduction (prokaryotic ultrastructure, viral lytic and lysogenic cycles, 70S vs 80S ribosomes underpinning selective antibiotic toxicity), Topic 1: Lifestyle, Health and Risk (cell-wall composition: peptidoglycan in bacteria, chitin in fungi, cellulose in plants), and Topic 8: Genetics, Populations, Evolution and Ecosystems (bacteria as recombinant-DNA vectors and as the source of restriction enzymes). The relevant statements concern: distinguishing bacteria, viruses, fungi and protoctista by cellular organisation, cell-wall and cell-membrane composition, mode of nutrition and reproduction; naming representative pathogens of each class (for example Mycobacterium tuberculosis, influenza virus, HIV, Candida albicans, ringworm dermatophytes, Plasmodium falciparum); and explaining how structural differences between host and pathogen underpin selective drug toxicity. Synoptic threads run into Topic 2 (binary fission and viral replication) and Topic 8 (antimicrobial resistance evolving by selection on bacterial populations) (refer to the official Pearson Edexcel 9BI0 specification document for exact wording).
Question (8 marks):
A microbiologist isolates four pathogens from clinical specimens: pathogen W is rod-shaped, 2,mum long, has a peptidoglycan cell wall and divides by binary fission; pathogen X is 100,nm across, has a protein capsid surrounding a single-stranded RNA genome, and replicates only inside human cells; pathogen Y is multicellular with a chitinous cell wall and grows as branching hyphae; pathogen Z is a single-celled eukaryote with a complex life cycle alternating between human and Anopheles mosquito hosts.
(a) Identify the broad class of each pathogen, justifying your classification with reference to the structural or biological features given. (4)
(b) Explain why an antibiotic that targets peptidoglycan synthesis would be effective against pathogen W but not against pathogens X, Y or Z. (4)
Solution with mark scheme:
(a) Step 1 — interpret each set of clues. W: rod-shaped, peptidoglycan wall, binary fission identifies a bacterium (prokaryote). X: capsid + RNA + obligate intracellular replication identifies a virus. Y: chitin wall + multicellular hyphae identifies a fungus. Z: single-celled eukaryote with a vector-borne life cycle alternating between human and Anopheles identifies a protoctistan (specifically Plasmodium causing malaria).
M1 (AO2.1) — bacterium identified from peptidoglycan + binary fission. Common error: candidates write "prokaryote" without naming it as bacterial, or write "rod" without linking the structural clue to classification.
M1 (AO2.1) — virus identified from capsid + RNA + obligate intracellular replication. The acellular nature is the key diagnostic feature.
M1 (AO2.1) — fungus identified from chitin + hyphae. Marks lost where candidates write "plant" because they remember "cell wall" without specifying its composition.
A1 (AO1.2) — protoctistan identified from "single-celled eukaryote with vector-borne life cycle alternating between human and Anopheles". Naming Plasmodium secures the A1; "protozoan" alone is also creditable.
(b) Step 1 — establish the molecular target. Peptidoglycan is found only in bacterial cell walls; it is absent from human cells, viruses, fungi (chitin) and protoctista (no rigid wall in Plasmodium).
M1 (AO1.1) — peptidoglycan is bacteria-specific.
Step 2 — apply selective toxicity reasoning to each pathogen.
M1 (AO2.1) — antibiotic effective against W because eta-lactam drugs (e.g. penicillin) inhibit transpeptidase, preventing peptidoglycan cross-linking and causing osmotic lysis.
M1 (AO2.1) — ineffective against X (virus) because viruses have no peptidoglycan and no cell wall at all; their capsid is protein.
A1 (AO3.1a) — ineffective against Y (chitin wall, not peptidoglycan) and Z (no rigid wall; Plasmodium membranes are unsuitable targets for eta-lactams); a single sentence connecting wall composition to drug specificity earns the AO3 evaluation mark.
Total: 8 marks.
Question (6 marks): A new antimicrobial agent inhibits 70S ribosomes but spares 80S ribosomes. Explain which microorganisms would be susceptible to this agent and which would be resistant, and discuss any side-effects you would predict in human patients.
Mark scheme decomposition by AO:
| Marking point | AO | Credit-worthy content |
|---|---|---|
| 1 | AO1.1 | States that bacteria have 70S ribosomes (susceptible) whereas eukaryotes (fungi, protoctista, human cells) have 80S cytoplasmic ribosomes. |
| 2 | AO1.2 | Explains that viruses have no ribosomes of their own and would not be directly targeted. |
| 3 | AO2.1 | Applies to fungi and protoctista: their 80S cytoplasmic ribosomes spare them, so this agent is not an antifungal or antiprotozoal. |
| 4 | AO2.1 | Applies to therapy: useful against bacterial pathogens such as Mycobacterium tuberculosis. |
| 5 | AO3.1a | Predicts a side-effect: human mitochondrial ribosomes are 70S (endosymbiotic origin), so off-target inhibition can cause mitochondrial toxicity. |
| 6 | AO3.2a | Concludes by linking dose to side-effect: ototoxicity, hepatotoxicity or marrow suppression are credible because of mitochondrial 70S binding. |
Total: 6 marks split AO1 = 2, AO2 = 2, AO3 = 2. This is a typical Section A "explain how" question — Edexcel rewards candidates who use the 70S/80S distinction synoptically (AO2/AO3) rather than merely stating it (AO1).
| AO | Typical share on this topic | Earned by |
|---|---|---|
| AO1 (knowledge) | 40–50% | Naming the four classes, recalling cell-wall composition, distinguishing 70S from 80S, naming representative pathogens, stating modes of reproduction |
| AO2 (application) | 35–45% | Applying class characteristics to identify unfamiliar pathogens from descriptions; predicting which drug class will work against a given organism; reasoning from structure to treatment |
| AO3 (analysis / evaluation) | 10–20% | Evaluating antimicrobial-resistance evolution; predicting side-effects from off-target conserved structures; discussing why viruses are difficult drug targets |
Examiner-rewarded phrasing: "bacteria possess a peptidoglycan cell wall, the target of eta-lactam antibiotics such as penicillin"; "viruses are acellular obligate intracellular parasites lacking metabolism and ribosomes of their own"; "fungi are eukaryotic with chitinous cell walls and 80S cytoplasmic ribosomes, so antifungal agents must target fungal-specific structures such as ergosterol biosynthesis"; "Plasmodium falciparum is a protoctistan whose life cycle alternates between an Anopheles mosquito vector and a vertebrate host".
Phrases that lose marks: "germs cause disease" (vague — credit requires naming the class); "viruses are alive" (the spec position is nuanced — viruses replicate and evolve but lack metabolism, growth and homeostasis, so do not fulfil the standard criteria of life); "all microorganisms are bacteria" (a category error that conflates four distinct kingdoms); "fungi are plants" (fungi are a separate kingdom with chitin, not cellulose, walls and heterotrophic, not autotrophic, nutrition); "Plasmodium is a bacterium" (a protoctistan, fully eukaryotic).
Question: State three structural or biological features that distinguish a virus from a bacterium. (3)
Grade C response (~140 words):
Bacteria are bigger than viruses. Bacteria have cell walls but viruses do not have cell walls. Bacteria can divide on their own but viruses need a host cell. Bacteria are alive and viruses are not really alive.
Examiner commentary: Awarded 2/3. The candidate identifies the size difference (M1, marginal), the cell-wall absence (M1) and the obligate-intracellular requirement (M1). However, "bacteria are alive and viruses are not really alive" is a vague, non-biological repetition that adds no new structural feature; examiners do not credit a fourth point that paraphrases the third. The candidate also misses precise vocabulary — "capsid" and "peptidoglycan" would have lifted the answer to the A* band.
Grade A response (~165 words):*
Bacteria are cellular prokaryotes typically 1–5,mum in size with a peptidoglycan cell wall, 70S ribosomes and a circular chromosome free in the cytoplasm; they reproduce by binary fission. Viruses are acellular, 20–300,nm in size, consist of a protein capsid enclosing a DNA or RNA genome (sometimes within a lipid envelope derived from the host membrane), have no ribosomes or metabolic machinery, and replicate only inside a living host cell by hijacking host ribosomes and nucleic-acid polymerases.
Examiner commentary: Full marks (3/3). The candidate gives three crisp axes of comparison (cellularity, biochemistry, mode of replication) and uses precise vocabulary (peptidoglycan, capsid, 70S, binary fission, obligate intracellular). Naming three axes rather than three loose facts is the structural move that distinguishes A* from A.
Question: Mycobacterium tuberculosis and Candida albicans are both treatable infectious agents but require different drug classes. Explain how their structural differences determine the choice of antimicrobial drug. (6)
Grade B response (~245 words):
M. tuberculosis is a bacterium and Candida is a fungus, so they need different drugs. Bacteria have peptidoglycan cell walls so antibiotics like penicillin can attack them by stopping the cell wall being made. Fungi have chitin cell walls so penicillin doesn't work. Antifungal drugs are needed instead. Bacteria also have 70S ribosomes which can be targeted by antibiotics like streptomycin. Fungi have 80S ribosomes so these drugs don't work on them.
Examiner commentary: Awarded 4/6. The candidate covers the key structural divide (peptidoglycan vs chitin walls; 70S vs 80S ribosomes) and links each to a representative drug class. However, the answer is mechanistically thin: the candidate does not name a specific antifungal target (e.g. ergosterol biosynthesis, the target of azole drugs, or eta-1,3-glucan synthase, the target of echinocandins), nor explain why M. tuberculosis specifically requires combination therapy (its waxy mycolic-acid envelope and slow growth necessitate prolonged multi-drug regimens). Mentioning that Candida membranes contain ergosterol (whereas human membranes contain cholesterol) is exactly the kind of biochemical specificity that examiners credit at A*.
Grade A response (~290 words):*
Mycobacterium tuberculosis is a bacterial prokaryote whose cell envelope combines a peptidoglycan cell wall with an outer waxy layer of mycolic acids. The peptidoglycan layer is the target of eta-lactam antibiotics, but the mycolic-acid coating renders the organism inherently slow to permeate, so first-line therapy uses isoniazid (which inhibits mycolic-acid synthesis) and rifampicin (which inhibits bacterial RNA polymerase) in a combination regimen designed to suppress resistance. M. tuberculosis also has 70S ribosomes, the target of streptomycin, used as a second-line agent. Treatment is prolonged (six months) because of the organism's slow growth and intracellular persistence in macrophages.
Candida albicans is a eukaryotic fungus with a chitin and eta-glucan cell wall and an ergosterol-rich plasma membrane. eta-lactam antibiotics are useless because there is no peptidoglycan target. Instead, azole drugs (e.g. fluconazole) inhibit lanosterol 14alpha-demethylase, blocking ergosterol biosynthesis, and echinocandins (e.g. caspofungin) inhibit eta-1,3-glucan synthase, weakening the fungal wall. Selective toxicity is achieved because human membranes contain cholesterol, not ergosterol, and human cells lack a eta-glucan wall altogether. Candida shares 80S cytoplasmic ribosomes with the human host, so ribosomal inhibitors used against bacteria are inappropriate.
Examiner commentary: Full marks (6/6). The candidate links each pathogen's specific cell-envelope chemistry to a named drug class and gives the molecular target in each case (transpeptidase for eta-lactams; lanosterol 14alpha-demethylase for azoles; eta-1,3-glucan synthase for echinocandins). The answer also reaches AO3 by reasoning about why combination therapy is required for M. tuberculosis — slow growth, intracellular persistence, and the suppression of resistance evolution. The cholesterol-versus-ergosterol contrast is the clinching A* detail.
Question: Compare and contrast the four major pathogen classes — bacteria, viruses, fungi and protoctista — and discuss how their structural and biological differences shape both pathogenicity and the design of antimicrobial drugs. (9)
Grade A response (~410 words):*
Bacteria are cellular prokaryotes (1–5,mum) with a peptidoglycan cell wall, 70S ribosomes, a circular chromosome free in the cytoplasm and frequently plasmids; they reproduce asexually by binary fission and are exemplified by Mycobacterium tuberculosis. Viruses are acellular (20–300,nm), consist of a protein capsid enclosing a DNA or RNA genome, lack ribosomes and metabolism, and replicate only inside a host cell by hijacking host ribosomes and polymerases; influenza (segmented −ssRNA) and HIV (retrovirus with reverse transcriptase) are paradigmatic. Fungi are eukaryotes with chitin and eta-glucan cell walls and ergosterol-containing membranes; they grow either as single-celled yeasts (e.g. Candida) or multicellular hyphae (dermatophytes such as Trichophyton causing ringworm) and reproduce by spores. Protoctista are a heterogeneous eukaryotic kingdom of single-celled (protozoan) organisms; the pathogens of interest include Plasmodium falciparum (malaria, vector-borne by Anopheles), Trypanosoma brucei (African sleeping sickness, vector-borne by tsetse flies) and Entamoeba histolytica (amoebic dysentery, faecal–oral transmission).
These structural differences shape pathogenicity. Bacterial pathogens cause disease through toxin secretion (exotoxins of Clostridium) or invasion and intracellular persistence (M. tuberculosis in macrophages). Viruses cause disease by lytic destruction of host cells (influenza), by integrating into host genomes during latency (HIV provirus), or by oncogenic transformation (HPV). Fungi cause disease either superficially (ringworm, oral candidiasis) or, in immunocompromised hosts, systemically (invasive aspergillosis). Protoctista exploit complex life cycles to evade immunity — Plasmodium alternates between hepatocytes and erythrocytes, presenting different surface antigens at each stage and frustrating vaccine development.
These differences also dictate drug design. eta-lactams target peptidoglycan, so they hit bacteria but are useless against the other three classes. Azoles target ergosterol biosynthesis, exploiting the cholesterol-versus-ergosterol distinction between host and fungal membranes. Antivirals (e.g. zidovudine inhibiting HIV reverse transcriptase, oseltamivir inhibiting influenza neuraminidase) must target viral-specific enzymes because the host machinery is otherwise indistinguishable. Antimalarials such as artemisinin act on Plasmodium-specific haem-detoxification machinery in the digestive vacuole. Across all four classes, the recurring theme is selective toxicity — the drug must exploit a molecular feature unique to the pathogen, and the more closely the pathogen resembles its host (fungi and protoctista, which are eukaryotic like us), the harder selective drug design becomes.
Examiner commentary: Full marks (9/9). The candidate organises the answer in three demanded stages — structural comparison, pathogenicity, drug design — and uses molecular detail (mycolic acids, ergosterol, reverse transcriptase, neuraminidase, artemisinin) to anchor each generality. The closing thesis (selective toxicity scales with host–pathogen divergence) is the kind of cross-topic synthesis Edexcel rewards at the very top.
Oxbridge-style interview prompt: "Antibiotic resistance arises in bacterial populations within a few years of a drug's introduction, but antifungal resistance has historically taken decades to emerge. What features of fungal versus bacterial biology might explain this difference, and how would you design an experiment to test your hypothesis?"
This topic links to Edexcel 9BI0 Core Practical 4 — the aseptic culture of bacteria and the measurement of bacterial growth on agar plates. The experimental craft involves flame-sterilising loops or pipettes, inoculating sterile nutrient agar plates within the still-air zone of a Bunsen flame, sealing plates (incompletely, to prevent anaerobic conditions) and incubating at 25°extC in a school setting (not at 37°extC, to discourage growth of human pathogens). Colony morphology — size, colour, edge profile and elevation — is recorded, and viable cell counts are estimated by serial dilution and spread-plating. The practical underpins this lesson by reinforcing how axenic (single-species) cultures are obtained and why aseptic technique is essential for unambiguous identification: a contaminated plate simply cannot be classified, because two pathogens may coexist. The same techniques scaled up underpin clinical microbiology laboratories' identification of patient pathogens prior to targeted antibiotic prescribing — the practical link from bench to bedside that Edexcel emphasises.
This content is aligned with the Pearson Edexcel GCE A Level Biology B (9BI0) specification, Paper 1 — Lifestyle, Transport, Genes and Health, Topic 6: Immunity, Infection and Forensics. For the most accurate and up-to-date information, please refer to the official Pearson Edexcel specification document.
graph TD
M["Microorganisms<br/>(four major classes)"]
M --> B["Bacteria<br/>(prokaryotic)<br/>peptidoglycan wall<br/>70S ribosomes<br/>e.g. M. tuberculosis"]
M --> V["Viruses<br/>(acellular)<br/>capsid + DNA/RNA<br/>no ribosomes<br/>e.g. influenza, HIV"]
M --> F["Fungi<br/>(eukaryotic)<br/>chitin wall<br/>80S ribosomes<br/>e.g. Candida, ringworm"]
M --> P["Protoctista<br/>(eukaryotic)<br/>varied morphology<br/>e.g. Plasmodium,<br/>Trypanosoma"]
B --> Bd["Drug target:<br/>peptidoglycan<br/>(beta-lactams)"]
V --> Vd["Drug target:<br/>viral enzymes<br/>(reverse transcriptase,<br/>neuraminidase)"]
F --> Fd["Drug target:<br/>ergosterol or chitin<br/>(azoles, echinocandins)"]
P --> Pd["Drug target:<br/>parasite-specific<br/>(artemisinin)"]
style M fill:#27ae60,color:#fff
style B fill:#3498db,color:#fff
style V fill:#e74c3c,color:#fff
style F fill:#e67e22,color:#fff
style P fill:#9b59b6,color:#fff