Memly's USMLE Step 1 Microbiology: 300 Organism Cards
300 organisms by structure, virulence and how they are identified.
Add every card on the free plan. Importing runs no AI generation and spends no AI credits. You'll need a Memly account.
Microbiology collapses into a list of names unless each organism carries a small set of features that separate it from the one next to it. Catalase splits the gram-positive cocci, coagulase splits the staphylococci, and novobiocin splits what is left. Non-septate hyphae branching at wide angles is a different mold from septate hyphae branching at acute ones. Narrow-based budding with a capsule is a different yeast from broad-based budding without one. Learn the discriminating feature and the name follows. Learn the name first and you have a list. That is how these 300 cards are built. Every one opens with a classification or a definition, and beyond that the fields follow what the organism actually turns on: 83 give the transmission route, and where two organisms are routinely mixed up, the card names the other one and says which single feature separates them. The weighting is 146 cards of bacteriology including 31 on laboratory identification alone, 74 on virology, 30 on parasites, 28 on fungi, and 22 on immunology and host defence patterns. Antimicrobials are not here. Mechanism, spectrum and adverse effects live in the Pharmacology Drug Classes deck, so the two fit together without repeating a card: this deck is the organism, that one is the agent. Cards are tagged by group and by sub-group, so you can drill just the gram negatives, just the DNA viruses, or just the helminths. Import it and the deck joins your spaced-repetition schedule, and what you end up with is the thing the subject is really testing: given a stain, a plate, and a growth condition, being able to say what it is and why.
What happens when you add it
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The button opens Memly and the whole deck lands in your account.
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Each card gets its own schedule, based on how well you actually recall it.
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They are your cards afterwards — rewrite, delete or reorganize them freely.
What's inside
Showing 100 representative cards from the full 300-card deck.
| Front | Back |
|---|---|
| Gram stain principle | Definition: A differential stain separating bacteria by how well the cell wall retains crystal violet after an alcohol wash. Reads out: Gram-positive cells keep the violet dye, gram-negative cells lose it and take up the counterstain. Why it matters: The result is a property of wall structure, so it also predicts susceptibility to agents that act on the wall. |
| Periplasmic space | Definition: The compartment between inner and outer membranes of a gram-negative cell, containing peptidoglycan and secreted enzymes. Why it matters: Beta-lactamases accumulate here, so an enzyme released into this space reaches its target before the agent does. |
| Catalase test | Definition: Detection of the enzyme converting hydrogen peroxide to water and oxygen, seen as bubbling. Reads out: Staphylococci are positive and streptococci are negative, which is the first split among gram-positive cocci. |
| Optochin sensitivity | Definition: A disc test separating alpha-hemolytic streptococci. Reads out: Streptococcus pneumoniae is sensitive, while viridans streptococci are resistant. |
| Bile solubility | Definition: Lysis of an organism by bile salts, which activate its own autolysin. Reads out: Streptococcus pneumoniae dissolves, while viridans streptococci do not, agreeing with the optochin result. |
| Urease test | Definition: Detection of the enzyme splitting urea into ammonia and carbon dioxide, raising the pH of the medium. Reads out: Proteus, Helicobacter pylori, Klebsiella, Ureaplasma, and Cryptococcus are positive. |
| Citrate utilization | Definition: Growth using citrate as the sole carbon source, raising the pH and turning the medium blue. Reads out: Klebsiella, Enterobacter, Serratia, and Salmonella are positive, while Escherichia coli and Shigella are negative. |
| Chocolate agar | Definition: Blood agar heated to lyse the red cells, releasing factor V and factor X. Grows: Haemophilus influenzae, which cannot obtain both factors from intact blood agar. |
| Lowenstein-Jensen medium | Definition: An egg-based selective medium for mycobacteria. Why it matters: Mycobacterial growth is very slow, so culture takes weeks rather than the overnight of routine bacteriology. |
| Obligate aerobe | Definition: An organism requiring oxygen as its terminal electron acceptor. Examples: Mycobacterium tuberculosis, Pseudomonas aeruginosa, Nocardia, and Bacillus species. |
| Microaerophile | Definition: An organism growing best at oxygen concentrations below atmospheric. Examples: Campylobacter jejuni, Helicobacter pylori, and Borrelia. |
| Staphylococcus aureus | Classification: Gram-positive cocci in clusters, catalase positive and coagulase positive, beta hemolytic. Virulence: Protein A binding the antibody Fc region, exotoxins including toxic shock syndrome toxin and exfoliative toxin, and enzymes that spread through tissue. Causes: Skin and soft tissue infection, abscess, osteomyelitis, endocarditis, pneumonia, and a rapid-onset food poisoning from preformed toxin. |
| Staphylococcus saprophyticus | Classification: Gram-positive cocci in clusters, catalase positive, coagulase negative, novobiocin resistant. Causes: Urinary tract infection, particularly in young women. Often confused with: Staphylococcus epidermidis, from which novobiocin separates it. |
| Streptococcus pyogenes | Classification: Gram-positive cocci in chains, catalase negative, beta hemolytic, bacitracin sensitive, Lancefield group A. Virulence: M protein blocking phagocytosis, streptolysin O, and pyrogenic exotoxins acting as superantigens. Causes: Pharyngitis, skin infection, scarlet fever, and the immune-mediated sequelae of rheumatic fever and post-streptococcal glomerulonephritis. |
| Viridans streptococci | Classification: Gram-positive cocci in chains, alpha hemolytic, optochin resistant, not bile soluble. Virulence: Dextran production allowing adherence to tooth surfaces and to damaged heart valves. Causes: Dental caries and subacute endocarditis on previously abnormal valves. |
| M protein | Definition: A surface protein of group A streptococci extending from the cell wall. Mechanism: Blocks phagocytosis by interfering with complement deposition, and its similarity to human proteins is the basis proposed for post-infectious immune damage. |
| Rheumatic fever mechanism | Definition: Immune-mediated damage following group A streptococcal pharyngitis, attributed to antibodies cross-reacting with host tissue. Why it matters: The damage is immunological rather than infectious, which is why it appears weeks after the infection has cleared. |
| Bacillus anthracis | Classification: Gram-positive spore-forming aerobic rod with a polypeptide capsule of D-glutamate. Virulence: A tripartite toxin of protective antigen, edema factor, and lethal factor. Transmission: Spores from animal products by cutaneous contact or inhalation. |
| Clostridium tetani | Classification: Gram-positive spore-forming obligate anaerobe with a terminal spore. Transmission: Spores entering through a puncture wound. Virulence: Tetanospasmin, which blocks release of the inhibitory transmitters glycine and GABA. |
| Botulinum toxin mechanism | Definition: A protease cleaving vesicle fusion proteins at the neuromuscular junction, preventing acetylcholine release. Often confused with: Tetanospasmin, which uses the same chemistry on the same protein family but acts on inhibitory neurons, so the two toxins produce opposite pictures. |
| Clostridioides difficile | Classification: Gram-positive spore-forming obligate anaerobe. Virulence: Toxin A damaging mucosa and toxin B disrupting the cytoskeleton by glucosylating regulatory GTPases. Why it matters: Its spores resist alcohol, which is why physical removal rather than alcohol matters for hand hygiene. |
| Diphtheria toxin mechanism | Definition: An AB toxin that ADP-ribosylates elongation factor 2, halting protein synthesis. Often confused with: Exotoxin A of Pseudomonas aeruginosa, which modifies the same target by the same chemistry in an unrelated organism. |
| Actin rocket motility | Definition: Polymerization of host actin at one pole of an intracellular bacterium, propelling it into the neighbouring cell. Used by: Listeria, Shigella, and Rickettsia. Why it matters: The organism never enters the extracellular space, so antibody has limited access to it. |
| Actinomyces israelii | Classification: Gram-positive branching filamentous rod, anaerobic, not acid fast. Where: Normal flora of the mouth. Causes: Slowly progressive cervicofacial lesions with draining sinus tracts containing yellow sulfur granules. |
| Spore-forming gram-positive rods | Definition: The genera Bacillus and Clostridium, separated by oxygen requirement. Why it matters: Spores survive heat, drying, and many disinfectants, so the organisms persist in environments that would clear vegetative bacteria. |
| Neisseria meningitidis | Classification: Gram-negative diplococci, oxidase positive, maltose and glucose fermenting, grown on Thayer-Martin. Virulence: Polysaccharide capsule, IgA protease, and endotoxin from lipooligosaccharide. Transmission: Respiratory droplets, with carriage in the nasopharynx. |
| Neisseria species compared | Definition: Both are oxidase-positive gram-negative diplococci. The meningococcus ferments maltose and has a polysaccharide capsule, the gonococcus does neither. Why it matters: Capsule presence explains why one has a polysaccharide-based vaccine and the other does not. |
| Bordetella pertussis | Classification: Gram-negative coccobacillus, highly fastidious, grown on charcoal-containing media. Virulence: Pertussis toxin, filamentous haemagglutinin for attachment, and tracheal cytotoxin that damages ciliated cells. Transmission: Respiratory droplets, with high transmissibility. |
| Legionella pneumophila | Classification: Gram-negative rod staining poorly, requiring iron and cysteine, grown on charcoal yeast extract. Transmission: Aerosols from water systems, with no person-to-person spread. Virulence: Survives inside alveolar macrophages by blocking phagosome-lysosome fusion. |
| Enterobacteriaceae common features | Definition: Gram-negative rods that are oxidase negative, ferment glucose, and reduce nitrate. Why it matters: A negative oxidase result on a gram-negative rod points to this family, which is the first branch in enteric identification. |
| Enterohemorrhagic Escherichia coli | Definition: A strain carrying shiga-like toxin, most recognized as serotype O157:H7. Mechanism: The toxin inactivates the 60S ribosomal subunit, and damage to endothelium underlies the associated microangiopathic syndrome. Identification: Does not ferment sorbitol, which separates it from most other strains. |
| Uropathogenic Escherichia coli | Definition: Strains carrying P fimbriae that bind uroepithelial receptors. Why it matters: Adherence against urine flow is the limiting step, so the fimbria rather than a toxin defines this group. |
| Proteus mirabilis | Classification: Gram-negative rod, non-lactose fermenting, highly motile with swarming growth, strongly urease positive. Why it matters: Urease raises urinary pH, which favours precipitation of struvite stones, so the enzyme links the organism to stone formation. |
| Non-typhoidal Salmonella | Classification: Gram-negative rod, non-lactose fermenting, motile, hydrogen sulfide producing. Transmission: Animal reservoirs including poultry, eggs, and reptiles. Often confused with: Shigella, which is non-motile, produces no hydrogen sulfide, and has a human-only reservoir. |
| Yersinia enterocolitica | Classification: Gram-negative rod growing at cold temperatures. Transmission: Contaminated milk, pork, and water. Why it matters: It can inflame mesenteric lymph nodes, producing a picture that has been described as resembling appendicitis. |
| Vibrio cholerae | Classification: Comma-shaped gram-negative rod, oxidase positive, growing in alkaline media. Virulence: Cholera toxin. Transmission: Contaminated water, requiring a large inoculum because the organism is acid sensitive. |
| Campylobacter jejuni | Classification: Comma or S-shaped gram-negative rod, oxidase positive, microaerophilic, growing at higher than usual incubation temperature. Transmission: Undercooked poultry, unpasteurized milk, and contact with animals. Why it matters: It is a recognized antecedent of an immune-mediated demyelinating neuropathy through molecular mimicry. |
| Pseudomonas aeruginosa | Classification: Gram-negative rod, oxidase positive, non-lactose fermenting, obligate aerobe, producing blue-green pigments and a grape-like odour. Virulence: Exotoxin A inhibiting elongation factor 2, phospholipase C, and biofilm formation. Where: Water sources, moist environments, and equipment. |
| Brucella | Classification: Small gram-negative coccobacillus, facultative intracellular within macrophages. Transmission: Unpasteurized dairy and contact with infected animals. Why it matters: Intracellular survival produces an undulating fever pattern and a prolonged course. |
| Bartonella henselae | Classification: Gram-negative rod. Transmission: Cat scratch or bite. Causes: Regional lymphadenopathy, and vascular proliferative lesions in people with impaired cell-mediated immunity. |
| Endotoxin | Definition: Lipopolysaccharide in the outer membrane of gram-negative bacteria, released on cell lysis. Mechanism: Lipid A activates macrophages through Toll-like receptor 4, releasing cytokines that drive fever, vasodilation, and coagulation activation. Often confused with: Exotoxin, which is secreted, protein, heat labile, and often has a specific molecular target. |
| Lipid A | Definition: The membrane-anchored lipid portion of lipopolysaccharide, and the component responsible for its biological activity. Why it matters: The toxic effects are host-derived, coming from the immune response lipid A provokes rather than from direct damage. |
| Superantigen | Definition: A toxin cross-linking a class II molecule and the T cell receptor outside the normal antigen groove. Why it matters: It activates a large fraction of T cells regardless of specificity, so the damage is cytokine-driven rather than caused by the toxin itself. |
| Type III secretion system | Definition: A needle-like apparatus injecting bacterial proteins directly into a host cell cytoplasm. Used by: Salmonella, Shigella, Yersinia, and Pseudomonas. Why it matters: Delivery bypasses the extracellular space entirely, so antibody cannot intercept the effector. |
| Mycobacterium tuberculosis | Classification: Acid-fast rod, obligate aerobe, slow growing on Lowenstein-Jensen medium. Transmission: Airborne droplet nuclei. Virulence: Cord factor, and sulfatides that inhibit phagosome-lysosome fusion, allowing survival inside macrophages. |
| Cord factor | Definition: A mycobacterial surface glycolipid causing organisms to grow in parallel cords. Mechanism: Inhibits neutrophil migration and damages mitochondria, and it is required for granuloma formation. |
| Latent tuberculosis | Definition: Persistence of viable organisms within granulomas without active disease, held in check by cell-mediated immunity. Why it matters: Loss of that immunity allows reactivation, which is why the balance rather than the organism determines the state. |
| Mycobacterium leprae | Classification: Acid-fast rod that cannot be grown on artificial media, preferring cool body regions. Why it matters: The disease form follows the host response, with strong cell-mediated immunity limiting the organism and weak responses allowing extensive multiplication. |
| Treponema pallidum | Classification: Spirochete too thin to be seen on Gram stain, visualized by darkfield microscopy, not culturable on artificial media. Transmission: Sexual contact and across the placenta. Why it matters: Its outer membrane carries few surface proteins, which is one explanation offered for its persistence despite an antibody response. |
| Borrelia recurrentis | Classification: Spirochete transmitted by the body louse. Mechanism: Antigenic variation of surface proteins, producing successive waves of bacteraemia as each new variant escapes the antibody raised against the last. |
| Mycoplasma pneumoniae | Classification: The smallest free-living bacteria, with no cell wall and sterols in the membrane, growing slowly on enriched media. Why it matters: Having no peptidoglycan, it is unaffected by agents acting on the cell wall and is invisible on Gram stain. Causes: A gradual-onset pneumonia, often with cold agglutinins. |
| Chlamydia trachomatis | Classification: Obligate intracellular bacterium that cannot make its own ATP. Transmission: Sexual contact, to the neonate during delivery, and by direct contact in the ocular serotypes. Why it matters: Its wall lacks classical muramic acid, which is part of why it behaves unlike a typical gram-negative organism. |
| Chlamydophila psittaci | Classification: Obligate intracellular bacterium. Transmission: Inhalation of dried droppings or secretions from birds. |
| Typhus group rickettsiae | Definition: Rickettsia prowazekii transmitted by the body louse and Rickettsia typhi by the rat flea. Often confused with: Spotted fever, whose rash starts peripherally. The typhus rash characteristically begins centrally and spreads outward. |
| Biofilm | Definition: A community of bacteria embedded in a self-produced polysaccharide matrix on a surface. Formed by: Staphylococcus epidermidis on prosthetic material, Pseudomonas aeruginosa on respiratory surfaces, and viridans streptococci on damaged valves. Why it matters: Organisms inside divide slowly and are shielded from both phagocytes and diffusion, so the state rather than the species explains persistence. |
| Siderophores | Definition: Secreted molecules that bind iron with very high affinity and are taken back up by the organism. Why it matters: The host withholds iron by binding it to transferrin and lactoferrin, so siderophore production is a counter to that defence. |
| Bacterial flagella | Definition: A rotating filament of flagellin driven by the proton gradient, giving directed motility. Why it matters: Flagellin is strongly immunogenic and is recognized by innate receptors, so motility carries a cost in detection. |
| Catalase as a virulence factor | Definition: A bacterial enzyme degrading hydrogen peroxide. Why it matters: It neutralizes part of the phagocyte oxidative burst, which is why catalase-positive organisms are the ones that trouble hosts whose phagocytes cannot generate that burst. |
| Facultative versus obligate intracellular bacteria | Definition: Facultative organisms can grow inside or outside host cells, while obligate ones cannot be cultured without them. Examples: Facultative include Salmonella, Listeria, Legionella, Brucella, Francisella, Mycobacterium, and Yersinia. Obligate include Rickettsia and Chlamydia. Why it matters: Both groups are controlled by cell-mediated rather than antibody-mediated immunity. |
| Viral genome classification | Definition: Viruses grouped by nucleic acid type, strandedness, and sense, since those determine what must happen before proteins can be made. Why it matters: The grouping predicts whether the virus must carry its own polymerase, which is a structural requirement rather than a naming convention. |
| Viral uncoating | Definition: Release of the genome from the capsid after entry, often triggered by endosomal acidification. Why it matters: The genome is inaccessible until this step, so anything blocking endosomal acidification blocks replication before transcription begins. |
| Negative-sense RNA genome | Definition: A genome complementary to messenger RNA, which must be transcribed before anything can be translated. Why it matters: Host cells have no enzyme that copies RNA into RNA, so the virus must carry its own polymerase inside the particle. |
| Antigenic drift | Definition: Gradual accumulation of point mutations in surface protein genes. Why it matters: It produces small annual changes, which is why immunity from a previous season is partial rather than absent. |
| Cytopathic effect | Definition: Visible change in infected cells in culture, including rounding, fusion into multinucleate cells, or lysis. Why it matters: It is how viral growth was detected before molecular methods, and the pattern of change differs between virus families. |
| DNA virus general features | Definition: Most are double stranded, linear or circular, and replicate in the nucleus using host machinery. Exceptions: Poxviruses replicate in the cytoplasm and carry their own polymerase, and parvoviruses are single stranded. Why it matters: The exceptions are the examinable part, since the general rule follows from needing host nuclear enzymes. |
| Varicella zoster virus | Classification: Enveloped double-stranded DNA herpesvirus. Transmission: Respiratory droplets and direct contact with vesicle fluid. Latency: Dorsal root and cranial nerve ganglia, with reactivation producing a dermatomal distribution. |
| Human herpesvirus 8 | Classification: Enveloped double-stranded DNA herpesvirus. Mechanism: Drives proliferation of endothelial cells, and the associated vascular tumour appears when cell-mediated immunity is impaired. |
| Human papillomavirus | Classification: Non-enveloped double-stranded circular DNA virus. Mechanism: In high-risk types, the E6 protein promotes degradation of p53 and E7 inactivates the retinoblastoma protein, releasing cell cycle control. Transmission: Direct contact, including sexual contact. |
| RNA virus general features | Definition: Most replicate in the cytoplasm and lack proofreading, so mutation rates are far higher than for DNA viruses. Exceptions: Influenza and retroviruses use the nucleus at some stage. Why it matters: High mutation rate underlies antigenic change, quasispecies diversity, and rapid emergence of resistance. |
| Coxsackievirus | Classification: Non-enveloped positive-sense RNA picornavirus, divided into groups A and B. Causes: Group A with vesicular lesions of the mouth and extremities and herpangina, group B with myocarditis and pleurodynia. |
| Dengue virus | Classification: Enveloped positive-sense RNA flavivirus with four serotypes. Transmission: Aedes mosquito. Mechanism: Antibody from a previous infection with one serotype can enhance uptake of a different serotype into cells, which is the proposed basis for more severe second infections. |
| Hepatitis C virus | Classification: Enveloped positive-sense RNA flavivirus. Transmission: Blood exposure, chiefly through shared injecting equipment. Why it matters: Its envelope proteins vary rapidly within one host, which is why infection frequently becomes chronic and why no vaccine has followed. |
| Influenza genome segmentation | Definition: Eight separate RNA segments packaged together in one particle. Why it matters: Co-infection of one cell by two strains allows whole segments to be exchanged, which is the mechanism of antigenic shift and of pandemic emergence. |
| Parainfluenza virus | Classification: Enveloped negative-sense RNA paramyxovirus. Mechanism: Inflames the subglottic airway, producing the barking cough and inspiratory stridor of croup. |
| Hantavirus | Classification: Enveloped segmented negative-sense RNA virus of the bunyavirus group. Transmission: Inhaled aerosols of rodent urine and droppings, with no arthropod vector and no person-to-person spread in most forms. |
| HIV effect on cell-mediated immunity | Definition: Progressive loss of CD4-positive T cells, removing the helper function that coordinates both cellular and antibody responses. Why it matters: The organisms that appear as immunity declines are those normally controlled by cell-mediated immunity, which is why the pattern is predictable from the defect. |
| Arbovirus transmission | Definition: Transmission by an arthropod vector in which the virus replicates before being passed on. Why it matters: Vector distribution and season determine where and when infection occurs, which is why these infections are geographically bounded. |
| Vertical transmission | Definition: Passage from mother to child across the placenta, during delivery, or through breastfeeding. Why it matters: Which route an agent uses determines when in gestation or delivery the risk falls, so timing rather than the agent alone shapes the outcome. |
| Fungal cell wall | Definition: A wall of chitin and glucans, with ergosterol rather than cholesterol as the principal membrane sterol. Why it matters: Both the wall polysaccharide and the membrane sterol are absent from human cells, which is why they are the two selective targets. |
| Potassium hydroxide preparation | Definition: A specimen treated with alkali, which dissolves keratin and host cells while leaving fungal walls intact. Why it matters: The fungal wall resists the alkali because of its chitin, so the method works by removing everything else. |
| Histoplasma capsulatum | Classification: Dimorphic fungus appearing as small yeasts within macrophages. Transmission: Inhaled spores from soil enriched by bird or bat droppings. Where: Associated with river valley regions of North America and with caves. |
| Candida albicans | Classification: Yeast forming pseudohyphae and true hyphae at body temperature, part of normal flora of mouth, gut, and vagina. Why it matters: It is already present, so disease follows a change in the host or in competing flora rather than new acquisition. |
| Mucormycetes | Classification: Molds with broad non-septate hyphae branching at wide angles, including Rhizopus and Mucor. Mechanism: Invade blood vessels and cause tissue infarction. Why it matters: The association is with acidosis and with high available iron, which is why the host state rather than exposure explains most disease. |
| Fungal spores and conidia | Definition: Reproductive structures released into the environment, whose shape and arrangement identify many molds. Often confused with: Bacterial endospores, which are survival structures rather than reproductive ones and are formed inside the cell. |
| Giardia lamblia | Classification: Flagellated protozoan with trophozoite and cyst forms. Transmission: Cysts in contaminated water, including streams and lakes. Mechanism: Adheres to the small intestinal surface without invading, producing fat malabsorption. |
| Trichomonas vaginalis | Classification: Flagellated protozoan with a trophozoite form only and no cyst stage. Transmission: Sexual contact. Why it matters: Having no cyst, it cannot survive long outside the host, which is why transmission is essentially direct. |
| Plasmodium falciparum sequestration | Definition: Infected erythrocytes expressing adhesive proteins that bind capillary endothelium, so they are held in small vessels. Why it matters: Sequestration keeps mature stages out of the circulating blood and obstructs microvasculature, which is why this species produces the most severe disease. |
| Trypanosoma cruzi | Classification: Flagellated protozoan. Transmission: Faeces of a reduviid bug rubbed into the bite site or mucosa. Mechanism: Damages autonomic ganglia over years, producing dilated hollow organs including the heart, oesophagus, and colon. |
| Nematodes | Definition: Roundworms with a cylindrical unsegmented body and separate sexes. Why it matters: Most intestinal species are acquired by ingesting eggs or by larvae penetrating skin, so the entry route separates them into two groups. |
| Strongyloides stercoralis | Classification: Nematode whose larvae penetrate skin. Mechanism: Can complete its cycle within one host, so the burden increases without re-exposure. Why it matters: That autoinfection can accelerate dramatically when cell-mediated immunity is suppressed. |
| Filarial worms | Classification: Tissue nematodes including Wuchereria bancrofti and Onchocerca volvulus. Transmission: Mosquito for the lymphatic species and blackfly for the river-associated species. Mechanism: Adults in lymphatics obstruct drainage, while microfilariae in skin and eye provoke inflammation. |
| Echinococcus granulosus | Classification: Tapeworm of dogs, with sheep as usual intermediate host. Transmission: Ingested eggs from dog faeces. Mechanism: Forms slowly enlarging fluid-filled cysts, most often in liver, whose contents are highly antigenic. |
| Definitive versus intermediate host | Definition: The definitive host harbours the sexually reproducing stage, while an intermediate host carries larval or asexual stages. Why it matters: For malaria the mosquito is definitive and the human intermediate, which reverses the assumption that the human is the main host. |
| Type I hypersensitivity | Definition: An immediate reaction in which antigen cross-links IgE bound to mast cells, releasing histamine and other mediators. Why it matters: It requires previous sensitization, so the first exposure produces the IgE and a later one produces the reaction. |
| Toll-like receptors | Definition: Innate receptors recognizing conserved microbial patterns such as lipopolysaccharide, flagellin, and unmethylated DNA motifs. Why it matters: They detect classes of organism rather than specific ones, which is why the innate response is immediate but does not improve with repeated exposure. |
| Natural killer cells | Definition: Innate lymphocytes killing cells that display too little class I molecule or that are coated with antibody. Why it matters: They detect the absence of a normal signal, which covers the gap left when a virus downregulates class I to hide from T cells. |
| Antibody isotypes | Definition: IgM as the first response and a strong complement activator, IgG the most abundant and the only one crossing the placenta, IgA in secretions, IgE on mast cells, and IgD on naive B cells. Why it matters: The heavy chain constant region rather than the binding site determines what an antibody can do once bound. |
| Mucosal secretory antibody | Definition: Dimeric IgA transported across epithelium and carrying a secretory component that resists proteolysis. Why it matters: It neutralizes organisms at the surface before attachment, which is precisely why several mucosal pathogens produce a protease against it. |
| B cell defects and organism pattern | Definition: Impaired antibody production, associated with recurrent infection by encapsulated bacteria and by enteroviruses. Why it matters: Encapsulated organisms need opsonizing antibody to be cleared, so the defect predicts the organism class. |
| Phagocyte defects and organism pattern | Definition: Impaired killing or migration, associated with catalase-positive bacteria and with molds. Why it matters: The pattern follows the failed mechanism rather than exposure, so knowing the defect predicts the organism. |
Frequently asked
How is each organism card built?
It opens with the classification, which for a bacterium means the Gram result, shape, arrangement and the key biochemical results. Then the fields that matter for that organism: virulence mechanism, transmission route on 83 cards, what it causes, and on 19 the organism it is most often confused with plus the single feature that separates them.
Where do the antimicrobials fit?
In the Pharmacology Drug Classes deck, deliberately. That deck covers mechanism, target, class suffix and adverse effect profile for every antimicrobial class. Keeping the agent and the organism in separate decks means neither one repeats the other, and you can drill either side on its own. The only drug names here are optochin, bacitracin and novobiocin, which appear as identification discs rather than as therapy.
Does it cover the laboratory identification tests?
Yes, as its own block of 31 cards: Gram stain and acid-fast staining, catalase and coagulase, hemolysis patterns, the optochin, bacitracin and novobiocin discs, oxidase, urease, indole and citrate, lactose fermentation on MacConkey, and the special media from chocolate agar to charcoal yeast extract. Each says what the test reads out and which organisms it separates.
Which groups get the most cards?
Bacteriology 146, made up of 31 laboratory identification, 35 gram-positive, 35 gram-negative, 23 virulence mechanisms and 22 mycobacteria, spirochetes and atypicals. Then virology 74, parasites 30, fungi 28, and immunology 22. Bacteriology is heaviest because that is where the discriminating features are densest.
How is it organized for studying one group at a time?
Every card carries a group tag and a finer sub-group tag, across laboratory identification, gram-positive bacteria, gram-negative bacteria, mycobacteria and spirochetes, bacterial virulence, virology, fungi, parasites and immunology. Filter by a tag to drill one group, or by the finer tag for a single block such as DNA viruses, helminths or biochemical tests.
Can I import the whole deck on the free plan?
Yes. Importing a saved deck runs no new AI generation and spends no AI credits, so the free plan imports every card. You can study, edit and delete them afterwards.
Will importing it twice create duplicates?
No. Cards you already have are skipped and only cards added in a revision come through. Including re-imports after deleting it, one official deck can be imported three times per account.
Can I edit the cards after importing?
Yes. Once imported they are your cards: edit either side, delete the ones you already know cold, retag them, or move them into another deck.
Memly's USMLE Step 1 Microbiology: 300 Organism Cards
Add every card on the free plan. Importing runs no AI generation and spends no AI credits. You'll need a Memly account.
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No official questions are reproduced, and every card is written by Memly. Compiled 2026-08-21.