Microbiology section 3 – Flashcards
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| Describe the bacteria that causes diphtheria. |
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| It is called Corynebacterium diphtheriae. It is a small, Gram positive club. |
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| What are the three domains of the diphtheria toxin. |
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| A: the section that is released into and damages the cell B: binds to cell membrane T: inserts into membrane of the endocytotic vesicle |
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| Which bacteria forms a pseudomembrane in the throat? |
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| Corynebacterium tuburculosae |
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| How is diphtheria transmits? |
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| Inhalation of droplets from an infected person. |
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| Why kind of Strep causes Strep throat and scarlet fever? |
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| Streptococcus pyogenes. (Group A Strep) |
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| What does DPT stand for? |
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| diphtheria, pertussis, tetanus |
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| What are exogenous bacteria? |
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| Those that are not normally found in the human body. They cause primary infections. |
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| What are opportunistic infections? |
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| They are caused by normal flora when conditions are right. |
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| What kind of bacteria are most enteric bacteria? |
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| Gram negative rods. |
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| Which bacteria causes Lyme disease? |
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| Borrelia burgdorferi |
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| Which kinds of bacteria (shape and Gram) cause most diseases? |
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| Gram+ cocci and Gram- rods |
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| Which major diseases are caused by Gram negative cocci? |
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| gonorrhea and meningitis |
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| Which two major diseases are caused by Mycobacterium species? |
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| tuberculosis and leprosy |
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| Describe the bacteria that causes whooping cough. (Shape, metabolism, Gram) |
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| Bordetella pertussis. Strictly aerobic, Gram negative rod. |
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| During a pertussis infection, when do you get the coughs with whooping sound? |
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| 2-4 wks |
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| Which area does B. pertussis colonize? |
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| the pharynx, larynx, trachea, and bronchi |
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| Why is B. pertussis virulent? |
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| It produces adhesins that prevent it from becoming swept away by binding to cilia. (Filamentous hemoglutin) Also, it produces the pertussis toxin. The toxin can act as an adhesin or harm host cells. |
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| What does pertussis toxin do? |
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| It increases intracellular cAMP, which interferes with normal signaling. |
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| What were the three original fungal phyla? |
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| Basidiomycota, Ascomycota, and Zygomycota. |
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| Are fungi mobile? Can they fix carbon? |
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| With very limited exception, they are non-motile. They are heterotrophs (they cannot fix carbon). |
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| Which fungal form consists of hyphae that form a mycelium? |
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| the mold form |
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| What does it mean for a fungus to be dimorphic? |
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| It can switch between the yeast and mold forms. |
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| Oftentimes, hyphae are divided into separate compartments by barriers called ____. |
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| septae |
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| Asexual spores are called _____ or ____, while sexual spores are called _____. |
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| anamorphs; conidia; teleomorphs |
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| Sometimes, spores simply ___ off of existing cells. Other times, they are released from a lollipop-shaped _____. |
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| bud; sporangiospore |
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| Polyenes bind to ____, interfering with cell ____. |
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| ergosterol; membranes |
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| Azoles prevent ____ synthesis, which prevents ____ synthesis. |
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| ergosterol; membrane |
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| What do echinocandins do? |
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| They prevent fungal cell wall synthesis. |
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| What two classes of fungal antibiotics are most commonly used? |
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| Azoles and echinocandins. |
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| Mircosporum, Trichophyton, and Epidermophyton cause _____ fungal infections, such as ringwom and athlete's foot. |
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| cutaneous |
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| Chromoblastomycosis, phaeohyphomycosis, mycetoma, and sporotrichosis are all examples of _____ fungal infections. |
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| subcutaneous |
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| ______ is sometimes called "valley fever" and is found in the southwest US and Mexico. |
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| Coccidioidomycosis |
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| Of the endemic fungal diseases we looked at, which is localized in the Ohio river valley area? |
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| Histoplasmosis |
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| C. albicans is ____, meaning it can switch from its blastoconidia form to hyphae. |
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| dimorphic |
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| What is a characteristic that all the opportunistic fungi share? |
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| They can grown well at 37 degrees C. |
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| Of the opportunistic fungi we looked at, which is inhaled and binds to fibrinogen? |
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| Aspergillus |
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| Which opportunistic fungus has a very thick capsule and can invade CSF? |
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| Cryptococcus |
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| What is a zygospore? |
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| When two fungi mate sexually, their hyphae are connected by the zygospore, from which a sporangiospore arises and releases spores. |
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| Where in the body is a Rhizopus infection typically localized? |
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| In the rhinocerebral region. It can spread to the orbits as well. |
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| All Staphylococci are ____ positive. However, only Staph aureus is ____ positive. |
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| catalase; coagulase |
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| Describe Staph. |
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| Gram positive facultative cocci. |
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| What are some diseases caused by Staph? |
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| abscesses, SSSS, TSS, and food poisoning |
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| What is exfoliatin? What disease is it involved in? |
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| Exfoliatin is a toxin produced by Staph. It is involved in SSSS. |
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| Superantigens cause many T cells to differentiate, leading to excess production of ___. |
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| interleukin-2 |
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| Streptococci are classified according to their hemolysis of RBCs. Describe the three different hemolysis patterns. |
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| Alpha: greenish zone around colony Beta (complete hemolysis): complete clearing around colony Gamma: colony does not cause hemolysis |
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| In what ages is strep throat most common? |
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| Kids 5-10 yrs old. |
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| Which genus causes impetigo and rheumatic fever? |
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| Streptococcus |
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| Which disease causes "strawberry tongue"? |
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| scarlet fever caused by Strep. pyogenes |
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| Which causes TSS from tampons, Strep or Staph? Which is more deadly? Which important virulence factor do both produce. |
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| Staph TSS is associated with tampons. Strep TSS is more deadly. Both produce superantigens. |
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| How is erisypelas different from impetigo? |
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| Both are Strep infections, but erisypelas occurs in a deeper layer of skin than impetigo. |
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| If strep pharyngitis is not treated with penicillin, the patient may later experience ____, a delayed sequela. |
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| rheumatic fever |
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| These are virulence factors for Strep: M-protein F-protein Streptolysin What do they do? |
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| M-protein: antiphagocytic F-protein: an adhesin Streptolysin: lyses leukocytes |
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| What is M protein? |
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| A virulence factor for Strep A. It's a long protein on the strep cell surface that prevents phagocytosis. |
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| What are three diseases causes by Strep pneumoniae? |
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| pneumonia, otitis media, and meningitis |
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| Describe the grouping of the cocci of Strep A and Strep pneumoniae. |
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| Strep A: long chains Strep pneumoniae: short chains, pairs, or solo |
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| What are two important diagnostic features for pneumococci? |
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| 1. bile solubility (due to autolysin) 2. resond to Quellung test (capsules swell) |
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| What feature of pneumococci allows them to resist phagocytosis in the lung? |
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| their capsule |
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| Pnemococci are able to cause meningitis because they can cross the _____. |
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| blood-brain barrier |
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| Which is more susceptible to penicillin, staph or strep? |
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| strep |
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| What is the most abundant bacteria in the gut? |
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| E. coli |
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| Which bacteria cause dysentery? |
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| Both E. coli and Shigella species. |
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| In a serotype, what do the O and H refer to? |
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| O-antigen: LPS side chains H-antigen: flagella (K-antigen: the capsule) |
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| Shigella has a ___ infectious dose. |
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| low |
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| Often, ____ infections occur at day cares. |
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| Shigella |
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| Is Salmonella part of normal flora? |
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| Not for humans. |
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| Like most enteric bacteria, Vibrio cholerae is a Gram _____ ____. |
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| negative rod (however, it is curved) |
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| In terms of colonization, what separates watery diarrhea from bloody diarrhea and dysentery? |
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| With watery diarrhea, bacteria only colonize the enteric cell surface. With more severe diarrhea, they invade the cells themselves. |
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| How do diarrhea causing bacteria survive the fast flow of the small intestine? |
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| They use their pili to attach to the tract. |
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| What are the two virulence factors of V. cholerae? |
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| Tcp pili and cholera toxin. |
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| Describe the structure of cholera toxin. Which subunit is released into the cell? |
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| There is one alpha subunit and 5 identical beta subunits. The A unit is released into cells (leads to excess cAMP). |
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| Which bacteria causes typhoid fever? |
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| Salmonella. It's a secondary infection from salmonella infection. (People can be carriers.) |
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| Salmonella can cause typhoid fever when it is able to invade what? |
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| lymph nodes and blood cells |
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| Which organ is the seat of chronic typhoid infection? |
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| the gallbladder |
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| Does V. cholerae invade the cell? |
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| No. It causes watery diarrhea. |
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| Describe the shape/Gram of Neisseria gonorrhoeae. |
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| Gram negative diplococci |
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| Who is more likely to contract gonorrhea after one exposure, men or women? |
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| women |
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| Where is the primary site of infection for gonorrhea? |
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| Men: urethra Women: endocervix |
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| If a young female has arthritis of the knee, which STD may be to blame? |
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| gonorrhea |
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| Does the gonococcus enter the host cell? |
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| Yes, via endocytosis. |
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| Which component of the gonococcus is responsible for most of the symptoms of gonorrhea? |
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| LOS (lipooligosaccharide), it's endotoxin |
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| What does P1 do for the gonococcus? |
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| Prevents fusion of lysosome with phagosome. |
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| Why has is been difficult to develop a vaccine against gonorrhea? |
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| The bacteria constantly undergoes antigenic variation. E.g. when the cell recognizes one kind of pilin, the bacteria will begin producing another. |
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| What class of drugs is used to treat gonorrhea? |
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| cephalosporins |
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| Which bacteria causes syphilis? |
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| Treponema pallidum |
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| In what stage of syphilis does chancre appear? |
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| primary syphilis |
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| In what stage of syphilis does a body-wide rash appear? |
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| secondary syphilis |
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| After syphilis becomes latent, what can happen? |
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| 1. nothing("cure") 2. secondary stage recurs 3. tertiary syphilis begins |
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| What happens during tertiary syphilis? |
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| Bacteria leaves the blood stream and invades the organs. |
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| What is used to treat syphilis? |
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| Penicillin |
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| What is the most common bacterial STD? |
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| chlamydia |
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| Chlamydia is very ____, allowing it to pass through some filters. It is an obligate _____ _____. |
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| small; intracellular parasite |
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| Is Chlamydia trachomatis Gram - or +? |
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| Gram - |
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| If you see the symptoms of gonorrhea, but cannot find any Gram negative cocci, what does the patient likely have? |
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| chlamydia |
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| If chlamydia is an obligate intracellular parasite, how can it be transmitted through a towel? |
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| They exist as EBs (elementary bodies), which can stay outside cells w/o replicating. |
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| What is trachoma? |
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| An eye infection caused by chlamydia. |
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| Chlamydia replicates within a cell as _____ bodies. When the cell lyses, it releases ____ bodies. |
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| reticulate; elementary |
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| What is used to treat chlamydia? |
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| Azithromycin and doxycycline. Erythromycin for children and pregnant women. |
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| Gram and shape of Heliocobacter pylori. |
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| Gram negative rod. Spiral shaped (not a spirochete). |
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| At what times is pain from gastritis and peptic ulcers likely to occur? |
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| 2-3 hours after a meal and during the middle of the night. |
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| H. pylori is safe within the mucin layer, but how does it survive its journey there? |
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| It secretes urease, which neutralizes the acid around itself. |
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| Why are ulcers vulnerable to acid? |
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| The LPS of H. pylori breaks down the mucin layer. |
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| H. pylori attaches to epithelial cells using several different kinds of _____. |
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| adhesins |
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| What is the purpose of a urease breath test? |
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| A pt drinks a solution with labeled urea. If H. pylori is present, the urea will be broken down to ammonia and exhaled. This test checks for H. pylori. |
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| For ___ percent of people, a ___ week course of antibiotics will cure ulcers. |
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| 80; 2 |
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| How is Borrelia burgdorferi visualized? |
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| dark-field microscopy |
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| Which bacteria causes Lyme disease? |
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| Borrelia burgdorferi |
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| Which kinds of ticks carry B. burgdorferi? |
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| Ixodes (deer tick) |
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| What is the symptom of stage 1 Lyme disease? |
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| erythema migrans |
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| What happens during stage 2 Lyme disease? |
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| Dissemination. Fatigue, headache, pain, fever, etc. It's kind of like the flu. |
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| What happens during stage 3 Lyme disease? |
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| Arthritis, Bell's palsy, meningitis, arrhythmia. |
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| What is the treatment for Lyme disease? |
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| Doxycyline and Lyme disease vaccine. |
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| How does tuberculosis grow? |
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| Slowly. In cords. |
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| How is tuberculosis transmitted? How many bacteria are needed? |
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| It is inhaled. Only a few bacteria are necessary for TB infection. |
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| How does TB survive in the lungs? |
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| The unique cell wall makes them resistant to destruction by macrophages. |
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| What happens during primary TB? |
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| Usually, not much if the patient is healthy. The body will form tubercles. |
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| What happens during secondary TB? |
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| Lesion break down. Tissue can become necrotic. Bloody sputa. TB is contagious. |
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| High lipid content and ____ acid make _____ species like the bacteria that causes Tb very tough. |
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| mycolic; Mycobacterium |
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| How does M. tuberculosis survive in the macrophage? |
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| Prevent fusion with the lysosome. Escapes into cytoplasm. Inhibits activation. |
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| How is Tb diagnosed? |
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| Tb skin test (most common), culture test, chest x-ray (for granulomas). |
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| What is unique about Tb treatment? |
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| It lasts 6-9 months. Several different drugs must be used in concert. |
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| What drug can cause intrinsic staining on teeth? |
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| Tetracycline used in utero. This is cosmetic only. The only treatment is veneers. |
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| What rinse may cause extrinsic staining? Why? |
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| Chlorhexidine. It kills bacteria, causing them to release their pigments. |
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| What is material alba? |
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| A loosely attached accumulation of host cells, bacteria, and food. |
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| How can dental plaque be removed? |
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| Only mechanically. |
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| What is the difference between calculus and plaque? |
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| Calculus is calcified plaque. It is always covered with a layer of uncalcified plaque. |
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| What is planktonic bacteria? |
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| The bacteria is suspended in solution. For my purposes, it's basically bacteria in saliva as opposed to bacteria in biofilm. |
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| Biofilms exhibit primitive "_____ systems." |
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| circulatory |
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| What are the three steps of biofilm formation? |
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| Attachment, growth, and detachment. |
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| How do the nutritional needs of plaque in the gingival sulcus differ from those on the tooth surface? |
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| In the gingival sulcus, bacteria will have to live off protein instead of carbs. This is because crevicular fluid is derived from serum, not saliva. |
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| How do the bacteria in a biofilm interact with one another? |
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| They can cooperate to enhance metabolic activity, or they can have antagonistic effects on one another. |
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| What four factors explain plaque's resistance to host defenses and antibiotics? |
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| 1. slow penetration 2. stress response of inner layers 3. altered microenvironment 4. persister cells |
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| What is quorum sensing? |
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| A process that allows bacterial cells to sense their own density. The result will lead to altered behavior. |
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| Describe the composition of the acquired pellicle. |
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| It is a cell-free film made mostly of proteins and glycoproteins. |
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| How long does it take the pellicle to appear after teeth cleaning? How long to mature? |
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| 2 hours to appear. 7 days to mature. |
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| What causes firm attachment of bacteria to the pellicle? |
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| Bacterial adhesins |
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| What types of bacteria attach to the pellicle during plaque initiation? |
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| Streptococcus and Actinomyces. Gram positive (both cocci and rods). |
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| At late stage of plaque formation, bacteria are likely to be Gram ____. |
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| negative |
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| What is happening to the tooth surface microenvironment as plaque forms? |
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| Oxygen and carb levels go down. Temperature increases. |
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| What happens to the prevalence of cocci as plaque matures? |
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| Cocci are replaced with rods and filaments. |
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| What characterizes the metabolism of late colonizers? |
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| They are increasingly anaerobic. |
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| How do bacteria in subgingival plaque differ from those in supragingival plaque? |
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| They are dominated by Gram -, anaerobic bacteria. They are mainly proteolytic. |
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| What are the three phases of plaque initiation? |
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| random contact, reversible adsorption, and firm attachment |
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| Re the acquired pellicle and the bacteria, what is the ligand and what is the receptor? |
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| The receptors are proteins on the pellicle and the ligands are adhesins on the surface of bacteria. |
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| What are the five initial colonizers? |
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| 1. Strep sanguis 2. Strep gordonii 3. Strep oralis 4. Strep mitis 5. Actinomyces naeslundii |
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| Large ____ microcolonies formed during early stages of plaque formation are made primarily of _____ shaped cells. |
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| columnar; coccoid |
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| Where will you find iron, in subgingival or supragingival plaque? |
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| subgingival (blood products derived from GCF) |
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| Describe the components of the corn cob. |
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| A rod or filamentous center surrounds by cocci. (Gram+ in early stages. Gram- in later stages.) |
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| When will you find early supragingival plaque? What kinds of organisms are there? |
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| 0-3 days. Gram+ rods and cocci. Facultative anaerobes. The organisms are NOT PATHOGENIC. They are well-tolerated by the host. |
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| Describe the organization of early supragingival plaque colonies. |
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| Columnar microcolonies. |
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| Name the six secondary colonizers. |
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| 1.Fusobacterium nucleatum 2. Tannerella forsythis 3. Prevotella intermedia 4. Porphyromonas gingivalis 5. Treponema denticola 6. Aggregatibacter actinomycetemcomitans |
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| When is the supragingival plaque fully matured? |
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| Around 3 weeks. Subgingival plaque continues to develop. |
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| What aspect of bacteria cause inflammation of the gingiva? |
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| The LPS of Gram- bacteria. (Bacteria is able to permeate the junctional epithelium.) |
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| The JE is more ____ than the SE. |
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| permeable |
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| What/where are capnophilic bugs found? |
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| They are found in subgingival plaque. They like carbon dioxide. |
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| What kinds of bacteria are found in subgingival plaque? |
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| Gram- anaerobes. |
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| The deepest layer of the subgingival plaque will have a wall of _____ between it an the junctional epithelium. |
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| neutrophils |
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| What are the plaque-induced periondontal diseases? |
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| gingivitis and periodontitis |
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| What is periodontitis? |
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| Inflammation and destruction of the attachment apparatus. |
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| How long does it take filamentous and slender rod-shaped bacteria to appear after cessation of OH? |
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| 2-4 days |
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| How long does it take spirochetal organisms to appear after cessation of OH? |
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| 10 days |
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| How many species of bacteria have been isolated in the oral cavity? |
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| over 700 |
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| What is the non-specific plaque hypothesis? |
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| Doesn't matter what the bugs are, just how many are there. |
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| What is the specific plaque hypothesis? |
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| Specific organisms in plaque cause gingivitis. |
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| Many oral bugs suspected in periodontal disease are anaerobic. How does that make it difficult to fulfill Koch's postulates? |
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| They are very difficult to grow in culture. |
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| Who is Sigmund Socransky? |
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| An oral microbiologist who modified Koch's postulates to work for periodontal disease. |
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| Describe Socransky's modification re numbers. |
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| The putative pathogen must be present in higher numbers in diseased individuals. |
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| (Socransky) The organism should exhibit _______ relevant to the initiation and progression of the disease. There should be a ___ response to the organism. |
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| virulence factors; host |
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| Is there a direct correlation between the amount of plaque on an individual's teeth and the severity of periodontal disease? Which hypothesis does this support? |
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| No. This supports the specific plaque hypothesis. |
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| What is the main thing you can do with dark field microscopy? |
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| Determine bug morphology. |
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| What are the two main recent advances that have improved the study of periodontal bugs? |
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| Advances in bacterial culturing and molecular genetic approaches. |
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| What are some other names for necrotizing ulcerative gingivitis? |
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| Trench mouth. Vincent's disease. |
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| Which periodontal disease is characterized by punched out papillae with a pseudomembrane? |
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| necrotizing ulcerative gingivitis |
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| Which bacteria are likely involved in necrotizing ulcerative gingivitis? |
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| Spirochetes, Fusobacteria species, Selenomonas species, and Prevotella species. It's difficult to say if there is a causal relationship. |
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| Which periodontal disease typically involves permanent incisors and first molars and typically self-arrests? |
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| Localized aggressive periodontitis (formerly called localized juvenile periodontitis) |
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| Which bacteria is most closely related with localized aggressive periodontitis? What are some characteristics of this bacteria? |
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| Aggregatibacter actinomycetemcomitans (Aa). Gram-, capnophilic, non-encapsulated, non-motile. In subgingival plaque. |
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| In chronic periodontitis, what correlates with the amount of attachment loss? |
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| the amount of microbial deposits |
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| Which bugs are associated with chronic periodontitis? |
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| P. gingivalis, Tannerella forsythia, Aa, Treponema denticola |
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| Is Aa implicated in chronic or aggressive periodontitis. |
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| Both, but much more in aggressive periodontitis. |
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| How are P. gingivalis and Aa similar? |
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| Both Gram-, both non-motile. |
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| How is P. gingivalis different from Aa? |
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| Pg is an obligate anaerobe. Aa is a capnophile. Pg has a capsule. Aa does not. |
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| Which virulence factors should a periodontal pathogen display? |
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| Colonize a niche, invade tissues, obtain nutrients, evade immune system. |
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| What are the three virulence factors of Aa I would like to remember? |
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| 1. Endotoxin 2. Leukotoxin 3. Cytolethal distending toxin |
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| What does Aa endotoxin do? |
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| Elicits bone resorption and inflammation. |
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| What does Aa leukotoxin do? |
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| Kills leukocytes. |
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| What does Aa cytolethal distending toxin do? |
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| Kills epithelial cells. |
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| Porphyromas gingivalis displays the ability to invade ________. |
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| human cells |
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| What are the three bugs that are suspecting in periodontal disease? |
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| P. gingivalis, Tannerella forsythia, and Treponema denticolis |
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| According to the ecoligic plaque hypothesis, with plaque accumulation, GCF flow is ____ and electrical potential is ____. |
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| high; low |
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| What is the ecologic plaque hypothesis (in a nutshell)? |
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| When the ecology supports the growth of disease causing bugs, they can proliferate past a certain threshold and cause periodontal disease. |
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| Does periodontal disease represent an exogenous or opportunistic infection? |
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| More so opportunistic. These bugs are likely part of our normal flora. But sometimes maybe they're not. |
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| Which bugs cause severe caries in gnotobiotic rats? |
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| Lactobacilli and S. mutans |
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| "Caries-resistant hamsters are not truly caries resistant." Explain. |
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| They just do not carry cariogenic bacteria as part of their normal flora, but when infected, they develop caries. |
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| What kinds of bacteria cause root surface caries? |
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| Actinomyces viscosus and Lactobacilli. |
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| Which bacteria have a strong association with SS, PF, and RS caries? |
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| Mutans Streptococci. (incl. S. mutans, S. sobrinus, S. rattus, and S. cricetus) |
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| Are S. sanguis and S. mitis cariogenic? |
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| They have a weak association with pit and fissure caries. |
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| What is aciduricity (re caries)? |
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| Capacity of a bacteria to maintain metabolism at low pH. |
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| What is antigen I/II? |
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| Strep adhesins that allow them to attach to the acquired pellicle and to each other. |
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| What goes glucan binding protein (GBP) do? |
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| Binds S. mutans to the extracellular glucanms. |
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| All E. coli have ____ pili. In addition, enterotoxigenic E. coli has ____ pili and _______, while uropathogenic E. coli have ____. |
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| common; Type 1; CFA I/II; P pili |
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| Other than pili, what is a bacterial adherence mechanism we discussed? |
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| Afimbrial adhesins (surface proteins) |
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| What are the two kinds of adhesins produced by B. pertussis? |
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| Filamentous hemagglutinin (Fha) and Pertussis toxin (Ptx) |
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| Initial attachment of gonococcus is mediated by ____. Then the surface protein ____ mediates a much tighter interaction. |
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| pili; P2 |
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| What are some kinds of bacteria that can invade cells? |
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| Chlamydia, Shigella, Salmonella |
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| How do bacteria enter non-phagocytic cells? |
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| 1. Zipper mechanism or 2. Trigger mechanism |
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| How does Yersinia enter cells? |
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| the Zipper mechanism |
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| How does Salmonella enter cells? |
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| The "trigger" mechanism. (Changes cytoskeletal structure of cell.) |
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| How can bacteria evade complement? |
answer
| 1. mask surface w/ capsule (S. aureus) 2. Coat themselves with IgA 3. Produce C5a peptidase (S. pyogenes) 4. LSP blocks access (Salmonella) |
question
| What is streptolysin? |
answer
| Enzyme produced by S. pyogenes. Capable of lysing a phagocyte. (also causes hemolysis) |
question
| Which two surface proteins will prevent opsonization? |
answer
| Protein M (staph, strep) and Protein A (S. pyogenes) |
question
| 1 gram of tetanus toxin is enough to kill _____ people. |
answer
| 10 million |
question
| How does cholera toxin work? (and AB toxin arrangement) |
answer
| It hijacks host cell signal transduction. (A-B5) |
question
| How does diphtheria toxin work? (and AB toxin arrangement) |
answer
| It blocks protein synthesis. (A-B single polypeptide) |
question
| How does TSS toxin work? |
answer
| As a superantigen (S. aureus) |
question
| Group A Strep releases the degradative enzyme ______. |
answer
| hyaluronidase |
question
| Why is lipid A (endotoxin) not toxic unless the bacteria is lysed? |
answer
| It is usually buried in the membrane. |
question
| How does endotoxin work? |
answer
| It activates a macrophage to activate PGs, ILs, TNF, complement, etc., leading to tissue damage and inflammation. |
question
| How can bacteria trigger an autoimmune response? |
answer
| Sometimes, the bacteria present an antigen that resembles the host cell. |
question
| With tuberculosis, it is not the bacteria themselves that cause damage, but rather inflammation due to _____. |
answer
| cytokines |
question
| What does the Shigella plasmid do? |
answer
| Encode for cell invasion properties. |
question
| What are pathogenicity islands? |
answer
| Gene segments that are transposable between bacteria. |
question
| What are pathogenicity islands? |
answer
| Gene segments that are transposable between bacteria. |
