Although mutants incapable of producing exotoxins are relatively easy to isolate, mutants incapable of producing endotoxins are much harder to isolate. From what you know of the structure and function of these types of toxins, explain the differences in mutant recovery.
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1. Although mutants incapable of producing exotoxins are relatively
easy to isolate, mutants incapable of producing endotoxins are
much harder to isolate. From what you know of the structure and
function of these types of toxins, explain the differences in mutant
recovery.
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- 1. Although mutants incapable of producing exotoxins are relatively easy to isolate, mutants incapable of producing endotoxins are much harder to isolate. Explain the differences in mutant recovery?Which statement among A-D is false regarding bacterial toxins? A) O Hemolysıns are cell membrane disrupters that can rupture red blood cells. B) O Second mesengar pathway disrupters like cholera toxin produces a debilitating respiratory condition of the lungs. C) O Shiga toxin, tetanus toxin, and hemolysins are all types of exotoxins. D) O Superantigens elicit a hyperactive response by the immune system and can lead to shock. E) O None are false, A-D are all true statements.Before development of a vaccine against this microbe, thedisease it caused accounted for two-thirds of bacterial meningi-tis cases during the first year of life but is still the number oneleading cause of mental retardation in patients who survive seri-ous disease due to permanent central nervous system disorders.What is the microorganism?(a) Haemophilus influenzae type B(b) Haemophilus influenzae type A(c) Neisseria meningitidis(d) Streptococcus pneumoniae(e) Listeria monocytogenes
- 41. Identify the MISMATCH pair from the following, if any Group of answer choices some toxins :::: helps bacteria scavenge iron from environment endotoxin :::: are difficult to inactivate pneumolysin :::: encoded by chromosomal DNA gene superantigens :::: compromises immune system exotoxins :::: secreted by Gr + and – ve bacteria none of the above is a mismatch pair 42. dentify the FALSE statement for cholera toxin, if any Group of answer choices adenylate cyclase is activated metabolic acidosis is a consequence of toxin activity subunit A enters intestinal epithelial cell; modifies a key component of target cells none of the above is a false statements it’s encoded by a phage gene toxin subunit has ADP ribosylation activity2) Describe the function of the key Agrobacterium proteins involved in the transfer and integration of the transfer DNA (T-DNA) into host cells24. Which of the following antibiotics would you use to stop the growth of mycoplasma. A) Penicillin, an antibiotic that blocks cell wall biosynthesis. B) Tetracycline, an antibiotic that inhibits bacterial protein synthesis by blocking the function of ribosomes.
- Compare endotoxins and exotoxins produced by bacteria to include: 1) the type(s) or source(s) of bacteria that produce each toxin2) what each toxin is composed of3) how each toxin is released into the environment10. In a secret cabinet of a lab, you find two Petri dishes in storage and a mysterious lab notebook. In an effort to identify the bacteria, you run some tests (taking all necessary safety precautions) and look through the lab notebook. You find that the two Petri dishes contain the same type of nutrient medium and both bacteria seem to be Escherichia sp., but that the bacteria in plate 1 are producing large amounts of a variety of neurotoxins. The bacteria in plate 2 are not producing any major exported product. You also find this chart in the lab notebook: A E. coli growth rate (biomass/hour) Given that Strain 2 is normal E.coli (the control) and Strain 1 is a genetically engineered strain of E.coli, which line is most likely to represent strain 1, and why? A. Line B, since strain 1 should exhibit lower than normal growth efficiency. B. Line B, since strain 1 should exhibit higher than normal growth efficiency. C. Line A, since strain 1 should exhibit lower than normal growth…Sp 23 E2.pdf bads/Sp%2023%20E2.pdf Read aloud E R x + + of 4 Q D 29) The life cycle of the virus that infects bacteria and allows the bacteria to survive is called: a) Phagic b) Recombinant c) lytic d) parasitic e) lysogenic 30) The enzyme present in the human immune virus which must be injected with the genetic material is called: a) Reverse Translatase b) Reverse Replicase c) Reverse Transcriptase d) Reverse Polymerase e) Retro Virase 31) If the electron donor for bacterial nutrient uptake is coming from H₂S then this mode of electron uptake is called: a) Electromotive trophy b) Electro-osmosis c) Lithotroph d) Heterotroph e) none of the above 32) The life cycle of the virus that infects bacteria and destroys the bacterial cell membrane: a) Phagic b) Cytotic c) Apoptotic d) lytic e) lysogenic. 3 33) If an organism feeds on dead or dying organisms that this mode of feeding is called: a) Heterotroph b) Chemoheterotroph c) Chemolithoautroph d) Chemolithoorganotroph e) Saprobic 34) One…
- 1. Precise words:Find the nonspecific terms in the following sentences. Replace the nonspecific choices with more preciseterms or phrases (It is not necessary to change the sentence structure).(i) All OVE mutants showed enhanced iP concentrations.(ii) Plants were kept in the cold overnight.(iii) To provide proof of concept for our hypothesis, we studied a virus in its host cell.(iv) The present paper reports on continuing experiments that were performed to clarify thissurprising effect.(v) The first transition state is a little lower in energy than the second transition state. 2. Simple words:Improve the word choice in the following examples by replacing the underlined terms or phrases withsimpler word choices (do not change the sentence structure).(i) These data substantiate our hypothesis.(ii) The difference in our results compared to those of Reuter et al. (1995) can be accounted forby the fact that different conditions were used.(iii) For the purpose of discussing cell migration we…9. Define adherence of the bacterial disease process. Why is this step so important for bacterial infections? 10. List the four ways that bacteria evade or subvert the immune system during the Establishment and Surviving Host Defenses stage of the bacterial disease process. 11. Define exotoxins. How do exotoxins damage and destroy cells? Can exotoxins affect all cell types in the human body? Explain your answer. 12. Create (draw) a table to compare and contrast the following respiratory agents: Streptococcus pneumonia, Listeria monocytogenes, and Mycoplasma pneumoniae for the 5 steps of the bacterial disease process (portal of entry. adherence, establishment, invasiveness, and portal of exit) (3 points)There have been recurring cases of mad-cow disease in the United Kingdom since the mid-1990s. Mad-cow disease is caused by a prion, an infectious particle that consists only of protein. In 1986, the media began reporting that cows all over England were dying from a mysterious disease. Initially, there was little interest in determining whether humans could be affected. For 10 years, the British government maintained that this unusual disease could not be transmitted to humans. However, in March 1996, the government did an about-face and announced that bovine spongiform encephalopathy (BSE), commonly known as mad-cow disease, can be transmitted to humans, where it is known as variant Creutzfeldt-Jakob disease (VCJD). As in cows, this disease eats away at the nervous system, destroying the brain and essentially turning it into a spongelike structure filled with holes. Victims experience dementia; confusion; loss of speech, sight, and hearing; convulsions; coma; and finally death. Prion diseases are always fatal, and there is no treatment. Precautionary measures taken in Britain to prevent this disease in humans may have begun too late. Many of the victims contracted it over a decade earlier, when the BSE epidemic began, and the incubation period is long (VCJD has an incubation period of 10 to 40 years). A recent study concluded that 1 in 2,000 people in Great Britain carry the abnormally folded protein that causes VCJD. In spite of these numbers, the death rate from VCJD remains low. It is not clear whether this means that the incubation period for the disease is much longer than previously thought, or whether they may never develop the disease. How can a prion replicate itself without genetic material?