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For the second half of the twentieth century, the development ofantibiotics greatly reduced the number of deaths from

bacterial infections
fungal infections
prion infections
viral infections

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Nelly Stracke
Nelly StrackeLv2
30 Sep 2019
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Related questions

.1 List the signs and symptoms of sepsis, and explain the most common types of infections that develop in to septic shock. Make sure to include information to differentiate between gram-positive sepsis and gram-negative sepsis. Lastly, describe what the two conditions are that define the systemic inflammatory response syndrome of sepsis.

2)

. List a viral, bacterial, and fungal microbe that can cause a respiratory infection. With these three microbes, include the following for each (16 points):

a. mode of transmission

b. disease symptoms

c. preferred treatment

d. a laboratory test that could be done to determine a patient has the microbe

16. All of the following are true about ear infections EXCEPT:

Middle ear infections (otitis media) often produce a puslike exudate (referred to as otitis media with effusion) due to infection by genera of Streptococcus, Haemophilus, or various species of anaerobes.

External auditory canal (otitis externa) infections are typically caused by Staphylococcus aureus or Pseudomonas aeruginosa.

After successful treatment of middle ear infections with antibiotics, sometimes tubes are inserted to prevent fluid accumulation, repeated infections, and hearing loss.

Pseudomonad infections are common in swimmers because these organisms are able to produce a soluble greenish-blue pigment.

Repeated ear infections in children often decrease markedly because as the child ages and the Eustachian tube changes shape and develops an angle that prevents most organisms from reaching the middle ear.

17. Why are colds difficult to treat and prevent?

Different cold viruses predominate during different seasons.

Because there are so many different types of rhino- and coronaviruses, each with different antigens, development and administration of vaccines are currently prohibitive.

Although some human interferons have been shown to block or limit rhinovirus infections, delivery to infection sites is difficult, and unwanted side effects can occur.

All of the above.

Both a and c.

18. Which of the following is NOT true about parainfluenza viruses?

Most infants by the age of 6 months have been exposed to and develop antibodies against all 4 parainfluenza viruses.

They cause rhinitis characterized by nasal, pharyngeal, and bronchial inflammation, primarily in children.

Parainfluenza virus infection can be prevented by vaccination.

They can cause noisy respiration (stridor) and acute obstruction of the larynx called croup.

The viruses are spread by direct contact or by large droplets.

19. In whooping cough, patients experience violent coughing episodes during the _________ stage and can have bluing of the skin or _________ due to lack of oxygen from massive mucus and bacterial airway blockage.

Paroxysmal; cyanosis

Catarrhal; pigmentation

Convalescent; osmosis

Pneumotic; hydrolysis

Primary; emesis

20. Penicillins have no effect on Mycoplasma pneumoniae because:

Mycoplasmas are viruses

Mycoplasmas possess beta lactamases

Mycoplasmas are too small

Mycoplasmas are eukaryotes

Mycoplasmas lack cell walls

21. How many cases of tuberculosis are reported globally each year?

10

10,000

100,000

3 million

10 million

22. Mycobacteria are difficult to Gram stain, and are termed “acid-fast” due to their:

Ability to survive in acidic conditions

Resistance to drying

Thick, waxy cell walls

Resistance to sunlight

Lack of a peptidoglycan layer

23. Which of the following is true about pathogenic mycobacteria?

They have a long generation time of 12 to 18 hours.

They are obligate anaerobes sensitive to small amounts of oxygen.

They are highly resistant to drying and can remain viable in dried sputum 6 to 8 months later.

Both a and b.

Both a and c.

24. Clinical symptoms of tuberculosis are primarily due to:

Host inflammatory response

Mycotoxins

Endotoxin

Mucus production

Exotoxin

25. What characteristic of Coxiella burnetii, the causative agent of Q fever, allows it to survive for up to 2 years?

Metachromatic granule

Exotoxin

Endospore

Hemagglutinin

Cilia

26. The normal microflora of the heart includes species of:

Gram-positive bacteria

Gram-negative bacteria

Fungi

Viruses

None of these

27. Which of the following is commonly directly responsible for causing septic shock today?

Bacterial hemagglutinins

Bacterial endotoxins

Bacterial exotoxins

Fungal aflatoxins

Bacterial neurotoxins

28. All of the following are symptoms of septic shock EXCEPT

Shock

Lymphangitis

Chills

Fever

Collapsed blood vessels

29. What is the most likely explanation of how Streptococcus pyogenes causes rheumatic fever?

Strep throat infections migrate down to the heart.

Endotoxin production causes septicemia.

Vegetation followed by fibrin deposition.

Cross-reactivity of an antibody for a Streptococcus pyogenes antigen to a heart cell antigen.

It is an opportunistic infection triggered by coronary artery disease and atherosclerosis.

30. Bacterial endocarditis is an infection and inflammation of the lining and valves of the heart and occurs as a result of transient bacteria attaching to fibrin from exposed collagen fibers of damaged valvular surfaces. True or false?

1- The drug chloroquine raises the pH of endosomes, How willthis affect antigen processing and presentation by class IIMHC?


2- A common approach to vaccine development has been the use ofa viral vector such as vaccinia virus to carry genetic informationof a pathogen into an individual. The vaccinia virus infection(which does not cause disease in most individuals) would then leadto production of proteins from the pathogen and an immune response.Such an approach has been very successful for viruses but has notbeen successful for most bacterial infections. Why?


3- The pathogen Listeria monocytogenes enters cellsthrough phagocytosis but escapes from the phagosome before it isdestroyed. Would patients who are deficient in class I MHC bebetter or worse hosts for this pathogen than normal individuals?Why?

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