Bauman Chapter 15 Answers to Critical Thinking Questions
p. 440
Some strains of Staphylococcus aureus produce exfoliative toxin, a chemical that causes portions of the entire outer layer of the skin to be sloughed off in a disease called scalded skin syndrome. Given that cells of the outer layers are going to fall off anyway, why is this disease dangerous?
The outer layers of dead skin cells are tightly connected to each other and make a formidable barrier against microbial invasion. Exfoliative toxin completely removes this barrier, providing entry to a wide range of microbes.
p. 447
A medical laboratory technologist argues that granulocytes are a natural group, whereas agranulocytes are an artificial grouping. Based on Figure 15.5, do you agree or disagree with the lab tech? What evidence can you cite to justify your conclusion?
The technologists’ statement is a reasonable one. Granulocyte cells (neutrophils, eosinophils and basophils) develop from a common progenitor (myeloid), whereas agranulocytes (lymphocytes and monocytes) develop from different progenitors (lymphoid and myeloid respectively).
p. 451
A patient has a genetic disorder that makes it impossible for her to synthesize complement protein 8 (C8). Is her complement system nonfunctional? What major effects of complement could still be produced?
Without C8 the complement system is unable to form Membrane Attack Complexes and damage bacteria. The complement cascade will still produce factors (C3a, C5b, which) to attract phagocytes and enhance inflammation, and other factors (C3b) that opsonizes pathogens, making phagocytic attack easier.
p. 457
While using a microscope to examine a sample of pus from a pimple, Maria observed a large number of macrophages. Is the pus from an early or a late stage of infection? How do you know?
The pus is from a late stage of infection. Neutrophils arrive early in infection in large numbers, and begin to die as they fight the infection. Monocytes arrive soon after, and mature into macrophages, but do not die as the neutrophils do, thus lots ofmany macrophages and few neutrophils is an indication that are found as the attack on the infection is winding down.
p. 458
How do drugs such as aspirin and ibuprofen act to reduce fever?
Aspirin and ibuprofen block the reactions that produce the molecules that “reset” the body’s’ thermostat in the hypothalamus.
p. 461
1. Neighbor A received a chemical burn on his arm and was instructed by his physician to take over-the-counter, anti-inflammatory medication for the painful, red, swollen lesions. When Neighbor B suffered pain, redness, and swelling from an infected cut on his foot, he decided to take the same anti-inflammatory drug because his symptoms matched Neighbor A’s symptoms. How is Neighbor B’s inflammation like that of Neighbor A? How is it different? Is it appropriate for B to medicate his cut with the same medicine A used?
Neighbor A has inflammation that is a response to tissue damage caused by the burn. Neighbor B is also experiencing inflammation in response to damage, but the damage was done by invading microbes. B should not use the same medicine A used: inflammation is an important process in fighting microbial invasion, and reducing inflammation too much may allow the microbes to spread.
2. What might happen to someone whose body did not produce C3? C5?
A body lacking C3 does not have a functional complement cascade: no factors that enhance inflammation, attract phagocytes, opsonize antigens will be produced, and MACs will not assemble.
The absence of C5 prevents the assembly of MACs, but the complement cascade proceeds far enough to produce C3a and C3b which contribute to inflammation and are chemotactic and opsonizing factors.
3. Duncan, age 65, has had diabetes for 40 years, with resulting damage to the small blood vessels in his feet and toes. His circulation is impaired. How might this condition affect his vulnerability to infection?
Impaired circulation reduces the bodys’ ability to develop an inflammatory response and to deliver the phagocytes and complement molecules needed to initiate the fight against infection: Duncan is very vulnerable to infection.
4. A patient’s chart shows that eosinophils make up 8% of his white blood cells. What does this lead you to suspect? Would your suspicions change if you learned that the patient had spent the previous 3 years as an anthropologist living among an African tribe? What is the normal percentage of eosinophils?
In the United States, the primary reason for eElevated eosinophils is allergies. However, eosinophilia may also indicate a strong indication of infection by parasitic worms. T, and the patient history verifies the likelihood that the patient has an helminth infection. Normal eosinophil levels are 2-4%.
5. There are two kinds of agranulocytes in the blood—monocytes and lymphocytes. Janice notes that monocytes are phagocytic and that lymphocytes are not. She wondered why two agranulocytes would be so different. What facts of hematopoiesis can answer her question?
Monocytes develop from myeloid stem cells while lymphocytes develop from lymphoid stem cells. “Agranulocyte” is a description of the appearance of the cytoplasm, not of function or lineage.
6. A patient has a genetic disorder that prevents him from synthesizing C8 and C9. What effect would this have on his ability to resist blood-borne Gram-negative and Gram-positive bacteria? What would happen if C3 and C5 fragments were also inactivated?
The lack of C8 and C9 results in the inability to form mMembrane aAttack Ccomplexes (MACs), which are particularly effective in damaging Gram-negative bacteria; therefore, so infections with Gram-negative bacteria may progress to dangerous levels. The complement cascade can progess far enough in this patient to produce C3a, C3b, and C5b, which contribute to inflammation and are chemotactic and opsonizing factors. A, as a result, the inflammatory response to both Gram-positive and Gram-negative bacteria is normal. If factors C3 and C5 are were also missing, the complement factor contribution to inflammation is would be destroyed, reducing the vigor of the response to any invading bacterium, Gram-positive or Gram-negative;, and the patient is would be more susceptible to dangerous bacterial infections.