Prescott’s Microbiology, 9th Edition
Chapter 39 –Human Diseases Caused by Bacteria
GUIDELINES FOR ANSWERING THE MICRO INQUIRY QUESTIONS
Figure 39.2 What organisms serve as the environmental reservoir for L. pneumophila?
The bacteria are inside protozoa as parasites.
Figure 39.5 How is the M protein also thought to be involved in poststreptococcal diseases?
Streptococcal M protein has been implicated in poststreptococcal diseases such as glomerulonephritis. It is thought that in glomerulonephritis deposition of antigen-antibody complexes involving M protein is responsible for the kidney damage. Also rheumatic fever, an autoimmune disease, is thought to be associated with crossreactive antibodies that were initially made against the M protein but also recognize heart tissue.
Figure 39.6 What causes the exudate seen in strep throat? Is it seen in all cases?
In half of human cases, an exudate builds up consisting of bacterial and host cell debris.
Figure 39.7 What are the three stages of Lyme disease? What other spirochete disease does this resemble?
The first stage of Lyme disease is a localized stage that occurs about a week after an infectious tick bite and results in a “bullseye” skin lesion. The disease is treatable at this point. The second, disseminated stage occurs weeks to months later. Symptoms include neurological abnormalities, heart inflammation, and bouts of arthritis. The late stage can occur years later and victims develop neuron demyelination and symptoms similar to Alzheimer’s disease. Syphilis, also due to spirochete infection, also has 3 stages of disease.
Figure 39.12 What are the chief differences between tuberculoid and lepromatous leprosy?
The main differences between tuberculoid and lepromatous leprosy is the T cell response. Those with tuberculoid leprosy have a protective T cell response that results in a delayed type hypersensitivity reaction to antigens on the surface of Mycobacterium leprae. The disease is a mild, nonprogressive form. In contrast, those with lepromatous leprosy do not produce a protective T cell response so do not develop delayed type hypersensitivity, and bacteria are allowed to multiply unimpeded resulting in progressive disease with disfiguring nodules. Immune formation of granuloma to contain the bacteria is a common host response to mycobacteria.
Figure 39.13 How does H. pylori increase the local pH in its gastric microenvironment?
The bacteria use motility to bury themselves under the mucous layer next to epithelial cells in the stomach. While there, they secrete urease enzyme, which cleaves urea into the weak base ammonia, thus raising the pH.
Figure 39.16 Which of these clinical manifestations are associated with syphilis transmission? Explain.
The primary syphilic chancre contains spirochetes so contact with it may result in disease transmission. Rash lesions of the secondary stage are also infectious. Gummas of the third stage are not considered infectious.
Figure 39.21 To what drugs, besides methicillin, are MRSA strains resistant?
Methicillin is used as a marker. If SA strains are resistant to methicillin, then they are usually resistant to multiple other antibiotics, including many other beta-lactams. MRSA can commonly be resistant to a dozen other antibiotics, or more.
Figure 39.22 What virulence factors enable the rapid invasion of certain step A strains?
These strains secrete extracellular protease, lipase, and other enzymes, which enhance spread through tissues.
Figure 39.25 How do the neurological effects of botulinum toxin differ from those of tetanus toxin?
While both toxins act on neurons at the neuromuscular junction, botulinum toxin (botox) blocks the release of the primary stimulatory neurotransmitter, acetylcholine. In contrast, tetanus toxin (tetanospasmin) blocks release of inhibitory neurotransmitters (GABA and glycine). Thus, botox results in flaccid paralysis while tetanospasmin results in spasmodic paralysis.
Figure 39.27 To which E. coli class does the strain O157:H7 belong?
E. coli O157:H7 is an enterohemorrhagic (EHEC) strain which produces the shiga-like toxins.
Figure 39.29 By what mechanisms do EF and LF kill macrophages?
In anthrax, Edema factor has adenylate cyclase activity which causes intracellular cAMP to increase which leads to fluid release or edema. Lethal factor prevents the transcription factor NF kappa B from regulating numerous cytokine and other immunity genes needed to promote macrophage survival.
Figure 39.31 What cells and tissues make up the pseudomembrane?
In pseudomembranous colitis the pseudomembrane is a collection of inflammatory cells, dead cells, necrotic tissue, and fibrin that obstructs the intestine.
Figure 39.33 How is tooth enamel demineralized by bacterial growth?
The bacteria ferment sugars, especially sucrose. The resulting acids move below the enamel surface where they dissociate and react with the hydroxyapatite of the enamel to form soluble calcium and phosphate ions, and the ions diffuse outward.
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