A fellow student asks you to explain how tuberculosis (TB) can remain dormant in some people. What explanation will you give?
It does not remain dormant but some host defenses can kill the bacteria
Virulence factors in the baciilli weaken over time leading to apoptosis
The bacilli can become isolated within tubercles in the lungs, possibly encapsulated
Macrophages attack and phagocytize new areas of infection
The Correct Answer is C
A. It does not remain dormant but some host defenses can kill the bacteria: While the immune system can kill some of the Mycobacterium tuberculosis bacilli, in many cases, the bacteria evade complete eradication and persist in a dormant state within the lungs. This does not mean the infection is fully eliminated, as it can reactivate later.
B. Virulence factors in the bacilli weaken over time, leading to apoptosis: Mycobacterium tuberculosis does not naturally lose its virulence over time. Instead, it can persist in a latent state due to immune containment, not because of a reduction in its ability to cause disease.
C. The bacilli can become isolated within tubercles in the lungs, possibly encapsulated: In latent tuberculosis, the immune system walls off the bacilli within granulomas (tubercles), preventing active disease. These granulomas may be encapsulated with fibrous tissue, restricting bacterial growth and spread. The bacteria remain dormant but can reactivate if the immune system weakens.
D. Macrophages attack and phagocytize new areas of infection: While macrophages do play a role in the immune response to tuberculosis, they are often unable to completely eradicate the bacilli. Instead, the bacteria can survive within macrophages and trigger the formation of granulomas, which help contain but not eliminate the infection.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
A. Hospital-acquired pneumonia: Pneumonia that develops 48 hours or more after hospital admission is classified as hospital-acquired pneumonia (HAP). It is caused by pathogens acquired in the hospital setting, often involving multidrug-resistant organisms such as Pseudomonas aeruginosa, Staphylococcus aureus (including MRSA), and Klebsiella pneumoniae. Patients who are intubated, have prolonged hospital stays, or have weakened immune defenses are at higher risk.
B. Immunocompromised pneumonia: Pneumonia in immunocompromised patients occurs due to weakened host defenses, such as in individuals with HIV/AIDS, those undergoing chemotherapy, or transplant recipients on immunosuppressive therapy. While these patients can develop HAP, pneumonia due to opportunistic infections like Pneumocystis jirovecii or fungal infections is categorized separately.
C. Community-acquired pneumonia: Pneumonia acquired outside the hospital or within the first 48 hours of admission is classified as community-acquired pneumonia (CAP). Typical pathogens include Streptococcus pneumoniae, Haemophilus influenzae, and Mycoplasma pneumoniae. CAP is usually less resistant to antibiotics compared to HAP.
D. Viral pneumonia: Pneumonia caused by viral pathogens such as influenza, respiratory syncytial virus (RSV), or SARS-CoV-2 is classified based on the causative agent rather than the setting in which it was acquired. Although viruses can cause both CAP and HAP, the classification of pneumonia is determined by the timing of onset and exposure risks.
Correct Answer is A
Explanation
A. Injury to the endothelial cells that line the artery walls: The development of atherosclerosis begins with damage to the endothelial cells of the arterial wall. This injury can be caused by various factors, including hypertension, smoking, high cholesterol, and diabetes. Once the endothelium is injured, it becomes more permeable, allowing lipids and inflammatory cells to penetrate and accumulate, leading to the formation of atherosclerotic plaques.
B. Release of the platelet-derived growth factor: While platelet-derived growth factor (PDGF) plays a role in the proliferation of smooth muscle cells and the progression of atherosclerosis, it is not the initiating event. PDGF is released in response to endothelial injury and inflammation but does not cause the initial damage itself.
C. Macrophages adhere to vessel walls: The adherence of macrophages to the vessel walls occurs after the initial endothelial injury. Once the endothelium is damaged, macrophages migrate to the site and contribute to the inflammatory response and plaque formation, but this is not the initiating event.
D. Release of inflammatory cytokines: Inflammatory cytokines are part of the response that follows endothelial injury and play a role in the progression of atherosclerosis. However, the release of these cytokines is a consequence of the initial injury rather than the initiating event.
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