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Western Governors University
D311 Microbiology with Lab: A Fundamental Approach
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1) What is the difference between pathogenesis and virulence?
Pathogenesis refers to the overall ability of an organism to cause disease, encompassing the mechanisms and processes by which the disease develops. Virulence, on the other hand, is a measure of the severity or harmfulness of the disease caused by a pathogen. In other words, while pathogenesis explains how a disease occurs, virulence quantifies how intense or severe the disease symptoms are.
2) What are the different types of virulence factors, and how do bacterial, viral, and eukaryotic factors differ?
Virulence factors are molecules or structures produced by pathogens that enable them to establish infection, evade the host immune response, and cause damage. These factors vary among bacteria, viruses, fungi, and helminths.
| Type of Pathogen | Virulence Factors | Examples and Description |
|---|---|---|
| Bacterial | Adhesion, evasion, invasion | Adhesion factors such as Protein F in Streptococcus pyogenes attach to respiratory epithelial cells causing strep throat. Evasion factors include capsules and mycolic acid that protect bacteria from phagocytosis, and antigenic variation that alters surface antigens to escape immune detection. Invasion factors include exoenzymes like collagenase, which breaks down collagen, facilitating bacterial spread. |
| Viral | Adhesion, immune evasion | Hemagglutinin adhesin in influenza virus binds to sialic acid on respiratory cells. Viruses evade immunity by antigenic drift (small mutations) and antigenic shift (major genetic reassortment), leading to changes in surface proteins. |
| Fungal | Adhesins, capsules, mycotoxins | Candida albicans uses glycoproteins for adhesion and produces proteases such as keratinase and phospholipase to invade tissues. Cryptococcus species have capsules made of glucuronoxylomannan that prevent phagocytosis. Claviceps purpurea produces ergot toxin causing gangrenous and convulsive ergotism. |
| Helminthic | Large size, protective cuticles, glycan mimicry | Helminths are large, making phagocytosis difficult. Roundworms have cuticles to resist immune damage. Some express glycans resembling host molecules, helping them avoid immune recognition. |
3) How do endotoxins and exotoxins differ?
| Feature | Endotoxins | Exotoxins |
|---|---|---|
| Source | Produced only by Gram-negative bacteria (part of LPS in outer membrane) | Produced by both Gram-positive and Gram-negative bacteria (secreted proteins) |
| Effect | Cause systemic symptoms like inflammation and fever | Cause specific damage based on receptor targeting |
| Heat stability | Heat stable | Mostly heat labile, some stable |
| Median lethal dose | High (less toxic) | Low (highly toxic) |
Endotoxins generally induce generalized inflammatory responses, whereas exotoxins have targeted actions causing specific cellular damage.
4) How does the Gram stain differentiate between Gram-positive and Gram-negative bacteria?
Gram-positive bacteria have a thick peptidoglycan layer that retains the crystal violet-iodine complex during staining, appearing purple. Gram-negative bacteria have a thinner peptidoglycan layer and an outer membrane; they lose the crystal violet stain during the alcohol decolorization step and take up the counterstain safranin, appearing pink or red
5) What are the differences between Acid-fast, Endospore, and Capsule staining?
| Staining Type | Purpose | Key Features |
|---|---|---|
| Acid-fast | Differentiate bacteria with waxy mycolic acid layers (e.g., Mycobacterium) | Acid-fast bacteria retain red carbolfuchsin dye due to thick mycolic acid; non-acid fast bacteria do not. |
| Endospore | Differentiate endospores from vegetative cells | Endospores stain green with malachite green; vegetative cells stain red with safranin. |
| Capsule | Visualize bacterial capsules | Negative staining technique; background stained black, capsules appear as clear halos around cells. |
6) What is a key difference between bacteria and protists?
Bacteria are prokaryotic cells, lacking a membrane-bound nucleus and typically possessing a single circular chromosome in a nucleoid region. Protists are eukaryotic, with complex membrane-bound nuclei and multiple linear chromosomes.
1) How does commensalism differ from mutualism?
In mutualism, both species benefit from the relationship. In commensalism, one organism benefits while the other remains unaffected.
2) What distinguishes a noncommunicable infectious disease from a noninfectious disease?
Noncommunicable infectious diseases are caused by pathogens but are not transmitted person-to-person, such as tetanus caused by Clostridium tetani. Noninfectious diseases are not caused by pathogens and may result from genetic, environmental, or immune system factors.
3) What is the difference between biological and mechanical vectors?
Mechanical transmission occurs when a vector physically carries pathogens on its body and transmits them through contact. Biological transmission involves the vector harboring the pathogen internally and transmitting it through biting or other invasive mechanisms.
4) How do vertical and horizontal direct contact transmission differ?
Vertical transmission is the passage of pathogens from mother to child during pregnancy, birth, or breastfeeding. Horizontal transmission occurs through direct contact between individuals outside of the maternal context.
5) What differentiates a passive carrier from an active carrier?
A passive carrier mechanically transmits a pathogen without being infected themselves (e.g., a healthcare worker transmitting pathogens via contaminated hands). An active carrier harbors and can transmit the infection because they are themselves infected.
6) How do the prodromal period and period of illness differ?
The prodromal period is characterized by early, nonspecific symptoms as the pathogen multiplies. The period of illness features the most severe and distinct signs and symptoms.
7) What differentiates the period of decline from the period of convalescence?
During the decline, symptoms and pathogen numbers decrease. Convalescence is the recovery phase where the patient returns to normal function, although some diseases may leave lasting damage.
8) What is the difference between morbidity rate and mortality rate?
| Rate | Definition |
|---|---|
| Morbidity rate | Number of individuals who become ill in a population |
| Mortality rate | Number or percentage of deaths caused by a disease in a population |
1) When is an autoclave preferred for microbial control?
Autoclaves are the preferred method for sterilizing surgical instruments and materials that require complete elimination of all microbial life, including spores.
2) How does beta-lactamase contribute to antibiotic resistance?
Beta-lactamase enzymes hydrolyze the β-lactam ring found in β-lactam antibiotics, such as penicillins, rendering the drug inactive. This enzymatic degradation is a primary mechanism by which bacteria resist β-lactam antibiotics.
3) What are the differences between cellular and humoral immunity?
Humoral immunity involves B cells producing antibodies that neutralize extracellular pathogens. Cellular immunity relies on T cells targeting and destroying intracellular pathogens.
4) How do the chickenpox and tetanus vaccines differ?
The chickenpox vaccine is a live attenuated vaccine that uses a weakened virus to induce immunity through a subclinical infection. The tetanus vaccine is a toxoid vaccine containing inactivated bacterial toxins, which stimulate humoral immunity to neutralize the toxin without exposing the host to the whole pathogen.
5) What are examples of anti-helminthic drugs, and why are helminth infections difficult to treat?
Anti-helminthic drugs include niclosamide, praziquantel, and ivermectin. Treating helminth infections is challenging because these parasites are multicellular eukaryotes, similar to humans, making it difficult to target the parasite without harming the host.
Madigan, M. T., Bender, K. S., Buckley, D. H., Sattley, W. M., & Stahl, D. A. (2018). Brock Biology of Microorganisms (15th ed.). Pearson.
Tortora, G. J., Funke, B. R., & Case, C. L. (2020). Microbiology: An Introduction (13th ed.). Pearson.
Murray, P. R., Rosenthal, K. S., & Pfaller, M. A. (2019). Medical Microbiology (9th ed.). Elsevier.
Ryan, K. J., & Ray, C. G. (2017). Sherris Medical Microbiology (6th ed.). McGraw-Hill.
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