MMG exam 3 short answers

Define empiric therapy and prophylaxis. Provide one clinical example of
each from nursing practice and explain the microbiological rationale behind
both. (6 points)

- Empiric therapy: Starting antibiotic treatment before the exact microorganism causing an infection has been identified, based on the suspected infection and the most likely pathogens.

• Clinical example: A nurse caring for a patient with a suspected bacterial infection may administer broad-spectrum antibiotics before culture results are available to avoid delaying treatment.

• Microbiological rationale: Different bacteria have different antibiotic susceptibilities. A Gram stain aids in identifying early characteristics of bacteria, including their Gram reaction (positive or negative) and shape, which can help guide initial antibiotic selection. Broad-spectrum antibiotics target a range of possible bacteria before the exact pathogen is known. Once culture and sensitivity results identify the specific bacterium and which antibiotics it is susceptible to, treatment can be adjusted to a more targeted antibiotic.

- Prophylaxis: The use of medication or other preventive measures to reduce the risk of infection or disease in a person who is at risk but does not currently have that infection. (preventing an infection before it occurs)

• Clinical example: A nurse may administer prophylactic antibiotics to a patient before surgery to reduce the risk of a surgical site infection.

• Microbiological rationale: Surgery can introduce microorganisms into normally sterile body tissues. Giving antibiotics before the procedure helps prevent bacteria from establishing an infection and multiplying at the surgical site.

Three mechanisms of antibiotic resistance

1. Enzymatic breakdown or inactivation

• Bacteria produce enzymes that destroy or chemically modify antibiotics, making them ineffective.

• Example: Some bacteria produce beta-lactamase enzymes that break down the beta-lactam ring in penicillin, preventing the antibiotic from working.

2. Modification of the antibiotic target

• Bacteria change the structure of the specific cellular target that an antibiotic normally binds to, preventing the antibiotic from attaching and working effectively.

• Example: MRSA (methicillin-resistant Staphylococcus aureus) produces an altered penicillin-binding protein (PBP2a) that has a low affinity for many beta-lactam antibiotics.

3. Efflux pumps

• Bacteria use transport proteins called efflux pumps to pump antibiotics out of the bacterial cell, reducing the amount of antibiotic inside the cell and preventing it from working effectively.

• Example: Some strains of Streptococcus pneumoniae use efflux pumps to pump out macrolide antibiotics, such as erythromycin, contributing to antibiotic resistance.

Define antigenic shift and antigenic drift and describe how each affects viral
evolution. State the likely role of antigenic shift in the development of the
influenza pandemic of 1918. (6 points)

- Antigenic drift: A gradual buildup of small genetic mutations in the genes that code for viral surface antigens, causing small changes in the proteins on the surface of a virus.

• Effect on viral evolution: Allows viruses to change over time and avoid being recognized by the host immune system, helping them continue to infect people who may already have some immunity. In influenza, antigenic drift contributes to seasonal flu epidemics. Because of these changes, new flu vaccines are made each year. The WHO predicts which strains are most likely to circulate during the upcoming flu season, and vaccines are updated to target those strains. When the predicted strains match the circulating strains, vaccination can reduce the risk of illness by approximately 60%.

- Antigenic shift: A sudden, major change in a virus that occurs when two different viral strains infect the same host cell and exchange genome segments through a process called reassortment.

• Effect on viral evolution: Can create a virus with a completely new combination of surface antigens that the host population may have little or no immunity against, allowing it to spread more easily. This can happen when animal and human influenza viruses infect the same host cell and exchange genome segments. In influenza, reassortment can create new combinations of hemagglutinin (H) and neuraminidase (N), potentially producing a new influenza A subtype and causing a worldwide pandemic.

- Role of antigenic shift in the 1918 influenza pandemic:

• The 1918 Spanish flu pandemic was caused by an H1N1 influenza A virus. Antigenic shift contributed to the emergence of this new strain because people had little preexisting immunity against it. The pandemic had unusually high mortality among young adults, partly associated with severe immune responses called cytokine storms.

A mother infected with RSV is concerned about her newborn becoming ill.
Explain the following (5 points):

a) The immunization strategies used for RSV prevention in three groups: pregnant women, newborns, and older adults
b) The role of passive immunity in this prevention strategy
c) Describe the vaccine type used to prevent RSV-related illness

a) Immunization strategies used for RSV prevention in three groups:

• Pregnant women: Pregnant women can receive the RSV vaccine (Pfizer’s Abrysvo), allowing them to produce antibodies that can be passed to the developing baby before birth.

• Newborns and infants: Babies whose mothers did not receive the RSV vaccine during pregnancy can receive nirsevimab (Beyfortus), an injection containing RSV antibodies. It is also recommended for certain children at increased risk of severe RSV during their second RSV season.

• Older adults: Adults ages 75 and older, as well as adults ages 60–74 who are at increased risk of severe RSV, are recommended to receive an RSV vaccine.

b) Role of passive immunity in RSV prevention:

• Passive immunity protects babies by providing them with antibodies made by another source rather than requiring them to produce their own.

• When a pregnant woman receives the RSV vaccine, her antibodies cross the placenta and provide protection to her baby after birth.

• Nirsevimab also provides passive immunity by directly giving the infant ready-made RSV antibodies through an injection.

c) Vaccine type used to prevent RSV-related illness:

• RSV vaccines are subunit vaccines that contain the RSV F protein antigen. They do not contain the entire virus.

• The F protein helps the virus enter host cells, so exposing the immune system to this antigen allows it to recognize RSV and produce an immune response.

• These vaccines stimulate the person's own immune system to produce antibodies, providing active immunity.

Describe antitoxin (include details on the following): what type of molecule
it is, how it is produced, how it can treat diphtheria and whether antitoxin
treatment provides passive or active immunity. Define toxoid. (5 points)

1. What type of molecule is an antitoxin?

-An antitoxin is an antibody (immunoglobulin) that specifically binds to and neutralizes a toxin produced by a bacterium.

2. How is antitoxin produced?

• Antitoxins are produced by exposing an animal, such as a horse, to an inactivated toxin (toxoid). The animal's immune system responds by producing antibodies against the toxin. These antibodies are then collected and prepared for use in humans.

• For diphtheria, horses are immunized to produce antibodies against diphtheria toxin. The collected antibodies are used to make diphtheria antitoxin (DAT).

3. How does antitoxin treat diphtheria?

-Diphtheria antitoxin is given as an injection and works by binding to and neutralizing diphtheria toxin in the body. This prevents the toxin from causing additional damage to host cells. Diphtheria causes a pseudomembrane in the throat from the accumulation of dead cells. It does not reverse damage that has already occurred.

4. Does antitoxin treatment provide passive or active immunity?

-Antitoxin treatment provides passive immunity because the patient receives already made antibodies produced by another organism. These antibodies immediately neutralize the toxin, providing immediate but temporary protection rather than requiring the patient's immune system to produce its own antibodies.

5. Define toxoid.

-A toxoid is a bacterial toxin that has been inactivated so it can no longer cause disease but can still stimulate the immune system to produce antibodies. The diphtheria toxoid is included in the DTaP toxoid vaccine to help protect against diphtheria by providing active immunity. The vaccine stimulated the production of antibodies within a host.

A child presents with fever, sore throat, and a sandpaper-like rash. A rapid
strep test is positive for Streptococcus pyogenes. (7 points)

a. Identify the relevant Lancefield group for S. pyogenes and explain the
basis of the Lancefield classification system
b. Define “superantigen” describe how this virulence factor contributes
to the symptoms observed
c. Define the term sequelae and provide one example that could result
from untreated Streptococcus pyogenes infection

a) Identify the relevant Lancefield group for S. pyogenes and explain the basis of the Lancefield classification system.

• Streptococcus pyogenes belongs to Group A Streptococcus (GAS).

• The Lancefield classification system, developed by Rebecca Lancefield, groups Streptococcus bacteria based on specific antigens on their surface. The groups are identified using an agglutination reaction with antibodies against different group-specific antigens.

• S. pyogenes reacts with Group A antibodies, which is why it is classified as Group A Streptococcus.

b) Define superantigen and describe how this virulence factor contributes to the symptoms observed.

• A superantigen is an extremely potent bacterial toxin and virulence factor that causes nonspecific, excessive activation of T helper cells, triggering an excessive immune response.

• Normally, an antigen-presenting cell (APC) presents a specific antigen on its MHC II molecule, which must be specifically recognized by the T-cell receptor (TCR) on a T helper cell. A superantigen binds to MHC II and the TCR at the same time, bypassing normal antigen-specific recognition and activating many T helper cells nonspecifically.

• This causes large numbers of T helper cells to release excessive amounts of cytokines, leading to severe inflammation.

• Some strains of Group A S. pyogenes produce an erythrogenic toxin that acts as a superantigen. It causes inflammation and dilation of capillaries, resulting in the characteristic red, sandpaper-like rash associated with scarlet fever.

c) Define sequelae and provide one example that could result from untreated S. pyogenes infection.

• Sequelae are conditions that occur as a consequence of a previous disease or infection.

• One example is rheumatic fever, which can develop after an untreated Group A S. pyogenes throat infection. The immune system produces antibodies against the bacterial M protein, but these antibodies can cross-react with similar proteins in human tissues. This causes the immune system to mistakenly attack the body's own tissues, potentially damaging the heart.

Describe the following relative to tuberculosis according to the assigned
video (7 points):

• Proportion of world population who are infected:
• Initial cell infected:
• What is at the center of a granuloma:
• Frequency of active TB:
• TB-related deaths in 2023
• Active TB case infected an additional how many people per year:
• Most deaths occurring in which areas of the world

• Proportion of world population who are infected: Approximately 1 in 4 people worldwide (25%).

• Initial cell infected: Macrophages in the lungs.They are engulfed by macrophages, which are immune cells that normally destroy invading bacteria. However, TB bacteria have a thick, waxy outer coating that allows them to resist the acidic environment inside the macrophage. They also modify the macrophage so they can use it as a host. The bacteria slowly consume the macrophage and replicate inside it. When the infected macrophage eventually dies, the bacteria can spread and infect new macrophages.

• What is at the center of a granuloma: A core of infected and dead macrophages. Other immune cells surround the core to contain the bacteria. Granulomas can also cause distinctive spots in the lungs that might be visible on chest X-rays.

• Frequency of active TB: Approximately 1 in 10 infected people will develop active TB.

• TB-related deaths in 2023: Approximately 1.3 million people.

• Active TB case infected an additional how many people per year: Approximately 5–15 people per year.

• Most deaths occurring in which areas of the world: Primarily Africa, South America, and Asia, with almost half of TB deaths occurring in Southeast Asia.

Describe the pathological progression of pertussis and discuss 3 factors
contributing to its reemergence. (6 points)

1. Pathological progression of pertussis

Pertussis, also known as whooping cough, is a serious upper respiratory tract infection caused by Bordetella pertussis, a Gram-negative bacterium.

• Incubation period: Approximately 7–10 days before symptoms begin.

• Catarrhal stage: Lasts 1–2 weeks and begins with cold-like symptoms.

• Paroxysmal stage: Lasts 2–6 weeks and involves severe, repeated coughing attacks (paroxysms) that can end with a characteristic “whoop” sound as the person breathes in. Complications can include vomiting, fractured ribs, and bleeding behind the eyes and in the brain.

• Convalescent stage: Lasts approximately 4 weeks, during which coughing attacks gradually become less frequent.

3 reasons for re-emergence:

1. Vaccine changes and waning immunity: The original whole-cell pertussis vaccine was replaced by an acellular (subunit) vaccine in the 1990s because of side effects. However, the newer vaccine does not provide the same long-term immunity, allowing vaccinated individuals to become susceptible to infection as their immunity decreases. So boosters are needed.

2. Genetic changes in Bordetella pertussis: Some strains of B. pertussis have undergone genetic changes that could help them avoid recognition by the immune system in vaccinated individuals. This could give these strains an advantage and contribute to the reemergence of pertussis.

3. Vaccine hesitancy: Some people may not trust vaccines in general, or might question why they need booster doses if they have already been vaccinated. They may feel that the vaccine should work after the first doses and become less willing to get additional boosters. This can lead people to skip recommended doses, leaving them less protected against pertussis and allowing it to spread.

You are caring for a patient with suspected pneumonia. The sputum Gram
stain shows many neutrophils and Gram-positive diplococci. (6 points)

a. Identify the most likely etiological agent and describe one diagnostic
test that could confirm this diagnosis.
b. Discuss why the quality of a sputum specimen is important and what
findings would cause the lab to reject it
c. Describe the vaccine available to prevent this infection

a. Identify the most likely etiological agent and describe one diagnostic test.

-The most likely etiological agent is Streptococcus pneumoniae (pneumococcus), a Gram-positive, lancet-shaped diplococcus that commonly causes pneumonia.

-A sputum culture can help confirm the diagnosis by growing and identifying the bacteria present in the sample.

b. Discuss why the quality of a sputum specimen is important and what findings would cause the lab to reject it.

Sputum samples can become contaminated with normal microbiota from the mouth during collection. This makes it difficult to determine which bacteria are actually causing the lung infection. This is important because normal microbiota in the mouth can include opportunistic pathogens that may cause infection if they enter other parts of the body, such as the lungs. A good-quality sample should contain minimal saliva. The lab would reject a specimen containing too many squamous epithelial cells, which indicate contamination with saliva.

c. Describe the vaccine available to prevent this infection.

The pneumococcal vaccine is a conjugate vaccine containing capsule antigens from S. pneumoniae attached to carrier proteins. This is because capsule is made of polysaccharides, which are less immunogenic than proteins, so when attached to a protein they are more immunogenic. These capsule antigens help the immune system recognize the bacterium and develop protection against infection.

10. A patient presents with painful blisters on the lip margin. Lab testing
confirms HSV-1. (5 points)

a. Explain what viral latency is and where HSV-1 establishes latency
b. Describe how reactivation occurs and why this can happen repeatedly
throughout life
c. Explain the molecular mechanism by which acyclovir reduces viral
replication but fails to eradicate latent infection

a. Explain what viral latency is and where HSV-1 establishes latency.

Viral latency is when a virus remains inside host cells in an inactive or dormant state. During this time, the virus is not actively replicating or producing new virus particles, but its genetic material remains inside the host cell. HSV-1 establishes latency in the trigeminal nerve cells (neurons), where it can remain for the person's lifetime.

b. Describe how reactivation occurs and why this can happen repeatedly throughout life.

Reactivation occurs when the latent virus becomes active again and begins replicating. The virus travels along the nerve back to the skin or lips, causing another outbreak of cold sores. Triggers that can cause reactivation include stress, UV light exposure, and hormonal changes. This can happen repeatedly because the virus remains in the nerve cells for life and is not completely eliminated by the immune system.

c. Explain the molecular mechanism by which acyclovir reduces viral replication but fails to eradicate latent infection.

Acyclovir is a nucleoside analog, meaning it mimics normal nucleotides, which are the building blocks of DNA. When incorporated into viral DNA, it creates a chemical dead end that stops further DNA replication. This prevents the virus from making new copies of itself. However, acyclovir only works against actively replicating viruses. It cannot eliminate HSV-1 DNA that remains dormant inside nerve cells, so the virus can reactivate later.

11. A wound culture from a diabetic patient reveals Gram-positive cocci in
clusters and a positive coagulase test. (4 points)

a. Identify the organism and describe one major virulence factor that
contributes to its pathogenicity
b. Explain how coagulase testing helps distinguish this pathogen from
coagulase-negative species
c. Discuss one reason why this organism poses a particular risk in
healthcare settings.

a. Identify the organism and describe one major virulence factor that contributes to its pathogenicity.

The organism is Staphylococcus aureus, a Gram-positive coccus that forms clusters. One major virulence factor is Protein A, which binds to the part of antibodies that is normally supposed to remain available for immune cells to recognize. This interferes with immune cells' ability to recognize the bacteria, helping S. aureus evade the immune system and cause infection.

b. Explain how coagulase testing helps distinguish this pathogen from coagulase-negative species.

Staphylococcus aureus is coagulase-positive, meaning it produces the enzyme coagulase, which causes plasma to clot. Coagulase-negative Staphylococcus species do not produce this enzyme and therefore do not cause plasma to clot. This test helps identify S. aureus and distinguish it from other Staphylococcus species. (different from agglutination)

c. Discuss one reason why this organism poses a particular risk in healthcare settings.

Staphylococcus aureus poses a risk in healthcare settings because some strains are resistant to multiple antibiotics, including methicillin-resistant S. aureus (MRSA). Hospitals frequently use antibiotics to treat infections, creating selective pressure that allows resistant bacteria to survive and multiply while susceptible bacteria are eliminated. This can contribute to the spread of antibiotic-resistant strains among hospitalized patients, especially those with wounds, surgical sites, or weakened immune systems, leading to opportunistic infections.

12.Describe 3 virulence factors of Pseudomonas species and describe the
diseases they cause. (6 points)

1. Exotoxin A

• Exotoxin A is a toxin released by P. aeruginosa that stops host cells from making proteins.

• Without the proteins they need, host cells become damaged and die.

• This contributes to tissue destruction during severe infections, including wound infections.

2. Pyocins

• Pyocins are antibacterial proteins produced by Pseudomonas aeruginosa that kill or inhibit the growth of other bacteria.

• They help Pseudomonas compete against other bacteria for resources and survive in its environment.

3. Biofilm formation

• P. aeruginosa can form biofilms, which are communities of bacteria surrounded by a protective layer. These can be polymicrobial colonies, meaning they contain multiple types of microorganisms living together.

• This protective layer makes it harder for the immune system and antibiotics to eliminate the bacteria.

• Biofilms contribute to persistent lung infections, especially in people with cystic fibrosis, and infections associated with medical devices such as catheters.

13. Describe the types and severity of skin mycoses (6 points)

- Superficial mycoses

• Involve only the outermost layers of the skin or hair and generally cause mild discoloration of the skin, hair, or nails. They do not invade deeply and are usually mild.

• Examples include infections caused by Piedraia, Trichosporon, and Malassezia species.

- Cutaneous mycoses

• Infect the skin, hair, and nails. Dermatophytes break down keratin, causing these tissues to become brittle and flaky. These infections are generally localized and treatable with topical or oral antifungals, although treatment can take a long time.

• Examples include ringworm and athlete's foot, caused by dermatophytes such as Trichophyton, Microsporum, and Epidermophyton. Cutaneous candidiasis, caused by Candida albicans, is another example. It produces a bright red, itchy or burning rash, especially in moist, friction-prone areas, and is more common in people with diabetes.

- Subcutaneous mycoses

• Involve deeper layers of the skin, including the dermis and sometimes muscle tissue. They are more serious than superficial or cutaneous infections because they invade deeper tissues.

• They often enter through wounds or punctures. An example is Sporothrix schenckii, which can enter the skin through a rose thorn prick. These infections can be more severe and may spread further, especially in immunocompromised individuals.

Severity: Most superficial and cutaneous mycoses are relatively mild and localized. However, subcutaneous infections and fungal infections in immunocompromised individuals can become more widespread, invade deeper tissues, or even cause systemic infections.

4. For Listeria meningitis, identify three populations at increased risk.
   Describe how L. monocytogenes can spread from the initial site of infection
   to the meninges. (6 points)

1. Identify three populations at increased risk for Listeria meningitis and explain why.

• Pregnant people: Pregnancy increases susceptibility to serious listeriosis, and L. monocytogenes can cross the placenta and infect the fetus, potentially causing serious complications.

• Newborns/neonates: Their immune systems are not fully developed, making them more vulnerable to serious infections, including meningitis. They can also acquire the infection through the placenta or during birth.

• Older adults (over 60): Their immune systems may become less effective with age, making it harder to fight off infections and increasing the risk of severe listeriosis and meningitis.

2. Describe how L. monocytogenes spreads from the initial site of infection to the meninges.

• Listeria monocytogenes is a Gram-positive, intracellular bacterium that is typically acquired through contaminated food. After entering the body, it can invade and survive inside macrophages by breaking out of the phagosome, allowing it to avoid being destroyed.

• The bacteria use the host cell's actin in the cytoskeleton to move within the infected cell and push into neighboring cells, allowing them to spread directly from cell to cell.

• The bacteria can spread throughout the body, including across the blood-brain barrier, and eventually reach and infect the meninges, causing meningitis.

15.Describe post-exposure prophylaxis for rabies infection and how each
components works as a treatment for rabies

Post-exposure prophylaxis (PEP) is given after a person may have been exposed to rabies through an animal bite or scratch. It includes three important components:

• Wound cleaning: The bite wound is thoroughly washed with soap and water to physically remove as much of the rabies virus as possible from the exposure site. This helps reduce the amount of virus that can enter the body.

• Human rabies immunoglobulin (HRIG): Provides ready-made antibodies that immediately bind to and neutralize the rabies virus at the site of the bite before it can spread through the nervous system. The antibodies also opsonize the virus, meaning they coat it and make it easier for immune cells to recognize and engulf it through phagocytosis. This provides passive immunity.

• Rabies vaccine: A whole-inactivated vaccine that stimulates the person's immune system to produce its own antibodies against the rabies virus. These antibodies help neutralize the virus and support its removal by immune cells. This provides active immunity and helps protect the person from developing the disease.

All three components are important because wound cleaning helps remove the virus, HRIG provides immediate protection, and the vaccine allows the body to develop its own longer-lasting immune response. PEP must be given before neurological symptoms begin because rabies is nearly always fatal once symptoms develop.

Describe trypanosomes and detail how they cause African sleeping sickness
(include details on transmission, infection and disease progression). (6 points)

• Description of trypanosomes: Trypanosoma brucei is a protozoan parasite, meaning it is a single-celled eukaryotic organism. It is a flagellate, meaning it has a whip-like flagellum that allows it to move. It is the causative agent of African sleeping sickness, a tropical disease found in Africa.

• Transmission: African sleeping sickness is a vector-borne disease transmitted through the bite of an infected tsetse fly. The fly introduces Trypanosoma brucei parasites into the person's body when it bites to feed on blood. Cattle and other livestock can serve as reservoirs for the parasite.

• Initial infection: A chancre, or sore, can form around the bite site. The infection may initially be asymptomatic, meaning the person may not experience noticeable symptoms.

• Spread of infection: The parasites enter the bloodstream and spread throughout the body, causing fever, headaches, and swollen lymph nodes.

• CNS infection and damage: The parasites eventually cross the blood-brain barrier and infect the central nervous system (CNS). They cause direct cytotoxic effects, meaning they directly damage host cells. They also trigger a strong immune response in which the host's neutrophils can damage the host's neurons.

• Disease progression: As the infection affects the CNS, patients develop characteristic sleep disturbances. They cannot sleep at night and cannot stay awake during the day. Without treatment, African sleeping sickness is fatal.