Micrbio 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.

Empiric Therapy

• Definition: The administration of broad-spectrum antimicrobial therapy initiated immediately based on clinical presentation and suspicion before laboratory culture and sensitivity results are finalized

• Clinical Example: Prescribing a broad-spectrum antibiotic (such as cephalosporin or vancomycin) to a patient presenting with acute, sever symptoms of bacterial meningitis or sepsis before CSF/blood culture results return

• Microbiological Rationale: Many serious infections progress rapidly and waiting 2-3 days for traditional culture and sensitivity results could lead to permanent neurological damage or death. Empiric therapy prevents unchecked microbial proliferation and buys time for the immune system while ensuring coverage against the most likely etiological agents

Prophylaxis

• Definition: The preventative administration of antimicrobial drugs or medical treatments designed to prevent an infection or disease in a person at risk before exposure or before signs of infection manifest

• Clinical Example: Administering Rabies Post-Exposure Prophylaxis. (PEP) - comprising Human Rabies Immunoglobulin (HRIG) and the whole inactivated vaccine - to a patient bitten by a stray animal. Another example is surgical antibiotic prophylaxis given right before an incision is made

• Microbiological Rationale: Once certain pathogens establish an infection or reach critical target organs (like the CNS), they are 100% fatal or exceptionally difficult to treat. Prophylaxis neutralizes or eliminates the pathogen before it can establish a foothold, replicate, and trigger irreversible tissue damage

Describe three mechanisms by which antibiotic resistance may develop and provide a specific example of each.

Inactivation by Enzymes

• The microbe acquires a gene encoding an enzyme that chemically modifies or destroys the antibiotic molecule, rendering it ineffective

• Production of beta-lactamases by Staphylococcus aureus, which hydrolyze the beta-lactam ring of penicillins, making them inactive

Efflux Pumps

• The microbe acquires genes encoding transport proteins that actively pump the antibiotic out of the cell, keeping intracellular drug concentrations below a therapeutic level

• Acquisition of the mefA gene in Streptococcus pyogenes, which encodes an efflux pump that removes macrolide antibiotics (like erythromycin)

Target Modification

• The microbe acquires mutations or new genes that alter the cellular target of the antibiotic so that the drug can no longer bind to it and exert its effect

• Acquisition of the mecA gene is S. aureus (yielding MRSA), which encodes an altered penicillin-binding protein (PBP2a) that has a very low binding affinity for beta-lactam drugs

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.

Antigenic Drift

• The gradual, progressive accumulation of point mutations over time in visual surface glycoproteins (Hemagglutinin and Neuraminidase). Occurs in both Influenza A and B viruses. Because these small changes allow the virus to partially evade host antibodies from previous infections or vaccinations, it drives seasonal influenza epidemics

Antigenic Shift

• An abrupt, major change in influenza surface antigens resulting from the reassortment of segmented genome strands when two different virus strains infect the same host cell. This creates novel, drastically different Influenza A subtypes to which the human population has little to no pre-existing immunity, frequently triggering worldwide pandemics

Role in the 1918 Influenza Pandemic:

• Antigenic shift introduced a completely unprecedented influenza subtype that swept through a immunologically naive global population. This massive shift, paired with hyper-aggressive immune reactions (cytokine storms) in young adults, drove the catastrophic mortality of the 1918 Spanish flu.

A mother infected with RSV is concerned about her newborn becoming ill. Explain the following: a) Immunization strategies used for RSA 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

Immunization strategies for RSV prevention

• Pregnant Women: Can receive an RSV subunit vaccine during pregnancy to generate maternal antibodies that can cross the placenta to protect the infant

• Newborns/Infants: Receive passive immunization via monoclonal antibody injections during their first RSV season, or protection via maternal vaccination

• Older Adults: Eligible for active immunization using RSV subunit vaccines targeting the viral F protein

The role of passive immunity in this prevention strategy

• Passive immunity provides immediate, pre-formed IgG antibodies that bind to and neutralize the RSV F protein, blocking the viral attachment and entry without requiring the infant’s immature immune system to mount an active response

Describe the vaccine type used to prevent RSV-related illness

• Subunit vaccines are used for older adults and pregnant individuals, utilizing purified viral components (specifically the fusion [F] protein antigens) to elicit a safe, targeted adaptive immune response

Describe antitoxin: 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.

Antitoxin:

• Type of molecule: It is an antibody molecule (specifically purified animal-derived IgG, such as from horses)

• How it is produced: Produced by immunizing large animals (like horses) with harmless toxoids or toxins, prompting their immune systems to generate high titers of neutralizing antibodies, which are then harvested, purified, and administered to humans

• How it treats diphtheria: Diphtheria antitoxin (DAT) circulates and binds directly to free, un-internalized circulating diphtheria exotoxins, neutralizing them and preventing them from entering host cells to inhibit protein synthesis.

• Type of immunity provided: Provides passive immunity because it introduces pre-formed antibodies rather than stimulating the patient’s own immune system

Toxoid:

• A toxoid is an inactivated bacterial exotoxin (treated with heat or chemicals) that retains its antigenicity (the ability to stimulate an immune responses and memory cells) but has lost its toxicity. It is used as a vaccine component (DTaP)

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

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

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

• Lancefield Group: Group A (Group A Streptococcus / GAS)

• Basis of System: Developed by Rebecca Lancefield, it is a serological classification system based on agglutination reactions between specific carbohydrate antigens on the bacterial cell wall and group-specific antibodies (A through O)

Define “superantigen” describe how this virulence factor contributes to the symptoms observed

• Definition: A superantigen is a virulence factor that binds nonspecifically outside the normal antigen-binding groove to MHC class II molecules and T-cell receptors (TCRs), causing massive, indiscriminate activation of up to 1 in 5 T-helper cells

• Contribution to Symptoms: In scarlet fever, the specific superantigen erythrogenic toxin causes an overwhelming systemic inflammatory response, capillary dilation, and fluid leakage, resulting in the characteristic red “sandpaper-like” rash and “strawberry tongue”

Define the term sequelae and provide one example that could result from untreated Streptococcus pyogenes infection

• Definition: Sequelae are pathological conditions that arise as a delayed consequence or direct aftermath of a previous disease or infection

• Example: Rheumatic fever resulting from molecular mimicry where antibodies against bacterial M-protein cross-react with host tissues in the heart, joints, or kidneys

Describe the following relative to tuberculosis according to the assigned video:

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

• 1 in 4 humans alive

Initial cell infected

• Alveolar macrophage

What is at the center of a granuloma

• A core of infected and dead macrophages surrounded by other immune cells

Frequency of active TB

• 1 in 10 infected individuals (10%) will develop acute active disease

TB-related deaths in 2023

• 1.3 million people

Active TB cases infected an additional how many people per year

• 5 to 15 people

Most deaths occurring in which areas of the world

• Africa, South America, and Asia

Describe the pathological progression of pertussis and discuss 3 factors contributing to its reemergence

Pathological Progression of Pertussis:

• Incubation period: 7-10 days with no symptoms

• Catarrhal Stage: Lasts 1-2 weeks, presenting with mild, cold-like upper respiratory symptoms

• Paroxysmal Stage: Lasts 2-6 weeks, characterized by severe, violent coughing fits ending in a characteristic “whoop” sound upon inhalation.

• Convalescent Stage: Lasts ~4 weeks as coughing spells gradually decrease in frequency

3 Factors Contributing to Reemergence

• Waning Immunity from Acellular Vaccines: The switch in the 1990s from the older whole-cell pertussis vaccine to the safer acellular (subunit) DTaP vaccine resulted in immunity that fades faster over time

• Async/Waning Booster Compliance: Adolescents and adults frequently fail to get routine DTaP boosters, creating a reservoir of susceptible transmitters who can pass the bacterium to vulnerable infants

• Pathogen Evolution / Antigenic Changes: Bordetella pertussis populations have undergone genetic shifts that allow them to better evade vaccine-induced immunity

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

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

Identify the most likely etiological agent and describe one diagnostic test that could confirm this diagnosis

• Etiological agent: Streptococcus pneumoniae

• Diagnostic test: Bacterial sputum culture combined with a positive Gram stain showing lancet-shaped Gram-positive diplococci, or NAAT/PCR testing

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

• Importance: Expectorated sputum passes through the oropharynx and can easily be contaminated by normal oral microbiota, making it difficult to distinguish true lower respiratory pathogens from mouth flora

• Rejection Criteria: The laboratory will reject a specimen if a low-power microscope scan reveals too many squamous epithelial cells (indicating saliva) and too few neutrophils

Describe the vaccine available to prevent this infection

A patient presents with painful blisters on the lip margin. Lab testing confirms HSV-1.

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

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

• Viral Latency: A latent persistent viral infection is a state where the virus remains inside host cells in a non-replicating or dormant form without producing active disease symptoms, escaping elimination by the immune system

• Site of Latency: HSV-1 establishes latency specifically in the trigeminal nerve ganglia

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

• Mechanism: Reactivation is triggered by stressors (such as UV/sunlight exposure, hormonal shifts, emotional stress, or fatigue) causing the virus to reactivate, travel back down the nerve axons to the epithelial border, and replicate

• Why Repeatedly: Because antiviral medications and host immune responses clear active viral replication episodes during outbreaks but cannot destroy viral genomes tucked away formant inside nerve cells, the latent reservoir remains intact for life

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

• Mechanism: Acyclovir is a nucleoside analog that mimics guanosine. Once activated by viral thymidine kinase, it is incorporated by viral DNA polymerase into replicating viral DNA, acting as a chemical dead end that terminates nucleic acid chain elongation

• Failure to Eradicate: It only holds active DNA synthesis during viral replication phases; it cannot target or destroy dormant viral genomes resting in non-replicating latency within nerve cells

A wound culture from a diabetic patient reveals Gram-positive cocci in clusters and a positive coagulase test.

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

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

• Organism: Staphylococcus aureus (Coagulate-positive Staphylococcus)

• Virulence Factor: Coagulase, which clots fibrin around the bacteria to shield them from phagocytes and immune clearance

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

• The coagulase test detects the presence of bound coagulase (clumping factor) or free coagulase enzymes. Staphylococcus aureus produces coagulase and yields a positive agglutination/clumping results, whereas all other staphylococcal species are coagulase-negative

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

• It readily colonizes skin and medical devices, and high rates of strains like MRSA are resistant to all beta-lactam antibiotics, making hospital-acquired infections exceptionally difficult to treat and control.

Describe 3 virulence factors of Pseudomonas species and describe the diseases they cause

Pyocyanin

• Virulence Factor: A blue-green phenazine pigment secreted by Pseudomonas aeruginosa that generates reactive oxygen species, damages host cells, and gives infected wounds or culture media a distinct blue-green hue

• Disease Caused: Wound and burn infections

Exotoxin A

• Virulence Factor: A potent protein toxin that inhibits host cell protein synthesis, leading to cell death and tissue destruction

• Disease Caused: Severe pneumonia, bacteremia, and aggressive burn/wound tissue damage

Capsule/Alginate Production (Biofilm formation)

• Virulence Factor: Secretion of a mucoid exopolysaccharide layer that shields the bacterium from phagocytosis, host antibodies, and antibiotic penetration

• Disease Caused: Chronic pulmonary infections in cystic fibrosis patients and ventilator-assisted pneumonia

Describe the types and severity of skin mycoses

Cutaneous Mycoses (Dermatophytosis / Ringworm / Tinea)

• Description: Fungal infections caused by dermatophytes that infect keratinized layers of the skin, hair, and nails

• Severity: Generally mild and non-serious, remaining superficial. Present as scaly, circular lesions (“ringworm”), athlete’s foot (tinea pedis), or discolored, thickened nails, and responds well to topical or oral antifungals

Cutaneous Candidiasis

• Description: Superficial yeast infections caused by Candida albicans affecting warm, moist, friction-prone skin folds

• Severity: Mild to moderate, presenting as a bright red, itchy macular rash with satellite lesions. Seen frequently in individuals with diabetes or immunosuppression, but rarely life-threatening unless it becomes systemic

For Listera meningitis, identify three populations at increased risk. Describe how L. monocytogenes can spread from the initial site of infection to the meninges

Three Populations at Increased Risk

• Pregnant individuals (vertical transmission)

• Elderly adults

• Immunocompromised individuals

Spread from Initial Site to Meninges

• Pathogenesis: Following ingestion of contaminated food, Listeria monocytogenes invades intestinal epithelial cells through phagocytosis, escapes the phagosome into the cytoplasm, and utilizes host cell actin filaments to form “actin tails” that propel it directly into neighboring cells without exiting into the extracellular space

• Dissemination: Inside macrophages and monocytes, the bacteria disseminate systemically via the bloodstream, allowing them to cross the selecting endothelial cells of the blood-brain barrier to infect the meninges and brain

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

Components of Rabies PEP

• Human Rabies Immunoglobulin (HRIG): Injected immediately directly into and around the wound site (passive immunity)

• Whole Inactivated Rabies Vaccine: Administered as a multi-dose series intramuscularly on specific days

How Each Component Works

• HRIG (Passive Immunization): Provides immediate, pre-formed neutralizing antibodies that bind to and neutralize virus particles right at the exposure site before the virus can enter peripheral nerve endings

• Inactivated Vacation (Active Immunization): Stimulates the patient’s own adaptive immune system to produce a rapid, active humoral and cellular immune response and neutralizing antibodies before the slow-moving virus can complete its lengthy incubation period (2-12 months) and reach the central nervous system

Describes typanosomes and detail how they cause African sleeping sickness (include details on transmission, infection and disease progression)

Description of Trypanosomes:

• Trypanosoma brucei: A single-celled, flagellated eukaryotic protozoan parasite that causes African trypanosomiasis

Tranmission:

• Vector-borne transmission via the bite of an infection tsetse fly, which injects infective metacyclic trypomastigotes into the mammalian host

Infection and Disease Progression:

• Initial Phase: Parasites multiply in blood, lymph, and fluid, causing a painful chancre at the bite site, intermittent fevers, headaches, and swollen lymph nodes

• CNS Invasion: The parasite eventually crosses the blood-brain barries to invade the central nervous system

• Neurological Progression: Causes severe neuropsychiatric symptoms, profound sleep-wake cycle inversion (inability to sleep at night and irresistible urge to sleep during the day)