Quorum sensing in biofilms US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Quorum sensing in biofilms. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Quorum sensing in biofilms US Medical PG Question 1: An 18-year-old male in his first year of college presents to the emergency room with a fever and a severe headache. He reports having unprotected sex with several partners over the past few weeks. Upon examination, the male demonstrates nuchal rigidity and photophobia. His past medical history is notable for a lack of vaccinations beginning from infancy due to his parents' belief that vaccinations may cause autism. The bacteria causing these symptoms would most likely demonstrate which of the following?
- A. Negative catalase test
- B. Gram-negative bacteria (Correct Answer)
- C. Urease positive
- D. Positive quellung reaction
- E. Lactose fermentation
Quorum sensing in biofilms Explanation: ***Gram-negative bacteria***
- The clinical picture of fever, severe headache, **nuchal rigidity**, and photophobia in an unvaccinated 18-year-old college student strongly suggests **bacterial meningitis** caused by *Neisseria meningitidis*.
- *Neisseria meningitidis* is a **Gram-negative diplococcus**, which is the most definitive laboratory characteristic for identifying this organism.
- College dormitory settings and unvaccinated status are major risk factors for **meningococcal meningitis**, and Gram stain is typically the first diagnostic step showing Gram-negative diplococci in CSF.
*Positive quellung reaction*
- The Quellung reaction (capsular swelling) is classically associated with **Streptococcus pneumoniae**, not *Neisseria meningitidis*.
- While *N. meningitidis* does have a polysaccharide capsule, the Quellung test is not the standard identification method for this organism.
- *S. pneumoniae* would be more common in older adults or those with specific risk factors like asplenia.
*Negative catalase test*
- *Neisseria meningitidis* is **catalase-positive**, so a negative catalase test would rule out this organism.
- Catalase-negative organisms include Streptococcus and Enterococcus species, which have different clinical presentations.
*Lactose fermentation*
- *Neisseria meningitidis* is a **non-lactose fermenter** and does not utilize lactose fermentation for energy.
- Lactose fermentation is characteristic of enteric Gram-negative bacteria like *E. coli* and *Klebsiella*, not Neisseria species.
- *N. meningitidis* ferments **maltose and glucose**, which distinguishes it from *N. gonorrhoeae* (glucose only).
*Urease positive*
- *Neisseria meningitidis* is **urease-negative**, so urease positivity would rule out this organism.
- Urease-positive bacteria include *Helicobacter pylori*, *Proteus* species, and *Klebsiella*, none of which typically cause meningitis in this clinical setting.
Quorum sensing in biofilms US Medical PG Question 2: A 37-year-old woman with a history of anorectal abscesses complains of pain in the perianal region. Physical examination reveals mild swelling, tenderness, and erythema of the perianal skin. She is prescribed oral ampicillin and asked to return for follow-up. Two days later, the patient presents with a high-grade fever, syncope, and increased swelling. Which of the following would be the most common mechanism of resistance leading to the failure of antibiotic therapy in this patient?
- A. Intrinsic absence of a target site for the drug
- B. Use of an altered metabolic pathway
- C. Production of beta-lactamase enzyme (Correct Answer)
- D. Altered structural target for the drug
- E. Drug efflux pump
Quorum sensing in biofilms Explanation: ***Production of beta-lactamase enzyme***
- The patient's symptoms of a rapidly worsening infection despite ampicillin treatment suggest the presence of a **beta-lactamase producing organism**. Ampicillin is a **beta-lactam antibiotic** that is inactivated by these enzymes.
- Anorectal abscesses and rapidly progressing soft tissue infections are often caused by **polymicrobial flora**, including staphylococci and enterococci, many of which can produce **beta-lactamase**.
*Intrinsic absence of a target site for the drug*
- While some bacteria inherently lack the target site for certain drugs (e.g., mycoplasma lacking a cell wall, thus being resistant to beta-lactams), this is less likely to be the **most common mechanism of acquired resistance** leading to treatment failure in a typical perianal infection.
- The rapid progression and failed initial treatment point towards an **acquired mechanism of resistance** rather than an intrinsic one.
*Use of an altered metabolic pathway*
- This mechanism, such as altered **folate synthesis pathways** in resistance to trimethoprim-sulfamethoxazole, is less common as the primary mechanism for ampicillin resistance.
- Ampicillin's mechanism of action primarily targets the **bacterial cell wall**, not a metabolic pathway in the same way.
*Altered structural target for the drug*
- This involves modifications to the **penicillin-binding proteins (PBPs)**, which are the targets of beta-lactam antibiotics like ampicillin. While a valid mechanism (e.g., in MRSA), the **production of beta-lactamase** is generally a more widespread and common cause of ampicillin failure, especially in infections involving mixed flora from the perianal region.
- Given the abrupt failure of ampicillin, **beta-lactamase inactivation** is a more immediate and common cause than a rapid mutational change in PBPs.
*Drug efflux pump*
- **Efflux pumps** actively remove antibiotics from the bacterial cell, contributing to resistance against various drug classes.
- While efflux pumps can play a role, the dominant mechanism for resistance to **ampicillin** in many common perianal pathogens is the **enzymatic degradation by beta-lactamases**.
Quorum sensing in biofilms US Medical PG Question 3: An investigator is studying the chemical structure of antibiotics and its effect on bacterial growth. He has synthesized a simple beta-lactam antibiotic and has added a bulky side chain to the molecule that inhibits the access of bacterial enzymes to the beta-lactam ring. The synthesized drug will most likely be appropriate for the treatment of which of the following conditions?
- A. Folliculitis (Correct Answer)
- B. Nocardiosis
- C. Atypical pneumonia
- D. Erythema migrans
- E. Otitis media
Quorum sensing in biofilms Explanation: ***Folliculitis***
- The bulky side chain provides **steric hindrance** that prevents **staphylococcal beta-lactamases** from accessing and degrading the **beta-lactam ring**.
- This modification creates an **anti-staphylococcal penicillin** (similar to methicillin, nafcillin, or oxacillin), which is effective against **methicillin-sensitive *Staphylococcus aureus* (MSSA)**.
- **Folliculitis** is most commonly caused by *S. aureus*, making this modified beta-lactam an appropriate treatment choice for MSSA-related folliculitis.
- The bulky side chain specifically protects against the **penicillinase** (beta-lactamase) produced by staphylococci.
*Otitis media*
- Otitis media is commonly caused by beta-lactamase-producing organisms like *Haemophilus influenzae* and *Moraxella catarrhalis*.
- However, the beta-lactamases produced by these gram-negative organisms are **not inhibited by bulky side chains** alone.
- Treatment of beta-lactamase-producing *H. influenzae* and *M. catarrhalis* requires **beta-lactamase inhibitors** (such as clavulanic acid combined with amoxicillin), not steric hindrance.
- The mechanism of protection differs: beta-lactamase inhibitors **suicide inhibitors** that bind to the enzyme, whereas bulky side chains provide **physical blocking**.
*Nocardiosis*
- Nocardiosis is caused by *Nocardia* species, which are **aerobic actinomycetes**.
- These bacteria are typically treated with **sulfonamides** (trimethoprim-sulfamethoxazole) for prolonged periods.
- Beta-lactam antibiotics are generally not first-line treatment, as *Nocardia* species often show intrinsic resistance or require specific antibiotic combinations.
*Atypical pneumonia*
- Atypical pneumonia is caused by organisms like *Mycoplasma pneumoniae*, *Chlamydophila pneumoniae*, and *Legionella pneumophila*.
- These organisms lack a **peptidoglycan cell wall**, which is the target of all **beta-lactam antibiotics**.
- Beta-lactams (regardless of modifications) are completely ineffective against atypical pneumonia pathogens.
- Treatment requires **macrolides** (azithromycin), **tetracyclines** (doxycycline), or **fluoroquinolones**.
*Erythema migrans*
- Erythema migrans is the characteristic rash of early **Lyme disease**, caused by *Borrelia burgdorferi*.
- While *Borrelia* is sensitive to certain beta-lactam antibiotics (amoxicillin, ceftriaxone), it does **not produce beta-lactamases**.
- The bulky side chain modification is unnecessary for treating *Borreria* infections, as there is no beta-lactamase to protect against.
- Standard treatment uses doxycycline, amoxicillin, or ceftriaxone—not anti-staphylococcal penicillins.
Quorum sensing in biofilms US Medical PG Question 4: An investigator is studying the genetic profile of an isolated pathogen that proliferates within macrophages. The pathogen contains sulfatide on the surface of its cell wall to prevent fusion of the phagosome and lysosome. She finds that some of the organisms under investigation have mutations in a gene that encodes the enzyme required for synthesis of RNA from a DNA template. The mutations are most likely to reduce the therapeutic effect of which of the following drugs?
- A. Pyrazinamide
- B. Ethambutol
- C. Rifampin (Correct Answer)
- D. Streptomycin
- E. Levofloxacin
Quorum sensing in biofilms Explanation: ***Rifampin***
- **Rifampin** specifically targets bacterial **DNA-dependent RNA polymerase**, inhibiting **RNA synthesis**. Mutations in the gene encoding this enzyme would directly reduce rifampin's binding and effectiveness.
- The description of the pathogen thriving within macrophages and using **sulfatide to evade lysosomal fusion** strongly suggests **Mycobacterium tuberculosis**, a bacterium for which rifampin is a cornerstone treatment.
*Pyrazinamide*
- **Pyrazinamide** is a prodrug that, once converted to **pyrazinoid acid**, disrupts **mycobacterial membrane potential** and metabolism. Its primary target is not RNA synthesis.
- Its efficacy is pH-dependent and it acts optimally in acidic environments, such as within macrophages, but mutations affecting RNA synthesis would not directly compromise its action.
*Ethambutol*
- **Ethambutol** inhibits **arabinosyl transferase**, an enzyme essential for the synthesis of the **mycobacterial cell wall component arabinogalactan**.
- Its mechanism of action is distinct from RNA synthesis, thus mutations affecting RNA polymerase would not impact its efficacy.
*Streptomycin*
- **Streptomycin** is an **aminoglycoside antibiotic** that binds to the **30S ribosomal subunit**, inhibiting bacterial **protein synthesis**.
- This mechanism is unrelated to DNA-dependent RNA polymerase, so mutations in RNA synthesis enzymes would not affect streptomycin's action.
*Levofloxacin*
- **Levofloxacin** is a **fluoroquinolone antibiotic** that inhibits **bacterial DNA gyrase (topoisomerase II)** and **topoisomerase IV**, thereby blocking DNA replication and transcription.
- While it affects processes related to DNA, its direct target is not the DNA-dependent RNA polymerase enzyme itself, distinguishing it from rifampin's specific mechanism.
Quorum sensing in biofilms US Medical PG Question 5: An 18-year old college freshman presents to his university clinic because he has not been feeling well for the past two weeks. He has had a persistent headache, occasional cough, and chills without rigors. The patient’s vital signs are normal and physical exam is unremarkable. His radiograph shows patchy interstitial lung infiltrates and he is diagnosed with atypical pneumonia. The patient is prescribed azithromycin and takes his medication as instructed. Despite adherence to his drug regimen, he returns to the clinic one week later because his symptoms have not improved. The organism responsible for this infection is likely resistant to azithromycin through which mechanism?
- A. Mutation in topoisomerase II
- B. Methylation of ribosomal binding site
- C. Presence of a beta-lactamase
- D. Decreased binding to RNA polymerase
- E. Insertion of drug efflux pumps (Correct Answer)
Quorum sensing in biofilms Explanation: ***Insertion of drug efflux pumps***
- **Azithromycin** is a macrolide antibiotic that inhibits bacterial protein synthesis by binding to the **50S ribosomal subunit**.
- In **Mycoplasma pneumoniae** (the most common cause of atypical pneumonia in young adults), the **most common** mechanism of macrolide resistance is through **efflux pumps**, particularly the **mef genes**.
- These efflux pumps actively transport macrolides out of the bacterial cell, reducing intracellular drug concentration and conferring resistance.
- This mechanism is responsible for the majority of macrolide-resistant *M. pneumoniae* isolates worldwide.
*Methylation of ribosomal binding site*
- **Methylation** of the ribosomal binding site (specifically the **23S rRNA** via erm genes) does prevent azithromycin from binding effectively.
- While this is a valid macrolide resistance mechanism seen in organisms like *Streptococcus pneumoniae* and *Streptococcus pyogenes*, it is **less common** in *Mycoplasma pneumoniae*.
- Efflux pumps (mef) are the predominant mechanism in *M. pneumoniae* resistant strains.
*Mutation in topoisomerase II*
- **Topoisomerase II** (DNA gyrase) is the target of **fluoroquinolone antibiotics**, not macrolides.
- Mutations in this enzyme lead to resistance against fluoroquinolones, such as **ciprofloxacin**.
*Presence of a beta-lactamase*
- **Beta-lactamase enzymes** inactivate **beta-lactam antibiotics** (e.g., penicillin, cephalosporins) by hydrolyzing their beta-lactam ring.
- Additionally, *Mycoplasma pneumoniae* **lacks a cell wall**, making it inherently resistant to all beta-lactam antibiotics regardless of beta-lactamase production.
*Decreased binding to RNA polymerase*
- **RNA polymerase** is the target for antibiotics like **rifampin**, which inhibits bacterial transcription.
- Decreased binding to RNA polymerase would lead to rifampin resistance, not azithromycin resistance.
Quorum sensing in biofilms US Medical PG Question 6: A 63-year-old female recovering from a total shoulder arthroplasty completed 6 days ago presents complaining of joint pain in her repaired shoulder. Temperature is 39 degrees Celsius. Physical examination demonstrates erythema and significant tenderness around the incision site. Wound cultures reveal Gram-positive cocci that are resistant to nafcillin. Which of the following organisms is the most likely cause of this patient's condition?
- A. Streptococcus pyogenes
- B. Escherichia coli
- C. Streptococcus viridans
- D. Staphylococcus epidermidis
- E. Staphylococcus aureus (Correct Answer)
Quorum sensing in biofilms Explanation: ***Staphylococcus aureus***
- The combination of **post-surgical infection**, **erythema**, and fever with **Gram-positive cocci** that are **nafcillin-resistant** is highly indicative of **Methicillin-Resistant Staphylococcus aureus (MRSA)**.
- *S. aureus* is a common cause of **surgical site infections**, and its resistance to nafcillin implies it is MRSA, a significant clinical concern for its difficulty in treatment.
*Streptococcus pyogenes*
- While *S. pyogenes* is a Gram-positive coccus that can cause skin and soft tissue infections, it is typically **susceptible to penicillin** and related antibiotics like nafcillin, unlike the organism described.
- It is more commonly associated with **streptococcal pharyngitis** or **cellulitis**, and while it can cause severe disease, its resistance profile doesn't match the clinical picture.
*Escherichia coli*
- *E. coli* is a **Gram-negative rod**, not a Gram-positive coccus.
- It is a common cause of **urinary tract infections** and **gastrointestinal infections**, making it an unlikely pathogen for a post-surgical joint infection unless contaminated from a visceral source.
*Streptococcus viridans*
- **Viridans streptococci** are Gram-positive cocci but are typically associated with **endocarditis** or dental infections, especially after poor dental hygiene or procedures.
- They are usually **susceptible to penicillin** and do not typically exhibit nafcillin resistance as the primary feature in a post-arthroplasty infection.
*Staphylococcus epidermidis*
- *S. epidermidis* is a **coagulase-negative Staphylococcus** known for forming **biofilms on prosthetic devices**, leading to chronic, low-grade infections.
- While it can be nafcillin-resistant, the **acute presentation** with fever and significant inflammation suggests a more virulent pathogen like *S. aureus*, as *S. epidermidis* infections are typically indolent.
Quorum sensing in biofilms US Medical PG Question 7: A 56-year-old woman comes to the emergency department because of worsening pain and swelling in her right knee for 3 days. She underwent a total knee arthroplasty of her right knee joint 5 months ago. The procedure and immediate aftermath were uneventful. She has hypertension and osteoarthritis. Current medications include glucosamine, amlodipine, and meloxicam. Her temperature is 37.9°C (100.2°F), pulse is 95/min, and blood pressure is 115/70 mm Hg. Examination shows a tender, swollen right knee joint; range of motion is limited by pain. The remainder of the examination shows no abnormalities. Arthrocentesis of the right knee is performed. Analysis of the synovial fluid shows:
Appearance Cloudy
Viscosity Absent
WBC count 78,000/mm3
Segmented neutrophils 94%
Lymphocytes 6%
Synovial fluid is sent for culture and antibiotic sensitivity. Which of the following is the most likely causal pathogen?
- A. Staphylococcus aureus
- B. Escherichia coli
- C. Pseudomonas aeruginosa
- D. Staphylococcus epidermidis (Correct Answer)
- E. Streptococcus agalactiae
Quorum sensing in biofilms Explanation: ***Staphylococcus epidermidis***
- This patient's symptoms (worsening pain and swelling in a knee with a history of **total knee arthroplasty 5 months ago**, increased WBC count and neutrophil predominance in synovial fluid), point towards a **prosthetic joint infection**.
- **Coagulase-negative Staphylococci**, particularly *S. epidermidis*, are the most common cause of **late prosthetic joint infections**, typically occurring months to years after surgery.
*Staphylococcus aureus*
- *Staphylococcus aureus* is a common cause of **acute prosthetic joint infections**, which usually manifest within the **first 3 months post-surgery**. This patient's symptoms began 5 months after surgery.
- While it can cause late infections, *S. epidermidis* is more characteristic for this timeline in prosthetic joint infections.
*Escherichia coli*
- *Escherichia coli* is typically associated with **urinary tract infections** or **gastrointestinal infections**.
- It is an uncommon cause of prosthetic joint infections unless there's a direct spread from a local infection or systemic sepsis, which is not suggested here.
*Pseudomonas aeruginosa*
- *Pseudomonas aeruginosa* is often associated with **healthcare-associated infections**, particularly in immunocompromised patients or those with indwelling catheters or extensive burns.
- While it can cause prosthetic joint infections, it's less common than Staphylococci and usually linked to specific clinical settings or water contamination.
*Streptococcus agalactiae*
- *Streptococcus agalactiae* (Group B Strep) is primarily known to cause serious infections in **neonates** and **pregnant women**, and in adults with underlying conditions like **diabetes** or **immunocompromise**.
- It is an infrequent cause of prosthetic joint infections in otherwise healthy adults without specific risk factors for GBS infection.
Quorum sensing in biofilms US Medical PG Question 8: A 13-year-old boy is brought to the emergency department because of vomiting, diarrhea, abdominal pain, and dizziness for the past 3 hours with fever, chills, and muscle pain for the last day. He had presented 5 days ago for an episode of epistaxis caused by nasal picking and was treated with placement of anterior nasal packing. His parents report that the bleeding stopped, but they forgot to remove the nasal pack. His temperature is 40.0°C (104.0°F), pulse is 124/min, respirations are 28/min, and blood pressure is 96/68 mm Hg. He looks confused, and physical exam shows conjunctival and oropharyngeal hyperemia with a diffuse, erythematous, macular rash over the body that involves the palms and the soles. Removal of the anterior nasal pack shows hyperemia with purulent discharge from the underlying mucosa. Laboratory studies show:
Total white blood cell count 30,000/mm3 (30 x 109/L)
Differential count
Neutrophils 90%
Lymphocytes 8%
Monocytes 1%
Eosinophils 1%
Basophils 0%
Platelet count 95,000/mm3 (95 x 109/L)
Serum creatine phosphokinase 400 IU/L
What is the most likely diagnosis for this patient?
- A. Stevens-Johnson syndrome
- B. Measles
- C. Disseminated gonococcal infection
- D. Herpes simplex virus type 2 (HSV-2) meningitis
- E. Toxic shock syndrome (Correct Answer)
Quorum sensing in biofilms Explanation: ***Toxic shock syndrome***
- The patient's presentation with **fever**, **hypotension**, **diffuse erythematous rash** involving palms/soles, **multisystem involvement** (vomiting, diarrhea, dizziness, confusion, elevated CPK), and the history of prolonged **nasal packing** (a common nidus for *Staphylococcus aureus* toxin production) is highly characteristic of **toxic shock syndrome (TSS)**.
- **Leukocytosis with neutrophilia** and **thrombocytopenia** are also common laboratory findings in TSS.
*Stevens-Johnson syndrome*
- Characterized by **mucocutaneous lesions** with epidermal detachment, forming **bullae** and **erosions**, often preceded by fever and flu-like symptoms.
- While it can involve mucous membranes, the **diffuse erythematous macular rash without bullae** and the rapid development of **shock** are not typical features.
*Measles*
- Presents with a **maculopapular rash** that typically starts on the face and spreads downwards, often coalescing. It is preceded by **prodromal symptoms** like cough, coryza, conjunctivitis, and **Koplik spots**.
- **Hypotension**, **severe multiorgan dysfunction**, and **nasal packing as a risk factor** are not features of measles.
*Disseminated gonococcal infection*
- Can cause **fever**, migratory **polyarthralgia**, and a **pustular or vesiculopustular rash** with hemorrhagic lesions, primarily on the extremities.
- The described **diffuse erythematous macular rash**, severe hypotension, and history of nasal packing do not fit the typical presentation of disseminated gonococcal infection.
*Herpes simplex virus type 2 (HSV-2) meningitis*
- Primarily causes **aseptic meningitis** with symptoms like fever, headache, stiff neck, and photophobia.
- It does not explain the **diffuse erythematous rash**, **hypotension**, **multisystem involvement**, or the role of **nasal packing** in the patient's presentation.
Quorum sensing in biofilms US Medical PG Question 9: A hospital implements silver-coated central venous catheters to reduce catheter-related bloodstream infections. Initial results show 60% reduction in infections at 1 week, but this benefit decreases to 20% reduction by 4 weeks. Electron microscopy of explanted catheters shows biofilm formation with embedded bacteria despite the silver coating. What mechanism best explains the loss of antimicrobial efficacy over time?
- A. Depletion of silver ions from the catheter surface through diffusion
- B. Matrix proteins binding silver ions and reducing bioavailability
- C. Development of silver-tolerant persister cell populations
- D. Bacterial mutation conferring genetic resistance to silver ions
- E. Host protein deposition creating a conditioning film blocking silver release (Correct Answer)
Quorum sensing in biofilms Explanation: ***Host protein deposition creating a conditioning film blocking silver release***
- Rapid adsorption of host proteins like **fibrinogen, fibronectin, and albumin** creates a **conditioning film** that physically masks the antimicrobial surface.
- This protein layer acts as a barrier to **ion release** and provides a scaffold for **bacterial adhesion**, facilitating the transition to a long-term **biofilm** state.
*Depletion of silver ions from the catheter surface through diffusion*
- Modern antimicrobial catheters are designed for **sustained release**, and the presence of silver on explanted microscopy suggests the reservoir is not yet empty.
- If diffusion were the only factor, efficacy would decline linearly rather than being linked to the physical observation of **biofilm formation** over the coating.
*Matrix proteins binding silver ions and reducing bioavailability*
- While some binding may occur, this is not the primary mechanism of clinical failure; the principal issue is the physical **obstruction of the surface**.
- This theory does not account for how bacteria are able to initially colonize and survive in **close physical contact** with the coated surface.
*Development of silver-tolerant persister cell populations*
- **Persister cells** are phenotypically dormant and survive antibiotics, but they do not typically cause the gradual, large-scale reduction in antimicrobial device efficacy seen here.
- The microscopy findings emphasize **structural biofilm layers** rather than a specific metabolic state of individual bacteria.
*Bacterial mutation conferring genetic resistance to silver ions*
- True **genetic resistance** to silver (via sil operons) is clinically rare and usually occurs through **efflux pumps**, not biofilm-mediated shielding.
- The scenario describes a loss of efficacy common across multiple hospital settings, whereas **mutational resistance** would be more sporadic or localized.
Quorum sensing in biofilms US Medical PG Question 10: A 28-year-old woman with cystic fibrosis undergoes lung transplantation. Pre-transplant sputum cultures show mucoid Pseudomonas aeruginosa. Post-transplant, she receives immunosuppression and antibiotic prophylaxis. Six months later, she develops pneumonia, and cultures grow non-mucoid P. aeruginosa with identical genetic fingerprint to pre-transplant isolates. What evolutionary adaptation most likely explains this phenotypic reversion?
- A. Horizontal gene transfer from colonizing respiratory flora
- B. Decreased selective pressure for biofilm formation in absence of mucus obstruction (Correct Answer)
- C. Selection pressure favoring planktonic phenotype in immunosuppressed state
- D. Loss of mucA mutations due to genetic reversion in new host environment
- E. Antibiotic prophylaxis eliminating mucoid variants selectively
Quorum sensing in biofilms Explanation: ***Decreased selective pressure for biofilm formation in absence of mucus obstruction***
- In the **Cystic Fibrosis (CF)** lung, the presence of thick **mucus plugs** and chronic inflammation exerts selective pressure that favors the **mucoid phenotype** (alginate production) for survival.
- Following **lung transplantation**, the new lungs lack the original CF environment, causing the bacteria to revert to a **non-mucoid** state which is more energetically efficient for **planktonic growth** and rapid replication.
*Horizontal gene transfer from colonizing respiratory flora*
- Genetic identity via **fingerprinting** confirms the post-transplant isolate is a direct descendant of the original strain, not a result of **recombination** with other flora.
- The change in phenotype is an **adaptive response** to environmental shifts rather than the acquisition of new genetic material from the host microbiome.
*Selection pressure favoring planktonic phenotype in immunosuppressed state*
- While **immunosuppression** affects the host's ability to clear infections, it is the **structural change** (removal of mucus) that primarily influences the bacterial transition from biofilm to planktonic form.
- Biofilms are generally more resistant to the host immune system; thus, a lack of immunity would not logically drive the bacteria *away* from a protective **biofilm phenotype**.
*Loss of mucA mutations due to genetic reversion in new host environment*
- The **mucoid phenotype** in CF is often caused by **mucA mutations**, but spontaneous **back-mutations** (genetic reversion) are extremely rare in large bacterial populations.
- Phenotypic changes are more likely due to **compensatory mutations** or changes in **gene expression** rather than a literal restoration of the wild-type DNA sequence.
*Antibiotic prophylaxis eliminating mucoid variants selectively*
- **Mucoid variants** and their associated **biofilms** typically show *increased* resistance to antibiotics compared to non-mucoid forms.
- Therefore, **antibiotic prophylaxis** would be expected to select *for* mucoid variants rather than eliminating them to favor non-mucoid ones.
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