Microbial genetics and drug resistance

Microbial genetics and drug resistance US Medical PG Question 1: A 42-year-old woman with a history of multiple sclerosis and recurrent urinary tract infections comes to the emergency department because of flank pain and fever. Her temperature is 38.8°C (101.8°F). Examination shows left-sided costovertebral angle tenderness. She is admitted to the hospital and started on intravenous vancomycin. Three days later, her symptoms have not improved. Urine culture shows growth of Enterococcus faecalis. Which of the following best describes the most likely mechanism of antibiotic resistance in this patient?

• A. Increased efflux across bacterial cell membranes
• B. Production of beta-lactamase
• C. Alteration of penicillin-binding proteins
• D. Alteration of peptidoglycan synthesis (Correct Answer)
• E. Alteration of ribosomal targets

Microbial genetics and drug resistance Explanation: ***Alteration of peptidoglycan synthesis*** - **Vancomycin** targets the **D-Ala-D-Ala terminus** on the peptidoglycan precursor, preventing cross-linking during bacterial cell wall synthesis. - **Vancomycin resistance in Enterococcus faecalis** occurs through acquisition of resistance genes (vanA, vanB) that encode enzymes modifying the peptidoglycan precursor from **D-Ala-D-Ala to D-Ala-D-Lac**. - This structural change reduces vancomycin's binding affinity by approximately 1000-fold, rendering the antibiotic ineffective. - The mechanism directly involves **alteration of the peptidoglycan synthesis pathway**, specifically the terminal amino acid residues of the pentapeptide precursor. *Increased efflux across bacterial cell membranes* - This mechanism involves **efflux pumps that actively transport antibiotics out of the bacterial cell**, reducing intracellular concentration. - While efflux pumps contribute to resistance for antibiotics like **tetracyclines, fluoroquinolones, and macrolides**, this is not the primary mechanism of vancomycin resistance in Enterococcus. *Production of beta-lactamase* - **Beta-lactamase enzymes** hydrolyze the **beta-lactam ring** of antibiotics like **penicillins and cephalosporins**, rendering them inactive. - **Vancomycin is a glycopeptide antibiotic, not a beta-lactam**, so its efficacy is not affected by beta-lactamase production. *Alteration of ribosomal targets* - This mechanism confers resistance to antibiotics that target **bacterial ribosomes** to inhibit protein synthesis, such as **macrolides, aminoglycosides, and tetracyclines**. - **Vancomycin acts on cell wall synthesis**, not protein synthesis, so alteration of ribosomal targets is not relevant to vancomycin resistance. *Alteration of penicillin-binding proteins* - **Penicillin-binding proteins (PBPs)** are the targets of **beta-lactam antibiotics** (penicillins, cephalosporins, carbapenems). - Alterations in PBPs cause resistance to beta-lactams, not to vancomycin. - **Vancomycin does not interact with PBPs**; it binds directly to the D-Ala-D-Ala terminus of peptidoglycan precursors in the cell wall.

Microbial genetics and drug resistance US Medical PG Question 2: 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)

Microbial genetics and drug resistance 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.

Microbial genetics and drug resistance US Medical PG Question 3: A 64-year-old female with type 2 diabetes mellitus comes to the physician because of a 1-week history of painful red swelling on her left thigh. Examination shows a 3- x 4-cm, tender, fluctuant mass. Incision and drainage of the abscess are performed. Culture of the abscess fluid grows gram-positive, coagulase-positive cocci that are resistant to oxacillin. Which of the following best describes the mechanism of resistance of the causal organism to oxacillin?

• A. Degradation of the antibiotic
• B. Decreased uptake of the antibiotic
• C. Decreased activation of the antibiotic
• D. Altered target of the antibiotic (Correct Answer)
• E. Acetylation of the antibiotic

Microbial genetics and drug resistance Explanation: ***Altered target of the antibiotic*** - The organism described (gram-positive, coagulase-positive cocci, oxacillin-resistant) is **methicillin-resistant *Staphylococcus aureus* (MRSA)**. - MRSA achieves oxacillin (and other beta-lactam) resistance by acquiring the ***mecA* gene**, which encodes for a **modified penicillin-binding protein (PBP2a)** with reduced affinity for beta-lactam antibiotics. *Degradation of the antibiotic* - This mechanism, primarily through the production of **beta-lactamase enzymes**, can degrade beta-lactam antibiotics. - While *Staphylococcus aureus* can produce beta-lactamases, oxacillin (a **penicillinase-resistant penicillin**) is specifically engineered to be stable against these enzymes. *Decreased uptake of the antibiotic* - Reduced permeability of the bacterial cell wall can lead to decreased uptake, a mechanism more commonly associated with **gram-negative bacteria** due to their outer membrane. - This is not the primary mechanism of resistance for MRSA to oxacillin. *Decreased activation of the antibiotic* - Some antibiotics are prodrugs that require activation by bacterial enzymes, and resistance can arise from mutations affecting this activation. - Oxacillin is active in its administered form and does not require bacterial activation. *Acetylation of the antibiotic* - **Enzymatic modification**, such as acetylation, adenylylation, or phosphorylation, is a common mechanism of resistance, particularly against **aminoglycoside antibiotics**. - This specific mechanism is not responsible for oxacillin resistance in MRSA.

Microbial genetics and drug resistance US Medical PG Question 4: A scientist is studying the mechanisms by which bacteria become resistant to antibiotics. She begins by obtaining a culture of vancomycin-resistant Enterococcus faecalis and conducts replicate plating experiments. In these experiments, colonies are inoculated onto a membrane and smeared on 2 separate plates, 1 containing vancomycin and the other with no antibiotics. She finds that all of the bacterial colonies are vancomycin resistant because they grow on both plates. She then maintains the bacteria in liquid culture without vancomycin while she performs her other studies. Fifteen generations of bacteria later, she conducts replicate plating experiments again and finds that 20% of the colonies are now sensitive to vancomycin. Which of the following mechanisms is the most likely explanation for why these colonies have become vancomycin sensitive?

• A. Point mutation
• B. Gain of function mutation
• C. Viral infection
• D. Plasmid loss (Correct Answer)
• E. Loss of function mutation

Microbial genetics and drug resistance Explanation: ***Plasmid loss*** - The initial **vancomycin resistance** in *Enterococcus faecalis* is often mediated by genes located on **plasmids**, which are extrachromosomal DNA. - In the absence of selective pressure (vancomycin), bacteria that lose the plasmid (and thus the resistance genes) have a **growth advantage** over those that retain the energetically costly plasmid, leading to an increase in sensitive colonies over generations. *Point mutation* - A **point mutation** typically involves a change in a single nucleotide and could lead to loss of resistance if it occurred in a gene conferring resistance. - However, since there was no selective pressure for loss of resistance, it is less likely that 20% of the population would acquire such a specific point mutation to revert resistance. *Gain of function mutation* - A **gain of function mutation** would imply that the bacteria acquired a *new* advantageous trait, not the *loss* of resistance. - This type of mutation would not explain why some colonies became sensitive to vancomycin after the drug was removed. *Viral infection* - **Viral infection** (bacteriophages) can transfer genes through transduction or cause bacterial lysis, but it's not the primary mechanism for a widespread reversion of resistance in the absence of antibiotic pressure. - It would not explain the observed increase in vancomycin-sensitive colonies due to evolutionary pressure. *Loss of function mutation* - While a **loss of function mutation** in a gene conferring resistance could lead to sensitivity, it's generally less likely to explain a 20% shift without selective pressure than **plasmid loss**. - Plasmids are often unstable and are easily lost in the absence of selection, whereas a specific gene mutation causing loss of function would need to arise and become prevalent in the population.

Microbial genetics and drug resistance US Medical PG Question 5: A 24-year-old male presents to the emergency room with a cough and shortness of breath for the past 3 weeks. You diagnose Pneumocystis jiroveci pneumonia (PCP). An assay of the patient's serum reveals the presence of viral protein p24. Which of the following viral genes codes for this protein?

• A. gag (Correct Answer)
• B. pol
• C. rev
• D. env
• E. tat

Microbial genetics and drug resistance Explanation: ***gag*** - The **gag gene** (group-specific antigen) in HIV codes for structural proteins of the virus, including **p24**, which forms the viral capsid. - The presence of **p24 protein** in the serum is a key marker for **HIV infection**, particularly in the early stages, as it indicates active viral replication. *pol* - The **pol gene** codes for essential viral enzymes such as **reverse transcriptase**, **integrase**, and **protease**, which are crucial for the HIV life cycle. - While vital for viral replication, the **pol gene products** are enzymes involved in processing and replication, not the structural capsid protein p24. *rev* - The **rev gene** (regulator of expression of virion proteins) codes for the **Rev protein**, which regulates the export of HIV mRNAs from the nucleus to the cytoplasm. - This regulatory protein ensures the efficient synthesis of structural and enzymatic proteins but does not directly code for the p24 capsid protein. *env* - The **env gene** (envelope) codes for the viral envelope glycoproteins **gp160**, which is cleaved into **gp120** and **gp41**. - These proteins are critical for viral entry into host cells by binding to CD4 receptors and co-receptors, but they are distinct from the p24 capsid protein. *tat* - The **tat gene** (trans-activator of transcription) codes for the **Tat protein**, a powerful trans-activator that enhances the transcription of HIV RNA. - Tat plays a crucial role in increasing the efficiency of viral gene expression but does not code for structural components like the p24 capsid.

Microbial genetics and drug resistance 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)

Microbial genetics and drug resistance 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.

Microbial genetics and drug resistance US Medical PG Question 7: A 35-year-old female presents to the emergency room complaining of diarrhea and dehydration. She has been experiencing severe watery diarrhea for the past 3 days. She reports that she has been unable to leave the bathroom for more than a few minutes at a time. The diarrhea is profuse and watery without visible blood or mucus. She recently returned from a volunteer trip to Yemen where she worked at an orphanage. Her past medical history is notable for psoriasis for which she takes sulfasalazine. The patient drinks socially and does not smoke. Her temperature is 99°F (37.2°C), blood pressure is 100/55 mmHg, pulse is 130/min, and respirations are 20/min. Mucous membranes are dry. Her eyes appear sunken. Capillary refill is 4 seconds. The patient is started on intravenous fluid resuscitation. Which of the following processes is capable of transmitting the genetic material for the toxin responsible for this patient's condition?

• A. Transposition
• B. Conjugation
• C. Endospore formation
• D. Transduction (Correct Answer)
• E. Transformation

Microbial genetics and drug resistance Explanation: ***Transduction*** - The patient's symptoms are highly suggestive of **cholera**, caused by *Vibrio cholerae*, which produces **cholera toxin**. - The genes for cholera toxin are carried on a **bacteriophage (CTXφ)**, and their transfer between bacteria occurs via **transduction**. *Transposition* - **Transposition** involves the movement of **transposons ("jumping genes")** within a genome or between DNA molecules. - While transposons can carry antimicrobial resistance genes or virulence factors, this mechanism is not typically associated with the transfer of the primary cholera toxin genes. *Conjugation* - **Conjugation** is the transfer of genetic material between bacteria through direct cell-to-cell contact, often involving a **pilus** and the transfer of **plasmids**. - While *Vibrio cholerae* can engage in conjugation, the cholera toxin genes are predominantly acquired via specialized transduction with the CTXφ phage, not typically plasmid-mediated conjugation. *Endospore formation* - **Endospore formation** is a survival mechanism used by certain bacteria (e.g., *Clostridium*, *Bacillus*) to withstand harsh environmental conditions. - It is not a mechanism for **horizontal gene transfer** or the transmission of toxin-encoding genetic material between bacteria. *Transformation* - **Transformation** is the uptake of **naked DNA** from the environment by a bacterial cell. - While *Vibrio cholerae* can be naturally competent for transformation, the cholera toxin genes are primarily acquired through **phage-mediated transduction**, not free DNA uptake.

Microbial genetics and drug resistance US Medical PG Question 8: A 27-year-old man presents to the emergency department with weakness and a fever for the past week. The patient is homeless and has a past medical history of alcohol and IV drug abuse. His temperature is 102°F (38.9°C), blood pressure is 107/68 mmHg, pulse is 120/min, respirations are 17/min, and oxygen saturation is 98% on room air. Physical exam is notable for a tremulous patient with antecubital scars and a murmur over the left lower sternal border. Blood cultures are drawn and the patient is started on vancomycin and ceftriaxone and is admitted to the ICU. The patient's fever and symptoms do not improve despite antibiotic therapy for which the initial identified organism is susceptible. Cultures currently reveal MRSA as one of the infective organisms. Which of the following is the best next step in management?

• A. Transesophageal echocardiography (Correct Answer)
• B. Obtain new blood cultures
• C. CT scan of the chest
• D. Nafcillin and piperacillin-tazobactam
• E. Vancomycin and gentamicin

Microbial genetics and drug resistance Explanation: ***Transesophageal echocardiography*** - The patient's history of **IV drug abuse**, **fever**, **new murmur**, and identification of **MRSA** strongly suggest **infective endocarditis**. - A Transesophageal echocardiography (TEE) is the **most sensitive and specific imaging modality** to detect vegetations, abscesses, or valvular damage, which is crucial for guiding further management. *Obtain new blood cultures* - While repeating blood cultures can be useful to confirm eradication or identify new pathogens, the initial blood cultures already revealed MRSA, which is a common cause of **endocarditis in IV drug users**. - The immediate priority given the lack of improvement and high suspicion of endocarditis is to visualize the heart valves for vegetations. *CT scan of the chest* - A CT scan of the chest would be useful to look for complications such as **septic emboli in the lungs** or other pulmonary pathologies. - However, it would not provide the detailed visualization of heart valves necessary to diagnose or rule out valvular vegetations characteristic of endocarditis. *Nafcillin and piperacillin-tazobactam* - **Nafcillin** is active against **methicillin-susceptible Staphylococcus aureus (MSSA)**, but the patient's cultures already identified **MRSA**. - **Piperacillin-tazobactam** is a broad-spectrum antibiotic but not a first-line treatment for MRSA infections and would not be appropriate given the identified pathogen. *Vancomycin and gentamicin* - The patient is already on **Vancomycin**, which is appropriate for MRSA, but adding **gentamicin** without clear indication would not be the best next step. - While gentamicin is sometimes used as an adjunct in specific endocarditis regimens (e.g., enterococcal), the primary concern here is the lack of clinical improvement despite appropriate MRSA coverage, pointing towards a structural cardiac issue.

Microbial genetics and drug resistance US Medical PG Question 9: A 46-year-old woman presents to her primary care physician with complaints of increasing left upper quadrant discomfort. She has a known history of type 1 Gaucher disease. On physical examination, her spleen is palpable 8 cm below the costal margin. Routine laboratory work reveals severe pancytopenia. After consultation with the patient on the risks of her condition, the patient decides to undergo a splenectomy. Which of the following is more likely to occur as a consequence of splenectomy in this patient?

• A. Thrombocytopenia
• B. Leukopenia
• C. Pneumococcal septicemia (Correct Answer)
• D. Staphylococcal septicemia
• E. Anemia

Microbial genetics and drug resistance Explanation: ***Pneumococcal septicemia*** - Patients who undergo splenectomy are at significantly increased risk of **overwhelming post-splenectomy infection (OPSI)**, particularly from **encapsulated bacteria** like *Streptococcus pneumoniae*. - The spleen plays a crucial role in filtering encapsulated bacteria and producing opsonizing antibodies, and its removal compromises this immune function. *Thrombocytopenia* - **Thrombocytopenia** is typically a symptom *before* splenectomy in Gaucher disease due to hypersplenism. - After splenectomy, the platelet count often **increases**, not decreases, due to the removal of the organ that sequesters platelets and destroys them. *Leukopenia* - **Leukopenia** (specifically neutropenia) is a pre-existing condition in severe Gaucher disease due to hypersplenism and bone marrow involvement. - Post-splenectomy, the white blood cell count, particularly neutrophils, generally **increases** as the sequestration and destruction in the spleen are eliminated. *Staphylococcal septicemia* - While *Staphylococcus* can cause serious infections, it is **not the primary pathogen** associated with OPSI in asplenic patients. - Encapsulated bacteria like *Streptococcus pneumoniae* are the most common and dangerous cause of post-splenectomy sepsis. *Anemia* - **Anemia** is a common finding in Gaucher disease due to hypersplenism and bone marrow infiltration. - Splenectomy typically **improves** anemia by removing the site of red blood cell destruction and reducing abnormal cytokine production that inhibits erythropoiesis.

Microbial genetics and drug resistance US Medical PG Question 10: A 35-year-old man comes to the emergency department with fever, chills, dyspnea, and a productive cough. His symptoms began suddenly 2 days ago. He was diagnosed with HIV 4 years ago and has been on triple antiretroviral therapy since then. He smokes one pack of cigarettes daily. He is 181 cm (5 ft 11 in) tall and weighs 70 kg (154 lb); BMI is 21.4 kg/m2. He lives in Illinois and works as a carpenter. His temperature is 38.8°C (101.8°F), pulse is 110/min, respirations are 24/min, and blood pressure is 105/74 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 92%. Examinations reveals crackles over the right lower lung base. The remainder of the examination shows no abnormalities. Laboratory studies show: Hemoglobin 11.5 g/dL Leukocyte count 12,800/mm3 Segmented neutrophils 80% Eosinophils 1% Lymphocytes 17% Monocytes 2% CD4+ T-lymphocytes 520/mm3(N ≥ 500) Platelet count 258,000/mm3 Serum Na+ 137 mEq/L Cl- 102 mEq/L K+ 5.0 mEq/L HCO3- 22 mEq/L Glucose 92 mg/dL An x-ray of the chest shows a right lower-lobe infiltrate of the lung. Which of the following is the most likely causal organism?

• A. Streptococcus pneumoniae (Correct Answer)
• B. Legionella pneumophila
• C. Pneumocystis jirovecii
• D. Staphylococcus aureus
• E. Cryptococcus neoformans

Microbial genetics and drug resistance Explanation: ***Streptococcus pneumoniae*** - This patient presents with **fever, chills, productive cough, dyspnea, leukocytosis with neutrophilia, and a lobar infiltrate on chest X-ray**, which are classic signs of **community-acquired bacterial pneumonia**. - Although the patient is **HIV-positive**, his CD4+ count is >500/mm3 and he is on antiretroviral therapy, indicating relatively preserved immune function, making *S. pneumoniae* the most common cause of pneumonia even in HIV-infected individuals with controlled disease. *Legionella pneumophila* - While *Legionella* can cause pneumonia with fever and dyspnea, it is often associated with **gastrointestinal symptoms** (e.g., diarrhea) and **hyponatremia**, which are not present here. - Exposure to contaminated water sources is a common risk factor, and the lobar infiltrate is less typical than diffuse or patchy infiltrates. *Pneumocystis jirovecii* - *Pneumocystis pneumonia (PJP)* is typically seen in **HIV patients with severely suppressed immune systems (CD4+ count <200/mm3)**. - The patient's CD4+ count (520/mm3) is above this threshold, and PJP usually presents with diffuse interstitial infiltrates rather than a lobar infiltrate. *Staphylococcus aureus* - *S. aureus* pneumonia often occurs in the context of recent **influenza infection, intravenous drug use, or hospitalization**, or can present rapidly with **necrotizing pneumonia** or **empyema**. - While possible, the absence of these specific risk factors or severe features makes it less likely than *S. pneumoniae* in this specific presentation. *Cryptococcus neoformans* - *Cryptococcus neoformans* is an opportunistic fungus that typically causes **pulmonary or central nervous system infections**, especially in severely immunocompromised patients (CD4+ count usually <100/mm3). - Pulmonary cryptococcosis often manifests as **nodules or cavitary lesions**, or can be asymptomatic, which differs from the acute lobar pneumonia presented.

Microbial genetics and drug resistance Flashcard 1 of 10

Question: Small DNA within the cells of bacteria that replicate independently are known as _____

Answer: plasmids

Microbial genetics and drug resistance Flashcard 2 of 10

Question: _____ is a -lactamase producing bacteria resistant to penicillin.

Answer: Staph aureus

Microbial genetics and drug resistance Flashcard 3 of 10

Question: Klebsiella, enterobacter, and serratia commonly exhibit multi-drug _____

Answer: resistance

Microbial genetics and drug resistance Flashcard 4 of 10

Question: In which type of immunity (innate or adaptive) does microbial resistance persist through generations?_____

Answer: Innate immunity

Microbial genetics and drug resistance Flashcard 5 of 10

Question: _____ of High Frequency bacterial strains allows us to perform genetic mapping

Answer: Conjugation

Microbial genetics and drug resistance Flashcard 6 of 10

Question: _____ bacterial DNA transduction stems from incorporation of viral DNA into bacterial DNA; excision of viral DNA results in excision of bacterial DNA as well

Answer: Specialized (Generalized or Specialized)

Microbial genetics and drug resistance Flashcard 7 of 10

Question: What glial cell type serves as the CNS phagocyte?

Answer: microglia mnemonic: Microglia (e.g. Macrophages) develop from Mesoderm

Microbial genetics and drug resistance Flashcard 8 of 10

Question: Microglia derive from what embryologial predecessor?

Answer: mesoderm mnemonic: Microglia (e.g. Macrophages) develop from Mesoderm

Microbial genetics and drug resistance Flashcard 9 of 10

Question: Where do the genes for bacterial exotoxins reside?

Answer: plasmids or transferred by bacteriophages

Microbial genetics and drug resistance Flashcard 10 of 10

Question: What bacteria are particularly adept at transformation of environmental DNA?

Answer: S. pneumoniae, H. influenzae B, Neisseria mnemonic: SHiN