Bacteriology — MCQs

A patient with second and third-degree burns developed a wound infection on the twelfth day of admission, characterized by a bluish-green exudate. Treatment with chloramphenicol and tetracycline was unsuccessful. A gram-negative, motile organism was isolated that was oxidase-positive, did not ferment lactose, sucrose, or glucose, but grew on MacConkey's agar and produced a fruity aroma on that medium. Which of the following organisms was most likely isolated?

Bacteriology Indian Medical PG Practice Questions and MCQs

Question 261: Which of the following is true about the cholera vibrio?

A. It is strongly anaerobic.
B. It grows best at 25°C.
C. It has marked tolerance of alkaline pH. (Correct Answer)
D. It grows over a wide range but best at a slight acid pH.

Explanation: **Explanation:** *Vibrio cholerae*, the causative agent of cholera, has distinct biochemical and physiological characteristics that are frequently tested in NEET-PG. **1. Why Option C is Correct:** *Vibrio cholerae* is a **strongly halophilic and alkaliphilic** organism. It has a marked tolerance for high pH, growing optimally at a pH of **8.2**, but can survive in environments with a pH as high as 9.2–9.6. This unique physiological trait is exploited in the laboratory using selective enrichment media like **Alkaline Peptone Water (APW)** and solid media like **TCBS (Thiosulfate Citrate Bile Salts Sucrose) agar**, which inhibit most other intestinal commensals that cannot tolerate such alkalinity. **2. Why the Other Options are Incorrect:** * **Option A:** *Vibrio cholerae* is a **strongly aerobic** organism; growth is poor under anaerobic conditions. * **Option B:** The optimum temperature for growth is **37°C** (human body temperature), not 25°C. * **Option D:** While it grows over a wide range, it is **highly sensitive to acid**. Gastric acidity is a primary host defense against cholera; patients with achlorhydria or those taking antacids are at a much higher risk of infection. **3. High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Described as "comma-shaped" (Vibrio) with a single polar flagellum showing **darting motility** (shooting star appearance). * **Culture:** On TCBS agar, it produces distinctive **yellow colonies** due to sucrose fermentation. * **String Test:** Used for biochemical identification; colonies become mucoid and form a "string" when mixed with 0.5% sodium deoxycholate. * **Transport Media:** Venkatraman-Ramakrishnan (VR) medium or Cary-Blair medium are used for stool samples.

Question 262: Which one of the following bacteria contains mycolic acid in the cell wall?

A. Escherichia
B. Mycoplasma
C. Mycobacteria (Correct Answer)
D. Staphylococcus

Explanation: ### Explanation **Correct Answer: C. Mycobacteria** **Underlying Medical Concept:** The hallmark of the genus *Mycobacterium* (e.g., *M. tuberculosis*, *M. leprae*) is a unique, lipid-rich cell wall. The most critical component is **mycolic acid**, which are long-chain fatty acids (C60 to C90). These lipids make the cell wall thick, waxy, and hydrophobic. This structure prevents traditional Gram staining (as dyes cannot penetrate) but allows the bacteria to resist decolorization by acid-alcohol after being stained with carbol fuchsin—a property known as **Acid-Fastness**. **Analysis of Incorrect Options:** * **A. Escherichia:** As a Gram-negative bacterium, *E. coli* has a thin peptidoglycan layer and an outer membrane containing Lipopolysaccharide (LPS), but it lacks mycolic acids. * **B. Mycoplasma:** These are unique because they **completely lack a cell wall**. Their cell membrane contains sterols for stability. Since they have no wall, they cannot contain mycolic acid. * **D. Staphylococcus:** This is a Gram-positive bacterium characterized by a thick layer of peptidoglycan and teichoic acids. It does not possess the waxy lipid coat found in acid-fast organisms. **NEET-PG High-Yield Pearls:** * **CMN Group:** Apart from *Mycobacteria*, other genera containing mycolic acids (though shorter chains) include ***C**orynebacterium*, ***M**ocardia*, and ***N**ocardia*. * **Staining:** Use **Ziehl-Neelsen (ZN) stain** or Kinyoun stain for identification. *Nocardia* is specifically "weakly acid-fast." * **Function:** Mycolic acids protect the bacteria from dehydration, antibiotics, and host immune responses (macrophage digestion). * **Cord Factor:** A derivative of mycolic acid (trehalose dimycolate) is responsible for the parallel "serpentine cord" growth pattern seen in virulent strains of *M. tuberculosis*.

Question 263: Which is the most common causative agent of gas gangrene?

A. Clostridium histolyticum
B. Clostridium novyi
C. Clostridium septicum
D. Clostridium perfringens (Correct Answer)

Explanation: **Explanation:** **Clostridium perfringens (Option D)** is the correct answer as it is the most common causative agent of gas gangrene (clostridial myonecrosis), isolated in approximately **80–95%** of clinical cases. The pathogenesis is primarily driven by the production of the **Alpha toxin (Lecithinase)**, which causes extensive tissue necrosis, hemolysis, and vascular damage, creating an anaerobic environment conducive to bacterial spread. **Analysis of Incorrect Options:** * **Clostridium novyi (Option B):** This is the second most common cause (approx. 40% of cases). It is often associated with more profound edema and is frequently seen in soil-contaminated wounds. * **Clostridium septicum (Option C):** While it can cause gas gangrene, it is uniquely associated with **atraumatic/spontaneous gas gangrene**, often linked to underlying gastrointestinal malignancies (e.g., colon cancer) or neutropenia. * **Clostridium histolyticum (Option A):** This species produces potent proteolytic enzymes (collagenases) and is a rare cause of gas gangrene, usually occurring in polymicrobial infections. **High-Yield Clinical Pearls for NEET-PG:** * **Nagler’s Reaction:** A biochemical test used for rapid identification of *C. perfringens* based on its lecithinase activity (opalescence on egg yolk agar, inhibited by antitoxin). * **Morphology:** It is a Gram-positive, boxcar-shaped anaerobic bacillus. Notably, it is **non-motile** and rarely shows spores in clinical samples. * **Clinical Sign:** Presence of **crepitus** (gas bubbles in tissue) and a "mousy" or "sweetly putrid" odor. * **Double Zone of Hemolysis:** On blood agar, *C. perfringens* produces a characteristic double zone (inner complete hemolysis by theta toxin, outer partial hemolysis by alpha toxin).

Question 264: Toxic shock syndrome caused by Staphylococcus infection is due to which of the following?

A. Superantigen (Correct Answer)
B. Alpha-hemolysis
C. Coagulase
D. Penton Valentine factor

Explanation: **Explanation:** **Correct Answer: A. Superantigen** Toxic Shock Syndrome (TSS) is primarily caused by **Toxic Shock Syndrome Toxin-1 (TSST-1)** produced by *Staphylococcus aureus*. TSST-1 acts as a **superantigen**, which bypasses the normal antigen-processing pathway. Instead of being processed by Antigen Presenting Cells (APCs), superantigens bind directly to the **MHC class II** molecules and the **Vβ region of T-cell receptors (TCR)**. This results in the non-specific activation of up to 20% of the body's T-cells, leading to a massive "cytokine storm" (release of IL-1, IL-2, TNF-α, and IFN-γ), which causes high fever, hypotension, and multi-organ failure. **Analysis of Incorrect Options:** * **B. Alpha-hemolysis:** This refers to partial hemolysis on blood agar (typical of *S. pneumoniae*). *S. aureus* typically exhibits **Beta-hemolysis** (complete lysis) due to alpha-toxin, which acts by forming pores in cell membranes, not by superantigenic activity. * **C. Coagulase:** This is an enzyme used to differentiate *S. aureus* (coagulase-positive) from other Staphylococci. It converts fibrinogen to fibrin to wall off lesions, but it does not trigger the systemic inflammatory response seen in TSS. * **D. Panton-Valentine Leukocidin (PVL) factor:** This is a cytotoxin that destroys white blood cells and is strongly associated with **necrotizing pneumonia** and severe skin/soft tissue infections (CA-MRSA), rather than classic TSS. **High-Yield Clinical Pearls for NEET-PG:** * **TSS Presentation:** Characterized by high fever, "sunburn-like" rash that desquamates (especially on palms/soles), hypotension, and involvement of ≥3 organ systems. * **Risk Factors:** Classically associated with prolonged use of highly absorbent tampons or infected surgical wounds. * **Other Superantigens:** *Streptococcus pyogenes* produces **SpeA and SpeC** (Pyrogenic exotoxins), which cause a similar Streptococcal Toxic Shock-like Syndrome.

Question 265: What is the incubation period of typhoid?

A. 1-2 days
B. 10-14 days (Correct Answer)
C. 1 month
D. None of the above

Explanation: **Explanation:** **Typhoid fever**, caused by the bacterium *Salmonella Typhi*, is a systemic infection characterized by a prolonged incubation period. The correct answer is **10-14 days**, though it can range from 3 to 21 days depending on the infectious dose. **Why 10-14 days is correct:** The pathogenesis of typhoid involves a complex "step-ladder" progression. After ingestion, the bacilli penetrate the intestinal mucosa and are sequestered within the mesenteric lymph nodes. They undergo primary multiplication within the reticuloendothelial system (liver, spleen, and bone marrow). The incubation period represents the time required for the bacteria to multiply sufficiently to cause a **secondary bacteremia**, at which point clinical symptoms like fever and malaise manifest. **Analysis of Incorrect Options:** * **A. 1-2 days:** This is too short for a systemic infection like typhoid. Such short incubation periods are typical of localized bacterial gastroenteritis (e.g., *Salmonella Enteritidis* or *Vibrio cholerae*). * **C. 1 month:** While rare cases can extend to 3 weeks, a 1-month incubation is atypical for *S. Typhi* and more characteristic of infections like Hepatitis A or certain parasitic infestations. **Clinical Pearls for NEET-PG:** * **Transmission:** Fecal-oral route; humans are the only natural reservoir. * **Diagnosis (WAT):** **W**idal test (positive in 2nd week), **A**ntigen detection, and **T**yphidot. * **Gold Standard:** Bone marrow culture is the most sensitive, but **Blood culture** is the investigation of choice in the **1st week**. * **Carrier State:** The **gallbladder** is the most common site of chronic colonization (e.g., the famous case of Typhoid Mary).

Question 266: All statements are true except,

A. Enteroaggregative Escherichia coli (EAEC) is associated with persistent diarrhea.
B. Enterohemorrhagic Escherichia coli (EHEC) can cause hemolytic uremic syndrome (HUS).
C. Enteroinvasive Escherichia coli (EIEC) produce disease similar to salmonellosis. (Correct Answer)
D. Enterotoxigenic Escherichia coli (ETEC) is a common cause of traveler's diarrhea.

Explanation: ### Explanation The correct answer is **C**. Enteroinvasive *Escherichia coli* (EIEC) produce a disease that is clinically and pathologically similar to **Shigellosis (Bacillary Dysentery)**, not Salmonellosis. **1. Why Option C is the correct choice (The False Statement):** EIEC invades the colonic epithelium using an invasion plasmid (pInv). Like *Shigella*, it utilizes actin-based motility to spread between cells, leading to mucosal ulceration and inflammation. This results in dysentery characterized by fever, abdominal cramps, and stools containing blood and mucus. Salmonellosis, conversely, typically presents as either enteric fever (*S. Typhi*) or inflammatory gastroenteritis with a different invasive mechanism. **2. Analysis of Incorrect Options (True Statements):** * **Option A:** **EAEC** is characterized by a "stacked-brick" adhesion pattern. It is a well-known cause of **persistent diarrhea** (lasting >14 days), especially in children and HIV-infected individuals. * **Option B:** **EHEC** (specifically O157:H7) produces Shiga-like toxins (Verotoxins). These toxins damage glomerular endothelial cells, leading to the triad of **Hemolytic Uremic Syndrome (HUS)**: microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. * **Option C:** **ETEC** is the leading cause of **Traveler’s diarrhea**. It acts via Heat-labile (LT) and Heat-stable (ST) toxins, which increase cAMP and cGTP respectively, leading to watery diarrhea. **High-Yield Clinical Pearls for NEET-PG:** * **EIEC:** Non-motile, non-lactose fermenters (resembling *Shigella*). * **EHEC:** Does **not** ferment Sorbitol (Sorbitol MacConkey Agar is the screening medium). * **ETEC:** "LT" (Labile Toxin) increases **A**denylate cyclase; "ST" (Stable Toxin) increases **G**uanylate cyclase (Mnemonic: **eL**ated **A**ir, **St**ationary **G**round). * **Infantile Diarrhea:** Primarily associated with **EPEC** (Enteropathogenic *E. coli*).

Question 267: A 25-year-old female presents with splenomegaly, leucopenia, and fever, and subsequently dies within a few days. Autopsy reveals longitudinal ulcers in the intestine. What is the probable diagnosis?

A. Tuberculosis
B. Hemorrhagic fever
C. Amoebiasis
D. Enteric fever (Correct Answer)

Explanation: ### Explanation The clinical presentation of fever, splenomegaly, and leucopenia, combined with the hallmark autopsy finding of **longitudinal ulcers** in the intestine, point directly to **Enteric Fever (Typhoid)** caused by *Salmonella Typhi*. **Why Enteric Fever is Correct:** In typhoid fever, the bacteria invade the **Peyer’s patches** of the terminal ileum. This leads to hyperplasia, followed by necrosis and sloughing of the overlying mucosa. Because Peyer’s patches are distributed along the long axis of the gut, the resulting ulcers are characteristically **longitudinal (oval)**. The systemic involvement explains the splenomegaly and the classic hematological finding of leucopenia (relative lymphocytosis). **Why Other Options are Incorrect:** * **Tuberculosis:** Intestinal TB typically presents with **transverse (circumferential)** ulcers because the bacilli spread via the lymphatics, which encircle the bowel wall. * **Amoebiasis:** Caused by *Entamoeba histolytica*, these ulcers are characteristically **flask-shaped** with narrow necks and broad bases, usually involving the colon rather than the ileum. * **Hemorrhagic Fever:** While it can cause systemic collapse and fever, it does not produce localized longitudinal intestinal ulceration. **High-Yield Clinical Pearls for NEET-PG:** * **Ulcer Orientation:** Typhoid = Longitudinal; Tuberculosis = Transverse. * **Complications:** Intestinal perforation (usually in the 3rd week) and hemorrhage are major causes of mortality. * **Diagnostic Tests:** Use the **ASU** mnemonic for timing: **A**ntigen/Blood culture (1st week), **S**erology/Widal (2nd week), **U**rine/Stool culture (3rd week). * **Pathology:** Look for "Typhoid nodules" (aggregates of macrophages/Kupffer cells) in the liver and bone marrow.

Question 268: Which serotype of Streptococcus pneumoniae most often produces mucoid colonies?

A. Type I
B. Type II
C. Type III (Correct Answer)
D. Type IV

Explanation: **Explanation:** **Streptococcus pneumoniae Type III** is the correct answer because it possesses an exceptionally large, prominent polysaccharide capsule. The capsule is the primary virulence factor of *S. pneumoniae*, protecting it from phagocytosis. In Type III strains, the excessive production of capsular material results in large, glistening, and **mucoid colonies** on blood agar, often described as having a "raindrop" appearance. * **Why Type III is correct:** Among the 90+ serotypes, Type III is the most virulent in adults and is notorious for its thick capsule. This heavy encapsulation not only leads to the characteristic mucoid morphology but also correlates with higher mortality rates in lobar pneumonia. * **Why Options A, B, and D are incorrect:** While Type I, II, and IV are significant human pathogens, they typically produce "smooth" (S) or "draughtsman" (checker-like) colonies. Draughtsman colonies occur due to autolysis of the center of the colony upon aging, a feature common to most pneumococci but less apparent in the heavily mucoid Type III. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Gram-positive, lancet-shaped diplococci. * **Quellung Reaction:** Gold standard for serotyping; involves capsular swelling when exposed to specific antisera. * **Culture Characteristics:** Alpha-hemolytic on blood agar; Optochin sensitive and Bile soluble (distinguishes it from *S. viridans*). * **Virulence:** The capsule is essential for pathogenicity; non-capsulated strains are non-pathogenic. * **Vaccines:** PPSV23 (Polysaccharide) and PCV13 (Conjugate) are used to prevent infection against the most common serotypes.

Question 269: Which of the following is EXCEPT true about pneumococci?

A. Optochin sensitive
B. Bile soluble
C. Inulin fermenter
D. Catalase positive (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Catalase positive**. This statement is false (except true) because **Pneumococci (*Streptococcus pneumoniae*) are Catalase-negative.** **1. Why Catalase positive is the correct (False) statement:** All members of the genus *Streptococcus*, including *S. pneumoniae*, lack the enzyme catalase, which breaks down hydrogen peroxide into water and oxygen. This is a fundamental biochemical test used to differentiate *Staphylococci* (Catalase-positive) from *Streptococci* (Catalase-negative). **2. Analysis of other options:** * **A. Optochin sensitive:** This is a hallmark feature of *S. pneumoniae*. It is inhibited by optochin (ethylhydrocupreine hydrochloride), which distinguishes it from other alpha-hemolytic viridans group streptococci (which are resistant). * **B. Bile soluble:** Pneumococci possess autolytic enzymes (amidases) that are activated by surface-active agents like bile salts (sodium deoxycholate). This results in the lysis of the colony, a key diagnostic test. * **C. Inulin fermenter:** *S. pneumoniae* is unique among streptococci for its ability to ferment inulin, producing acid (detected by a change in indicator color). **Clinical Pearls for NEET-PG:** * **Morphology:** Gram-positive, lancet-shaped diplococci. * **Quellung Reaction:** Swelling of the capsule when mixed with specific antiserum; the "Gold Standard" for identification. * **Virulence Factor:** The polysaccharide **capsule** is the most important virulence factor (anti-phagocytic). * **Hemolysis:** Shows **Alpha-hemolysis** (partial/green) on blood agar under aerobic conditions. * **Commonest Cause:** It is the #1 cause of Community-Acquired Pneumonia (CAP) and bacterial meningitis in adults.

Question 270: A patient with second and third-degree burns developed a wound infection on the twelfth day of admission, characterized by a bluish-green exudate. Treatment with chloramphenicol and tetracycline was unsuccessful. A gram-negative, motile organism was isolated that was oxidase-positive, did not ferment lactose, sucrose, or glucose, but grew on MacConkey's agar and produced a fruity aroma on that medium. Which of the following organisms was most likely isolated?

A. Candida albicans
B. Clostridium perfringens
C. Escherichia coli
D. Pseudomonas aeruginosa (Correct Answer)

Explanation: ### Explanation The clinical presentation and laboratory findings are classic for **Pseudomonas aeruginosa**. **1. Why the Correct Answer is Right:** * **Clinical Context:** *P. aeruginosa* is the most common cause of nosocomial infections in **burn patients**. * **Pigment Production:** The characteristic **bluish-green exudate** is due to the production of **Pyocyanin** (blue-green) and **Pyoverdin** (fluorescent yellow-green). * **Biochemical Profile:** It is a **Gram-negative, motile** rod. It is **Oxidase-positive** (a key differentiator from Enterobacteriaceae) and a **Non-fermenter** (does not utilize sugars like lactose or glucose fermentatively). * **Culture Characteristics:** It grows on MacConkey agar as **Non-Lactose Fermenting (NLF)** pale colonies and produces a distinct **fruity/sweet grape-like odor** (due to aminoacetophenone). * **Resistance:** It is inherently resistant to many common antibiotics, including chloramphenicol and tetracycline, explaining the treatment failure. **2. Why the Other Options are Wrong:** * **Candida albicans:** A yeast (fungus), not a Gram-negative motile rod. It typically causes white "curdy" discharge. * **Clostridium perfringens:** A Gram-positive, anaerobic, non-motile spore-former associated with gas gangrene, not bluish-green pus. * **Escherichia coli:** A Gram-negative rod, but it is a **Lactose Fermenter** (pink colonies on MacConkey), **Oxidase-negative**, and does not produce blue-green pigments. **3. NEET-PG High-Yield Pearls:** * **Ecthyma Gangrenosum:** A necrotic skin lesion pathognomonic for *Pseudomonas* sepsis. * **Exotoxin A:** Its primary virulence factor (mechanism identical to Diphtheria toxin: inhibits EF-2). * **Cystic Fibrosis:** *Pseudomonas* is the most common cause of respiratory infections in these patients (Alginate-producing mucoid strains). * **Drug of Choice:** Antipseudomonal penicillins (Piperacillin-Tazobactam), Ceftazidime (3rd gen), Cefepime (4th gen), or Carbapenems.

Practice by Chapter

Staphylococci

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Streptococci and Enterococci

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Neisseria and Moraxella

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Corynebacterium and Listeria

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Bacillus and Clostridium

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Enterobacteriaceae

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Vibrio, Aeromonas, and Plesiomonas

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Pseudomonas and Related Bacteria

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Haemophilus and HACEK Group

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Bordetella and Brucella

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Mycobacteria

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Spirochetes

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