Persons with heterozygous sickle cell trait are protected from infection by:
All are true regarding the development of T-cells, except?
Which of the following statements about interleukin-1 is false?
Which of the following is a superantigen ?
What is the primary use of the Hybridoma technique?
An adolescent male developed vomiting and diarrhea 1 hour after having food from a restaurant. The most likely pathogen is?
Rosette formation with sheep RBCs (SRBCs) indicates functioning of -
What is the typical bacterial count in the duodenum?
Which of the following bacteria is known to exhibit antigenic variation?
Most common organism causing ventilator associated pneumonia -
NEET-PG 2013 - Microbiology NEET-PG Practice Questions and MCQs
Question 11: Persons with heterozygous sickle cell trait are protected from infection by:
- A. Pneumococcus
- B. P. falciparum (Correct Answer)
- C. P. vivax
- D. Salmonella
Explanation: ***P. falciparum*** - Individuals with heterozygous sickle cell trait have a **protective effect** against severe malaria caused by *P. falciparum* due to altered red blood cell morphology [1][2]. - The sickle hemoglobin (HbAS) provides a **selective advantage**, reducing the severity of malaria infections and the parasitic load [2][3]. *P. vivax* - Sickle cell trait does not confer significant protection against *P. vivax*, which primarily infects non-sickled red blood cells [2]. - The infection still occurs in individuals with the trait because it specifically affects the reticulocyte count, which is less impacted by sickling. *Salmonella* - While sickle cell disease is linked with increased susceptibility to **Salmonella infections**, the sickle cell trait itself does not provide protection against it [2]. - The trait does not influence immunity or susceptibility to bacterial pathogens like *Salmonella*. *Pneumococcus* - Individuals with sickle cell trait still have a normal risk of **invasive pneumococcal disease**, similar to those without the trait [2]. - Protection against *Pneumococcus* primarily relates to vaccination status and not to hemoglobinopathies. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 398-400. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 50-51.
Question 12: All are true regarding the development of T-cells, except?
- A. T-cells are formed in bone marrow
- B. In lymph nodes, T-cells are found in paracortical area
- C. Maturation of T-cells take place in thymus
- D. T-cells are located in mantle layer of spleen (Correct Answer)
Explanation: ***T-cells are located in mantle layer of spleen*** - The **mantle layer** (or marginal zone) of the spleen is primarily associated with **B-lymphocytes**, which are involved in antibody production. - While T-cells are present in the spleen, they are predominantly found in the **periarteriolar lymphoid sheath (PALS)**, which is part of the white pulp, rather than the mantle layer. *T-cells are formed in bone marrow* - **Hematopoietic stem cells** in the **bone marrow** are the progenitors of all blood cells, including lymphocytes. - These stem cells differentiate into **lymphoid stem cells**, which then travel to the thymus to become T-cells. *Maturation of T-cells take place in thymus* - **T-cell precursors** migrate from the bone marrow to the **thymus**, where they undergo a complex process of differentiation and selection. - In the thymus, T-cells acquire their **T-cell receptors (TCRs)** and undergo positive and negative selection to ensure they are self-MHC restricted and tolerant to self-antigens. *In lymph nodes, T-cells are found in paracortical area* - The **paracortical area** (or paracortex) of the lymph node is the **T-cell zone**, rich in T-lymphocytes and dendritic cells. - This region is crucial for the interaction between T-cells and antigen-presenting cells, initiating adaptive immune responses.
Question 13: Which of the following statements about interleukin-1 is false?
- A. IL-1 is an endogenous pyrogen.
- B. The primary source of IL-1 is the monocyte-macrophage system.
- C. IL-1 inhibits IL-2 production by T-cells. (Correct Answer)
- D. IL-1 promotes acute phase protein synthesis in the liver.
Explanation: ***IL-1 inhibits IL-2 production by T-cells*** - This statement is false because **IL-1** actually **enhances the production of IL-2** by T-cells, which is crucial for T-cell proliferation and immune response. - **IL-1 acts synergistically with IL-6 and TNF-α** to promote inflammation and immune cell activation, where IL-2 plays a key role. *The primary source of IL-1 is the monocyte-macrophage system* - This statement is true; **monocytes and macrophages** are the main producers of **IL-1α and IL-1β** upon activation by various stimuli. - Other cells, such as neutrophils, dendritic cells, and endothelial cells, can also produce IL-1, but monocytes and macrophages are the predominant source. *IL-1 is an endogenous pyrogen* - This statement is true; **IL-1** is a potent **endogenous pyrogen** that acts on the hypothalamus to induce fever, a hallmark of the acute phase response. - It triggers prostaglandin synthesis in the hypothalamus, leading to an elevation in the body's thermoregulatory set point. *IL-1 promotes acute phase protein synthesis in the liver* - This statement is true; **IL-1** is a key mediator that stimulates **hepatocytes** to produce **acute phase proteins**, such as C-reactive protein and serum amyloid A. - This hepatic response is part of the innate immune system's effort to control infection and inflammation.
Question 14: Which of the following is a superantigen ?
- A. Cholera toxin
- B. Diphtheria toxin
- C. TSST (Correct Answer)
- D. Vero-cytoxin
Explanation: ***TSST*** - **Toxic Shock Syndrome Toxin-1 (TSST-1)** is a classic example of a superantigen produced by *Staphylococcus aureus*. - Superantigens **bind directly to MHC class II molecules and T-cell receptors (TCRs)** outside of the antigen-binding groove, leading to non-specific activation of a large percentage of T cells and a massive release of cytokines. *Cholera toxin* - **Cholera toxin** is an exotoxin produced by *Vibrio cholerae* that causes massive fluid secretion in the intestine by **activating adenylate cyclase** in enterocytes. - It functions by **ADP-ribosylating the Gs alpha subunit**, leading to constitutive activation of cyclic AMP production, but it is not a superantigen. *Diphtheria toxin* - **Diphtheria toxin**, produced by *Corynebacterium diphtheriae*, inhibits protein synthesis in eukaryotic cells by **ADP-ribosylating elongation factor-2 (EF-2)**. - This action leads to cell death and the characteristic pseudomembrane formation in diphtheria, but it does not act as a superantigen. *Vero-cytoxin* - **Vero-cytoxin** (also known as Shiga toxin or Shiga-like toxin) is produced by *E. coli* O157:H7 and other Shiga toxin-producing *E. coli* (STEC). - It inhibits protein synthesis by **cleaving ribosomal RNA**, primarily causing damage to intestinal cells and renal endothelial cells, but it is not a superantigen.
Question 15: What is the primary use of the Hybridoma technique?
- A. Monoclonal antibodies (Correct Answer)
- B. Antigen
- C. Specific antibodies
- D. Cytokines
Explanation: ***Monoclonal antibodies*** - The **hybridoma technique** is primarily used to produce **monoclonal antibodies (MAbs)**, which are highly specific antibodies derived from a single B-cell clone. - These antibodies recognize a **single epitope** on an antigen, providing exceptional specificity and uniformity. - The technique involves **fusing a B-lymphocyte** (antibody-producing cell) with a **myeloma cell** (immortal cancer cell) to create a hybridoma that continuously produces identical antibodies. - This is the **gold standard** for producing large quantities of identical, highly specific antibodies for diagnostic and therapeutic use. *Specific antibodies* - While monoclonal antibodies are indeed specific, this term is **too vague** and could refer to any antibody with specificity, including polyclonal antibodies. - **Polyclonal antibodies** are also specific but are produced through conventional immunization, not the hybridoma technique. - The defining characteristic of the hybridoma technique is that it produces **monoclonal** (single clone) antibodies, not just "specific" ones. *Antigen* - An **antigen** is a molecule that elicits an immune response and is used to immunize animals during antibody production. - However, antigens are the **input** for antibody production, not the **product** of the hybridoma technique. *Cytokines* - **Cytokines** are signaling molecules involved in immune cell communication and regulation. - They are not produced by the hybridoma technique, which is specifically designed for **antibody production**.
Question 16: An adolescent male developed vomiting and diarrhea 1 hour after having food from a restaurant. The most likely pathogen is?
- A. Clostridium perfringens
- B. Vibrio parahaemolyticus
- C. Staphylococcus aureus (Correct Answer)
- D. Salmonella
Explanation: ***Staphylococcus aureus*** - The rapid onset of symptoms (within 1 hour) strongly suggests **pre-formed toxin ingestion**, which is characteristic of *Staphylococcus aureus* food poisoning. - While the typical incubation period is **1-6 hours** (average 2-4 hours), onset within 1 hour can occur with **high toxin loads** in contaminated food. - **Vomiting** is often the predominant symptom, occurring shortly after consuming contaminated food, which distinguishes it from other bacterial causes. *Clostridium perfringens* - Onset of symptoms caused by *Clostridium perfringens* is typically **8-16 hours** after ingestion, which is much longer than observed here. - It primarily causes **diarrhea and abdominal cramps** due to toxin production in the intestine, with minimal vomiting. *Vibrio parahaemolyticus* - Symptoms usually appear **4-96 hours** (average 12-24 hours) after consuming contaminated seafood, which is a longer incubation period than described. - It typically causes **watery diarrhea**, abdominal cramps, nausea, and occasional vomiting, but not within 1 hour. *Salmonella* - The incubation period for *Salmonella* infection is typically **6-72 hours** (average 12-36 hours), making it highly unlikely for symptoms to appear within 1 hour. - **Diarrhea, fever, and abdominal cramps** are common with *Salmonella*, but rapid-onset vomiting from pre-formed toxin is not its mechanism.
Question 17: Rosette formation with sheep RBCs (SRBCs) indicates functioning of -
- A. T-cells (Correct Answer)
- B. B-cells
- C. Neutrophils
- D. Monocytes
Explanation: ***T-cells*** - **T-cells** possess specific receptors, like **CD2** on their surface, that can bind to ligands on sheep red blood cells (SRBCs). - This binding leads to the formation of characteristic **rosettes**, where SRBCs cluster around the T-lymphocytes, indicating functional T-cells. *B-cells* - **B-cells** primarily function in **humoral immunity** by producing antibodies and do not typically form rosettes with sheep RBCs. - While B-cells have surface receptors, they are not CD2 and thus do not facilitate this specific type of rosette formation. *Neutrophils* - **Neutrophils** are **phagocytic cells** involved in innate immunity, primarily combating bacterial and fungal infections. - They lack the specific surface receptors (like CD2) required to form rosettes with sheep RBCs. *Monocytes* - **Monocytes** are precursors to macrophages and dendritic cells, involved in phagocytosis and antigen presentation. - They do not possess the necessary surface markers to form rosettes with sheep RBCs.
Question 18: What is the typical bacterial count in the duodenum?
- A. 10^2 per gram (Correct Answer)
- B. 10^1 per gram
- C. 10^10 per gram
- D. 10^5 per gram
Explanation: ***10^2 per gram*** - The duodenum has a **relatively low bacterial count** (typically 10^2-10^4 CFU/gram) due to the **acidic environment** from gastric acid and **rapid transit** of contents. - A count of **10^2 CFU/gram** represents the **lower end of the normal range** for the proximal duodenum, where gastric acid effects are strongest. - This sparse bacterial population contrasts sharply with the dense colonization seen in the distal gut. *10^1 per gram* - This represents an **extremely low count** more characteristic of the **stomach**, not the duodenum. - Such minimal bacterial presence is due to the **hostile acidic environment** (pH 1-3) in the stomach. - The duodenum, while having low counts, consistently has higher bacterial densities than this. *10^5 per gram* - This count is characteristic of the **distal small intestine (ileum)**, where bacterial concentrations progressively increase. - A bacterial count of **10^5 per gram in the duodenum** would be considered **abnormal** and suggest **small intestinal bacterial overgrowth (SIBO)**. - SIBO occurs when colonic-type bacteria colonize the small intestine inappropriately. *10^10 per gram* - This bacterial density is typical of the **colon** (which harbors 10^11-10^12 CFU/gram), the most densely colonized part of the human gut. - Such a high count in the duodenum would indicate **severe bacterial overgrowth** or gross contamination. - The colon's anaerobic environment supports this massive bacterial population.
Question 19: Which of the following bacteria is known to exhibit antigenic variation?
- A. Yersinia
- B. Bordetella
- C. Brucella
- D. Borrelia (Correct Answer)
Explanation: ***Borrelia*** - *Borrelia* species, particularly *Borrelia burgdorferi* (causing **Lyme disease**), are known for extensive **antigenic variation** of their outer surface proteins (Osps), especially OspC. - This variation helps the bacteria evade the host's immune response, contributing to persistent infection. *Yersinia* - While *Yersinia* species produce various virulence factors, including proteins that interfere with immune cell function, they are not primarily known for the type of rapid and extensive **antigenic variation**seen in *Borrelia*. - Their immune evasion strategies often involve modifying host cell signaling pathways and resisting phagocytosis. *Bordetella* - *Bordetella pertussis*, causative agent of **whooping cough**, varies its expression of adhesins and toxins through **phase variation**, which is a form of phenotypic switching. - However, this is distinct from the frequent and sequential changes in surface antigens (antigenic variation) observed in *Borrelia*. *Brucella* - *Brucella* species are **intracellular pathogens** that primarily evade the immune system by surviving and replicating within host cells. - They do not typically engage in significant **antigenic variation** of their surface components as a primary immune evasion mechanism.
Question 20: Most common organism causing ventilator associated pneumonia -
- A. Legionella
- B. Pneumococcus
- C. Pseudomonas (Correct Answer)
- D. Coagulase negative staphylococcus
Explanation: ***Pseudomonas*** - **Pseudomonas aeruginosa** is one of the most common causes of **ventilator-associated pneumonia (VAP)**, particularly in **late-onset VAP** (≥5 days) and in patients with prolonged mechanical ventilation, prior antibiotic exposure, or underlying lung disease. - Its ability to form **biofilms** and its intrinsic antibiotic resistance contribute to its prevalence in hospital-acquired infections. - Along with **Staphylococcus aureus** (especially MRSA), Pseudomonas is consistently among the leading causes of VAP in ICU settings. *Legionella* - **Legionella** is a less common cause of VAP and is typically associated with contaminated water sources, manifesting as **Legionnaires' disease**. - It usually causes severe, rapidly progressive pneumonia and is often harder to culture than other bacteria. *Pneumococcus* - **Streptococcus pneumoniae (Pneumococcus)** is the most common cause of **community-acquired pneumonia (CAP)**, but it is less frequently implicated in VAP. - While it can cause severe pneumonia and may be seen in **early-onset VAP**, its incidence in late-onset VAP is lower compared to Gram-negative rods like Pseudomonas. *Coagulase negative staphylococcus* - **Coagulase-negative Staphylococci** (e.g., *Staphylococcus epidermidis*) are common **contaminants** in cultures and primarily cause device-related infections, such as those associated with central venous catheters. - They are rarely a primary cause of VAP, as they typically have low virulence in the respiratory tract.