RUHS II MBBS Microbiology Paper-I with Answer Key | 4th August 2025 (New Scheme)

04-08-2025
II-MBBS
Second M.B.B.S. (Main) Examination (New Scheme)
July-2025
MICROBIOLOGY
Paper-I
Time: Three Hours
Maximum Marks: 100
Attempt all questions from both sections
(Use a separate answer book for each section)
Section-A
Q.1 Fill in the blanks
a) New taxonomical name for Clostridium difficile is _______
b) _______ are extrachromosomal ds circular DNA molecule that exist in free state in
cytoplasm of bacteria
c) _______ refers to any substance that enhances the immunogenicity of an antigen
d) Classical pathway of complement system is triggered by _______
e) Cytotoxic drugs are discarded in _______ colour container
f) Niger seed agar medium is selective medium for _______ culture
Q.2 Answer the following (Multiple Choice Questions)
1. All are DNA viruses except
a) Human adenovirus
b) Hepatitis B virus
c) Human papillomavirus
d) Influenza A virus
2. Weil’s disease is caused by
a) Leptospira interrogans
b) Borrelia recurrentis
c) Treponema pallidum
d) Brucella abortus
3. Monitoring the response to antiretroviral therapy include all except
a) CD4 T cell count b) CD8 T cell count
c) HIV RNA load d) P24 antigen detection
4. Amplifier host of Japanese B encephalitis virus is
a) Monkey b) Rabbit c) Pig d) Cattle
Dr. Shivankan Kakkar, MD 2

Q.3 A 30 year old female sex worker presented with unexplained severe weight loss, chronic
diarrhea for more than one month and unexplained persistent fever for one month.
a) What is the most probable diagnosis for this condition?
b) Write down in brief about pathogenesis of this condition
c) Describe in detail about laboratory diagnosis of this disease
d) Write briefly about treatment for this condition
Q.4 Write short notes on
a) Louis Pasteur
b) Inclusion body
c) Enumerate fungi causing systemic mycoses
d) Adoptive immunity
e) Enumerate complement deficiency diseases
Q.5 Explain briefly (any three)
a) Major histocompatibility complex
b) Cytokines
c) Plasma sterilization
d) Autoimmunity
Section-B
Q.6 Define hypersensitivity reactions. Write down in brief about its classification. Write in
detail about type IV hypersensitivity reactions.
Q.7 Explain briefly (any five)
a) Acute hemorrhagic conjunctivitis
b) Microorganism causing acute suppurative otitis media
c) Enumerate "TORCH" infection
d) Enumerate oncogenic viruses
e) Laboratory diagnosis of visceral leishmaniasis
f) Structure of Gram negative cell wall
Q.8 Explain briefly (attempt any four and question a is compulsory)
a) Demonstrate how to maintain confidentiality of patient identity regarding
laboratory results when an HIV-positive patient's report is requested over the phone
while the patient is in the operation theatre.
b) Transfusion - Transmitted infection
c) Clinical types of human plague and its Laboratory diagnosis
d) Bioterrorism
e) Scrub typhus

Answer Key: II MBBS Microbiology Examination
SECTION-A
Q.1 Fill in the blanks
a) New taxonomical name for Clostridium difficile is Clostridioides difficile.
b) Plasmids are extrachromosomal ds circular DNA molecules that exist in a free state in the
cytoplasm of bacteria.
c) An adjuvant refers to any substance that enhances the immunogenicity of an antigen.
d) The classical pathway of the complement system is triggered by an antigen-antibody
complex (specifically involving IgG or IgM).
e) Cytotoxic drugs are discarded in a yellow colour container.
f) Niger seed agar medium is a selective medium for Cryptococcus neoformans culture.
Q.2 Answer the following (Multiple Choice Questions)
1. All are DNA viruses except:
* d) Influenza A virus (This is an Orthomyxovirus, which is an RNA virus).
* Rationale: Adenovirus, Hepatitis B virus (a Hepadnavirus), and Papillomavirus are all
DNA viruses.
2. Weil’s disease is caused by:
* a) Leptospira interrogans
* Rationale: Weil's disease is the severe, icteric form of leptospirosis.
3. Monitoring the response to antiretroviral therapy includes all except:
* d) P24 antigen detection
* Rationale: CD4 T cell count measures immune reconstitution, and HIV RNA load measures
viral suppression. Both are standard for monitoring ART. The p24 antigen is primarily used
for the early diagnosis of HIV infection (before seroconversion) and typically becomes
undetectable as antibodies develop, making it unsuitable for monitoring therapy response.
While the CD8 count is monitored in research, it is not a primary tool for routine therapy
response.
4. The amplifier host of Japanese B encephalitis virus is:
* c) Pig
* Rationale: Pigs act as amplifier hosts because they develop a high and prolonged viremia,
which effectively infects mosquito vectors, thus amplifying the transmission cycle. Humans
and cattle are dead-end hosts.
Q.3 Case Study
a) What is the most probable diagnosis for this condition?
The most probable diagnosis is Acquired Immunodeficiency Syndrome (AIDS), which is
the advanced stage of Human Immunodeficiency Virus (HIV) infection. The patient presents
with the classic triad of AIDS-defining symptoms:
1. Severe, unexplained weight loss ("wasting syndrome").
2. Chronic diarrhea for more than one month.
3. Unexplained persistent fever for more than one month.
Her occupation as a female sex worker places her in a high-risk category for HIV
transmission.
b) Write down in brief about the pathogenesis of this condition.
The pathogenesis of HIV/AIDS is centered on the progressive destruction of the host's
immune system.
 Causative Agent: Human Immunodeficiency Virus (HIV), an RNA retrovirus.

 Primary Target: The virus primarily targets cells expressing the CD4 molecule, most
notably CD4+ T-helper lymphocytes. It also infects macrophages and dendritic cells.
 Mechanism of Entry: The viral envelope protein gp120 binds to the host cell's CD4
receptor and a coreceptor (CCR5 or CXCR4). This is followed by the fusion of the
viral and host cell membranes, mediated by gp41.
 Replication: Inside the host cell, the viral RNA is converted into double-stranded
DNA by the enzyme reverse transcriptase. This viral DNA is then integrated into the
host's own genome by the enzyme integrase, forming a provirus.
 Cell Destruction: The provirus can remain latent or become activated to produce new
virions, which bud from the cell, eventually leading to its death (lysis). This leads to a
progressive and profound depletion of CD4+ T-cells.
 Immunodeficiency: Since CD4+ T-cells are central to coordinating the adaptive
immune response, their depletion cripples the immune system. When the CD4 count
falls below 200 cells/μL, the patient becomes severely immunocompromised and
susceptible to opportunistic infections (OIs) and certain malignancies, which define
the clinical state of AIDS.
c) Describe in detail the laboratory diagnosis of this disease.
Laboratory diagnosis of HIV infection involves a multi-pronged approach for screening,
confirmation, and monitoring.
1. Screening Tests (Antibody Detection):
 ELISA (Enzyme-Linked Immunosorbent Assay): The most common
screening method. Detects antibodies against HIV-1 and HIV-2. Modern 4th
generation ELISAs simultaneously detect both HIV antibodies and the p24
antigen, shortening the "window period."
 Rapid Tests: Immunochromatographic or immunoconcentration assays that
provide results in minutes. Useful for point-of-care testing and in resource-
limited settings.
2. Confirmatory Tests:
 Western Blot: Previously the gold standard. It detects antibodies against
specific viral proteins of different molecular weights (e.g., gp120, gp41, p24).
A positive result requires reactivity to specific band combinations.
 Line Immunoassay (LIA): A more modern and automated alternative to the
Western Blot.
3. Direct Detection of Virus or Viral Components:
 p24 Antigen Detection: Useful for diagnosing acute/early infection before
antibodies are formed (window period) and for neonatal diagnosis.
 Nucleic Acid Amplification Tests (NAATs):
 HIV RNA PCR (Viral Load): Detects and quantifies viral RNA in the
plasma. It is the most sensitive test for early diagnosis, diagnosing
infection in newborns (maternal antibodies interfere with serology),
and for monitoring the effectiveness of antiretroviral therapy (ART).
4. Staging and Monitoring:
 CD4+ T-cell Count: Measured by flow cytometry. It is the primary indicator
of the patient's immune status. A normal count is 500-1500 cells/μL. A count
<200 cells/μL defines AIDS. It helps in deciding when to start prophylaxis for
opportunistic infections.
5. Diagnosis of Opportunistic Infections (OIs):

 Depending on clinical suspicion, specific tests are done (e.g., sputum for
AFB/GeneXpert for TB, India ink stain of CSF for Cryptococcus, BAL fluid
for Pneumocystis jirovecii).
d) Write briefly about the treatment for this condition.
The treatment for HIV/AIDS is Antiretroviral Therapy (ART), often referred to as Highly
Active Antiretroviral Therapy (HAART).
 Goal: The primary goal is to suppress HIV replication to undetectable levels (<50
copies/mL), which allows for immune reconstitution (rise in CD4 count), prevents
further immune damage, reduces the risk of transmission, and improves quality of
life.
 Principle: A combination of at least three drugs from two or more different classes is
used to prevent the development of drug resistance.
 Classes of Antiretroviral Drugs:
1. Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTIs): e.g.,
Tenofovir (TDF), Lamivudine (3TC).
2. Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs): e.g.,
Efavirenz, Nevirapine.
3. Protease Inhibitors (PIs): e.g., Atazanavir, Darunavir (often "boosted" with
Ritonavir).
4. Integrase Strand Transfer Inhibitors (INSTIs): e.g., Dolutegravir (DTG),
Raltegravir.
5. Entry Inhibitors: e.g., Enfuvirtide, Maraviroc.
 Current Regimen: The WHO-recommended first-line regimen for most adults is a
combination of two NRTIs and one INSTI (e.g., Tenofovir + Lamivudine +
Dolutegravir).
 Prophylaxis: Patients with low CD4 counts also receive prophylactic medication to
prevent opportunistic infections (e.g., Cotrimoxazole for Pneumocystis
jirovecii and Toxoplasma gondii).
Q.4 Write short notes on
a) Louis Pasteur:
Considered the "Father of Microbiology," Louis Pasteur (1822-1895) was a French scientist
whose discoveries revolutionized medicine and biology.
 Germ Theory of Disease: He provided conclusive proof for the germ theory,
demonstrating that microorganisms cause disease and fermentation.
 Pasteurization: He developed this process of gentle heating to kill pathogenic
microorganisms in beverages like milk and wine, preventing spoilage and disease
transmission.
 Vaccination: He developed the first effective vaccines against rabies and anthrax,
pioneering the principles of immunization using attenuated (weakened) organisms.
 Spontaneous Generation: He definitively disproved the theory of spontaneous
generation using his famous swan-neck flask experiment.
b) Inclusion Bodies:
Inclusion bodies are distinct, abnormal structures, often aggregates of protein or viral
components, found within the nucleus or cytoplasm of a host cell.
 Nature: They can be viral replication sites, accumulations of viral proteins, or a
cellular response to infection.
 Diagnostic Importance: The presence, location, and staining characteristics of
inclusion bodies are highly diagnostic for certain viral infections.

 Examples:
 Negri bodies: Eosinophilic cytoplasmic inclusions in neurons of rabies-
infected animals.
 Owl's eye inclusions: Large, basophilic intranuclear inclusions seen in cells
infected with Cytomegalovirus (CMV).
 Guarnieri bodies: Eosinophilic cytoplasmic inclusions in cells infected with
Poxviruses.
 Babes-Ernst granules: Metachromatic granules (volutin) in Corynebacterium
diphtheriae, which are not viral but bacterial inclusions.
c) Enumerate fungi causing systemic mycoses:
Systemic mycoses are fungal infections that can disseminate throughout the body. The
primary pathogens are dimorphic fungi that are typically acquired through inhalation.
1. Histoplasma capsulatum (Histoplasmosis)
2. Blastomyces dermatitidis (Blastomycosis)
3. Coccidioides immitis/posadasii (Coccidioidomycosis or Valley Fever)
4. Paracoccidioides brasiliensis (Paracoccidioidomycosis)
(Note: Opportunistic fungi like Cryptococcus neoformans and Aspergillus fumigatus
can also cause systemic disease, especially in immunocompromised hosts.)
d) Adoptive Immunity:
Adoptive immunity refers to the transfer of immunity from a sensitized individual to a non-
immune individual by transferring immune cells, primarily lymphocytes.
 Mechanism: It involves the transfer of active T-cells (e.g., cytotoxic T lymphocytes)
or B-cells that are already programmed to respond to a specific antigen.
 Contrast with Other Immunity:
 Active Immunity: Host produces their own immune response
(infection/vaccination).
 Passive Immunity: Host receives pre-formed antibodies
(maternal/antiserum).
 Application: It is largely experimental but has significant therapeutic potential,
especially in immunotherapy for cancer (e.g., CAR-T cell therapy) and in treating
certain viral infections and immunodeficiencies.
e) Enumerate complement deficiency diseases:
Deficiencies in components of the complement system lead to increased susceptibility to
infections and autoimmune diseases.
1. Early Classical Pathway (C1, C4, C2) Deficiency: Associated with an increased
risk of immune-complex diseases like Systemic Lupus Erythematosus (SLE).
2. C3 Deficiency: Leads to severe, recurrent pyogenic infections (e.g., with S.
pneumoniae, H. influenzae) as C3 is a central component for opsonization and
phagocytosis.
3. Membrane Attack Complex (C5-C9) Deficiency: Characterized by recurrent
infections with Neisseria species (N. meningitidis, N. gonorrhoeae).
4. C1 Inhibitor Deficiency: Causes Hereditary Angioedema (HAE).
5. Deficiency of Regulatory Proteins (CD59, DAF): Leads to Paroxysmal Nocturnal
Hemoglobinuria (PNH).
Q.5 Explain briefly (any three)
a) Major Histocompatibility Complex (MHC):
The MHC is a tightly linked cluster of genes on chromosome 6 in humans, encoding cell

surface glycoproteins essential for the adaptive immune system. They are also known as
Human Leukocyte Antigens (HLA).
 Function: Their primary role is to bind peptide fragments derived from pathogens
and display them on the cell surface for recognition by T-lymphocytes. This process is
called antigen presentation.
 Classes:
 MHC Class I: Expressed on all nucleated cells. They present endogenous
antigens (e.g., viral proteins, tumor antigens) to CD8+ cytotoxic T-
lymphocytes.
 MHC Class II: Expressed only on professional Antigen-Presenting Cells
(APCs) like macrophages, dendritic cells, and B-cells. They present
exogenous antigens (e.g., bacteria) that have been phagocytosed to CD4+ T-
helper lymphocytes.
 Clinical Relevance: MHC molecules are the primary determinants of tissue
compatibility in transplantation, and certain MHC alleles are strongly associated with
autoimmune diseases.
b) Cytokines:
Cytokines are a broad category of small, soluble proteins that act as signaling molecules in
the immune system, mediating cell-to-cell communication.
 Properties: They are potent, act at low concentrations, and typically act locally
(paracrine) or on the same cell that produced them (autocrine), although some can act
systemically (endocrine). Their effects are often pleiotropic (one cytokine, multiple
effects) and redundant (multiple cytokines, same effect).
 Major Families & Examples:
 Interleukins (ILs): Mediate communication between leukocytes (e.g., IL-1
for fever, IL-2 for T-cell proliferation).
 Interferons (IFNs): Primarily involved in antiviral responses (e.g., IFN-α,
IFN-β) and immune activation (IFN-γ).
 Tumor Necrosis Factor (TNF): A key mediator of acute inflammation (e.g.,
TNF-α).
 Chemokines: Mediate chemotaxis, directing immune cells to sites of
inflammation (e.g., IL-8).
 Colony-Stimulating Factors (CSFs): Promote the differentiation and
proliferation of hematopoietic stem cells.
c) Plasma Sterilization:
Plasma sterilization is a low-temperature sterilization method used for heat-sensitive and
moisture-sensitive medical instruments.
 Principle: It uses hydrogen peroxide (H O ) vapor and an electromagnetic field
₂ ₂
(radiofrequency or microwave) to create a plasma state. In this state, the H O is
₂ ₂
broken down into highly reactive free radicals (e.g., hydroxyl radicals). These free
radicals are potent oxidizing agents that effectively kill all microorganisms, including
spores, by destroying their proteins, nucleic acids, and lipids.
 Process: Instruments are placed in a chamber, a vacuum is created, H O vapor is
₂ ₂
injected, and an RF field is applied to generate plasma.
 Advantages:
 Low temperature (around 50°C).
 Fast cycle time (approx. 1 hour).
 No toxic residues (byproducts are water and oxygen).

 Uses: Ideal for sterilizing endoscopes, cameras, plastic instruments, and other delicate
equipment that would be damaged by autoclaving.
d) Autoimmunity:
Autoimmunity is a pathological condition arising from an abnormal immune response
directed against the body's own cells, tissues, or self-antigens. It represents a failure of
immunological tolerance.
 Mechanism: It results from a breakdown of the normal mechanisms of self-tolerance,
which include central tolerance (deletion of self-reactive T and B cells in the thymus
and bone marrow) and peripheral tolerance (anergy, suppression by regulatory T-
cells).
 Triggers: The exact cause is often unknown, but contributing factors include genetic
predisposition (e.g., certain HLA types), environmental triggers (e.g., infections,
drugs), and hormonal factors.
 Classification & Examples:
 Organ-specific: The immune response is directed against a single organ or
tissue (e.g., Hashimoto's thyroiditis, Type 1 Diabetes Mellitus, Myasthenia
Gravis).
 Systemic: The response is directed against widespread antigens, affecting
multiple organs and systems (e.g., Systemic Lupus Erythematosus (SLE),
Rheumatoid Arthritis, Scleroderma).
SECTION-B
Q.6 Define hypersensitivity reactions. Write down in brief about its classification. Write
in detail about type IV hypersensitivity reactions.
Definition:
Hypersensitivity reactions are exaggerated, inappropriate, or damaging immune responses to
an antigen. These reactions occur in a pre-sensitized host and are the underlying cause of
allergic diseases and many autoimmune disorders.
Classification (Gell and Coombs):
The most widely used classification divides hypersensitivity into four types based on the
mechanism of immunological injury.
 Type I (Anaphylactic/Immediate Hypersensitivity):
 Mediator: IgE antibody.
 Mechanism: IgE binds to mast cells and basophils. On re-exposure, the
antigen cross-links the bound IgE, causing degranulation and release of
vasoactive mediators (histamine, leukotrienes).
 Examples: Allergic rhinitis, asthma, systemic anaphylaxis.
 Type II (Cytotoxic Hypersensitivity):
 Mediator: IgG or IgM antibodies.
 Mechanism: Antibodies bind to antigens on the surface of host cells, leading
to their destruction via complement activation or antibody-dependent cell-
mediated cytotoxicity (ADCC).
 Examples: Transfusion reactions, autoimmune hemolytic anemia,
Goodpasture's syndrome.
 Type III (Immune Complex Hypersensitivity):
 Mediator: Antigen-antibody (IgG or IgM) complexes.
 Mechanism: Soluble immune complexes are formed in excess and deposited
in tissues (e.g., blood vessel walls, glomeruli). This activates complement,
leading to neutrophil recruitment and inflammatory tissue damage.

 Examples: Serum sickness, Arthus reaction, SLE glomerulonephritis.
 Type IV (Delayed-Type Hypersensitivity - DTH):
 Mediator: T-lymphocytes (cell-mediated).
 Mechanism: Mediated by antigen-specific T-cells, not antibodies. The
response is delayed, appearing 24-72 hours after antigen exposure.
Detailed Description of Type IV Hypersensitivity Reaction:
Type IV hypersensitivity is a purely cell-mediated immune reaction that does not involve
antibodies. It is orchestrated primarily by T-lymphocytes and macrophages.
Phases of the Reaction:
1. Sensitization Phase:
 On first exposure, the antigen is processed by Antigen-Presenting Cells
(APCs), such as macrophages or Langerhans cells.
 The APCs migrate to regional lymph nodes and present the processed antigen
(peptide) via MHC class II molecules to naive T-helper (Th) cells.
 The Th cells differentiate into antigen-specific Th1 and Th17 memory cells.
This phase takes 1-2 weeks and produces no clinical lesion.
2. Elicitation Phase:
 On subsequent exposure to the same antigen, the pre-sensitized memory Th1
cells are activated.
 These activated Th1 cells release a cascade of cytokines, including:
 IFN-γ (Interferon-gamma): The key cytokine. It is a powerful
activator of macrophages, enhancing their phagocytic and microbicidal
activity. Activated macrophages appear as large, eosinophilic
"epithelioid cells."
 TNF-α (Tumor Necrosis Factor-alpha): Promotes inflammation and
increases endothelial adhesion molecule expression, helping to recruit
more leukocytes.
 Chemokines (e.g., IL-8): Recruit macrophages and other leukocytes
to the site of antigen exposure.
 This influx of cells, particularly activated macrophages, and the release of
their lytic enzymes and reactive oxygen species cause local inflammation,
induration, and tissue damage. The reaction peaks at 48-72 hours, hence the
term "delayed-type."
Clinical Examples of Type IV Hypersensitivity:
 Tuberculin (Mantoux) Test: Intradermal injection of tuberculin protein (PPD). A
positive test (induration) indicates prior sensitization to Mycobacterium tuberculosis.
 Contact Dermatitis: Skin inflammation caused by contact with substances like
nickel, poison ivy (urushiol), or latex. Langerhans cells act as APCs.
 Granulomatous Inflammation: A hallmark of chronic Type IV reactions, seen in
diseases where the antigen is persistent (e.g., tuberculosis, leprosy, sarcoidosis). It
involves the formation of granulomas—organized collections of epithelioid
macrophages, giant cells, and lymphocytes—to wall off the pathogen.
 Graft Rejection: T-cell-mediated rejection of allogeneic organ transplants.
Q.7 Explain briefly (any five)
a) Acute Hemorrhagic Conjunctivitis (AHC):
AHC is a highly contagious viral infection of the conjunctiva characterized by a sudden
onset.
 Causative Agents: Primarily Enterovirus 70 and Coxsackievirus A24.

 Clinical Features: Sudden onset of severe eye pain, photophobia, foreign body
sensation, copious watery discharge, and prominent subconjunctival hemorrhages,
giving the eye a dramatic, bright red appearance.
 Transmission: Spreads rapidly via fomites and direct contact with eye secretions.
Epidemics are common.
 Course: Usually self-limiting, resolving within 1-2 weeks.
b) Microorganisms causing Acute Suppurative Otitis Media:
Acute Suppurative Otitis Media (ASOM) is a bacterial infection of the middle ear, common
in children. The three main causative organisms are:
1. Streptococcus pneumoniae (most common)
2. Haemophilus influenzae (usually non-typeable, not the vaccine-preventable type b)
3. Moraxella catarrhalis
c) Enumerate "TORCH" infections:
TORCH is an acronym for a group of perinatal infections that can be transmitted from mother
to fetus and cause significant congenital abnormalities.
 T - Toxoplasmosis (Toxoplasma gondii)
 O - Other (Syphilis, Varicella-Zoster Virus, Parvovirus B19)
 R - Rubella
 C - Cytomegalovirus (CMV)
 H - Herpes Simplex Virus (HSV)
d) Enumerate oncogenic viruses:
Oncogenic viruses are viruses that can cause or contribute to the development of cancer.
 DNA Viruses:
1. Human Papillomavirus (HPV) - Cervical cancer, oropharyngeal cancer
2. Epstein-Barr Virus (EBV) - Burkitt's lymphoma, nasopharyngeal carcinoma
3. Hepatitis B Virus (HBV) - Hepatocellular carcinoma
4. Human Herpesvirus 8 (HHV-8) - Kaposi's sarcoma
 RNA Viruses:
1. Hepatitis C Virus (HCV) - Hepatocellular carcinoma
2. Human T-cell Lymphotropic Virus 1 (HTLV-1) - Adult T-cell
leukemia/lymphoma
e) Laboratory diagnosis of visceral leishmaniasis:
Visceral leishmaniasis (Kala-azar), caused by Leishmania donovani complex, is diagnosed by
detecting the parasite or an immune response to it.
 Microscopy: The definitive diagnosis is the demonstration of Leishman-Donovan
(LD) bodies (amacistigotes) within macrophages in Giemsa-stained smears of tissue
aspirates. Bone marrow aspirate is the safest and most common specimen; spleen
aspirate has the highest sensitivity but carries a risk of bleeding.
 Culture: Aspirates can be cultured on NNN (Novy-MacNeal-Nicolle) medium,
where promastigotes develop.
 Serology:
 rk39 Immunochromatographic Test: A rapid, sensitive, and specific dipstick
test detecting antibodies to the k39 antigen. Widely used for field diagnosis.
 Direct Agglutination Test (DAT) and ELISA are also used.
 Molecular Methods: PCR on blood or tissue aspirates is highly sensitive and
specific.
f) Structure of Gram-negative cell wall:
The Gram-negative cell wall is a complex, multi-layered structure outside the cytoplasmic
membrane.

1. Inner Cytoplasmic Membrane: Standard phospholipid bilayer.
2. Periplasmic Space: A gel-like space between the inner and outer membranes. It
contains a variety of enzymes and a thin layer of peptidoglycan.
3. Thin Peptidoglycan Layer: Provides some structural rigidity but is much thinner
than in Gram-positive bacteria.
4. Outer Membrane: This is the most unique feature. It is an asymmetric bilayer:
 The inner leaflet is composed of phospholipids.
 The outer leaflet is composed of Lipopolysaccharide (LPS).
5. Lipopolysaccharide (LPS): Also known as endotoxin, it consists of three parts:
 Lipid A: The toxic component, embedded in the membrane, responsible for
the fever and shock seen in Gram-negative sepsis.
 Core Polysaccharide: Connects Lipid A to the O antigen.
 O Antigen: A long polysaccharide chain extending outwards. It is highly
variable and used for serotyping (e.g., in E. coli O157:H7).
 The outer membrane also contains porin proteins that form channels for the passage
of small, hydrophilic molecules.
Q.8 Explain briefly (attempt any four and question a is compulsory)
a) Demonstrate how to maintain confidentiality of patient identity regarding laboratory
results when an HIV-positive patient's report is requested over the phone while the
patient is in the operation theatre.
This is a critical issue of medical ethics and patient confidentiality. The guiding principle is to
protect the patient's private information at all costs.
Correct Professional Conduct:
1. Do Not Disclose Information Over the Phone: Politely but firmly refuse to give the
result over the phone. You cannot verify the identity of the caller, and verbal
communication of such sensitive information is a breach of confidentiality.
2. State the Policy, Not the Result: Inform the caller, "I am sorry, but due to hospital
policy and our strict ethical duty to maintain patient confidentiality, I cannot provide
any laboratory results over the phone. This policy is in place to protect all our
patients."
3. Do Not Confirm or Deny: Do not even confirm that a test for HIV was performed on
the patient. Simply stating that "the HIV test is positive" or "the HIV test is negative"
confirms that the test was done, which itself is confidential information.
4. Provide Secure Alternatives: Offer a secure and verifiable method for the
information to be transmitted. Suggest the following options:
 "The result is available in the hospital's secure Hospital Information System
(HIS). The authorized treating surgeon or anesthesiologist can access it using
their login credentials."
 "A printed copy of the report can be sent in a sealed envelope to the Operation
Theatre via a designated hospital attendant or pneumatic tube system,
addressed specifically to the primary surgeon."
5. Document the Interaction: Make a note of the time, the caller's name (if given), and
your response. This is important for medico-legal purposes.
Rationale: An HIV diagnosis carries significant social stigma and personal implications.
Unauthorized disclosure can have devastating consequences for the patient. The clinical team
in the OT requires this information for universal precautions and potential post-exposure
prophylaxis (PEP) decisions, but the information must be obtained through a secure,
documented, and professional channel.

b) Transfusion-Transmitted Infections (TTIs):
TTIs are infections that can be transmitted from a donor to a recipient through the transfusion
of blood or blood products. To ensure blood safety, all donated blood units are mandatorily
screened for a panel of major TTIs.
 Mandatory Screened Infections (in India):
1. HIV-1 and HIV-2: Using 4th or 5th generation ELISA.
2. Hepatitis B Virus (HBV): Screening for Hepatitis B surface antigen
(HBsAg).
3. Hepatitis C Virus (HCV): Screening for anti-HCV antibodies.
4. Syphilis: Screening for antibodies to Treponema pallidum.
5. Malaria: Screening for malarial parasites (Plasmodium species).
 Emerging Threats: Other agents like CMV, Dengue virus, Chikungunya virus, and
Zika virus can also be transmitted but are not part of routine mandatory screening.
 Prevention: Prevention relies on a multi-layered approach: careful donor selection,
mandatory screening of all donated units, and the use of Nucleic Acid Amplification
Testing (NAAT) to detect infections during the window period.
c) Clinical types of human plague and its Laboratory diagnosis:
Plague is a zoonotic disease caused by the Gram-negative bacterium Yersinia pestis.
Clinical Types:
1. Bubonic Plague: The most common form (80-95% of cases). Results from the bite of
an infected flea. Bacteria travel to regional lymph nodes, causing them to become
extremely swollen, tense, and painful. These swollen nodes are called buboes (most
often in the groin, axilla, or neck).
2. Septicemic Plague: Occurs when the bacteria spread directly into the bloodstream
without forming a bubo (primary) or from a ruptured bubo (secondary). It is
characterized by fever, chills, prostration, shock, and Disseminated Intravascular
Coagulation (DIC), leading to bleeding and tissue necrosis (blackening of extremities,
"Black Death").
3. Pneumonic Plague: The most virulent and dangerous form. Can be primary
(inhalation of infectious droplets from another person/animal) or secondary (spread to
the lungs from septicemic plague). It is characterized by a rapid onset of pneumonia,
bloody sputum, and is highly fatal if not treated early. It is the only form that can
spread from person-to-person.
Laboratory Diagnosis:
 Specimen: Aspirate from a bubo, blood for culture (in septicemia), or sputum (in
pneumonic plague). Extreme care (BSL-3 precautions) must be taken when handling
specimens.
 Microscopy: Gram stain or Wayson stain of the specimen shows Gram-negative
coccobacilli with characteristic bipolar staining, giving them a "safety pin"
appearance.
 Culture: The organism can be cultured on blood agar or MacConkey agar. Colonies
appear after 48 hours.
 Rapid Diagnostic Test: Detection of the F1 capsular antigen using
immunochromatographic dipstick tests is a rapid and useful method.
 Molecular Methods: PCR is highly sensitive and specific for detecting Y.
pestis DNA.
d) Bioterrorism:
Bioterrorism is the deliberate and malicious use of biological agents—such as bacteria,

viruses, fungi, or their toxins—to cause illness, death, and panic in humans, animals, or
plants.
 Goal: To create widespread fear, social disruption, and economic damage, often with
a small amount of agent.
 CDC Categorization: The US Centers for Disease Control and Prevention (CDC)
categorizes bioterrorism agents into three categories based on risk:
 Category A: Highest priority agents. They pose the greatest risk to national
security because they are easily disseminated, result in high mortality rates,
and require special public health preparedness.
 Examples: Bacillus anthracis (Anthrax), Yersinia pestis (Plague),
Variola major (Smallpox), Clostridium botulinum toxin
(Botulism), Francisella tularensis (Tularemia), and Viral Hemorrhagic
Fevers (Ebola, Marburg).
 Category B: Second highest priority. Moderately easy to disseminate and
result in moderate morbidity but low mortality.
 Category C: Third highest priority. Emerging pathogens that could be
engineered for mass dissemination in the future.
e) Scrub Typhus:
Scrub typhus is an acute, febrile zoonotic disease caused by the obligate intracellular
bacterium Orientia tsutsugamushi.
 Vector and Transmission: It is transmitted to humans by the bite of larval mites
(chiggers) of the Leptotrombidium genus, which are found in areas with heavy scrub
vegetation.
 Clinical Features:
 The classic presentation includes fever, headache, myalgia, and conjunctival
injection.
 A pathognomonic sign, present in about 50% of patients, is an eschar: a
painless, black, necrotic lesion at the site of the chigger bite.
 A maculopapular rash may also develop. Severe cases can lead to
pneumonitis, meningitis, and multi-organ failure.
 Laboratory Diagnosis:
 Serology: This is the mainstay of diagnosis.
 Immunofluorescence Assay (IFA): Considered the gold standard.
 ELISA: Widely used to detect IgM and IgG antibodies.
 Weil-Felix Test: An older, less specific test where patient serum is
tested for agglutination of Proteus strains. A positive reaction with
the OX-K strain is suggestive.
 Molecular Methods: PCR on blood or eschar biopsy material is highly
specific and useful for early diagnosis.

RUHS II MBBS Microbiology Paper-I with Answer Key | 4th August 2025 (New Scheme)

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RUHS II MBBS Microbiology Paper-I with Answer Key | 4th August 2025 (New Scheme)