Free ASCP MLS Exam Practice Questions Mock Test: Part 32 – Immunology – Serological Infectious Disease

The IgG avidity assay is used to distinguish recent from long-standing HIV infections.

• Low avidity: Indicates a recent infection (typically within the past 4–6 months), as antibodies produced early bind weakly to antigens.

• High avidity: Suggests a mature immune response, characteristic of an infection that occurred months to years ago.

Other markers:

• p24 antigen (a): Appears early (acute phase) but declines; not reliable for timing.

• HIV RNA load (b): High during acute infection but variable in chronic stages; used for monitoring, not dating.

• Total anti-HIV antibody titer (d): Rises after infection but plateaus; cannot differentiate recent vs. chronic.

A four-fold or greater rise in antibody titer (e.g., from 1:8 to 1:32) between acute-phase (collected early in illness) and convalescent-phase (collected 2–4 weeks later) serum samples typically indicates:

• Recent or ongoing infection, as the immune response is actively increasing.

• This is a standard serological criterion for diagnosing acute infections (e.g., viral diseases like COVID-19, influenza, or Epstein-Barr virus).

Other scenarios:

• Vaccine response (a): Usually shows a rise but is timed after vaccination, not illness.

• Chronic infection (b): Titers are stable or fluctuate mildly (no sharp rise).

• Prior immunity (d): Titers are stable (e.g., from past infection or vaccination).

• Mumps confirmation can be done by:

  • Detection of mumps-specific IgM antibody → indicates recent or acute infection.

  • Seroconversion or ≥4-fold rise in IgG titers between acute and convalescent sera → confirms infection.

Why not the others?

• a) Too specific in timing; IgM appears soon after symptoms, but confirmation relies on IgM + IgG rise, not just timing.

• b) Rash is not a characteristic feature of mumps (that’s more for measles/rubella).

• d) IgG at >6 months just shows immunity (infection or vaccination), not acute confirmation.

Hepatitis A virus (HAV) does not have a chronic carrier state. It causes only acute, self-limiting infection and is always cleared by the immune system without progression to chronic hepatitis. In contrast:

• HBV (b): Can lead to chronic infection (carrier state).

• HCV (c): High rate of chronicity (~75-85%).

• HDV (d): Requires HBV and can cause chronic infection if HBV persists.

The combination of HBsAg (positive), anti-HBc (positive), and often HBeAg (positive) is the classic serological profile for the early acute phase of hepatitis B virus (HBV) infection.

Here’s why the other options are incorrect:

• b) Early convalescent phase HBV hepatitis: In the convalescent (recovery) phase, HBsAg and HBeAg disappear, and anti-HBe and anti-HBs begin to appear.

• c) Recovery phase of acute HBV hepatitis: In the recovery phase, HBsAg is negative, anti-HBc is positive (typically IgG), and the protective antibody anti-HBs is positive.

• d) Past HBV infection: This is characterized by a positive anti-HBc and a positive anti-HBs, indicating immunity from a past infection that has cleared. HBsAg and HBeAg are negative.

The hepatitis B vaccine is produced using recombinant DNA technology. Specifically:

• The gene for HBsAg (hepatitis B surface antigen) is inserted into yeast cells (e.g., Saccharomyces cerevisiae).

• The yeast then produces and secretes HBsAg, which is purified and used as the vaccine antigen.

• This recombinant HBsAg is non-infectious and stimulates the production of protective anti-HBs antibodies.

The classic antibody response to hepatitis A virus (HAV) infection follows this pattern:

1. Increase in IgM antibody: IgM anti-HAV appears early (at symptom onset), peaks during acute infection, and indicates recent infection.

2. Decrease in IgM antibody: IgM levels decline and typically become undetectable within 3–6 months.

3. Increase in IgG antibody: IgG anti-HAV rises later, persists for life, and provides long-term immunity.

The persistence of HBsAg (hepatitis B surface antigen) for more than 6 months defines chronic hepatitis B infection. This indicates the immune system has not cleared the virus, leading to long-term carriage and risk of liver complications (e.g., cirrhosis, hepatocellular carcinoma). In contrast:

• Acute hepatitis B (a): HBsAg is positive but typically clears within 6 months.

• Recovery (c): HBsAg is negative, and anti-HBs appears.

• Immunized (d): Only anti-HBs is positive (due to vaccination, not infection).

Hepatitis C virus (HCV) is the most likely to cause chronic cirrhosis due to its high rate of chronic infection (75-85%) and persistent liver inflammation over decades. Key points:

• HCV often progresses silently to cirrhosis, liver failure, or hepatocellular carcinoma.

• It is a leading cause of liver transplants worldwide.

While HBV (b) also causes cirrhosis, HCV’s chronicity and progressive fibrosis make it particularly associated with this outcome. In contrast:

• HAV (a) and HEV (d): Do not cause chronic infection or cirrhosis.

The measles vaccine is a live attenuated vaccine. It is typically administered as part of the MMR (measles, mumps, rubella) vaccine, which contains live viruses that have been weakened (attenuated) to stimulate an immune response without causing disease.

• Rabies (a): The rabies vaccine is an inactivated (killed) vaccine, not live attenuated.

• Tetanus (b): The tetanus vaccine is a toxoid vaccine (made from inactivated toxin), not live attenuated.

• Hepatitis B (c): The hepatitis B vaccine is a recombinant subunit vaccine (contains viral surface antigens produced in yeast cells), not live attenuated.

The late stage (also known as late disseminated stage) of Lyme disease is characterized by manifestations that can occur months to years after the initial infection. Key features include:

• Arthritis: Recurrent, often affecting large joints like the knee.

• Neurological complications: Such as peripheral neuropathy (numbness, tingling, or pain in the extremities) and encephalomyelitis (inflammation of the brain and spinal cord).

Hepatitis A virus (HAV) is classified under the Picornaviridae family (genus Hepatovirus). It is a small, non-enveloped, single-stranded RNA virus resistant to environmental degradation. In contrast:

• HBV (b): Belongs to Hepadnaviridae (DNA virus).

• HCV (c): Belongs to Flaviviridae (RNA virus).

• HEV (d): Belongs to Hepeviridae (RNA virus).

Hepatitis D virus (HDV) is a defective RNA virus that requires the presence of hepatitis B virus (HBV) to replicate. HDV lacks the genes to produce its own envelope proteins and instead uses the HBsAg (surface antigen) from HBV to form complete viral particles and infect liver cells. Therefore, HDV can only cause infection as:

• A coinfection (simultaneous infection with HBV and HDV).

• A superinfection (HDV infection in a person already chronically infected with HBV).

HBeAg (hepatitis B e-antigen) is a marker of active viral replication in HBV infection. It indicates:

• High levels of HBV DNA in the blood.

• Increased infectivity.

• Ongoing liver inflammation.

In contrast:

• anti-HBc IgG (a): Indicates past or chronic infection (not replication).

• anti-HBe (c): Appears as HBeAg disappears, signaling reduced replication (seroconversion).

• anti-HBs (d): Indicates immunity/recovery (not replication).

Hepatitis C virus (HCV) currently has no commercially available vaccine. Challenges include:

• High genetic variability (multiple genotypes and quasispecies).

• Rapid mutation allowing immune evasion.

• Lack of durable natural immunity after infection hindering vaccine design.

In contrast:

• HAV (a): Effective inactivated vaccine exists.

• HBV (b): Recombinant vaccine widely used.

• HEV (d): Vaccine exists (e.g., in China) though not globally universal.

Hepatitis B virus (HBV) is the most likely to cause hepatocellular carcinoma (HCC), especially in endemic regions. It is a leading cause of liver cancer worldwide due to:

• Direct oncogenic effects (viral DNA integration into host genome).

• Chronic inflammation and cirrhosis.

HCV (c) also significantly increases HCC risk (often through chronic cirrhosis), but HBV has a stronger direct carcinogenic role and can cause cancer even without cirrhosis. In contrast:

• HAV (a) and HEV (d): Do not cause chronic infection or HCC.

In HBV infection, IgM anti-HBc (IgM antibody against the hepatitis B core antigen) is the first antibody to appear. It arises during the acute phase, shortly after HBsAg becomes detectable, and is a key marker for recent acute infection. Other antibodies appear later:

• anti-HBe (d): Follows HBeAg decline.

• IgG anti-HBc (c): Replaces IgM anti-HBc and persists for life.

• anti-HBs (a): Appears last, after HBsAg clearance, indicating recovery/immunity.

IgM anti-HBc is critical for diagnosing acute HBV.

Hepatitis C virus (HCV) has the highest risk of progressing to chronic infection:

• ~75-85% of infected adults develop chronic infection.

• Chronic HCV can lead to cirrhosis, liver failure, or hepatocellular carcinoma over decades.

In contrast:

• HAV (a): No chronic infection (acute only).

• HBV (b): Chronic risk is ~5-10% in adults (higher in infants).

• HEV (d): No chronic infection typically (except in immunocompromised persons).

Hepatitis A virus (HAV) is most commonly transmitted via the fecal-oral route, typically through contaminated food, water, or close personal contact. This contrasts with other hepatitis viruses:

• HBV (a): Transmitted via blood, sexual contact, or perinatal exposure.

• HCV (b): Primarily blood-borne (e.g., IV drug use, transfusions).

• HDV (d): Requires HBV coinfection; transmission mirrors HBV (blood/sexual).

The incubation period for hepatitis B virus (HBV) ranges from 30 to 180 days, with an average of about 60–90 days. This prolonged period reflects the time from viral exposure to the onset of symptoms or detectable serological markers (like HBsAg). Shorter periods are typical for other viruses:

• HAV: 15–45 days (b).

• Influenza-like illnesses: 1–7 days (a/d are too short).

Flocculation tests for syphilis, such as the VDRL (Venercal Disease Research Laboratory) and RPR (Rapid Plasma Reagin) tests, detect the presence of reagin antibody. This is a non-treponemal antibody produced by the host in response to lipoidal material (like cardiolipin) released from damaged host cells during Treponema pallidum infection. It is not specific to T. pallidum itself, which is why these tests are used for screening and require confirmation with more specific treponemal tests.

Here’s why the other options are incorrect:

• b) Antigen: Flocculation tests detect antibodies, not antigens. The test uses cardiolipin-lecithin-cholesterol antigen to detect reagin antibodies.

• c) Hemolysin: Hemolysin is not involved in syphilis serology. It is associated with tests like the complement fixation test or hemolysis-based assays.

• d) Forssman antigen: This is a heterophilic antigen found in some animals and bacteria, but it is not related to syphilis testing.

• anti-HBs (Hepatitis B surface antibody): Appears after clearance of HBsAg or following vaccination → indicates recovery and protective immunity.

• HBsAg: Marker of active infection.

• HBeAg: Marker of replication and infectivity.

• Viral DNA polymerase: Reflects viral replication, not immunity.

Hepatitis C virus (HCV) is the most common cause of post-transfusion hepatitis in regions where donor blood is not routinely screened for HCV. This is due to:

• High chronicity: Many carriers are asymptomatic, leading to undetected infections.

• Blood-borne transmission: HCV spreads efficiently via blood products.

While screening has reduced risk dramatically, historical data and rare breakthrough cases still implicate HCV. Other viruses:

• HAV (a): Rarely transfusion-related (fecal-oral route).

• HBV (b): Now rare due to vaccination and screening.

• HEV (d): Primarily waterborne; transfusion transmission is possible but uncommon.

After vaccination against hepatitis B, a healthcare worker (or any individual) should be tested for anti-HBs (antibody to hepatitis B surface antigen). This test:

• Confirms an adequate immune response (typically a titer ≥10 mIU/mL indicates protection).

• Ensures immunity against HBV, which is critical for high-risk groups like healthcare workers.

Other markers are irrelevant post-vaccination:

• anti-HBc IgM (a): Indicates acute infection (not produced by vaccine).

• HBsAg (c): Indicates current infection (should be negative).

• HBeAg (d): Indicates high viral replication (not related to vaccination).

The combination of HBsAg (surface antigen), anti-HBc (core antibody), and often HBeAg (e-antigen) is characteristic of the early acute phase of hepatitis B virus (HBV) infection. During this phase:

• HBsAg appears first, indicating active infection.

• Anti-HBc (IgM) rises early, marking acute infection.

• HBeAg is a marker of high viral replication and infectivity, typically present in the acute phase.

Anti-HBs positivity alone (without other HBV markers) typically indicates immunity due to vaccination. The hepatitis B vaccine stimulates the production of anti-HBs antibodies, providing protection against infection. In contrast:

• Past infection (a): Usually shows both anti-HBs and anti-HBc positivity.

• Chronic carrier state (c): Characterized by HBsAg positivity, not anti-HBs.

• Early acute infection (d): Marked by HBsAg and IgM anti-HBc positivity; anti-HBs appears later.

The 20 nm spheres and filamentous structures observed in the blood of individuals infected with hepatitis B virus (HBV) are non-infectious circulating aggregates of hepatitis B surface antigen (HBsAg). These particles are produced in excess during viral replication and are composed of lipid and protein (HBsAg) but lack the viral genome and core components. They are not infectious because they do not contain the viral DNA or polymerase required for infection.

• a) Infectious: Incorrect, as these particles are not infectious due to the absence of viral nucleic acid.

• b) Circulating aggregates of HBeAg: Incorrect, as HBeAg (hepatitis B e-antigen) is a soluble protein, not particulate, and is not associated with these structures.

• d) Highly infectious when present in great abundance: Incorrect, as these particles remain non-infectious regardless of quantity. The infectious virion (Dane particle) is a larger, 42 nm double-shelled particle that contains the viral genome.

C3 is the central complement component common to both the classical and alternative pathways.

• In the classical pathway, C3 is cleaved by the C3 convertase (C4b2a).

• In the alternative pathway, C3 is cleaved by the C3 convertase (C3bBb).

This convergence at C3 activation leads to the formation of the membrane attack complex (MAC) via the terminal pathway (C5–C9). Other components:

• C1q (a): Unique to the classical pathway (initiates binding to antibodies).

• C2 (b): Part of the classical and lectin pathways.

• C5 (d): Activated after C3 in the terminal pathway.

The “Australia antigen” was the original name for HBsAg (hepatitis B surface antigen). It was discovered in 1965 by Dr. Baruch Blumberg in the blood of an Australian Aboriginal person and was later identified as the surface antigen of the hepatitis B virus. This landmark finding led to:

• Development of HBV diagnostics and screening.

• The first hepatitis B vaccine.

Other markers:

• HBeAg (a): Associated with viral replication.

• anti-HBc (c): Antibody to the core antigen.

• anti-HBs (d): Protective antibody against HBsAg.

Anti-HBs (antibody to hepatitis B surface antigen) is the specific test that indicates protective immunity after HBV vaccination. A positive anti-HBs test with a titer ≥10 mIU/mL confirms adequate immune response and protection against HBV infection. Other markers:

• anti-HBc IgM (a): Indicates acute infection (not related to vaccination).

• HBsAg (b): Indicates current infection (should be negative post-vaccination).

• HBeAg (d): Indicates active viral replication (irrelevant to vaccination).

The persistence of HBsAg (hepatitis B surface antigen) in serum for more than 6 months defines chronic hepatitis B infection. This indicates the immune system has failed to clear the virus, leading to long-term carriage and potential complications (e.g., cirrhosis, liver cancer). In contrast:

• Acute HBV (a): HBsAg is present but typically clears within 6 months.

• Immunity (c): Characterized by anti-HBs (with or without anti-HBc), not HBsAg.

• Recovery (d): HBsAg is negative, and anti-HBs appears.

For diagnosing congenital infections (e.g., syphilis, toxoplasmosis, CMV, rubella), the most reliable methods directly confirm infection in the neonate:

• Neonatal IgM detection: Pathogen-specific IgM antibodies do not cross the placenta, so their presence in the newborn indicates endogenous production (recent infection).

• PCR testing: Detects pathogen DNA/RNA (e.g., Treponema pallidum in congenital syphilis) with high specificity.

Other options are inadequate:

• Maternal serology (a): Only indicates maternal exposure, not fetal infection.

• Neonatal IgG (b): Passively transferred from mother; not diagnostic of congenital infection.

• Clinical signs (d): Supportive but nonspecific and may be absent at birth.

The Anti-Streptolysin O (ASO) antibody titer is the most common and standard serological test used to indicate a recent group A streptococcal infection (such as strep throat or scarlet fever). It measures the immune response to streptolysin O, a toxin produced by the bacteria. A rising ASO titer is a key diagnostic marker for post-streptococcal complications like rheumatic fever or glomerulonephritis.

In a precipitation reaction, both the antigen and antibody are initially soluble. When they combine in optimal proportions, they form insoluble immune complexes that precipitate out of solution. This is the basis for tests like:

• Radial immunodiffusion (e.g., Mancini method).

• Ouchterlony double diffusion.

• Immunoelectrophoresis.

Hepatitis D virus (HDV) is a defective RNA virus that cannot replicate on its own. It requires the presence of hepatitis B virus (HBV) to provide HBsAg (surface antigen) for its viral envelope and transmission. Without HBV, HDV cannot cause infection. In contrast:

• HAV (a): Independent picornavirus (RNA).

• HCV (b): Independent flavivirus (RNA).

• HEV (d): Independent hepevirus (RNA).

The prozone phenomenon (or hook effect) occurs when an excess of antibody interferes with the formation of antigen-antibody lattices, resulting in false-negative or weakly positive reactions. This is common in agglutination or precipitation tests (e.g., VDRL for syphilis). Key points:

• In antibody excess, each antigen molecule is saturated by antibodies, preventing cross-linking and visible clumping/precipitation.

• Diluting the sample resolves the prozone by reducing antibody concentration to optimal levels.

Other options:

• Antigen excess (a): Causes postzone phenomenon (also false negatives).

• Equivalence (c): Ideal for lattice formation and visible reaction.

• Complete precipitation (d): Occurs at equivalence, not prozone.

Hepatitis E virus (HEV) is associated with a high mortality rate (10–30%) in pregnant women, particularly during the third trimester. This is due to a higher risk of fulminant hepatic failure (acute liver failure) and other complications. In contrast:

• HAV (a): Generally mild in pregnancy; no increased mortality.

• HBV (b): Can cause chronic infection but no specific increased acute mortality in pregnancy.

• HCV (c): Chronic infection risk but no elevated acute mortality during pregnancy.

• gM anti-HBc: Appears during acute HBV infection and is a marker of recent infection.

• Chronic HBV: Typically IgM anti-HBc is absent, but IgG anti-HBc persists.

• anti-HBs: Indicates recovery or immunity.

• IgG anti-HBc: Persists for life, cannot distinguish acute vs chronic.

• HBeAg: Indicates viral replication, not infection timing.

IgG anti-HBc (antibody to the hepatitis B core antigen) persists for life and is a reliable marker of past or resolved HBV infection. It appears during the acute phase (after IgM anti-HBc) and remains detectable indefinitely, even after recovery. In contrast:

• IgM anti-HBc (a): Indicates recent acute infection (lasts ~6 months).

• HBeAg (c): A marker of active viral replication, not an antibody.

• HBsAg (d): Indicates current infection (acute or chronic); disappears upon recovery.

After infection with Epstein-Barr virus (EBV), the first antibody to appear is IgM against the viral capsid antigen (VCA-IgM). It becomes detectable during the acute phase of infectious mononucleosis and typically persists for 4–6 weeks. This makes it a key marker for diagnosing recent primary EBV infection.

Other markers appear later:

• VCA-IgG (a): Rises shortly after VCA-IgM and persists for life.

• EA (d): Early antigen antibodies appear in the acute phase but are less specific.

• EBNA (c): Antibodies to EBV nuclear antigen appear weeks to months after infection and indicate past infection/recovery.

Following a fetal infection with rubella (or any primary infection), the first class of antibodies produced is IgM. This is part of the initial humoral immune response. IgM antibodies are detectable early and are a marker of acute or recent infection. In the case of congenital rubella syndrome, the fetus produces IgM antibodies because the infection occurs before the full development of the immune system, and IgM is the first immunoglobulin to be synthesized.

• IgG (a) is produced later and indicates a matured immune response or past infection/memory response. It can cross the placenta, but in a primary fetal infection, IgM is the initial antibody generated.

• IgA (b) is primarily involved in mucosal immunity and is not the first antibody produced in a systemic fetal infection.

• Both IgG and IgA (d) is incorrect because IgA is not typically the initial response, and IgG production follows IgM.

HBeAg (hepatitis B e-antigen) is the antigen marker most closely associated with the transmissibility (infectivity) of HBV infection. Its presence indicates:

• High levels of viral replication,

• High viral load in the blood, and

• Increased infectivity (e.g., higher risk of perinatal transmission, sexual transmission, or blood-borne spread).

HBeAg is a soluble protein derived from the viral core and is secreted during active replication. Its detection correlates strongly with high transmissibility.

• a) HBsAg: While HBsAg (surface antigen) indicates active infection, it does not directly correlate with the degree of infectivity. Non-infectious HBsAg particles (spheres and filaments) are produced in large quantities.

• c) HBeAg: This appears to be a duplicate option (likely a typo); the correct choice is HBeAg.

• d) HBV: This is too vague; the virus itself is infectious, but HBeAg is the specific marker used clinically to assess transmissibility.

HCV RNA (detected by PCR) is the most reliable marker for ongoing hepatitis C infection. It directly measures viral replication and confirms active viremia. Key points:

• HCV RNA appears early (within 1–2 weeks post-exposure), before antibodies.

• It is used to diagnose active infection, monitor treatment response, and confirm viral clearance.

Other markers:

• anti-HCV IgM (a): Not routinely used; IgM is unreliable for HCV.

• HCV core antigen (c): Correlates with viremia but is less sensitive than RNA.

• anti-HCV IgG (d): Indicates exposure (past or current) but cannot differentiate resolved vs. ongoing infection.

The HBsAg (hepatitis B surface antigen) of HBV is utilized for:

• a) Diagnostic screening: It is the primary marker for detecting current HBV infection (acute or chronic) in blood tests.

• b) Immunization: The hepatitis B vaccine is composed of recombinant HBsAg, which stimulates protective anti-HBs antibodies.

• c) Carrier detection: Persistence of HBsAg for >6 months defines chronic carriage.

The most frequently used laboratory technique to diagnose and follow the course of therapy for secondary syphilis is the FTA-ABS (Fluorescent Treponemal Antibody Absorption) test, which is an indirect immunofluorescence assay. This test is highly sensitive and specific for detecting Treponema pallidum antibodies and is often used to confirm a diagnosis after a positive non-treponemal screening test.

Here’s why the other options are incorrect:

• a) Flocculation and b) Precipitation: These are types of non-treponemal tests (e.g., VDRL, RPR). While they are used for screening and monitoring treatment response (because antibody titers decline with therapy), they are less specific and not the most frequently used for definitive diagnosis of secondary syphilis. They are prone to false positives.

• c) Complement fixation: This is an older method (e.g., Wassermann test) that is largely obsolete and has been replaced by more modern techniques like immunofluorescence and ELISA.

• In the FTA-ABS (Fluorescent Treponemal Antibody Absorption) test, a smooth, uniform fluorescence of the treponemes indicates a true positive result.

• A beaded or speckled pattern of fluorescence is considered nonspecific and is reported as a false-positive reaction.

• That’s why FTA-ABS is used as a confirmatory treponemal test, but results must be interpreted carefully.

IgA is the most abundant immunoglobulin class on mucosal surfaces and in secretions (e.g., saliva, tears, breast milk, respiratory and gastrointestinal tracts). It exists primarily as:

• Secretory IgA (sIgA): A dimeric form linked by a J-chain and secretory component, which protects it from enzymatic degradation.

• Key role: Prevents pathogen attachment and invasion at mucosal entry points (first-line defense).

Other immunoglobulins:

• IgG (a): Most abundant in serum but not secretions.

• IgM (b): Pentamer; important in blood, less so in mucosa.

• IgE (d): Involved in allergies; low abundance everywhere.

In chronic hepatitis B infection, HBsAg (hepatitis B surface antigen) remains persistently positive (for more than 6 months), indicating ongoing infection and the carrier state. Other markers:

• anti-HBs (b): Typically negative in chronic infection (it appears only if the virus is cleared, which is rare in chronic cases).

• IgM anti-HBc (c): Usually negative; it is a marker of acute infection and declines over time.

• anti-HAV IgM (d): Not related to HBV; it indicates acute hepatitis A infection.

HBsAg (hepatitis B surface antigen) is the primary and earliest serological marker of active hepatitis B virus (HBV) infection. It appears in the blood during the incubation period, before symptoms or liver enzyme elevations, and indicates current infection (acute or chronic). Its detection is used for:

• Screening blood donations.

• Diagnosing HBV infection.

• Monitoring chronic carriers.

Other markers:

• anti-HBs (a): Indicates recovery/immunity (after infection or vaccination).

• anti-HBc (c): Appears during acute infection and persists for life; indicates past or current infection.

• HBeAg (d): Suggests high viral replication and infectivity, but is not the primary screening marker.

ELISA (Enzyme-Linked Immunosorbent Assay) is the method routinely used for detecting HBsAg due to its high sensitivity and specificity. It is capable of detecting very low levels of antigen, making it ideal for screening blood donations and diagnosing hepatitis B infections. Older methods like:

• Hemagglutination (a): Less sensitive and rarely used today.

• Counterimmunoelectrophoresis (b): Low sensitivity and obsolete.

• Radial immunodiffusion (c): Insensitive and slow.

Hepatitis B virus (HBV) is a DNA virus (hepadnavirus family), making it unique among the major hepatitis viruses. It has a partially double-stranded DNA genome. In contrast:

• HAV (a): Hepatitis A virus is an RNA virus (picornavirus).

• HCV (c): Hepatitis C virus is an RNA virus (flavivirus).

• HEV (d): Hepatitis E virus is an RNA virus (hepevirus).

The QuantiFERON-TB Gold test is an interferon-gamma release assay (IGRA) used to detect latent Mycobacterium tuberculosis infection. It measures the release of interferon-gamma (IFNγ) by sensitized T cells (specifically CD4+ and CD8+ T lymphocytes) in response to specific M. tuberculosis antigens (ESAT-6, CFP-10, and sometimes TB7.7). These antigens are not present in the BCG vaccine or most nontuberculous mycobacteria, making the test highly specific.

• Macrophages (b) may produce IFNγ but are not the primary cells measured in this assay.

• Neutrophils (c) and B cells (d) are not the source of IFNγ in this context; the test is designed to detect T-cell-mediated immunity.

In a direct immunofluorescence assay (DFA) to detect Legionella pneumophila, a primary antibody that is specific to Legionella antigens is directly conjugated to a fluorescent tag. This labeled antibody binds directly to the bacterium in the clinical sample, allowing it to be visualized under a fluorescence microscope.

Anti-HBs (antibody against hepatitis B surface antigen) is the specific serological marker that confirms immunity to hepatitis B virus. Its presence indicates either:

• Recovery from a past infection (with subsequent immunity), or

• Successful vaccination (where it is the only antibody produced).

A positive anti-HBs test (with adequate titer, typically ≥10 mIU/mL) confirms protective immunity. Other options:

• HBsAg (a): Indicates current active infection.

• IgM anti-HBc (c): Indicates recent acute infection.

• Hepatitis C Ag (d): Not related to HBV immunity; it’s a marker for hepatitis C virus.

• The patient sample (containing the target antigen) is mixed with a labeled antigen (e.g., enzyme-linked).

• Both compete for binding to a limited number of antibody sites coated on the plate.

• As patient antigen concentration increases, it outcompetes the labeled antigen, resulting in less labeled antigen bound to the antibody.

• After washing and substrate addition, the signal (e.g., color intensity) decreases proportionally to the patient antigen concentration.

This inverse relationship allows quantification of antigen levels (e.g., hormones, drugs). In contrast:

• Signal increase (a): Occurs in sandwich ELISA (for large antigens).

• No change (c): Suggests assay failure or saturation.

• Background only (d): Implies no competition or improper washing.

• anti-HBs (antibody to hepatitis B surface antigen) indicates recovery from a past HBV infection and the development of immunity. It is also the marker that appears after successful vaccination against hepatitis B.

• Viral DNA polymerase (a) is an enzyme involved in viral replication and is a marker of active viral replication, not immunity.

• HBe antigen (b) is a marker of active viral replication and high infectivity.

• HBsAg (d) (hepatitis B surface antigen) indicates an ongoing infection, either acute or chronic.

• IgM anti-HAV is the first antibody to appear during an acute hepatitis A virus (HAV) infection. It is detectable at the onset of symptoms and typically persists for about 3 to 6 months. Therefore, its presence is the best serological marker for diagnosing an acute HAV infection.

Here’s why the other options are incorrect:

• a) Presence of IgG antibodies to hepatitis A virus: IgG anti-HAV appears later in the infection and remains detectable for life, providing lifelong immunity. Its presence indicates a past infection or vaccination, not an acute one.

• c) Sharp decline in IgG antibodies to hepatitis A virus: IgG levels do not decline sharply during acute infection; they rise and then persist.

• d) Rise in both IgM and IgG antibodies to hepatitis A virus: While both may rise during acute infection, the specific and definitive indicator of an acute infection is the presence of IgM. The rise of IgG alone is not specific for acute disease.

Chemiluminescent immunoassays (CLIA) offer higher sensitivity and faster turnaround times compared to standard ELISA (enzyme-linked immunosorbent assay). This is because:

• Chemiluminescent substrates produce light signals that can be detected with very low background, allowing for a broader dynamic range and the ability to detect smaller amounts of analyte.

• Automated systems often used with CLIA enable rapid processing of sample

The measles vaccine is a live attenuated vaccine, meaning it contains a weakened form of the virus that cannot cause disease but stimulates a strong and lasting immune response. It is often combined with mumps and rubella vaccines (MMR). In contrast:

• Rabies (a) is typically an inactivated vaccine.

• Tetanus (b) is a toxoid vaccine (inactivated toxin).

• Hepatitis B (c) is a recombinant subunit vaccine.

• ANA testing: Commonly performed using indirect immunofluorescence (IIF) on HEp-2 cells, which allows visualization of antinuclear antibody patterns.

• ELISA: Can detect specific autoantibodies but is less commonly used for broad ANA screening.

• Agglutination & Western blot: Not standard for ANA detection.

• Secondary immune responses are faster, stronger, and more efficient because they are launched by memory B cells that were created during the primary response.

• These memory cells lead to a rapid production of large amounts of high-affinity IgG antibodies.

• The other options are incorrect because:

  • a) IgM is the first and main antibody of the primary response, not the secondary.

  • b) Secondary responses are faster, not slower.

  • d) IgA is produced, but it is not the only antibody; IgG is the dominant isotope in the secondary response. IgA is more associated with mucosal immunity.

Anti-HBs (antibodies against hepatitis B surface antigen) is the assay that confirms immune status to hepatitis B virus. The presence of anti-HBs indicates either:

1. Recovery from a past infection (with subsequent immunity), or

2. Successful vaccination (the hepatitis B vaccine is designed to elicit anti-HBs).

• HBsAg (a): This detects the presence of the hepatitis B surface antigen and indicates an active infection (acute or chronic), not immunity.

• IgM anti-HBc (c): This antibody against the hepatitis B core antigen is a marker of acute infection (recent exposure), not immunity.

• Hepatitis C Ag (d): This is unrelated to hepatitis B immunity; it detects hepatitis C virus antigen.

Hepatitis E virus (HEV) is strongly associated with zoonotic transmission, particularly from:

• Pigs and wild boars, which serve as reservoirs.

• Consumption of undercooked pork or game meat.

HEV genotypes 3 and 4 are common in developed countries and linked to animal-to-human transmission. In contrast:

• HAV (a): Primarily human-specific (fecal-oral route).

• HBV (b) and HCV (c): Human-specific (blood/body fluids).

IgM anti-HAV is the best serological marker for acute hepatitis A virus (HAV) infection. It appears early in infection, peaks during the acute illness, and typically becomes undetectable within 3–6 months. Its presence confirms recent or acute infection. In contrast:

• IgG anti-HAV (a): Indicates past infection or vaccination and persists for life, but does not differentiate acute from resolved infection.

• A sharp decline in IgG (c): Not characteristic; IgG rises and remains stable.

• A rise in both IgM and IgG (d): While both may rise, IgM alone is specific for acute infection.

• Chronic carriers of HBV are defined by the persistent presence of HBsAg in their blood for more than six months. They continue to harbor and carry the virus, often for life.

Here’s why the other options are incorrect:

• a) Have chronic symptoms of hepatitis: This is not always true. Many chronic carriers are asymptomatic and may have no signs of liver disease, though they are still at risk for long-term complications like cirrhosis and liver cancer.

• c) Do not transmit infection: This is false. Chronic carriers can transmit the virus to others through blood, sexual contact, or from mother to child during childbirth.

• d) Carry HBV but are not infectious: This is incorrect. While infectivity can vary (e.g., it is higher if HBeAg is positive and lower if anti-HBe is positive), carriers are still potentially infectious. The presence of HBsAg itself is a marker of potential infectivity.

Hepatitis E virus (HEV) closely resembles hepatitis A virus (HAV) in several key aspects:

• Transmission: Both are primarily spread via the fecal-oral route (contaminated water/food).

• Clinical course: Typically cause acute, self-limiting hepatitis (no chronic infection).

• Virology: Both are single-stranded RNA viruses (HAV is a picornavirus; HEV is a hepevirus).

In contrast:

• HBV (a): DNA virus, blood/sexual transmission, can become chronic.

• HCV (c): RNA virus, blood-borne, often chronic.

• HDV (d): Defective RNA virus, requires HBV coinfection.

The serologic pattern described—disappearance of HBsAg and HBeAg, persistence of anti-HBc, and appearance of anti-HBs and anti-HBe—is classic for the recovery phase of acute hepatitis B virus (HBV) infection.

This pattern contrasts with:

• a) Early acute HBV hepatitis: Characterized by presence of HBsAg, HBeAg, and IgM anti-HBc (anti-HBs and anti-HBe are absent).

• b) Early convalescent phase: HBsAg and HBeAg may still be detectable while anti-HBe appears; anti-HBs is not yet present.

• d) Carrier state: Persistence of HBsAg (and often HBeAg) without anti-HBs or anti-HBe development.

Chronic active hepatitis B is characterized by persistent infection. The pattern shows:

• HBsAg positive: Indicates ongoing infection.

• IgM anti-HBc negative: Rules out recent acute infection (IgM is for acute phase).

• anti-HBc positive: Confirms past or chronic infection (IgG anti-HBc).

• anti-HBs negative: No protective immunity (vaccination or clearance); the virus is still present.

The yellow fever vaccine is a live attenuated vaccine made from the weakened 17D strain of the yellow fever virus. It provides long-lasting immunity with a single dose. In contrast:

• Hepatitis B (a): Recombinant subunit vaccine (HBsAg protein).

• Rabies (b): Typically inactivated (killed) virus vaccine.

• Tetanus (d): Toxoid vaccine (inactivated toxin).

The CSF-VDRL (Cerebrospinal Fluid-Venereal Disease Research Laboratory) test is the recommended serological test for detecting syphilis antibodies in cerebrospinal fluid. It is a non-treponemal flocculation test specifically adapted for use with CSF and is the only test universally accepted for diagnosing neurosyphilis. A positive CSF-VDRL is highly specific for neurosyphilis, though it may lack sensitivity (meaning a negative result does not entirely rule out neurosyphilis).

Here’s why the other options are incorrect:

• a) Non-treponemal antibody: This is a category of tests (e.g., VDRL, RPR) but not a specific test name. The standard non-treponemal test for CSF is the CSF-VDRL.

• c) FTA-ABS (Fluorescent Treponemal Antibody Absorption): While the FTA-ABS test is highly sensitive for treponemal antibodies, the CSF FTA-ABS is not recommended for routine diagnosis of neurosyphilis. It is overly sensitive and can yield false positives due to blood contamination or passive antibody transfer from serum, making it unreliable for confirming neurosyphilis.

• d) MHA-TP (Microhemagglutination Assay for Treponema pallidum): This is a treponemal test used for serum confirmation, but it is not validated or recommended for use with cerebrospinal fluid.

• Hepatitis C (HCV) has a high rate of chronic infection (approximately 55-85% of infected individuals), which can lead to chronic hepatitis, cirrhosis, and hepatocellular carcinoma.

• In contrast, Hepatitis A (HAV) does not result in a chronic carrier state; infection is always acute and self-limiting, with lifelong immunity after recovery.

Here’s why the other options are incorrect:

• a) Has a highly stable incubation period: The incubation period for HCV (2 weeks to 6 months) is actually quite variable, similar to HAV (15-50 days). Neither is “highly stable.”

• b) Is associated with a high incidence of icteric hepatitis: HCV infection is often subclinical or anicteric (without jaundice). Only about 20-30% of acute HCV cases present with jaundice, whereas HAV more commonly causes icteric illness (especially in adults).

• d) Is seldom implicated in cases of posttransfusion hepatitis: This is false. Before widespread screening, HCV was a major cause of post-transfusion hepatitis. It is now routinely screened for in blood donations to prevent transmission.

• ELISA is the routinely used test for the detection of hepatitis B surface antigen (HBsAg) due to its high sensitivity and specificity. It is a widely available, cost-effective, and automated method that can detect very low levels of HBsAg, making it ideal for screening blood donations and diagnosing infections.

Here’s why the other options are incorrect:

• a) Hemagglutination: This method is less sensitive and specific compared to ELISA and is not routinely used for HBsAg detection.

• b) Counterimmunoelectrophoresis: This is an older, less sensitive technique that has been largely replaced by more advanced methods like ELISA.

• c) Radial immunodiffusion: This method is relatively insensitive and slow, and it is not suitable for routine screening of HBsAg.

Hepatitis D virus (HDV) is a defective RNA virus that requires the presence of hepatitis B virus (HBV) to replicate and cause infection. HDV uses the HBsAg (hepatitis B surface antigen) produced by HBV to form its own viral coat and infect liver cells. Therefore, HDV can only occur as:

• A coinfection (simultaneous infection with HBV and HDV), or

• A superinfection (HDV infecting a person already chronically infected with HBV).

This serological pattern describes the resolution of an acute HBV infection:

• Disappearance of HBsAg and HBeAg: Indicates clearance of the virus and end of active replication.

• Persistence of anti-HBc: Remains as a lifelong marker of past infection.

• Appearance of anti-HBs: Confirms immunity and recovery.

• Appearance of anti-HBe: Suggorts reduction in viral replication.

• Rheumatoid factor (RF): An IgM antibody that binds the Fc portion of IgG.

• In serological assays (e.g., ELISA, indirect tests), RF can bind IgG antibodies nonspecifically, leading to false-positive results.

• Enhancing specificity or causing false negatives: Not typical effects.

• No effect: Incorrect; RF can interfere significantly in some assays.

For Lyme disease diagnosis, the Western blot is used as a confirmatory test after an initial positive or equivocal ELISA (or IFA) screening. This two-tier testing approach is recommended by the CDC:

• First tier: ELISA (or IFA) for high sensitivity.

• Second tier: Western blot for high specificity, detecting antibodies against multiple Borrelia burgdorferi antigens (e.g., OspC, p41, p93).

Other options:

• ELISA (a): Sensitive but prone to false positives (used for screening, not confirmation).

• RPR (b): For syphilis, not Lyme disease.

• IFA (d): Similar to ELISA; used in some labs but less standardized.

• Hepatitis A virus (HAV):

  • A non-enveloped RNA virus, making it more resistant to heat, acids, and detergents compared with enveloped viruses.

• HBV, HCV, HEV: Enveloped (except HEV is partially non-enveloped), generally more sensitive to heat and detergents.

Vertical transmission (mother to child during childbirth) is most common with hepatitis B virus (HBV). Without prophylaxis, the risk can be as high as 90% if the mother is HBeAg-positive. This is a major route of HBV endemicity. In contrast:

• HAV (a): Rarely vertically transmitted; primarily fecal-oral.

• HCV (c): Vertical transmission occurs but at a lower rate (~5-10%).

• HEV (d): Vertical transmission can occur (with high fetal mortality) but is not as common as with HBV.

Hepatitis C virus (HCV) is an RNA virus belonging to the Flaviviridae family (genus Hepacivirus). It is characterized by:

• A single-stranded, positive-sense RNA genome.

• High genetic variability, contributing to chronicity and vaccine challenges.

In contrast:

• HAV (a): RNA virus from Picornaviridae family.

• HBV (b): DNA virus from Hepadnaviridae family.

• HEV (d): RNA virus from Hepeviridae family.

For diagnosis of late latent or tertiary syphilis, the FTA-ABS (Fluorescent Treponemal Antibody Absorption) test is the most appropriate assay. This is because:

• Treponemal tests (like FTA-ABS) remain positive for life in most patients, even after treatment, and are highly sensitive in all stages of syphilis.

• Non-treponemal tests (like RPR or VDRL) may become non-reactive or show low titers in late latent or tertiary syphilis due to a declining antibody response, leading to false negatives.

Here’s why the other options are incorrect:

• a) RPR (Rapid Plasma Reagin) and b) VDRL (Venereal Disease Research Laboratory): These are non-treponemal tests. They are useful for screening and monitoring treatment response but lack sensitivity in late stages. Up to 30% of patients with tertiary syphilis may be non-reactive with these tests.

• d) FTA-ABS IgM: This test detects IgM antibodies, which are typically present in early or acute infection. In late latent or tertiary syphilis, IgM levels are often low or absent, making this test less reliable for diagnosis at this stage.

The first stage of Lyme disease (early localized infection) caused by Borrelia burgdorferi is characterized by the erythema migrans (EM) rash, which typically appears 3–30 days after a tick bite (not within 4–6 hours). Patients often have no other symptoms or only mild flu-like symptoms. The rash gradually expands and can persist for weeks if untreated (not just 7–10 days). Serologic testing is usually negative early in the infection because antibodies have not yet developed; it becomes positive weeks later. Thus, option b is accurate as patients may be asymptomatic aside from the rash.

• a) Incorrect: Rash develops days to weeks post-bite, not hours.

• c) Incorrect: Rash can last weeks, not just 7–10 days.

• d) Incorrect: Serology is often negative in the first week; it takes 2–4 weeks for antibodies to appear.

• Neutralization assays:

  • Measure the ability of antibodies in serum to inhibit the infectivity of a virus or toxin.

  • Reflect functional, protective immunity rather than just the presence of antibodies.

• Measuring antigen concentration or total antibody levels: Done by ELISA or similar assays.

• Detecting autoantibodies: Done by ANA tests or specific autoimmune assays.

Interferon gamma (IFNγ) is the hallmark cytokine produced by Th1 cells (T helper type 1 cells). Th1 cells are involved in cell-mediated immunity, activating macrophages and promoting responses against intracellular pathogens (e.g., Mycobacterium tuberculosis, Leishmania).

• Interleukin-4 (IL-4) (a) is associated with Th2 cells, which drive humoral immunity and allergic responses.

• Interleukin-5 (IL-5) (c) is also produced by Th2 cells and is involved in eosinophil activation.

• Interferon alpha (IFNα) (d) is a type I interferon produced by various cells (e.g., plasmacytoid dendritic cells) in response to viral infections, not specifically by Th1 cells

Serum is the most common sample type used in serological tests for antibody detection because:

• It is free of fibrinogen, clotting factors, and cells (unlike plasma or whole blood), reducing interference.

• It contains high concentrations of antibodies after centrifugation of clotted blood.

• It is standardized for most immunoassays (e.g., ELISA, chemiluminescence).

Other samples:

• Plasma (a): Contains anticoagulants that may affect some assays.

• Whole blood (b): Used in rapid tests but less common for lab-based serology.

• Urine (d): Not typical for antibody detection; used for certain antigens (e.g., Legionella) but not standard serology.

IgM is the most effective immunoglobulin at agglutination (clumping) of particulate antigens (e.g., bacteria, red blood cells) due to its:

• Pentameric structure (10 antigen-binding sites),

• High valence (ability to bind multiple antigens simultaneously),

• Large size, which facilitates rapid formation of antigen-antibody complexes.

IgM is also the first antibody produced in a primary immune response, making it critical for early defense. Other immunoglobulins:

• IgG (a): Monomeric; less efficient at agglutination but important in secondary responses.

• IgA (c): Dimeric; mainly protects mucosal surfaces.

• IgE (d): Involved in allergies and parasitic infections.

Albumin is not an acute phase reactant. In fact, its levels decrease during acute inflammation (negative acute phase reactant). Acute phase reactants are proteins whose plasma concentrations increase (positive) or decrease (negative) in response to inflammation. Key examples:

• Positive acute phase reactants:

  • C-reactive protein (CRP) (a): Rapidly increases.

  • Fibrinogen (b): Promotes clotting and rises.

  • Haptoglobin (d): Binds free hemoglobin and increases.

• Negative acute phase reactants (decrease):

  • Albumin (c): Synthesized less during inflammation, leading to lower levels.

The incubation period for hepatitis E virus (HEV) typically ranges from 2 to 9 weeks, with an average of about 40 days. This period reflects the time from exposure (e.g., consuming contaminated water) to the onset of symptoms. In contrast:

• 2–4 days (b): Typical for short-incubation pathogens like norovirus.

• 30–180 days (c): Characteristic of hepatitis B virus (HBV).

• 15–20 hours (d): Too short; seen in toxins or bacterial food poisoning.

Biological false-positive (BFP) VDRL reactions occur when the test is positive in the absence of syphilis. These are frequently encountered in patients with autoimmune diseases, particularly systemic lupus erythematosus (SLE). The false positivity is due to the presence of autoantibodies (e.g., against cardiolipin) that react with the lipoidal antigen used in the non-treponemal test.

Here’s why the other options are less likely or incorrect:

• b) Acquired immune deficiency syndrome (AIDS): While HIV patients may have a higher prevalence of syphilis, biological false positives are not frequently associated with AIDS itself. However, autoimmune phenomena can occur in HIV, but SLE is a more classic association.

• c) Gonorrhea: This bacterial STI does not typically cause biological false-positive VDRL reactions. Co-infections with syphilis may occur, but gonorrhea itself is not a common cause of BFP.

• d) Tertiary syphilis: In tertiary syphilis, the VDRL may be negative or weakly positive due to a declining antibody response, but this is not a false positive—it is a true positive (if detected) or a false negative. BFP reactions are unrelated to actual syphilis infection.

Superinfection with hepatitis D virus (HDV) in a person who is already a chronic HBV carrier frequently leads to fulminant hepatitis (severe acute liver failure) or a rapid worsening of liver disease. This occurs because:

• HDV causes direct cytopathic damage to liver cells.

• It accelerates liver inflammation and fibrosis, overwhelming the already compromised organ.

Outcomes are often severe, including high mortality, rather than recovery (a), immunity (c), or mild infection (d). Superinfection poses a greater risk than coinfection (simultaneous HBV+HDV infection).

Fulminant hepatitis (acute liver failure) is most commonly associated with HDV (hepatitis D virus) co-infection or superinfection with HBV. Hepatitis D is a defective virus that requires HBV to replicate, and the combination often leads to more severe disease, including a higher risk of rapid liver failure. While other viruses can cause fulminant hepatitis:

• HAV (a) and HEV (b): Can cause acute liver failure but less frequently than HDV+HBV.

• HCV (c): Rarely causes fulminant hepatitis on its own.

Hemagglutination inhibition (HAI) tests rely on the principle that specific antibodies in a patient’s serum can block (inhibit) the agglutination of red blood cells (RBCs) by a viral antigen. For example:

• Viruses like influenza or measles can naturally agglutinate RBCs.

• If patient serum contains antibodies against the virus, they bind to the virus and prevent it from agglutinating RBCs.

• No agglutination = positive inhibition (antibodies are present).

• Agglutination = negative inhibition (no antibodies).

The incubation period for hepatitis A virus (HAV) is typically 15 to 50 days, with an average of about 28–30 days. This range (15–45 days) reflects the time from exposure to the onset of symptoms. In contrast:

• HBV has a longer incubation (30–180 days).

• HCV ranges from 2 weeks to 6 months.

• Short periods like 2–4 days (c) or 7–10 days (d) are typical for other infections (e.g., influenza), not hepatitis.

The incubation period for hepatitis C virus (HCV) ranges widely from 2 weeks to 6 months (approximately 14 days to 26 weeks), with an average of about 6–9 weeks. This variability is due to factors like viral dose and host immunity. In contrast:

• 2–4 days (a): Typical for influenza or common cold viruses.

• 15–45 days (b): Characteristic of hepatitis A virus (HAV).

• 1–2 years (d): Not applicable to acute HCV; resembles chronic diseases.

The “window period” in hepatitis B virus (HBV) infection is a brief phase during the resolution of acute infection where:

• HBsAg has become undetectable (cleared by the immune system).

• anti-HBs has not yet risen to detectable levels.

• The only serological marker of infection is anti-HBc (particularly IgM anti-HBc initially, then IgG).

This gap between HBsAg disappearance and anti-HBs appearance is the “window period.” Diagnosis during this time relies on detecting anti-HBc.

A heterophile antigen is a type of antigen that is found in two or more unrelated species (e.g., humans and certain animals like sheep or horses) and is capable of inducing a cross-reacting immune response. The most classic example is the Paul-Bunnell antigen in Epstein-Barr virus (mononucleosis) infection, where antibodies produced against the virus also react with sheep red blood cells.

Why not the others?

• a) Auto-antigen → self-antigen (not heterophile).

• c) Anamnestic response → secondary immune response (memory), unrelated.

• d) Adjuvant → substance that enhances immune response, not an antigen type.

• The enzyme-linked immunosorbent assay (ELISA) is used as the initial screening test. If it is positive or equivocal, a confirmatory test is performed.

• The Western blot is the immunoblot test recommended by the CDC as the second step to confirm the diagnosis. It detects antibodies to specific proteins (bands) of Borrelia burgdorferi .

• This two-tiered approach is designed to maintain high specificity and avoid false positives, though sensitivity can be limited, especially in early stages of the disease

The Mantoux test (tuberculin skin test) for Mycobacterium tuberculosis is a classic example of a Type IV (delayed-type) hypersensitivity reaction. This cell-mediated immune response involves T-cells and macrophages, rather than antibodies. After intradermal injection of purified protein derivative (PPD), a localized induration (hard swelling) typically appears at the injection site within 48–72 hours if the person has been previously sensitized to the antigen. This delayed timeline is characteristic of Type IV hypersensitivity.

• Type I (immediate) hypersensitivity involves IgE antibodies and allergens (e.g., allergies).

• Type II hypersensitivity involves IgG/IgM antibodies attacking cell surfaces (e.g., hemolytic anemia).

• Type III hypersensitivity involves immune complex deposition (e.g., serum sickness).

• Nontreponemal antibodies (reagins) produced in response to host tissue damage (e.g., cardiolipin-lecithin-cholesterol antigens) caused by Treponema pallidum infection.

• It is not specific for treponemal antigens but is used for initial screening due to its sensitivity.

In contrast:

• Direct antigens (a): Detected via PCR or dark-field microscopy.

• Specific anti-Treponema antibodies (b): Detected by treponemal tests (e.g., FTA-ABS, TP-PA).

• Treponema pallidum DNA (d): Detected by molecular methods (e.g., PCR).