Infectious Diseases Practice Questions

Q: What is the most characteristic clinical finding in a patient with tetanus?

Masseter spasm. **Explanation:** **Tetanus** is caused by the neurotoxin **tetanospasmin** produced by *Clostridium tetani* [1]. The toxin blocks the release of inhibitory neurotransmitters (GABA and glycine) from Renshaw cells in the spinal cord, leading to unopposed muscle contraction and spasms. **Why Masseter Spasm is correct:** **Trismus**, or "lockjaw" due to **masseter spasm**, is the most characteristic and often the earliest presenting sign of generalized tetanus. The masseter muscles are highly sensitive to the toxin, leading to the classic facial expression known as **risus sardonicus** (a fixed, sardonic grin). **Analysis of Incorrect Options:** * **Option A:** The incubation period for tetanus typically ranges from **3 to 21 days** (average 8 days). A shorter incubation period is generally associated with more severe disease and a poorer prognosis. * **Option C:** Isolation of *C. tetani* from a wound is **not required** for diagnosis. The organism is recovered in only about 33% of cases, and its presence does not prove tetanus (as it can be present without toxin production). The diagnosis is strictly **clinical**. * **Option D:** CSF examination in tetanus is typically **normal**. Elevated protein is more characteristic of conditions like Guillain-Barré Syndrome, which is a common differential for acute weakness, not spasticity. **NEET-PG High-Yield Pearls:** * **Spatula Test:** Touching the oropharynx with a spatula triggers a reflex contraction of the jaw (positive result) instead of a gag reflex; it has high specificity for tetanus. * **Autonomic Instability:** This is the leading cause of death in modern intensive care settings (labile BP, tachycardia, hyperpyrexia). * **Management:** Neutralize unbound toxin with **Human Tetanus Immune Globulin (HTIG)** and use **Metronidazole** as the preferred antibiotic.

Q: A 30-year-old HIV positive patient presents with fever, dyspnoea and non-productive cough. The patient is cyanosed. His chest X-ray reveals bilateral, symmetrical interstitial infiltrates. What is the most likely diagnosis?

Pneumocystis jirovecii pneumonia. ### Explanation **Pneumocystis jirovecii Pneumonia (PCP)** is the most common opportunistic infection in HIV patients with a CD4 count <200 cells/µL. **Why Option C is Correct:** The clinical triad of **fever, progressive dyspnoea, and non-productive cough** in an HIV-positive patient is classic for PCP [1]. The presence of **cyanosis** and exercise-induced desaturation is common due to significant alveolar-capillary block. Radiologically, the hallmark is **bilateral, symmetrical perihilar interstitial infiltrates** (ground-glass opacities), which matches the description provided [1]. **Why Other Options are Incorrect:** * **A. Tuberculosis:** Usually presents with a productive cough, hemoptysis, and weight loss. Radiologically, it typically shows focal infiltrates, cavitary lesions (in the upper lobes), or miliary patterns rather than symmetrical interstitial infiltrates [1]. * **B. Cryptococcosis:** Primarily presents as meningitis in HIV patients. Pulmonary involvement is less common and usually manifests as well-defined nodules or pleural effusions . * **C. Toxoplasmosis:** Most commonly affects the CNS, presenting with seizures or focal neurological deficits and "ring-enhancing lesions" on MRI. Pulmonary toxoplasmosis is rare and clinically indistinguishable from PCP, but PCP is statistically much more likely . **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Definitive diagnosis is made via **Gomori Methenamine Silver (GMS) stain** of induced sputum or Bronchoalveolar Lavage (BAL), showing "crushed ping-pong ball" cysts [1]. * **Lab Marker:** Elevated **Serum LDH** levels are highly sensitive but non-specific for PCP. * **Treatment:** **DOC is IV Trimethoprim-Sulfamethoxazole (TMP-SMX)** [1]. * **Steroid Indication:** Add Prednisone if $PaO_2 35$ mmHg to prevent respiratory failure triggered by dying organisms [1].

Q: HIV post-exposure prophylaxis can be given up to what duration?

72 hours. **Explanation:** The correct answer is **72 hours**. Post-exposure prophylaxis (PEP) is a medical intervention aimed at preventing HIV infection after a potential exposure (e.g., needle-stick injury, sexual assault). **Why 72 hours is correct:** The effectiveness of PEP is highly time-dependent. The goal is to initiate antiretroviral therapy (ART) before the virus can disseminate from the initial site of entry to the regional lymph nodes and establish a systemic infection. Clinical guidelines and animal models indicate that the window of opportunity for PEP is **up to 72 hours**. Beyond this timeframe, the virus is likely to have integrated into the host genome, making PEP significantly less effective or ineffective. **Analysis of Incorrect Options:** * **A, B, and C (1-2, 14, and 18 hours):** While PEP is most effective when started as soon as possible (ideally within **2 hours**), these options are incorrect because they represent the "ideal" window rather than the "maximum" duration. PEP is still recommended and indicated up to the 72-hour mark. **High-Yield Clinical Pearls for NEET-PG:** * **Ideal Timing:** "The sooner, the better." Ideally within 2 hours of exposure. * **Duration of Treatment:** Once started, PEP must be continued for a total of **28 days**. * **Standard Regimen (NACO/WHO):** Usually a 3-drug regimen (e.g., Tenofovir + Lamivudine + Dolutegravir). * **Testing Protocol:** Baseline HIV testing is mandatory for the exposed person. Follow-up testing is typically done at 6 weeks, 3 months, and sometimes 6 months. * **Contraindication:** PEP is not indicated if the source person is confirmed to be HIV-negative.

Q: What is the typical C.S.F. cell count range in tubercular meningitis?

100 to 499. ### Explanation **Correct Answer: B (100 to 499)** Tubercular Meningitis (TBM) typically presents with a **lymphocytic pleocytosis** of moderate intensity [1]. In TBM, the CSF cell count usually ranges between **100 and 500 cells/mm³**. While the count can occasionally reach up to 1000, it rarely exceeds this threshold. The predominant cell type is lymphocytes, though an early "neutrophilic shift" may be seen in the hyperacute phase. **Analysis of Options:** * **Option A (0 to 99):** This range is too low. While viral meningitis or partially treated bacterial meningitis can sometimes fall here, TBM typically elicits a more robust inflammatory response. * **Option C (500 to 999):** While possible in severe TBM, this is less common than the 100–500 range. This range is more characteristic of fungal meningitis (like Cryptococcus) or severe viral encephalitis. * **Option D (1000 to 5000):** This range is diagnostic of **Acute Pyogenic (Bacterial) Meningitis**, where the response is predominantly neutrophilic [2]. TBM almost never reaches these high levels. **NEET-PG High-Yield Pearls for TBM:** 1. **CSF Biochemistry:** Characterized by **markedly low glucose** (<40 mg/dL or <ratio of 0.5) and **very high protein** (often 100–500 mg/dL) [2]. 2. **Cobweb Coagulum:** If CSF is left standing, a "pellicle" or cobweb formation may occur due to high fibrinogen levels. 3. **Basal Meningitis:** TBM typically involves the base of the brain [3]; look for **cranial nerve palsies** (CN VI is most common) and hydrocephalus on imaging [2]. 4. **Adenosine Deaminase (ADA):** An ADA level >10 U/L in CSF is highly suggestive of TBM in the appropriate clinical context.

Q: A patient with undulating fever presents with features of encephalitis. He is treated successfully with doxycycline and rifampicin. What is the most probable diagnosis?

Brucellosis. ### Explanation **Correct Answer: A. Brucellosis** The clinical triad of **undulating fever** (fever that rises and falls like a wave), neurological involvement (**neurobrucellosis** presenting as encephalitis), and a dramatic response to **Doxycycline and Rifampicin** is classic for Brucellosis. Brucellosis is a zoonotic infection caused by *Brucella* species (e.g., *B. melitensis* from goats/sheep). It is an intracellular pathogen, necessitating drugs with good intracellular penetration. While osteoarticular involvement is the most common complication, neurobrucellosis occurs in 5–10% of cases and can manifest as meningitis or encephalitis [1]. The WHO-recommended regimen for uncomplicated brucellosis is Doxycycline + Rifampicin for 6 weeks; however, for neurobrucellosis, treatment is often extended and may include a third drug like Ceftriaxone [1]. **Why other options are incorrect:** * **B. Bordetella pertussis:** Causes "Whooping Cough." It presents with paroxysmal cough and post-tussive vomiting, not undulating fever or encephalitis. The treatment of choice is Macrolides (Azithromycin). * **C. Francisella tularensis:** Causes Tularemia. While it is zoonotic, it typically presents with ulceroglandular disease or oculoglandular syndromes. The drug of choice is Streptomycin or Gentamicin. * **D. Mycoplasma:** Causes "Walking Pneumonia." While it can have extrapulmonary manifestations, it does not present with an undulating fever pattern. **High-Yield Clinical Pearls for NEET-PG:** * **Most common source:** Consumption of unpasteurized dairy products or contact with infected livestock. * **Gold Standard Diagnosis:** Bone marrow culture (more sensitive than blood culture) [1]. * **Serology:** Standard Agglutination Test (SAT); titers >1:160 are significant [1]. * **Rose Bengal Test:** Used as a rapid screening tool. * **Castaneda Medium:** A specialized biphasic medium used for culturing *Brucella*.

Q: What is the recommended treatment for CMV retinitis in an AIDS patient?

Valganciclovir. **Explanation:** **CMV Retinitis** is the most common opportunistic ocular infection in patients with AIDS, typically occurring when the CD4+ T-cell count falls below **50 cells/mm³**. It is characterized by a "pizza-pie" or "cheese and ketchup" fundus appearance due to retinal necrosis and hemorrhage. **Why Valganciclovir is correct:** The mainstay of treatment for CMV retinitis is anti-CMV agents that inhibit viral DNA polymerase. **Valganciclovir** (an oral prodrug of Ganciclovir) is the preferred treatment because it offers high oral bioavailability, achieving plasma levels comparable to intravenous Ganciclovir. It is used for both induction and maintenance therapy, significantly reducing the pill burden and the need for indwelling catheters. **Why the other options are incorrect:** * **Amantadine:** An antiviral used primarily for Influenza A and Parkinson’s disease; it has no activity against CMV. * **Fludarabine:** A purine analog chemotherapy agent used in the treatment of chronic lymphocytic leukemia (CLL), not an antiviral. * **Oseltamivir:** A neuraminidase inhibitor used specifically for the treatment and prophylaxis of Influenza A and B. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Oral Valganciclovir is the first-line treatment. For sight-threatening lesions (near the macula or optic nerve), **Intravitreal Ganciclovir or Foscarnet** may be added. * **Alternative Agents:** Foscarnet and Cidofovir (used if there is resistance or systemic toxicity). * **Side Effects:** Ganciclovir/Valganciclovir can cause **bone marrow suppression** (neutropenia), while Foscarnet is notably **nephrotoxic**. * **HAART:** Initiation of Highly Active Antiretroviral Therapy is crucial for long-term management to restore immune function.

Q: Diagnosis of acute viral hepatitis A is primarily established by which of the following findings?

Variable increase in transaminase levels.. **Explanation:** The diagnosis of **Acute Viral Hepatitis A (HAV)** relies on a combination of clinical presentation, biochemical markers of liver injury, and serological confirmation. **Why the correct answer is right:** In acute viral hepatitis, the hallmark biochemical finding is a **variable increase in serum transaminases (ALT and AST)**. These enzymes are released into the bloodstream due to hepatocellular necrosis and inflammation. In symptomatic cases, these levels typically exceed 500 U/L and can often reach into the thousands. The degree of elevation is "variable" because it depends on the timing of the test relative to the onset of symptoms and the severity of the hepatic insult. **Analysis of Incorrect Options:** * **Option A:** While hepatic injury is present, "significant" is subjective. Transaminase levels do not always correlate linearly with the degree of liver cell necrosis or the ultimate prognosis. * **Option C:** **IgG anti-HAV** indicates past infection or immunity (post-vaccination). It is **not** used to diagnose acute infection. The gold standard serological marker for acute HAV is **IgM anti-HAV**. * **Option D:** An absence of a rise in transaminases would effectively rule out acute viral hepatitis, as these are the primary indicators of active liver inflammation. **NEET-PG High-Yield Pearls:** * **Route of Transmission:** Fecal-oral (most common). * **Incubation Period:** 15–45 days (Average: 4 weeks). * **Serology:** **IgM anti-HAV** is the diagnostic marker of choice for acute infection. It appears at the onset of symptoms and persists for 3–6 months. * **Prognosis:** HAV is typically self-limiting and **never** progresses to chronic hepatitis. * **Complication:** The most feared (though rare) complication is **Fulminant Hepatic Failure**, especially in patients with underlying chronic liver disease.

Q: What is the empirical treatment for pneumococcal meningitis?

Vancomycin + ceftriaxone. The empirical treatment for suspected bacterial meningitis must cover the most common and aggressive pathogens, primarily *Streptococcus pneumoniae* and *Neisseria meningitidis* [2]. **1. Why Option D is Correct:** The current standard of care for empirical treatment of pneumococcal meningitis is the combination of **Vancomycin plus a third-generation cephalosporin (Ceftriaxone or Cefotaxime)** [1]. This is due to the rising global prevalence of penicillin-resistant and cephalosporin-resistant *S. pneumoniae* [1]. Vancomycin provides synergistic coverage against highly resistant strains, while Ceftriaxone offers excellent CSF penetration and covers *N. meningitidis* and *H. influenzae* [1]. **2. Why Other Options are Incorrect:** * **Option A (Penicillin G):** While historically the drug of choice, it is no longer used empirically due to widespread high-level penicillin resistance in *S. pneumoniae*. It is only used if the isolate is proven to be susceptible. * **Options B & C (Doxycycline/Tetracycline):** These are bacteriostatic agents and have poor penetration into the cerebrospinal fluid (CSF). They are not indicated for the treatment of acute bacterial meningitis. **3. NEET-PG High-Yield Pearls:** * **Dexamethasone:** Should be administered **before or with the first dose** of antibiotics to reduce neurological sequelae (like hearing loss) caused by the inflammatory response to bacterial lysis [2]. * **Listeria Coverage:** If the patient is >50 years old or immunocompromised, **Ampicillin** must be added to the regimen to cover *Listeria monocytogenes* [2]. * **Ceftriaxone Caution:** Avoid Ceftriaxone in neonates; use Cefotaxime instead to prevent biliary sludging and kernicterus. * **Drug of Choice (DOC):** Once sensitivity results are back, if the strain is penicillin-susceptible, Penicillin G becomes the DOC.

Q: A 34-year-old person presents with rapidly developing cough, dyspnea, expectoration, and blood-tinged sputum. The patient is febrile, cyanosed, and appears toxic. Chest examination reveals crepitations and rhonchi. What is the most likely diagnosis?

Pneumonic plague. **Explanation:** The clinical presentation of **rapidly developing** respiratory distress, blood-tinged (watery/frothy) sputum, and a highly toxic state in a febrile patient is classic for **Pneumonic Plague**, caused by *Yersinia pestis*. **Why Pneumonic Plague is correct:** Pneumonic plague is the most severe and fatal form of the disease. It has a very short incubation period (1–3 days) and progresses aggressively. Key diagnostic features include sudden onset of fever, cyanosis, and the production of **blood-tinged (hemoptysis)** or "prune-juice" sputum. It is highly infectious, spreading via respiratory droplets, and leads to death within 24–48 hours if untreated. **Why other options are incorrect:** * **Legionella:** Typically presents as "atypical pneumonia" with high fever, hyponatremia, and often diarrhea. It does not usually cause such a rapid, toxic decline or frank hemoptysis. * **Septicemic Plague:** This is a systemic infection where the bacteria multiply in the blood. While it causes DIC and necrosis (Black Death), it does not primarily present with cough and expectoration unless it leads to secondary pneumonia. * **Pulmonary Tuberculosis:** This is a **chronic** infection. While it causes cough and hemoptysis, it does not present with "rapidly developing" symptoms or an acute toxic state over hours/days. **High-Yield Clinical Pearls for NEET-PG:** * **Causative Agent:** *Yersinia pestis* (Gram-negative coccobacillus showing **bipolar staining** or "safety-pin appearance" with Wayson/Giemsa stain). * **Virulence Factors:** V and W antigens, F1 capsular antigen. * **Drug of Choice:** **Streptomycin** (Gentamicin is an alternative; Doxycycline for prophylaxis). * **Public Health:** It is a mandatory reportable disease under International Health Regulations.

Question 1

What is the most characteristic clinical finding in a patient with tetanus?

Accepted Answer

Masseter spasm

Answer

Incubation period of 2-3 days

Answer

Isolation of Clostridium tetani from the wound

Answer

Cerebrospinal fluid examination showing elevated protein

Question 2

A 30-year-old HIV positive patient presents with fever, dyspnoea and non-productive cough. The patient is cyanosed. His chest X-ray reveals bilateral, symmetrical interstitial infiltrates. What is the most likely diagnosis?

Accepted Answer

Pneumocystis jirovecii pneumonia

Answer

Tuberculosis

Answer

Cryptococcosis

Answer

Toxoplasmosis

Question 3

A 45-year-old male with a history of unprotected sexual intercourse 15 years ago presents with what pupillary condition?

Accepted Answer

Accommodation reflex positive, and pupillary reaction negative

Answer

Accommodation reflex negative, and pupillary reaction positive

Answer

Accommodation reflex positive, and pupillary reaction positive

Answer

Accommodation reflex negative, and pupillary reaction negative

Question 4

HIV post-exposure prophylaxis can be given up to what duration?

Accepted Answer

72 hours

Answer

1-2 hours

Answer

14 hours

Answer

18 hours

Question 5

What is the typical C.S.F. cell count range in tubercular meningitis?

Accepted Answer

100 to 499

Answer

0 to 99

Answer

500 to 999

Answer

1000 to 5000

Question 6

A patient with undulating fever presents with features of encephalitis. He is treated successfully with doxycycline and rifampicin. What is the most probable diagnosis?

Accepted Answer

Brucellosis

Answer

Bordetella pertussis

Answer

Francisella tularensis

Answer

Mycoplasma

Question 7

What is the recommended treatment for CMV retinitis in an AIDS patient?

Accepted Answer

Valganciclovir

Answer

Amantadine

Answer

Fludrabine

Answer

Oseltamivir

Question 8

Diagnosis of acute viral hepatitis A is primarily established by which of the following findings?

Accepted Answer

Variable increase in transaminase levels.

Answer

Significant hepatic injury indicated by transaminase levels.

Answer

Detection of IgG anti-HAV antibodies.

Answer

Absence of any rise in transaminase levels.

Question 9

What is the empirical treatment for pneumococcal meningitis?

Accepted Answer

Vancomycin + ceftriaxone

Answer

Penicillin G

Answer

Doxycycline

Answer

Tetracycline

Question 10

A 34-year-old person presents with rapidly developing cough, dyspnea, expectoration, and blood-tinged sputum. The patient is febrile, cyanosed, and appears toxic. Chest examination reveals crepitations and rhonchi. What is the most likely diagnosis?

Accepted Answer

Pneumonic plague

Answer

Legionella

Answer

Septicemic plague

Answer

Pulmonary tuberculosis

Infectious Diseases — MCQs

Infectious Diseases — MCQs

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