Serious & Notifiable Infections — MCQs
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In the UK, which one of the following baseline investigations is NOT routinely required before initiating standard first-line anti-tuberculosis therapy with rifampicin, isoniazid, pyrazinamide, and ethambutol?
A 48-year-old man from Nepal who has been living in the UK for 6 months presents with a 12-week history of progressive lower back pain, night sweats, and weight loss. He reports difficulty walking due to pain. On examination, he has tenderness over the L2-L3 vertebrae and reduced power (4/5) in both lower limbs. MRI spine shows destruction of L2 and L3 vertebral bodies with a paravertebral abscess. What is the most appropriate next step in investigation to establish the diagnosis?
A 26-year-old man presents to the emergency department with an 8-hour history of severe headache, fever, vomiting, and photophobia. On examination, he has temperature 39.2°C, heart rate 118/min, blood pressure 105/68 mmHg, and a purpuric non-blanching rash on his trunk and legs. He is confused with GCS 13/15 (E3, V4, M6). Blood tests show: WBC 18.2 × 10⁹/L, CRP 156 mg/L, platelets 98 × 10⁹/L, APTT 42 seconds, fibrinogen 1.2 g/L. What is the most appropriate immediate management?
A 44-year-old woman with rheumatoid arthritis managed with methotrexate and adalimumab has been diagnosed with latent tuberculosis infection based on a positive interferon-gamma release assay (IGRA) and normal chest X-ray. She is started on rifampicin and isoniazid for 3 months as preventive therapy. Her adalimumab was discontinued 4 weeks before starting TB treatment. When would it be most appropriate to restart her adalimumab therapy?
What is the primary immunological mechanism by which adjunctive dexamethasone therapy reduces mortality in adult patients with acute bacterial meningitis caused by Streptococcus pneumoniae?
A 55-year-old man is diagnosed with smear-positive pulmonary tuberculosis. Molecular testing using GeneXpert MTB/RIF confirms Mycobacterium tuberculosis but shows rifampicin resistance. He is started on an appropriate MDR-TB regimen. His 8-year-old daughter, who lives with him and has had close daily contact for the past 3 months, is asymptomatic with a normal clinical examination. Her Mantoux test shows 12 mm induration. Chest X-ray is normal. What is the most appropriate management for the daughter?
A 38-year-old man from Romania presents with a 10-week history of headache, vomiting, and personality change. He is known to be HIV-positive but has not been taking antiretroviral therapy. His CD4 count is 55 cells/mm³. Lumbar puncture shows: opening pressure 26 cmH2O, glucose 2.1 mmol/L (serum 5.8 mmol/L), protein 2.4 g/L, white cells 180/mm³ (80% lymphocytes). India ink staining is positive. MRI brain shows multiple small enhancing lesions in the basal ganglia. What is the most appropriate initial antifungal therapy?
A 67-year-old man with a cochlear implant presents with a 12-hour history of fever, severe headache, and confusion. Lumbar puncture shows: opening pressure 32 cmH2O, white cells 2800/mm³ (95% neutrophils), protein 2.8 g/L, glucose 1.2 mmol/L (serum glucose 6.4 mmol/L). Gram stain shows Gram-positive diplococci. Blood cultures are pending. Which empirical antibiotic regimen should be started immediately?
According to UK Public Health notification requirements and clinical management protocols, which one of the following scenarios requires notification to the local Health Protection Team within the shortest timeframe?
A 35-year-old man with HIV infection (CD4 count 80 cells/mm³, not on antiretroviral therapy) is diagnosed with tuberculous meningitis. He is started on rifampicin, isoniazid, pyrazinamide, ethambutol, and dexamethasone. Five days after starting tuberculosis treatment, antiretroviral therapy (ART) is initiated with tenofovir, emtricitabine, and dolutegravir. Two weeks later, he develops worsening confusion, new onset right hemiparesis, and deteriorating Glasgow Coma Scale. Repeat CT head shows new enhancing lesions and increased oedema. What is the most likely explanation for his clinical deterioration?
Serious & Notifiable Infections UK Medical PG Practice Questions and MCQs
Question 61: In the UK, which one of the following baseline investigations is NOT routinely required before initiating standard first-line anti-tuberculosis therapy with rifampicin, isoniazid, pyrazinamide, and ethambutol?
- A. Liver function tests (ALT, AST, bilirubin)
- B. Renal function (urea, creatinine, eGFR)
- C. Visual acuity and colour vision assessment using Ishihara charts
- D. Chest X-ray
- E. Serum uric acid level (Correct Answer)
Explanation: ***Serum uric acid level*** - While **pyrazinamide** is known to cause **hyperuricaemia** and can potentially trigger gout, routine measurement of **serum uric acid** is not recommended as a baseline investigation in UK guidelines. - Uric acid levels are only typically monitored if the patient develops **clinical symptoms of gout** or has pre-existing risk factors during the course of treatment. *Liver function tests (ALT, AST, bilirubin)* - Baseline **liver function tests** are mandatory because **rifampicin**, **isoniazid**, and **pyrazinamide** are all potentially **hepatotoxic**. - Establishing a baseline is critical for monitoring the development of **drug-induced hepatitis** and managing treatment interruptions if enzymes rise significantly. *Renal function (urea, creatinine, eGFR)* - **Renal function** must be assessed because **ethambutol** is primarily cleared by the kidneys and requires **dose adjustment** in cases of impairment. - Maintaining correct dosing is vital as renal dysfunction increases the risk of **ethambutol-related optic neuritis** toxicity. *Visual acuity and colour vision assessment using Ishihara charts* - Formal documentation of **visual acuity** and **Ishihara colour vision** is mandatory before starting **ethambutol** to detect baseline deficits. - These baseline results are essential for identifying early **optic neuritis**, a known side effect that warrants immediate cessation of the drug. *Chest X-ray* - A **chest X-ray** is a fundamental baseline investigation used to document the **extent of disease** and identifying cavitary lesions. - It serves as the primary radiological reference to evaluate **treatment response** and resolution of infection over the 6-month therapy period.
Question 62: A 48-year-old man from Nepal who has been living in the UK for 6 months presents with a 12-week history of progressive lower back pain, night sweats, and weight loss. He reports difficulty walking due to pain. On examination, he has tenderness over the L2-L3 vertebrae and reduced power (4/5) in both lower limbs. MRI spine shows destruction of L2 and L3 vertebral bodies with a paravertebral abscess. What is the most appropriate next step in investigation to establish the diagnosis?
- A. Sputum sample for acid-fast bacilli smear and culture
- B. CT-guided biopsy of the vertebral lesion for histology and microbiological culture (Correct Answer)
- C. Mantoux tuberculin skin test
- D. Blood cultures for Mycobacterium tuberculosis
- E. Serum inflammatory markers (ESR and CRP) and trial of anti-tuberculosis therapy
Explanation: ***CT-guided biopsy of the vertebral lesion for histology and microbiological culture***- A tissue diagnosis is essential to confirm **Pott's disease (spinal TB)** and rule out mimics like **malignancy** or **pyogenic osteomyelitis** before starting long-term treatment.- Biopsy allows for **histological examination** (caseating granulomas), **GeneXpert** testing, and **drug susceptibility testing**, which is vital given the risk of **MDR-TB**.*Sputum sample for acid-fast bacilli smear and culture*- This investigation assesses for **pulmonary TB**, which may not be present or active in cases of isolated **extrapulmonary spinal tuberculosis**.- A negative sputum result does not rule out the diagnosis, especially since the patient presents primarily with **spinal involvement** and neurological signs.*Mantoux tuberculin skin test*- The **Mantoux test** measures immune reactivity but cannot distinguish between **latent TB infection** and **active disease**.- It has limited diagnostic value in a patient from an **endemic region** (Nepal) who may have had prior **BCG vaccination** or exposure.*Blood cultures for Mycobacterium tuberculosis*- **M. tuberculosis** is rarely isolated from blood cultures unless the patient has **miliary TB** or is severely **immunocompromised** (e.g., HIV).- This method has a very **low diagnostic yield** for focal spinal infections compared to direct tissue sampling.*Serum inflammatory markers (ESR and CRP) and trial of anti-tuberculosis therapy*- While **ESR and CRP** are often elevated, they are **non-specific** and cannot confirm the underlying cause of vertebral destruction.- Starting **empirical therapy** without a tissue diagnosis is inappropriate due to the risk of **drug toxicity** and the failure to identify **resistant strains**.
Question 63: A 26-year-old man presents to the emergency department with an 8-hour history of severe headache, fever, vomiting, and photophobia. On examination, he has temperature 39.2°C, heart rate 118/min, blood pressure 105/68 mmHg, and a purpuric non-blanching rash on his trunk and legs. He is confused with GCS 13/15 (E3, V4, M6). Blood tests show: WBC 18.2 × 10⁹/L, CRP 156 mg/L, platelets 98 × 10⁹/L, APTT 42 seconds, fibrinogen 1.2 g/L. What is the most appropriate immediate management?
- A. Perform lumbar puncture immediately to confirm the diagnosis before starting any treatment
- B. Administer intravenous ceftriaxone 2 g immediately without delay, defer lumbar puncture (Correct Answer)
- C. Arrange urgent CT head before lumbar puncture, then start antibiotics after CSF obtained
- D. Administer intravenous aciclovir and await viral PCR results
- E. Administer intravenous benzylpenicillin and perform lumbar puncture after 2 hours of antibiotics
Explanation: ***Administer intravenous ceftriaxone 2 g immediately without delay, defer lumbar puncture*** - The patient presents with a severe headache, fever, photophobia, confusion (GCS 13), and a **purpuric non-blanching rash**, strongly suggestive of **meningococcal sepsis** with meningitis, which is a life-threatening emergency requiring immediate broad-spectrum antibiotics. - **Lumbar puncture** is contraindicated due to signs of **raised intracranial pressure** (altered GCS) and a significant **coagulopathy** (low platelets, prolonged APTT, low fibrinogen), which increase the risk of brain herniation or spinal hematoma. *Perform lumbar puncture immediately to confirm the diagnosis before starting any treatment* - Delaying **antibiotic administration** for a diagnostic procedure like lumbar puncture significantly increases mortality in suspected **bacterial meningitis/sepsis**. - Performing an LP in a patient with altered mental status and **coagulopathy** carries a high risk of adverse events, including **brain herniation** and **spinal hematoma**. *Arrange urgent CT head before lumbar puncture, then start antibiotics after CSF obtained* - Obtaining a **CT head** and then a **lumbar puncture** would cause critical delays in administering **life-saving antibiotics**, which must be given immediately in suspected meningococcal disease. - While a CT scan may be indicated to rule out mass lesions before LP if no contraindications exist, it should never delay the prompt administration of **empiric antibiotics**. *Administer intravenous aciclovir and await viral PCR results* - **Aciclovir** is an antiviral agent used for conditions like **Herpes Simplex Encephalitis**, but the prominent **purpuric rash** and rapid progression to sepsis strongly indicate a **bacterial etiology**, such as *Neisseria meningitidis*. - Awaiting viral PCR results before initiating definitive treatment for suspected bacterial meningitis is inappropriate and could be fatal due to the rapid progression of the disease. *Administer intravenous benzylpenicillin and perform lumbar puncture after 2 hours of antibiotics* - While **benzylpenicillin** is effective against *Neisseria meningitidis*, **ceftriaxone** is generally preferred in the hospital setting for its broader coverage against other potential bacterial meningitis pathogens, such as *Streptococcus pneumoniae*. - The decision to perform a lumbar puncture should be based on the resolution of contraindications (e.g., improved GCS, corrected coagulopathy), not on a fixed time interval after starting antibiotics.
Question 64: A 44-year-old woman with rheumatoid arthritis managed with methotrexate and adalimumab has been diagnosed with latent tuberculosis infection based on a positive interferon-gamma release assay (IGRA) and normal chest X-ray. She is started on rifampicin and isoniazid for 3 months as preventive therapy. Her adalimumab was discontinued 4 weeks before starting TB treatment. When would it be most appropriate to restart her adalimumab therapy?
- A. After completing 1 month of TB preventive therapy (Correct Answer)
- B. Immediately, as concurrent treatment is safe
- C. After 2 weeks of TB preventive therapy
- D. After completing the full 3-month course of TB preventive therapy
- E. After 6 months, regardless of completion of TB treatment
Explanation: ***After completing 1 month of TB preventive therapy*** - For patients with **latent tuberculosis infection (LTBI)**, current guidelines recommend starting **anti-TNF therapy** (like adalimumab) after at least **one month** of appropriate preventive treatment has been completed. - This duration ensures a sufficient reduction in the **mycobacterial load** and provides protection against the reactivation of TB once **immunosuppression** is reintroduced. *Immediately, as concurrent treatment is safe* - Starting biologics immediately increases the risk of **TB reactivation** before the preventive antibiotics have had time to work. - **TNF-alpha inhibitors** are potent immunosuppressants that can worsen an underlying latent infection into **disseminated disease** if not preceded by treatment. *After 2 weeks of TB preventive therapy* - Two weeks is considered an **insufficient duration** to achieve the clinical consensus for safety when reintroducing high-potency biologics. - Guidelines specifically advocate for the **4-week (1 month) threshold** to mitigate the risk of developing active tuberculosis. *After completing the full 3-month course of TB preventive therapy* - While this is safe, it is **unnecessarily restrictive** and delays the management of the patient's **rheumatoid arthritis**. - Delaying biological therapy for three months can lead to significant **joint damage** and disease flares that could have been avoided by restarting after the first month. *After 6 months, regardless of completion of TB treatment* - This timeframe is **arbitrary and inconsistent** with clinical standards for managing LTBI in patients on biologics. - Waiting six months would pose an extreme and unnecessary risk to the patient's **rheumatological health** without offering additional benefit over the standard 1-month rule.
Question 65: What is the primary immunological mechanism by which adjunctive dexamethasone therapy reduces mortality in adult patients with acute bacterial meningitis caused by Streptococcus pneumoniae?
- A. Direct antimicrobial activity through disruption of bacterial cell wall synthesis
- B. Reduction of inflammatory cytokine release and attenuation of subarachnoid space inflammatory response (Correct Answer)
- C. Enhancement of antibiotic penetration across the blood-brain barrier through increased vascular permeability
- D. Stimulation of neutrophil recruitment to improve bacterial clearance from cerebrospinal fluid
- E. Blockade of bacterial adhesion molecules preventing further CNS invasion
Explanation: ***Reduction of inflammatory cytokine release and attenuation of subarachnoid space inflammatory response*** - Dexamethasone, a corticosteroid, primarily acts by **suppressing the exaggerated inflammatory response** in the subarachnoid space. - It reduces the production and release of **pro-inflammatory cytokines** (e.g., TNF-α, IL-1β) that are triggered by bacterial components and lysis, thereby attenuating cerebral edema and neuronal damage. *Direct antimicrobial activity through disruption of bacterial cell wall synthesis* - Dexamethasone is a **glucocorticoid** and possesses no direct **antimicrobial properties** or ability to disrupt bacterial cell walls. - **Antibiotics** are responsible for bacterial clearance, while dexamethasone modulates the host's inflammatory response. *Enhancement of antibiotic penetration across the blood-brain barrier through increased vascular permeability* - Dexamethasone actually works to **stabilize the blood-brain barrier** and reduce its permeability, thereby **decreasing** rather than increasing vascular permeability. - This can potentially decrease the penetration of some antibiotics, but its overall benefit in reducing inflammation outweighs this effect. *Stimulation of neutrophil recruitment to improve bacterial clearance from cerebrospinal fluid* - Corticosteroids like dexamethasone generally **reduce inflammation** by inhibiting the recruitment and activity of immune cells, including neutrophils. - The primary mechanism of bacterial clearance is through **antibiotic therapy**, not enhanced neutrophil activity due to corticosteroids. *Blockade of bacterial adhesion molecules preventing further CNS invasion* - Dexamethasone does not act by blocking **bacterial adhesion molecules** or directly preventing the invasion of the central nervous system. - Its role is centered on modulating the host's immune response to **already established infection** within the subarachnoid space.
Question 66: A 55-year-old man is diagnosed with smear-positive pulmonary tuberculosis. Molecular testing using GeneXpert MTB/RIF confirms Mycobacterium tuberculosis but shows rifampicin resistance. He is started on an appropriate MDR-TB regimen. His 8-year-old daughter, who lives with him and has had close daily contact for the past 3 months, is asymptomatic with a normal clinical examination. Her Mantoux test shows 12 mm induration. Chest X-ray is normal. What is the most appropriate management for the daughter?
- A. Observe with clinical review in 3 months and repeat chest X-ray
- B. BCG vaccination
- C. Isoniazid monotherapy for 6 months
- D. Rifampicin and isoniazid for 3 months
- E. Specialist referral for individualized MDR-TB contact prophylaxis regimen (Correct Answer)
Explanation: ***Specialist referral for individualized MDR-TB contact prophylaxis regimen*** - The daughter has **Latent TB Infection (LTBI)**, indicated by a **positive Mantoux test (12mm induration)** in a high-risk contact (child living with an active TB case), with a **normal chest X-ray**. - Her father has **rifampicin-resistant pulmonary TB (MDR-TB)**, meaning standard LTBI prophylaxis (e.g., isoniazid monotherapy) is likely ineffective. Therefore, an **individualized regimen** based on the source case's drug susceptibility testing is crucial, necessitating **specialist consultation**. *Observe with clinical review in 3 months and repeat chest X-ray* - **Passive observation** is insufficient for a child, especially one exposed to **MDR-TB** and having a **positive Mantoux test**, due to their significantly higher risk of progression from LTBI to **active TB disease**. - Delaying effective prophylaxis increases the risk of developing severe forms of active TB, such as **TB meningitis** or **miliary TB**, which are more common and devastating in young children. *BCG vaccination* - **BCG vaccination** is primarily a prevention strategy for uninfected individuals, particularly infants in high-burden settings, and is **contraindicated** in someone with **latent TB infection** (positive Mantoux). - Administering BCG to an individual with a positive Mantoux test provides no additional benefit against existing infection and can cause unnecessary local reactions. *Isoniazid monotherapy for 6 months* - **Isoniazid monotherapy** is the standard for drug-susceptible LTBI, but the source patient has **MDR-TB**, which by definition includes resistance to at least **isoniazid** and **rifampicin**. - Administering **isoniazid alone** when the infecting strain is likely resistant would be ineffective, providing **no prophylactic benefit** and potentially fostering further drug resistance. *Rifampicin and isoniazid for 3 months* - This combined regimen is a common choice for drug-susceptible LTBI, but the father's TB is confirmed as **rifampicin-resistant** by molecular testing (GeneXpert). - Using drugs (specifically **rifampicin** and **isoniazid**) to which the source strain is resistant makes the prophylaxis **ineffective** and exposes the child to medication side effects without any protective benefit.
Question 67: A 38-year-old man from Romania presents with a 10-week history of headache, vomiting, and personality change. He is known to be HIV-positive but has not been taking antiretroviral therapy. His CD4 count is 55 cells/mm³. Lumbar puncture shows: opening pressure 26 cmH2O, glucose 2.1 mmol/L (serum 5.8 mmol/L), protein 2.4 g/L, white cells 180/mm³ (80% lymphocytes). India ink staining is positive. MRI brain shows multiple small enhancing lesions in the basal ganglia. What is the most appropriate initial antifungal therapy?
- A. Intravenous amphotericin B and oral flucytosine for 2 weeks, followed by oral fluconazole (Correct Answer)
- B. Oral fluconazole 400 mg daily for 8 weeks
- C. Intravenous caspofungin 70 mg loading dose then 50 mg daily
- D. Intravenous voriconazole 6 mg/kg twice daily for 2 doses, then 4 mg/kg twice daily
- E. Oral itraconazole 200 mg twice daily
Explanation: ***Intravenous amphotericin B and oral flucytosine for 2 weeks, followed by oral fluconazole*** - The patient presents with **Cryptococcal meningitis**, confirmed by severe immunosuppression (**CD4 count 55 cells/mm³**), classic CSF findings (low glucose, high protein, lymphocytic pleocytosis), and a **positive India ink stain**.- The recommended **induction therapy** for cryptococcal meningitis in HIV-positive patients is a combination of **amphotericin B** and **flucytosine** for at least 2 weeks, followed by oral fluconazole for consolidation. *Oral fluconazole 400 mg daily for 8 weeks* - **Fluconazole monotherapy** is insufficient for the **initial induction phase** of cryptococcal meningitis, especially in severely immunocompromised patients.- Using fluconazole alone for induction leads to **slower CSF sterilization** and higher mortality rates compared to combination therapy.*Intravenous caspofungin 70 mg loading dose then 50 mg daily* - **Caspofungin**, an echinocandin, has **no significant clinical activity** against *Cryptococcus neoformans*. - Echinocandins primarily target fungal cell walls of *Candida* and *Aspergillus*, not *Cryptococcus*.*Intravenous voriconazole 6 mg/kg twice daily for 2 doses, then 4 mg/kg twice daily* - While **voriconazole** has some *in vitro* activity against *Cryptococcus*, it is **not a first-line therapy** for cryptococcal meningitis. - Its efficacy for this condition has not been shown to be superior to **amphotericin B-based regimens**, making it an alternative for refractory cases only.*Oral itraconazole 200 mg twice daily* - **Itraconazole** exhibits **poor central nervous system (CNS) penetration**, rendering it largely ineffective for treating cryptococcal meningitis. - It is not recommended for either the **induction** or **consolidation phases** of treatment due to its inferior efficacy and limited CSF levels.
Question 68: A 67-year-old man with a cochlear implant presents with a 12-hour history of fever, severe headache, and confusion. Lumbar puncture shows: opening pressure 32 cmH2O, white cells 2800/mm³ (95% neutrophils), protein 2.8 g/L, glucose 1.2 mmol/L (serum glucose 6.4 mmol/L). Gram stain shows Gram-positive diplococci. Blood cultures are pending. Which empirical antibiotic regimen should be started immediately?
- A. Intravenous ceftriaxone 2 g twice daily
- B. Intravenous ceftriaxone 2 g twice daily and vancomycin 15-20 mg/kg twice daily (Correct Answer)
- C. Intravenous benzylpenicillin 2.4 g every 4 hours and gentamicin 5-7 mg/kg once daily
- D. Intravenous meropenem 2 g three times daily
- E. Intravenous ceftriaxone 2 g twice daily and metronidazole 500 mg three times daily
Explanation: ***Intravenous ceftriaxone 2 g twice daily and vancomycin 15-20 mg/kg twice daily*** - The patient's presentation with fever, headache, confusion, and classic CSF findings (elevated pressure, high neutrophils, high protein, low glucose) points to bacterial meningitis, likely caused by **Streptococcus pneumoniae** (Gram-positive diplococci). - The presence of a **cochlear implant** is a significant risk factor for infection with **penicillin-resistant** and **cephalosporin-resistant *S. pneumoniae***, necessitating the addition of **vancomycin** to ceftriaxone for adequate empirical coverage. *Intravenous ceftriaxone 2 g twice daily* - While **ceftriaxone** is a cornerstone for bacterial meningitis, its use as monotherapy is insufficient for empirical treatment in patients at high risk for resistant strains, such as those with **cochlear implants**. - Without **vancomycin**, there is a critical gap in coverage for highly drug-resistant **pneumococci**, which can lead to treatment failure and increased mortality. *Intravenous benzylpenicillin 2.4 g every 4 hours and gentamicin 5-7 mg/kg once daily* - **Benzylpenicillin** alone is inadequate as empirical therapy for meningitis in a patient with a **cochlear implant** due to the high prevalence of **penicillin-resistant *S. pneumoniae*** in this population. - **Gentamicin** provides poor penetration into the **cerebrospinal fluid (CSF)** and is not effective against Gram-positive organisms like *S. pneumoniae* in meningitis treatment. *Intravenous meropenem 2 g three times daily* - **Meropenem** is a broad-spectrum carbapenem with excellent CSF penetration, but it is typically reserved for meningitis caused by highly resistant Gram-negative bacteria or in cases of treatment failure. - For suspected pneumococcal meningitis with risk factors for resistance, the combination of **ceftriaxone and vancomycin** is the preferred empirical regimen due to its targeted coverage and stewardship principles. *Intravenous ceftriaxone 2 g twice daily and metronidazole 500 mg three times daily* - **Metronidazole** provides coverage against **anaerobic bacteria**, which are not typically the primary cause of meningitis presenting with Gram-positive diplococci unless there is an associated brain abscess or chronic ear infection. - This regimen lacks the crucial **vancomycin** component, leaving the patient vulnerable to potentially **drug-resistant *Streptococcus pneumoniae***, especially given the presence of a cochlear implant.
Question 69: According to UK Public Health notification requirements and clinical management protocols, which one of the following scenarios requires notification to the local Health Protection Team within the shortest timeframe?
- A. A 45-year-old man with culture-confirmed pulmonary tuberculosis who completed 2 weeks of standard treatment
- B. A 28-year-old woman with a positive interferon-gamma release assay (IGRA) and normal chest X-ray diagnosed with latent tuberculosis infection
- C. A 19-year-old university student with suspected meningococcal meningitis presenting to the emergency department with fever, headache, and non-blanching purpuric rash (Correct Answer)
- D. A 52-year-old man with confirmed Mycobacterium avium complex (MAC) pulmonary infection
- E. A 34-year-old woman with confirmed viral meningitis secondary to enterovirus on CSF PCR
Explanation: ***A 19-year-old university student with suspected meningococcal meningitis presenting to the emergency department with fever, headache, and non-blanching purpuric rash*** - **Meningococcal disease** is a flagship notifiable condition because it carries significant risk for **rapid outbreaks**, high mortality, and requires **immediate public health action** (chemoprophylaxis for contacts). - Notification must occur **urgently** (usually by telephone) as soon as the diagnosis is suspected, even before **microbiological confirmation** or laboratory results are available. *A 45-year-old man with culture-confirmed pulmonary tuberculosis who completed 2 weeks of standard treatment* - While **active tuberculosis** is a notifiable disease in the UK, it generally requires notification within **3 days** rather than the immediate urgency of meningococcal cases. - Notification usually happens upon **diagnosis**; once the patient has completed two weeks of treatment, they are generally considered **non-infectious** to the public. *A 28-year-old woman with a positive interferon-gamma release assay (IGRA) and normal chest X-ray diagnosed with latent tuberculosis infection* - **Latent tuberculosis infection (LTBI)** is not included in the statutory list of notifiable diseases under UK Public Health regulations. - Notification is only required for **active disease** where there is a risk of transmission or a requirement for collective monitoring. *A 52-year-old man with confirmed Mycobacterium avium complex (MAC) pulmonary infection* - Unlike *M. tuberculosis*, **Mycobacterium avium complex (MAC)** consists of environmental organisms that are not transmitted **person-to-person**. - Because there is no **public health risk** of transmission, non-tuberculous mycobacteria infections are not classified as **notifiable diseases**. *A 34-year-old woman with confirmed viral meningitis secondary to enterovirus on CSF PCR* - **Viral meningitis** is typically not on the statutory list of notifiable diseases in the UK; the regulations specifically emphasize **bacterial meningitis** due to its severity. - While the pathogen (enterovirus) may be monitored via laboratory reporting, it does not trigger the same **immediate clinical notification** pathway as **Neisseria meningitidis**.
Question 70: A 35-year-old man with HIV infection (CD4 count 80 cells/mm³, not on antiretroviral therapy) is diagnosed with tuberculous meningitis. He is started on rifampicin, isoniazid, pyrazinamide, ethambutol, and dexamethasone. Five days after starting tuberculosis treatment, antiretroviral therapy (ART) is initiated with tenofovir, emtricitabine, and dolutegravir. Two weeks later, he develops worsening confusion, new onset right hemiparesis, and deteriorating Glasgow Coma Scale. Repeat CT head shows new enhancing lesions and increased oedema. What is the most likely explanation for his clinical deterioration?
- A. Drug-resistant tuberculosis with treatment failure
- B. Tuberculous meningitis-associated immune reconstitution inflammatory syndrome (IRIS) (Correct Answer)
- C. Dexamethasone-induced hyperglycaemia causing cerebral oedema
- D. Progressive multifocal leukoencephalopathy
- E. Isoniazid-induced hepatic encephalopathy
Explanation: ***Tuberculous meningitis-associated immune reconstitution inflammatory syndrome (IRIS)*** - Paradoxical **TB-IRIS** occurs due to a restored immune response against mycobacterial antigens shortly after starting **ART**, especially in patients with a low **CD4 count** (<100 cells/mm³). - Clinical deterioration with **new enhancing lesions** and worsening cerebral oedema 2 weeks after ART initiation is classic for **CNS-IRIS**, often requiring high-dose **corticosteroids**. *Drug-resistant tuberculosis with treatment failure* - Clinical failure due to **drug resistance** typically presents as a gradual lack of improvement or slow decline rather than sudden **neurological deterioration** immediately following ART. - The timing of this patient's collapse specifically matches the **immune recovery** phase rather than the expected progression of resistant TB. *Dexamethasone-induced hyperglycaemia causing cerebral oedema* - While **dexamethasone** can cause significant **hyperglycaemia**, it does not typically result in focal **enhancing brain lesions** or focal deficits like hemiparesis. - Steroids are actually the primary treatment to **reduce cerebral oedema** in CNS TB; their use should theoretically prevent, not cause, these radiological changes. *Progressive multifocal leukoencephalopathy* - **PML** (caused by JC virus) usually presents as **non-enhancing**, white matter lesions without significant mass effect or widespread oedema. - It is a condition of **severe immunosuppression** rather than an inflammatory worsening triggered by the initiation of ART and TB treatment. *Isoniazid-induced hepatic encephalopathy* - **Isoniazid** toxicity would manifest with **elevated liver enzymes**, jaundice, and potentially asterixis, rather than **focal neurological deficits** and new brain lesions. - **Hepatic encephalopathy** causes global cerebral dysfunction and diffuse oedema on imaging, not localized **enhancing masses** or hemiparesis.
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