Medical Mycology Q&A Section B — MCQ Bank OmpathStudy

Medical Virology — Section B: Short Answer Questions Unit: MBMM 3300 Medical Virology & Mycology MBChB Year 3 --- --- Q: In what respect do mycoses caused by true pathogenic fungi differ from mycoses caused by fungi associated with opportunistic infections? What are the general consequences of these infections to the human host? A: True Pathogenic Fungi cause disease in healthy, immunocompetent individuals. They possess intrinsic virulence factors that allow them to overcome normal host defenses. Infection is primarily by inhalation of conidia from an environmental source. Examples include Histoplasma capsulatum , Coccidioides immitis , and Blastomyces dermatitidis . Opportunistic Fungi cause disease only in immunocompromised hosts — HIV/AIDS patients, transplant recipients, diabetics, or those on prolonged corticosteroids. They have low intrinsic virulence and rely entirely on a weakened host immune system. Examples include Candida albicans , Cryptococcus neoformans , Aspergillus fumigatus , and Pneumocystis jirovecii . General Consequences to the Human Host: Pulmonary involvement — pneumonia, cavitation, respiratory failure Disseminated infection spreading to the brain, liver, spleen, and adrenal glands Chronic granulomatous inflammation Severe immunological damage in susceptible individuals Death in untreated or severely immunocompromised patients --- Q: Match the common name of the disease with the clinical name. Common Name Clinical Name --- --- Darling's disease Histoplasmosis Valley fever Coccidioidomycosis South American / Brazilian Blastomycosis Paracoccidioidomycosis Mycotic Mycetoma Pseudoallescheriasis Balanitis Candidiasis of the penis --- Q: A child born in Muranga was vaccinated with an attenuated vaccine. Explain briefly how it is supposed to protect the child from the particular viral infection. A: 1. The attenuated (live, weakened) vaccine strain is administered and undergoes limited replication in the host without causing full disease 2. This mimics natural infection and stimulates both humoral immunity (B cells produce specific IgG, IgM, and IgA antibodies) and cell-mediated immunity (CD4+ T-helper and CD8+ cytotoxic T lymphocytes are activated) 3. Long-lived memory B and T cells are generated that retain specific recognition of viral antigens 4. Upon natural exposure to the virulent pathogen, the immune system mounts a rapid, amplified secondary immune response before the virus can cause significant disease 5. Neutralizing antibodies block viral entry into host cells; cytotoxic T lymphocytes destroy already-infected cells 6. The child is therefore protected from the disease --- Q: Name the portal of entry of the herpes simplex viruses HSV-1 and HSV-2. A: HSV-1: Oral mucosa, conjunctiva, respiratory mucosa, and breaks in skin HSV-2: Genital mucosa (primary route via sexual contact); also skin and mucous membranes Both viruses enter through mucous membranes or broken skin, replicate locally, and then travel retrogradely along sensory nerve axons to establish latency in sensory ganglia — the trigeminal ganglion for HSV-1, and the sacral ganglia S2–S4 for HSV-2. --- Q: Mention three diseases caused by herpes simplex viruses HSV-1 and HSV-2. A: 1. Orolabial herpes (cold sores / herpes labialis) — HSV-1; recurrent vesicular lesions on lips and perioral skin 2. Genital herpes — primarily HSV-2; painful genital vesicles, ulcers, and dysuria 3. Herpes encephalitis — HSV-1; most common cause of fatal sporadic encephalitis, involving the temporal lobe 4. Neonatal herpes — HSV-2, acquired during delivery; potentially fatal disseminated infection in the newborn 5. Herpes keratitis — corneal infection that can lead to blindness --- Q: Explain how interferon helps virus-infected cells fight back the infection. A: When a cell is infected by a virus, it detects viral nucleic acid through pattern recognition receptors (TLR3, RIG-I, MDA5), triggering the production of Type I interferons (IFN-α and IFN-β) . Mechanism of Action: Step 1 — Interferon Production and Secretion: The infected cell produces and secretes interferons that act on the same cell (autocrine) and on neighbouring uninfected cells (paracrine). Step 2 — JAK-STAT Signalling: Interferon binding to surface receptors activates the JAK-STAT pathway, driving transcription of interferon-stimulated genes (ISGs) that establish an antiviral state . Step 3 — Antiviral Mechanisms Activated: Protein Kinase R (PKR) is activated → phosphorylates eIF-2α → inhibits viral protein synthesis RNase L is activated → degrades viral RNA Mx proteins directly interfere with viral replication machinery 2',5'-oligoadenylate synthetase amplifies RNase L activation Step 4 — Immune Cell Activation: Stimulate B cells to produce antiviral antibodies Activate Natural Killer (NK) cells to destroy virus-infected cells Upregulate MHC Class I molecules on all cells, enhancing recognition and killing by cytotoxic T lymphocytes The net result is that interferon-treated cells beco