Cryptococcal Meningitis: Symptoms, Causes & OmpathStudy

UNIT CODE: MBMM 3300 MEDICAL VIROLOGY AND MYCOLOGY Mount Kenya University — School of Medicine, Department of Medical Microbiology Bachelor of Medicine and Bachelor of Surgery (MBChB) Degree — Year 3 University Examinations 2018/2019 Main Exam Date: Wed 17th February, 2021 Time: 3 Hours Paper 2 Instructions: Answer ALL questions in Sections A & B and ANY OTHER TWO from Section C Some answers on this page were completed with AI assistance where the source material had no answer key. These are provided as a study aid — please verify against your course materials. --- SECTION B: SHORT ANSWER QUESTIONS (5 MARKS EACH) --- Q36. Give the main characteristics that differentiate prions from other pathogens and describe the diseases caused to humans (5 marks) (2 repeats — refer to previous answer) Model answer: Prions are misfolded, infectious proteins (PrPSc) that contain no nucleic acid (no DNA or RNA) — unlike viruses, bacteria, and fungi, they carry no genetic material and so cannot be destroyed by nucleases, standard formalin fixation, or routine autoclaving. Disease is caused not by replication in the conventional sense but by conformational templating: abnormal PrPSc binds normal host prion protein (PrPC) and converts it to the same misfolded, protease-resistant, β-sheet-rich isoform, which then accumulates. They provoke no inflammatory or immune response (no antibody or cytotoxic T-cell reaction) and are associated with very long incubation periods before clinical onset. Pathologically they cause spongiform (vacuolar) change in neurons, reactive astrogliosis, and amyloid plaque deposition, with no evidence of an infectious genome on staining. Human prion diseases: Creutzfeldt-Jakob disease (sporadic, familial, iatrogenic, and variant forms), Kuru, Gerstmann-Sträussler-Scheinker syndrome, and Fatal Familial Insomnia — all presenting with rapidly progressive dementia, myoclonus, and ataxia, and all uniformly fatal. --- Q37a. Describe the pathogenesis of viral encephalitis (3 marks) (2 repeats — refer to previous answer) Model answer: Viruses reach the CNS either haematogenously (viraemia crossing the blood-brain barrier, e.g. arboviruses, enteroviruses) or by retrograde axonal transport along peripheral/cranial nerves (e.g. herpes simplex virus via the olfactory or trigeminal route, rabies virus via peripheral nerves). Within the CNS the virus infects neurons and glial cells, producing direct cytopathic injury — cell lysis, intranuclear/intracytoplasmic inclusion bodies, and neuronophagia — with a predilection for grey matter (e.g. temporal lobes in HSV encephalitis). This triggers a host immune response with perivascular ("cuffing") lymphocytic infiltration, microglial nodule formation, and diffuse mononuclear inflammation, which compounds the direct viral damage and produces cerebral oedema, the combination accounting for the clinical picture of fever, altered consciousness, seizures, and focal neurological deficits. --- Q37b. Name two viruses which cause encephalitis (2 marks) (2 repeats — refer to previous answer) Model answer: Herpes simplex virus (HSV-1) — the commonest cause of sporadic, non-epidemic viral encephalitis, typically necrotising and affecting the temporal lobes. Japanese encephalitis virus (a mosquito-borne flavivirus) — the leading cause of epidemic viral encephalitis in Asia; other accepted examples include rabies virus and West Nile virus. --- Q38. Outline risk factors for fungal infections (5 marks) (2 repeats — refer to previous answer) Model answer: Immunosuppression: HIV/AIDS (especially with low CD4 counts), long-term corticosteroid or cytotoxic chemotherapy, and solid-organ or bone-marrow transplantation on immunosuppressive regimens. Broad-spectrum antibiotic use: disrupts normal protective bacterial flora, allowing overgrowth of endogenous fungi such as Candida . Diabetes mellitus: particularly poorly controlled disease, predisposing to mucormycosis and candidiasis. Medical devices and procedures: indwelling central venous catheters, urinary catheters, and prosthetic heart valves promote biofilm formation and candidaemia. Environmental/occupational exposure and host factors: agricultural, construction, or cave-related occupational exposure (e.g. Histoplasma , Aspergillus ), malnutrition, and extremes of age (neonates and the elderly). --- Q39. Explain any two virulence factors used by fungi (5 marks) (2 repeats — refer to previous answer) Model answer: Polysaccharide capsule (e.g. Cryptococcus neoformans ) — masks fungal cell-wall antigens from host pattern-recognition receptors, inhibits phagocytosis by macrophages and neutrophils, and interferes with complement activation and opsonisation, allowing the organism to survive and disseminate. Thermal dimorphism (e.g. Histoplasma capsulatum , Blastomyces dermatitidis , Candida albicans ) — the ability to switch between a mould/hyphal form in the environment (25°C) and a yeast form in host tissue (37°C) allows tissue invasion and intr