Lecturesyouwill
see happen.

The lab sheet, organism by organism: diphtheria, sputum, tuberculosis, Haemophilus influenzae and Bordetella pertussis, then Mycoplasma, Legionella, the fungi and RSV. For each, the specimen, the stain, the culture, the identifying test and the report.

The influenza virus taken apart — its eight RNA segments, HA and NA — then followed into an airway cell and out again; why it changes every winter and now and then turns into a pandemic; the disease it causes; and how we diagnose, treat and prevent it.

Why did amoxicillin cure Omar’s pneumonia but not Sami’s? A bacterium taken apart, layer by layer — nucleoid, plasmids, ribosomes and cytosol inside; the membrane and peptidoglycan wall; capsule, flagella and pili outside; the endospore it becomes to survive — and the answer: a good antibiotic hits a structure our cells lack.

One family, one winter, five coughs: parainfluenza and croup; respiratory syncytial virus, bronchiolitis and the antibodies that now protect babies; human metapneumovirus; adenovirus, tough without an envelope; the coronaviruses, from colds to SARS, MERS and COVID-19; and rhinovirus, the commonest cause of the common cold.

Why did the stain miss Sami’s bacterium, and what named it instead? The same two students, now in the laboratory — how bacteria are ranked and named; their shapes and arrangements; the Gram stain read on the wall itself; the acid-fast stain for waxy mycobacteria; and the molecular methods (PCR, G+C, 16S rRNA, whole genome sequencing, MALDI-TOF) that name what stains and culture miss.

One house, two coughs: the pneumococcus, its capsule and how the laboratory recognises it; how it gets from the throat to the lung; lobar pneumonia, otitis media and their treatment; why only the conjugate vaccine protects babies; and Bordetella pertussis, its toxins, the three stages of whooping cough, and how to protect a newborn.

Two pneumonias whose Gram stain shows pus but no bacteria: Mycoplasma pneumoniae, which has no cell wall, grips the cilia and causes walking pneumonia and cold agglutinins; and Legionella pneumophila, which grows in warm water inside amoebae, lives inside macrophages, and causes Legionnaires’ disease and Pontiac fever.

One house, one bacillus: an acid-fast, slow-growing rod with a waxy mycolic-acid wall; spread by droplet nuclei; survival inside macrophages and the granuloma; primary TB, the Ghon complex and latent infection; reactivation, cavities and miliary spread; how active and latent TB are found (smear, PCR, culture, skin test, IGRA); the BCG vaccine; and treatment with four drugs.

The lecturer’s slides in five stops after the identification tree: the staphylococci and their tests, diseases and toxins; the streptococci by haemolysis; the spore-formers Bacillus and Clostridium; and the non-spore-forming rods Listeria, Corynebacterium and Mycobacterium.

The lecturer’s slides in four stops after the identification tree: the diplococci (Neisseria); the coccobacilli Haemophilus, Bordetella and Brucella; the bacilli sorted by lactose, with Shigella and Pseudomonas; and the curved bacteria Vibrio cholerae and Helicobacter pylori.