BIO6 Mid-Term Flashcards

Germ Theory

Specific microorganisms cause specific diseases

Pasteur

Disproved spontaneous generation; showed microbes cause spoilage

Koch's postulates (4)

Present in all cases; isolated and grown in pure culture; causes same disease in healthy host; re-isolated from that host

Epidemiology

Study of how disease is distributed in populations and what causes it, used to control disease

Chain of infection

Reservoir > portal of exit > transmission > portal of entry > susceptible host

Why the chain of infection matters

Break any one link and transmission stops

Natural reservoir

Where a pathogen normally lives: humans, animals or the environment

Portals of entry

Skin, gut, respiratory tract, urogenital tract, placenta, eyes

Direct vs indirect transmission

Direct: contact, droplets. Indirect: airborne, food, objects, vectors

Vector

An organism (usually an arthropod) that carries a pathogen between hosts

Incidence

Number of NEW cases in a set time

Prevalence

TOTAL cases (new + existing) at a point in time

Endemic

Normal baseline level of a disease in a community

Epidemic

Sudden increase in cases in one population

Pandemic

Epidemic spread across continents

Pathogenicity

Ability to cause disease (qualitative: yes or no)

Virulence

Degree of harm a pathogen causes (quantitative)

LD50

Dose that kills 50% of infected hosts; a measure of virulence

Incubation time

Time from exposure to first symptoms

Morbidity vs mortality

Morbidity: illness. Mortality: deaths

Acute vs chronic

Acute: fast onset, short. Chronic: slow onset, long or recurring

Latent infection

No symptoms now, but can reactivate

Bacteria

Single-celled prokaryotes

Peptidoglycan

Polymer in bacterial cell walls; unique to bacteria

Gram-positive

Thick peptidoglycan, no outer membrane; stains purple

Gram-negative

Thin peptidoglycan + outer membrane with LPS; stains red/pink

Why gram-positive stays purple

Ethanol dehydrates the thick peptidoglycan, trapping crystal violet

Why gram-negative turns red

Ethanol dissolves the outer membrane, violet washes out, red counterstain shows

Bacterial shapes

Cocci (spheres), bacilli (rods), spirilla (spirals)

Two parts of bacterial pathogenicity

Invasiveness (invade tissue) and toxigenesis (make toxins)

Adhesins

Surface structures that let bacteria stick to host cells

Invasins

Enzymes that break down host tissue so bacteria can spread

How bacteria avoid host defences

Avoid phagocytes, survive inside them, or kill them

Endotoxin

LPS in gram-negative outer membrane; released when cells multiply or die

Exotoxin

Protein secreted by living bacteria (mainly gram-positive)

Endotoxin vs exotoxin: potency

Exotoxins far more toxic; endotoxins need a high dose

Endotoxin vs exotoxin: heat and immunity

Endotoxins: heat stable, no antitoxin. Exotoxins: antibodies can neutralise them

Virus

Nucleic acid in a protein coat; replicates only inside living cells

Obligate intracellular parasite

Must live inside a host cell to reproduce

Virion structure

Nucleic acid, protein capsid, sometimes a lipid envelope with spikes

Viral life cycle

Attachment, penetration, uncoating, biosynthesis, assembly (maturation), release

Tissue tropism

A virus infects only certain cell types

Reverse transcriptase

Enzyme in RNA viruses (e.g. HIV) that makes DNA from viral RNA

Why HIV infection is permanent

Its DNA copy integrates into the host chromosome

Viral transmission routes

Respiratory, faecal-oral, blood, sexual, vectors

How viruses cause tumours

Viral DNA integrates, changes gene expression, cells divide uncontrollably

Tumour virus examples

HPV - cervical cancer; Epstein-Barr - Burkitt's lymphoma; hepatitis C - liver cancer

Where pathogenic fungi are found

Air, dust, soil, objects (fomites), normal flora

Mycoses

Fungal diseases

True fungal pathogen

Infects healthy hosts; high virulence; thermally dimorphic; restricted regions

Opportunistic fungal pathogen

Infects only weakened hosts; low virulence; worldwide

Thermal dimorphism

Fungus switches from hyphae (cool) to yeast (37 C) inside the host

Fungal portals of entry

Inhaled spores, damaged skin, skin surface

Dermatophytes

Fungi that feed on keratin; infect skin, hair and nails

Three parasite groups

Protozoa, helminths, arthropod vectors

Trophozoite

Protozoan feeding stage; motile

Cyst

Protozoan dormant stage; thick protective wall

How protozoa are classified

By motility and life cycle

Helminths

Multicellular parasitic worms: roundworms, flukes, tapeworms

Why arthropods are vectors

They carry viruses, bacteria and parasites between hosts, e.g. mosquito - malaria

Prion

Infectious misfolded protein; contains no nucleic acid

PrPC vs PrPSc

PrPC: normal protein. PrPSc: misfolded, disease-causing form

How prions cause disease

PrPSc is a template that misfolds normal PrPC; it builds up in the brain

Prion structural change

Alpha-helices refold into beta-sheets

Why prions are hard to destroy

Resist heat and chemicals; no cure or vaccine

Prion disease examples

CJD and kuru (humans), scrapie (sheep), BSE (cattle)

Three types of prion disease

Sporadic, familial, acquired

Why 'innate' immunity

Present from birth, non-specific, needs no prior exposure

Three lines of defence

1: skin and mucous membranes. 2: phagocytes, inflammation, fever. 3: B-cells, T-cells, antibodies

How skin protects

Physical barrier, resident microbes, shedding, chemical secretions

Other first-line defences

Lysozyme in tears and saliva, mucus, stomach acid

Lysozyme

Enzyme that breaks bacterial cell walls

Blood clotting steps

Damaged cells and platelets release clotting factors > prothrombin becomes thrombin > fibrinogen becomes fibrin > fibrin mesh traps cells > scab

Platelet plug

Platelets clump at the wound as emergency protection against blood loss

Why clots matter for immunity

Stop blood loss and block pathogens from entering

Phagocyte

White blood cell that engulfs and destroys microbes

Neutrophil

Most abundant phagocyte; short-lived; dead ones form pus

Macrophage

Long-lived phagocyte; also presents antigens to lymphocytes

Dendritic cell

Antigen-presenting cell linking innate and adaptive immunity

Natural Killer cell

Kills virus-infected and cancer cells without prior exposure

Mast cells and basophils

Release histamine and heparin

Four signs of inflammation

Redness, heat, swelling, pain

Inflammation steps

Damaged cells release histamine and prostaglandins > vessels dilate and leak > phagocytes arrive and engulf microbes > tissue repair

Histamine

Dilates blood vessels and makes them leaky: redness, heat, swelling

Prostaglandins

Increase blood flow and cause pain

Cause of redness and heat

More blood flow from dilated vessels

Cause of swelling

Fluid leaking from permeable vessels into tissue

Pus

Dead phagocytes, damaged tissue and fluid

Fever

Body-wide response that slows microbes and boosts immunity

Interferon

Protein released by virus-infected cells that helps other cells resist viruses

Complement system

~30 blood proteins that tag microbes, boost inflammation and burst bacteria

Cytokines

Signalling molecules that coordinate immune cells

Self vs non-self

Body cells carry MHC markers; unrecognised markers trigger a response

Antigen

Any substance that triggers antibody production

Antibody structure

Y-shaped protein; two heavy and two light chains; two antigen-binding sites

Antibody function

Binds a specific antigen and marks it for destruction

How antibodies inactivate antigens

Neutralisation (toxins, viruses), clumping (cells), precipitation (soluble antigens); all aid phagocytosis

Humoral immunity

B-cells make antibodies against pathogens OUTSIDE cells

Cell-mediated immunity

T-cells destroy infected, foreign or cancerous CELLS

B-cells mature in

Bone marrow