MSE-2019 Pathogenicity

Commensalism

One pair of organism benefits whereas the other is unaffected

Mutualism

Interdependent with both beneficting

Parasitic

Exploit human body to detriment

Pathogenic

Disease-producing

Infection

Colonisation of pathogenic bacteria

Disease

when infection causes change in health state

Communicable

Ability to spread from host to another

Contagious

Easily spread

Requirement for pathogenicity

- Be transmitted from reservior

- Enter into body

- Invade target cells

- Produce molecules that deteriorate host

- Means of exit to transmit infection further

Reservior in infection

- Infected/carriers (Diphtheria, typhoid, TB, gonorrohea)

- Zoonoses/animal reserviors (Borrelia)

- Non-living: soil/water (C. botulinum, C. tetani)

Means of transmission

- Direct contact (touching, kissing, sexual intercourse)

- Indirect contact (syringes, tissues, cups)

- Droplet (coughing, sneezing, talking)

- Vehicle (contaminated water/food or airborne)

- Biological (contaminated water/food by insects/anthropods or direct biting)

Physical barriers to infection

- Lysozyme in tears

- Cilia in trachea

- Mucus membranes

- Lungs (airway turbulence)

- Nose hairs

- Moisture in skin

- Gastric pH

Portals of entry

- respiratory tract

- gastrointestinal tract

- genitourinary system

- skin

- blood

Bacterial penetration of defences

- Capsule (prevent frimbriae attachment and phagcytosis)

- Loss of plasmid (decrease virulence)

Examples of preventing spread of bacteria

Modify components of cell material (protease, collagenase, hyaluronidase, kinase and coagulase)

Symptoms of toxins to host

- Fever

- Cardiovascular disturbances

- Diarrhoea

- Shock

- Inhibition of proteinsynthesis

- Haemolysis

- Disruption of CNS

Haemolysis

Destruction of erythrocytes

Toxigenicity

Capacity of bacteria to produce toxins

Toxemia

presence of toxins in the blood

Enterotoxins

effect upon gastrointestinal system

Neurotoxins

effect on nervous system

Exotoxins

- Enzymes that destroy cells/inhibit metabolic function

- Produced by gram +ve and -ve

- Most genes encoded by plasmids or phages

Examples of exotoxins

gas gangrene, diphtheria, cholera, scarlet fever

Examples of neurotoxins

Botulism and tetanus exotoxins

Endotoxins

LPS that are part of gram -ve bacteria that releases when cell lyses/dies

Process of endotoxins

- Stimulates macrophage to release cytokines to high toxic levels

- Activate blood-clotting -> capillary obstruction and tissue death

Symptoms of endotoxins

Chills, fever, aches, shock and death

Why are antibiotics ineffective against endotoxins

Antibiotics leads to cell death -> more release of endotoxins

Nosocomial infection

Opportunistic/Hospital acquired (e.g. UTI)

Factors used for bacterial identification

- Salinity (imitate sweat gland)

- Antibiotics (kill off some bacteria)

- Bio-salts

- Temperature

- Anaerobic/aerobic (swap O2 for N)

- Culture medium

Factors used in culture medium for bacterial identification

- pH indicators

- nutrients

- electrolytes

- density

Sensitivity

Isolating bacteria to understand which antibiotic to use on patient (collect info on resistance and dosage)

Botulism

Clostridium botulinum

Gas gangrene

Clostridium perfringens

Diphtheria

Corynebacterium diphtheriae

scarlet fever

Streptococcus pyogenes

Traveller's diarrhoea

E.coli and shigella species

Botulism symptoms

double vision, drooping eyelids, slurred speech, facial muscle weakness, breathing difficulties

Gas gangrene symptoms

pain, swelling, darkening skin, death

Diphtheria symptoms

thick white coating at back of throat, fever, sore throat

scarlet fever symptoms

strawberry tongue, rash, fever