Lecture 10 Flashcards
how exotoxins damage host cells, an example of a bacterium and the disease they cause
- electrolyte secretion - Vibrio cholerae - Diarrhoea
- necrosis - Staphylococcus aureus - the death of host cells (e.g. leukocidin production)
- apoptosis (programmed cell death) - Escherichia coli - triggered by Shiga toxins
- nerve synapse inhibition - Clostridium species - nerve terminals are blocked and muscles can’t contract (paralysis, tetani, botulism)
- superantigens - Staphylococcus aureus - trigger cytokine release e.g. toxic shock syndrome toxin (can be lethal)
how endotoxins damage host cells and an example of a bacterium
lipopolysaccharide (LPS) in the cell wall of Gram Negative bacteria causes an inflammatory cascade (TLR4 agonist)
how cell wall fragments (other than LPS) damage host cells and an example of a bacterium
Lipoteichoic acid in Gram-positive bacteria causes an inflammatory cascade
how hydrolytic enzymes damage host cells and an example of a bacterium
matrix remodelling/tissue digestion (allow bacteria to spread through tissues), e.g. using hyaluronidase and proteases from Staphylococcus aureus
how inhibition of secretory products damages host cells and an example of a bacterium
- Inhibition of stomach acid secretion by Helicobacter pylori
- Inhibition and degradation of digestive enzymes by Giardia lamblia (protozoan)
how invasion and intracellular multiplication damage host cells and an example of a bacterium
damage/lysis of to host tissue, immune evasion, certain pathogens infect cells to get to another place by using them as trogen horses, e.g. malaria parasite to get to the brain. viruses, parasites (malaria), bacteria (salmonella, mycobacterium tuberculosis)
how induction of autoantibodies damage host cells and an example of a bacterium
immune damage to host tissue (microbial antigens similar to the host antigens evoke an autoantibody response) e.g. Rheumatic fever by Streptococcus pyogenes
how mutation damage host cells and an example of a bacterium
uncontrolled cell growth (tumour), some viruses carry oncogenes which when inserted into DNA cause tumours. removal of virus doesn’t remove tumour
how obstruction damage host cells and an example of a bacterium
blocking blood or lymphatic vessels, occurs particularly with parasites which form large masses, e.g. hydatid cysts of the parasite Echinococcus granulosus (tape worm)
host responses to microorganisms
- inflammation (non-specific, basic, primitive protection against invading pathogens)
- immune response (specific)
types of tissue injury (not mechanisms)
ischaemic, physical, chemical, infectious, immunological
suffix for inflammation
-itis
what is pyrexia?
fever
cardinal signs of inflammation
heat, redness, swelling, pain, loss of function (context dependent - where’s being affected)
what is suppuration?
injury to solid tissue (e.g. kidney, brain, dermis, liver) and the causal agent is a pyogenic (pus-forming) organism
what is an abscess?
tissue injury localised by a fibroblastic boundary and has a necrotic pus-filled centre
what is an ulcer?
inflammatory lesions on the epithelial surfaces (pus forms, result of neutrophil phagocytosis)
what is cellulitis?
an inflammatory reaction spreading through CT planes
Inflammatory process:
- release of mediators from activated cells and plasma 2. vasodilation, increased vasopermeability, abnormal movement of fluid and plasma proteins into extravascular sites. hyperaemia (increase blood flow) causing redness, heat and swelling (related to capillaries). increased outflow of fluid due to increase in the net pressure in the capillaries and post capillary venules
- migration and activation of leukocytes in response to attractant substances
role of pre-capillary sphincters during acute inflammation
opens during acute inflammation to enable hyperaemia in the capillaries and for WBC’s to be fit in them (capillaries too narrow to allow WBC’s in with normal blood flow)
during infection how quickly and often does acute inflammation occur?
quickly and continuously
Systemic effects of inflammation:
a) pyrexia (fever) - mediated by cytokine IL-1 from monocytes and macrophages
b) leukocytosis - increased production and release of neutrophils and monocytes from bone marrow
c) acute phase proteins - increased production of liver proteins which limit tissue damage and resolve infection and inflammation, e.g. fibrinogen and complement proteins
d) endocrine changes - increased production of glucocorticoid and other steroid hormones in response to stress. other endocrine organs may be affected when physiological stress is severe or sustained
e) uptake of debris by dendritic cells (APC) which move to the lymph nodes via lymphatic vessels
what drug can reduce pyrexia?
paracetamol
function of primary lymphoid organs and examples
production of lymphocytes - bone marrow (B lymphocytes), thyroid (T lymphocytes)
