Infection Flashcards
Infection
Occurs through invasion of body by pathogenic micro-orgnisms Eg: Bacteria Viruses Fungi Protozoa Parasites
Invasion (routes of entry)
Skin + Mucous membranes
Ingestion
Inhalation
Establishing factors of infection
To cause disease organisms have to overcome body’s defense mechanisms
Infection is aided by
Quantity
Virulence [resistance to phagocytosis, adhesiveness, co-enzyme production]
Defence mechanisms against infection
Physical barriers - skin + filtration (nasal cilla)
Secretions - tears, urine + mucin
Chemical actions
Chemical defence mech
Acid - stomach + urinary tract
Lysozyme enzymes - dissolve bacterial capsule in tears
IgA - tears and GI
Non-specific - urine, sweat, sebum
IgA
Immunoglobulin A - any of a class of proteins present in the serum and cells of the immune system, which function as antibodies.
Lysozyme
enzymes that damage bacterial cell walls by catalyzing hydrolysis of 1,4-beta-linkages
Factors in the course of infection
Acute Inflamm limits spread
Chronic Inflamm (Fibrosis) localize infection
Phagocytosis - can fail with multiplication within phagocyte
Immune response
Interferon production (IFN)
Interferons
Interferons (IFNs) are a group of signaling proteins[1] made and released by host cells in response to the presence of several pathogens, such as viruses, bacteria, parasites, and also tumor cells. In a typical scenario, a virus-infected cell will release interferons causing nearby cells to heighten their anti-viral defenses.
Immune response
Humoral - antibody reactions
Cell mediated - T-lymphocytes
Local reaction to infection
usually inflammatory evoked by cell damage and death
Bacterial infection - genesis
Bacterial infections can cause:
Production of toxins - Endo vs ExoToxins
Hypersensitivity reactions - part of immune response resulting in tissue damage
Tissue invasion - lymphocyte spread + bacterial invasion of bloodstream [causes 3-aemias] Primary entry via lymphatic system
3-aemias
Bacteraemia - low amt of bact in blood [dental = bact endocarditis]
Septicaemia - more bact in blood - baneful
Pyaemia - clumps of purulence forming bacterial - emboli + septic infarction
Pyrexia
Increase in body temp due to imbalance between heat production and heat loss
- increase heat production due to increased metabolism
- increase temp in attempt to kill mico-organisms
- increased heat loss due to vasodilation in skin + perspiration
- changes assoc with increased pulse + dehydration
Wound Healing
2 processes
- regeneration = complete [no scar, full function]
- healing = partial [tissue replaced by fibrin]
Healing by 1st intention
Occurs with clean sterile wound
No micro-organisms + strong intact edges
No significant cell loss
2-3 hours, early inflamm near edges + epithelial cells move across from wound edges
2-3 days, epithelial growth + macrophages remove clots
10-14 days, epithelial covering complete with weak wound covering
weeks, hyperaemic with good union
months, remodeling with collagen
Healing by 2nd intention
Large open wounds (significant tissue loss)
Necrosis + infection
Cavity fills with blood + fibrin clots (acute inflamm)
Scab dries out, mitotic activity in epithelium with fibroblasts, neutrophils + macropahges present. (wound contracts)
Surface debris sheds, epithelium grows across + loose connective tissue formed by fibroblasts
Cappilary loops may form at wound basse
Epithelium recovers + scar tissue forms
Fibrosis may result with chronic inflamm + organization.
Factors delaying wound healing
Local:
- Infection
- poor blood supply
- excessive movement
- presence of foreign matter (infectious)
Systemic
- Deficiencies of Vit C, amino acids + zinc
- debilitating chronic disease
- (above factors affect collagen synthesis)
