Causes Of Infection Flashcards by Amarah Nasar

What is this?
Smaller than cellular organisms
Metabollically inert
Simple structure
Needs host cell to replicate
1/100th size of bacteria
Infects animals plants and bacteriophages

Virus

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Components of a virus

CAPSD IS PROTEIN COAT
GENES (DNA OR RNA)
Cell wall
Sheath
Core
Some have lipid envelope derived from host cell

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What is this?
Have genetic material no organelles

Rely on host organelles or systems to reproduce

Use surface proteins to bind to a cell and put their genetic material in it

Virus replication

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can lay dormant for decades, emerging to cause shingles

Chickenpox

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infects hosts for days, causing a cold

Rhinovirus

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causes chronic
liver infection over years

Hepatitis C VIRUS

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Unicellular organisms
Cell membrane
Cell wall
No nucleus
• Genetic material is DNA but not bounded by a membrane
Reproduce asexually
Some move using flagella and attach via fimbriae

Bacteria

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stain pink
stain purple

Gram -ve
Gram +ve

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Meningococcal sepsis
Bacterial endocarditis
Cellulitis
Streptococcal throat infection

Bacterial diseases

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Eukaryotes
Cell membrane
cell wall
nucleus
cytoplasmic structures
Reproduce sexually and asexually

Fungi

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Mild infections-
• thrush
•athletes foot
• ringworm

• Severe infections –In the Immunocompromised
• Cryptococcal meningitis in HIV patients
• Invasive candida in ICU –Or Immune competent

Fungal infections

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Ectoparasites
– live outside body
• Fleas
• Ticks

Endoparasites
– Iive inside body
• Worms

Epiparasites
– a parasite which lives on another parasite
• Malaria (mosquito)

Parasites

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Giardia
Cause bloody diarrhoea

Caught from drinking infected water

May be seen in stool under a light microsope

Cyst form aids survival + spread

Parasitic diseases

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One of the biggest killers worldwide

• Complex life cycle

• Reproduce in female anopheles mosquito

Malaria

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Cestodes (tapeworms)
Segmented, flat

Trematodes (flukes)
Unsegmented, flat

Nematodes (round worms)
Cylindrical, have digestive tract with lips, teeth and anus

Worm helminths

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Tapeworms – Fish, pork, beef tapeworms

• Cause
– Malabsorption
– Malnutrition in chronic disease
– Cysts in muscle or brain

Cestodes

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Round worms
Biggest

Cause diarrhoea and malabsorption

Nematodes

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Flukes
-lung flukes
-liver flukes
- pancreatic
-intestinal
-blood= schistosoma

Trematodes

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Smallest infective agents known

Proteinaceous Infectious particles

Lack nucleic acid - not a ‘living organism’

Proteins fold abnormally and accumulate

mainly in neural tissue

They are very difficult to destroy

• Concerns over cleaning surgical instruments

Prions

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CJD- fatal, degenerative neurological disease – Affects 1 in a million people each year – Transmitted through contaminated human growth hormone, surgical instruments and corneal grafts

• Variant CJD- typically occurs in young adults

• BSE- occurs in cattle

• Scrapie- occurs in sheep

• Kuru- similar to vCJD
– occurred in Papua New Guinea in 1950s
– thought to be spread by cannibalism

Prions diseases

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Nutrients - carbon, hydrogen, oxygen, nitrogen

Synthesise of new molecules

Energy

Growth requirements

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Break down molecules to produce energy. (lerger substrates, smaller products)

Catabolic metabolism

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Use energy to combine small molecules into macromolecules (energy+ source of elements especially carbon)

Anabolic pathway

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Phototrophs: uses sunlight energy to produce its energy
(photophosphoryla tion)

• Chemotrophs: extract energy from chemical bonds mainly by oxidation of electron donor compounds.

Source of energy

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• Organic compunds (organotrophs) e.g. Sugar, fat...etc • Inorganic molecules: (lithotrophs) • e.g. Ferrous iron ferric iron • Amonia nitrite

Source of electron donor

Autotrophs: produce complex organic compounds from simple inorganic ones • Heterotrophs: consume organic molecules as a source of carbon.

Source of carbon

availability of the main building blocks (protien, DNA, RNA, cell membrane….etc)

Growth and reproduction

fatty acids, amino acids, nucleic acids, carbohydrates…

Are precursors

vitamins.

Act as catalyst in the synthesis process

Consumed in the food

If organism can't make those precursors carbs,nucleic acids amino acids fatty acids

No energy needed driven by concentration gradient

Passive diffusion

Need energy Needs receptors and works against conc gradient

Active transport

Less energy involved phosphorylation of molecule

Group translocation

Temp Water,ph, osmolarity, oxygen, pressure. Light, physical space availablity

Physical requirements

Temperature affect protein structure and fluidity of the cytoplasm and the cytoplasmic membrane.

Temp

lowest temperature that a given organism can carry out its metabolic activities

Minimum growth temp

temperature at which metabolic activity is at its peak and thus growth rate is the highest.

Optimum Growth

Essential for life Bacteria usually require at least Aw= 0.8 (G-ve requires higher 0.97), and fungi at least 0.7 (water Aw= 1).

Water

vapour pressure of a sample divided by that of pure water at the same temperature.

Water activity

reflects high concentrations of solutes (hypertonic solution).

Low AW water effect

PH effect: High or low PH inhibit microbial growth except for few! Acidic conditions are body defense mechanism e.g. stomach and vagina (via fermentation by normal flora) Acidophiles can tolerate acidic conditions. Some are obligate acidophiles Alkalinophile lives in alkaline media like soil and alkaline water (e.g. Vibrio cholerae).

Ph effect

requires O2 for energy production (respiration)

Obligate aerobes

do not use O2 for energy production

Anaerobes

can survive with or without O2

Facultative anaerobes

can tolerate oxygen levels from 2-10% (limited ability to detoxify hydrogen peroxide and superoxide radicals)

Microaerophiles

Anaerobes but have some enzymes that detoxify oxygen’s poisonous forms.

Aerotolerant

Skin Mucus membrane Stomach Commensal microflora Immune system: innate learnt Behavioural: good hygiene

Defence mechanism

immune cell non-reactivity to antigens.

Self tolerance

Tolerance to innate antigens

Self tolerance

Antigens encountered within hours after birth

Neonatal tolerance

Acquired tolerance

Self tolerance with self recognition is key in maturation of both Tand B cells

When immunological tolerance breakdown what does it lead to

Autoimmune disease

What is this: T cells have to recognise s LF MHCs (self recognition) and display S T

Self tolerance

Loss of B CELLS leads to A I D

Auto Immune Disease

Pre T cells develop in the THymus via P S

Positive Selection

Self tolerance happens by the opposite of positive selection

Negative selection

Of the T cells produced what percentage become fully mature immunocompetent cells

1-5

deletion of self reactive T cells happen if they leave the thymus and meet what? What type of protein does it meet

Contact unrecognised self protein

B cells also develop what? S TOL

Self tolerance

Non reactivity to an antigen that should cause immune response is what

Acquired tolerance

What are these examples of? Failure of immune system to destroy sperm and fertilised eggs

Acquired tolerance

Which type of tolerance can be linked to inflammatory bowel disease

Oral

IgE-mediated, immediate type hypersensitivity (IgE-mediated degranulation of mast cells) (e.g. allergic rhinitis, allergic asthma, urticaria)

Type 1

Cytotoxic reaction (complement lysis/ADCC) (e.g. drug allergy)

Type 2

Immune complex reaction- complement activation) (e.g. allergic vasculitis)

Type 3

T-cell mediated, delayed type hypersensitivity (e.g. allergic contact eczema)

Type 4

Small 15-40,000 Mw proteins Soluble Long lasting in environment Low dose of allergen Mucosal exposure. Often proteases Most allergens promote a Th2 immune

Properties of antigens

Atopic diseases caused by individuals’ tendency to mount over zealous IgE responses Example - Dust allergens

Type 1 IgE mediated

Protease allergens can potentially activate PAR receptors

Protease mediated type 1 IgE hypersensitivity

IgE mediated reaction to inhaled allergens Upper airways: rhinitis • nasal itch; • Sneeze; • Rhinorhoea; • nasal obstruction. Lower airways: asthma • bronchoconstriction , mucus hypersecretion; • Wheeze; • Breathlessness; • Cough.

Asthma/ rhinitis

Direct/rapid route in to blood stream (sting, ingestion) Route and dose greatly affect out come

Urticaria/ anaphlaxis

Cold induced urticaria- triggered by NLP3 mutants Overly sensitive mechanotransduction induces mast cell degranulation Vibrational urticaria over activation of the GPCR- EMR2

Mast cell role in urticaria

mainly kill parasites via reacting towards opsonised parasites. large amounts of IL5 / IL3 in allergy cause degranulation

Eosinophils

IgE response evolved to expel/destroy helminth/protozoal pathogens

IgE EVOLUTION

IgG mediated destruction of blood cells/platelets-autoimmune hemolytic anemia. Hemolytic disease of the newborn Thrombocytopenia. Change in signalling Type IV

Non IgE allergic diseases: Type 2

Antibodies attach to epitopes on self cells Induces activation of compliment Results in vasodilatation and migration of phagocytic cells to the effected tissue. Promotes activation of membrane attack complex. Used to refer to antibodies that attacked self blood cells, but now is used to describe antibodies that target other tissues.

Type 2

Caused by antigen antibody complexes. Antigen can be self antigens (i.e., nuclear material as in Lupus) or non-self antigens such as bacteria. Promotes inflammatory response. Can be either : Local form Type 3 Hypersensitivity Systemic form Type 3 Hypersensitivity

Type 3

individual is immunised against an antigen, subcutaneous injection of a high concentration of that antigen induces an inflammatory response peaking within seven hours at that site. Example - inhaled spores causing extrinsic allergic alveolitis.

Type 3 local

Antigen complexes may form systemically - promoting system wide inflammatory responses. Example – Post infectious glomerulonephritis - antibody complexes become stuck in the glomeruli of the kidney inducing an inflammatory response. Can be caused by any bacterial infection, but most common complication with streptococcal pharyngitis

Type 3 systemic

1. Antigen injected into subcutaneous tissue and processed by local antigen presenting cells 2. A TH1 effector cell recognises antigen and releases cytokines that act on vascular endothelium 3. Phagocytes to site of antigen injection causes visible lesion is recruited

Type 4 delayed hypersensitivity

1. Contact sensitising agent penetrates the skin and bids to self proteins that are taken up by Langerhans cells 2. Langerhans present self peptides haptenated with the contact sentising agent to TH1 cells which secrete IFN-Y and other cytokines 3. Activated keratinocytes secrete cytokines like IL 1 AND TNF-A and chemokiens such as CXCL8 CXCL11 and CXCL9 4. Products of keratinocytes and TH1 CELLS ACTIVATE MACROPHAGES TO SECRETE MEDIATORS OF INFLAMMATION

Type 4 hypersensitivity

Related to Helper T cells interacting with activated cytotoxic T cells, NK cells or macrophages. Response is delayed and cannot be transferred in the serum. Examples BCG – injection of inactivated M. bovis will cause a localised inflammatory response after 2 days. Indicates that the individual has already encountered the TB bacillus. Contact dermatitis Donor organ rejection

Type. 4

Mediated via lipid soluble urushiol oil haptens binding MHCI

Allergic contact dermatitis

Binds α-gliadin (derivatised by transglutaminase-enzyme)

Coeliac disease

1. Peptides naturally produced from gluten do not bind to MHC class 2 molecules 2. An enzyme tissues transglutaminase modifies the peptides so they now can bind to the MHC class 2 molecules 3. The bound peptide activates gluten specific CD4 T cells 4. Activated T CELL can kill mucosal epithelial cells by binding FAS. They also secrete IFN-y which activates the epithelial cell

Cellular destruction in coeliac disease

Causes Of Infection Flashcards

(85 cards)