12.3.17

Medically Important Fungi

My revised pnemonic for ADP ribosylation A-B toxins

Boring     and      serious      people score high in usmle…

Bordetella pertussis and B.cereus  increases   cAMP by inhibiting Gi

Cool    and     Vibrant   people  also score high…

E. coli  and Vibreo cholerae increases cAMP by  activating Gs

Exception: Please please please remember that  Bacillus anthracis has an edema factor which it self acts as adenylate cyclase…. no ADP ribosylation involved..so hence  cAMP level increases.

PSEUDOmonas aeroginosa.

Pneumonia 

Sepsis (black lesion on skin).

External otitis (swimmers ear)

UTI,Drug use .

Diabetic osteomylitis

Aminoglycoside„,extended spectrum penicillin(pipracilin,ticarcillin)

Think pseudomonas in burn victims

Normal Flora

Blood, Spinal Fluid, Urine: sterile

Cutaneous surfaces (urethra, outer ear included): Staph epidermidis, Staph aureus, Corynobacteria (dyphteroids),Streptocci, Candida spp

Nose: Staph aureus, Staph epidermidis, dyphteroids, assorted streptococci

Gingival crevices: anaerobes = Bacterioides/Prevotella, Fusobacterium, Streotococci, Actinomyces

Oropharynx: Viridans group (alpha hemolytic strep), Neisseria (non pathogenic), H. influenzae (non typeable, meaning, w/o capsule), Candida albicans

Stomach: none

Breast-fed babies colon: microaerophilic/anaerobic = Bifidobacterium, Lactobacillus, streptococci.

Adult Colon: microaerophilic/anaerobic = Bacteroides/Prevotella, E.coli, Bifidobacterium, Eubacterium, Fusobacterium, Gram- anaerobic rods, Lactobacillus, E.faecalis, streptococci

Vagina: Lactobacillus, streptococci, diphteroids, yeasts, Veillonella, Gram- rods

fungal infectors by systems 

Sorry guys haven’t been updating much lately 

Innate Immunity - intro

First line of defence + first to act

A primitive response (exists in animals and some plants)

Non-specialised and without ‘memory’

Consists of:

Physical barriers (eg skin and mucosa//tight junctions, airflow)

Chemical barriers (eg enzymes, lung surfactant, antimicrobals)

Soluble mediators of inflammation (eg cytokines)

Microbal defence (eg commensal competition, secreted antimicrobals)

Cells (eg phagocytes)

Receptors to recognise presence of pathogen/injury - results in inflammation

Soluble Mediators

Complement Proteins

liver-derived 

circulate in serum in inactive form

activated by pathogens during innate response

functions include lysis, chemotaxis and opsonisation

Auxiliary Cells

Mediate inflammation as part of the immune response. The main auxiliary cells involved in the immune response are Basophils, Mast cells and Platelets.

Basophils 

Leukocyte containing granules 

on degranulation release histamine + platelet activating factor

causing increased vascular permeability and smooth muscle contraction

also synthesise and secrete other mediators that control the development of immune system reactions

Mast Cells

Also contain granules 

However they are not circulating cells - found close to blood vessels in all types of tissue especially mucosal and epithelial tissues.

rapidly release inflammatory histamine but this is IgE dependant so not innate

Platelets 

normally function in blood clotting

also release inflammatory mediators

Cytokines and chemokines

Produced by many cells but especially mØ (macrophages), initiate inflammatory response and act on blood vessels 

interferons - antiviral protection

chemokines - recruit cells

interleukines - fever inducing, IL-6 induces acute phase proteins 

IL-1 - encourages leukocytes to migrate to infected/damaged tissue

as does tumour necrosis factor (TNFa)

Acute phase proteins

Liver derived proteins 

plasma concentrations increase (positive acute-phase proteins) or decrease (negative acute-phase proteins) in response to inflammation

called the acute-phase reaction 

triggered by inflammatory cytokines ( IL-1, IL-6, TNFα)

help mediate inflammation ( fever, leukocytosis, increased cortisol, decreased thyroxine, decreased serum iron, etc)

activate complement opsonisation 

Inflammation 

Cells

Cytotoxic Cells

Eosinophils/natural killer cells, cytotoxic T cells

kill target via release of toxic granules 

dendritic cell derived IL-12 helps activate NK cells

Phagocytes

mono-nuclear = long-lived; polynuclear = short-lived

engulf, internalize and destroy 

phagosome forms around microbe

enzyme filled with lysosomes fuses to form phagolysosome

organism is digested

fragments are either ‘presented’ or exocytosed

phagocytosis requires recognition of microbe via receptors for

PAMPs (pathogen associated molecular patterns - eg flagella or capsule) - recognised by toll-like receptors 

activated complement

antibody

The innate immune response primes for the adaptive 

B-cells are primed by activated complement

Th1 cell differentiation needs pro-inflammatory cytokines

Microbial Genetics

It’s Medical Mnemonics Monday!

Renal Papillary Necrosis is a form of nephropathy characterized by coagulative necrosis of the renal medullary pyramids and papillae.  

Causes of Papillary Necrosis can be remembered by the mnemonic “POSTCARDS”.

P yelonephritis

O bstruction of the urogenital tract

S ickle cell disease

T uberculosis

Chronic liver disease,

A nalgesia /A lcohol abuse,

R enal transplant rejection

D iabetes mellitus

S ystemic vasculitis

Check out the list of the previous Medical Mnemonics here.