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Name 3 gram positive cocci?
- Staphylococcus aureus
- Group A strep [scarlet fever]
- B-haemolytic strep
- Strep Pneumoniae
- Strep Viridans
Name 3 gram negative cocci?
- Neisseria Meningitidis; mild sore throat → meningitis
- Neisseria Gonoccocus
- Moraxella Catarrhalis
Name 3 Gram positive Bacilli?
- Listeria → bacteraemia & meningitis [v young & old]
- Clostridia species → C. Diff, C perfingens, C tetani
Give 3 gram negative bacilli?
- H. Influenzae
Virulence = ability of organism to cause disease [ability to invade host tissue
What is a pathogen?
Microbial organism that can produce symptomatic disease
What is non-sterilising immunity?
- when a Pt grows up in a disease endemic area
- initial infection → symptoms
- subsequent infections have a decreasing severity of symptoms [asymptomatic]
- but pathogen still in blood
- e.g. malaria
Outline the pathogenesis of MTB infection
- Mycobacterium Tuberculosis
- [inhaled droplet spread]
- Inhaled droplets
- 95% individuals → dromant lesions
- replicate in macrophages
- Reactivation of MTB [HIV, immunosuppression, smoking]
- disease progresses to cavitating MTB
- cavities open onto bronchi facilitating spread via coughing
- 5% get full blown TB after 1st infection
Outline the range of disease caused by MTB
- Miliary TB
- Lots in both lung feilds
- looks like millet seed [CXR]
- CNS TB
- Tuberculomata across brain
- epileptic fits & space occupying lesions
Describe a granuloma
Formed when pathogen cannot be digested
- Central necrosis
- epitheliod cells [macrophages]
- Giant cells
- Lymphocytes [outermost, mainly T cells]
Outline the Ix of suspected MTB?
- CXR → apical destruction & cavity formation
- ZN stain for acid fast bacilli
- Mantoux RXN/ Heaf test
- inject MTB cell walll extract into dermis
- ?prev infection → area of inflammation
- no RXN? → no previous exposure
- not perfect, some cross reactin w BCG
What is the Tx for MTB?
MTB is RIPE for Tx
- Rifampicin → red urine, CYP450 inducer
- 6m R & I
- Drop P & E if sensitive to RI after 2m
What is the most common cause of community acquired pneuomonia?
Name 2 other typical organisms.
Most common → Strep Pneumoniae
- Haemophilus influenzae
- Mraxella Catarrhalis
Give 4 risk factors for CAP?
- ^ alcohol intake
- Existing airway disease [COPD/ Asthma]
- Influenza infection
What are the S&S of CAP?
What would be found O/E?
- Productive cough
- Pleuritic chest pain
- Lobar consolidation
- Coarse creps
- ^vocal resonance
- Dull percussion
Outline the Tx of CAP
[beware resisitance, check travel Hx]
What are the atypical causes of Pneumonia?
Mycoplasma Pneumoniae → flu symptoms, insiduous onset, Tx = Macrolides [clarithromycin]
Legionella Pneumonia → contaminated water supply, headache & fever, Tx = macrolides
How is the severity of pneumonia assesed?
- Urea >7mmol/l
- RR >30
- BP → sys >90, dia <60
- Age >65
Scor >3 = admission, ^^mortality
Which classes of antibiotics inhibit cell wall synthesis?
Which classes of antibiotics inhibit Nucleic Acid synthesis?
Which classes of antibiotics inhibit protein synthesis?
- Fusidic Acid
Which antibiotics inhibit folate?
For the betalactams give some examples, MoA & sensitivities
- Penicillins → pen/ amoxicillin etc
- Cephalosporins → cephtriaxone
- Carbopenems → meropenem
- inhibit bacterial cell wall synthesis
- most gram +ve
- MSSA = resistant to pen & amox
- Enterococci = resistant to all cephalosporins
- P aeruginosa = resistant to all [except → tazocin, meropenem & cephtazidime]
For Glycopeptides give some examples, MoA, & sensitivites
e.g. Vancomycin/ Teicoplanin
- Inhibit cell wall synthesis
- Only gram +ves
For the aminoglycosides give some examples, MoA & sensitivities
e.g. Gentamicin/ Streptomicin
- Inhibit protein sythesis → irreversibly bind to 30S ribosomal unit
- mostly gram neg
- esp sepsis
For the tetracyclines give some examples, MoA & sensitivities
e.g. tetracycline, doxycycline
- Inhibit protein synthesis → reversibly bind to 30S ribosomal unit
- Staph & strep
- some gram -ve [NO e. coli]
- active against intracellular organisms [chlamydia, coxiella burnetti, plasmodium]
For the Macrolides give some examples, MoA & sensitivities
e.g. Erythromycin, Clarithromycin
- reversibly bind to 30S ribosomal unit → inhibit protein synthesis
- ~mycobacteria [not MTB]
- Erythromycin → CAP, Campylobacter gastroenteritis
- Calrithromycin → CAP, H. Pylori, mycobacter
Ouline the features of influenza virus? [Virology]
How is type A classified?
- Segmented virus
- 3 subtypes [A, B & C]
- A = Pandemic Flu
- A & B = 8 RNA segments, cause epidemics
- C = 7 RNA, milder
- Classification of type a
- Haemagluttinin → cell entry [16 types], antigenic drift
- Neurominidase → exit cells [9 types]
- e.g. H5N1
What are the symptoms & complications of flu?
- Incubation ~1-4d
- 'flu like symptoms' → fever, malaise, sore throat, joint pain
- pneumonia [secondary bacterial infections]
- otitis media etc
How is 'flu treated?
- Oseltamivir [tamiflu]
- Neurominidase blocker
- pre-exposure prophylaxis in at risk groups [pregnant]
- soon after Pc
- A/E → CNS & GI
- trivalent [2 A strains & 1 B]
Outline the Life cycle of HIV?
- ssRNA retrovirus
- reverse transcribed into host DNA → latent infection
- mainly in T4 [also DC & macrophages]
- antiretrovirals only target circulating virus.
What are the seroconversion symptoms of HIV?
Seroconversion = development of detectable antibodies [i.e. finding out your HIV+]
- Sore throat
- Also → headache, lymphadenopathy, myalgia
Give 4 AIDS defining symptoms
- Palatal Kaposis Sarcoma [purple macules, herpes virus]
- Oesophageal Candida
- Oral KS
- Apthous Ulcers
- Cerebral Toxoplasmosis
- CMV retinits → Late stage
What are the different types of antiviral therapies available for HIV infection?
Reverse Transcriptase inhibitors → nucleoside analogoues or allostearic inhibitors
Protease inhibitors → e.g. Atazanivir
Co-receptor binding inhibitors → maraviroc [block CCR5 receptor]
Aim of therapy is to decrease viral load.
How does bacterial resisitance evolve?
- Spotaneous Mt in selective environment
- confers advantage
- rapid proliferation → resisitant
What are the 4 mechanisms of drug resisitance in bacteria?
Alter drug target → block antibiotic/ create new target
Alter access to drug → decrease cellular permeability
Enzymatic inactivation → destroy/alter anti-b
New metabolic pathway → bypass inhibited RXN
How are resistant genes spread between bacteria?