BACTERIAL MENINGITIS Timeline, Organisms, Presentation

(Day 4/100 days of productivity) - Haemophilus Influenzae card!

Today was mostly spent working on research, textbooks, but and making flashcards like this for microbiology!

Pneumonia

 “Pneumonia is called the old man’s friend because, left untreated, the sufferer often lapses into a state of reduced consciousness, slipping peacefully away in their sleep, giving a dignified end to a period of often considerable suffering.” -Dr John Pillinger

Pneumonia is a major cause of morbidity and mortality worldwide, the 6th largest cause of death in the USA. It is also economically costly in antibiotics, time off work, and hospitalisation

In half the cases the cause is not identified

In those where a cause is identified, S. pneumoniae is the most common cause

The reservoir is usually humans (oneself or a contact) 

spread is through respiratory droplets

Community acquired eg Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Mycoplasma pneumoniae, Chlamydia pneumoniae

Noscomial (hospital acquired) eg Enterobacteriaceae, Staphylococcus aureus, Anaerobes, Pseudomonas aeruginosa

Many patients have an underlying condition, e.g. bronchitis, asthma, a viral infection, tumours

Characterised by the alveolar sacs filling up with pus, giving rise to a purulent sputum

Symptoms

Results in chest tightness or pain, difficulty in breathing, fever or hypothermia, reduced blood oxygen, coughing to clear mucus, chest will sound “dull” when tapped, tachypnea, tachycardia (>100 bpm) or bradycardia (< 60 bpm), central cyanosis, altered mental status.

Streptococcus pneumoniae: Rust-colored sputum

Pseudomonas, Haemophilus, and pneumococcal species: May produce green sputum

Klebsiella species pneumonia: Red currant-jelly sputum

Anaerobic infections: Often produce foul-smelling or bad-tasting sputum

Diagnosis

X-ray showing infiltrates

Elevated temperature

Changes in WBC counts

Culture confirmation

Serum chemistry panel

Arterial/venous blood gas 

Serum free cortisol value and lactate level

Treatment

Intensive treatment, potentially to ITU level

Tailored antimicrobials if possible - limited options with viruses

Treatments include: analgesia and antipyretics, physiotherapy,  bronchodilators and N-acetylcysteine, suctioning and bronchial hygiene, ventilation 

Pathogenesis 

Causative agents can enter the lungs through inhalation, aspiration, spread across mucous membrane (some viruses), haematogenous spread (occasionally, e.g. IV drug users with S. aureus septicaemia) and penetrating injury (rare).

Immune response is triggered in the lung and there are local defence factors in the respiratory secretions

Cilia, if functioning, will move material up the respiratory tract, but if damaged this physical defence is impaired

The lungs also have a resident macrophage population (alveolar macrophages) but they are of limited use against several respiratory pathogens that possess a capsule

some organisms can even replicate in these cells

Damage to the lung is caused by the microbes and the immune response

 Enzymes released by the bacteria

Factors released by immune cells that cause local irritation and cell apoptosis

Systemic manifestations follow eg

Oxygen deprivation – thickening of the membranes reduces gas transfer

Systemic shock – especially with Gram-negative bacilli such as Haemophilus influenzae

Different anatomy notes form this semester Supplies used (not all at once, I mix and match): Faber-Castell Coloured Pencils (48 Pack) - https://amzn.to/2Kd1mUy Staedtler Triplus Fineliners - http://amzn.to/2pghonI Stabilo Point 88 Fineliner - https://amzn.to/2qU8fC9 Sharpie Pens - https://amzn.to/2HTRmP2 Uni Pin 0.1 Fineliner - https://amzn.to/2HmXp1z Crayola Supertips - https://amzn.to/2HVW1jr Bic Ballpoint Pen - https://amzn.to/2HmCjk0 Stabilo Swing Cool Highlighters - https://amzn.to/2HKxPTu

Influenza

Happy flu season! I’ve just been stuck inside for 5 days with a mild case, so this is a bit bitter

There are 3–5 million cases of flu per year, and ~375,000 deaths, usually in older, younger, and immunocompromised individuals.

Enveloped, Single-stranded RNA virus

First identified in 1933, but existed long before

Generally considered an infection of the bronchi

so effectively a form of bronchitis – i.e. it causes inflammation of the bronchi 

There are 3 types - A, B and C

B & C appear restricted to humans 

C is less common

A is found in wide range of species including pigs and poultry as well as man

Type A appears to be responsible for more severe disease

Basics

Transmission by aerosols

Incubation ~2 days

Contagious during first 3-5days of illness

Symptoms – fever, myalgia, headache, dry cough, sore throat, aches, fatigue

Recovery ~7-10 days for most

Complications – most frequent = secondary bacterial pneumonia, rarely = viral pneumonia, myocarditis, encephalitis

No specific treatment

Vaccination for high risk groups including the elderly, health care workers, those with underlying respiratory conditions.

Avian

The main reservoir is wildfowl that are resistant to the disease

doesn’t usually affect animals other than poultry and pigs

However some transfer events occur

Seasonal

Incidence highest in winter

Strains vary from year to year -  hard to predict and vaccinate (this year’s vaccine has been pretty rubbish)

Pandemic

Can be caused by any strain that has not been seen in the human population for many years

New strains evade the herd immunity that exists to previously encountered strains

1918 /19 –( Spanish) estimated 40-50 million deaths worldwide

1957 – Influenza A/H1N1 (Asian)

1968 – Influenza A/H3N2 (Hong Kong)

Eventually the virus runs out of susceptible hosts and the epidemic fizzles out

Experts generally agree another pandemic is inevitable, and may be imminent – maybe we have had some minor pandemics 

16000 confirmed H1N1 deaths in 2009 affecting over 200 countries

Consensus is that the prompt action of the Hong Kong authorities probably prevented a pandemic in 1997

The prediction is scary - for industrialised countries they predic 1.0 – 2.3 million hospitalisations

280,000-650,000 deaths 

in two years

A network of 112 centres monitor flu isolates to identify unusual strains that can then be examined further

The WHO has a Pandemic Preparedness Plan in place http://www.who.int/influenza/preparedness/pandemic/en/

Diagnosis

Generally based on GP diagnosis

Virus isolation / virus demonstration from nasopharyngeal secretions during acute phase

Demonstration of viral antigen in secretions

Antibody rise using paired sera ( 1st sample taken between days 1-3 of illness, 2nd taken around day 12 of illness) by haemagglutination inhibition or complement fixation test

Molecular methods evolving rapidly – in particular in response to the recent epidemic/pandemic strains emerging

A range of respiratory illnesses have the same symptoms, only laboratory testing can confirm the aetiological agent

Treatment/Vaccination 

In the UK NICE argue that immunisation against predicted strains is the best form of defence – traditionally focused on the elderly and those with underlying lung problems, but recently started rolling out a childhood vaccine (nasal spray)

Vaccines generally based on the H & N surface structures which mutate, however hopes of an M protein based vaccine which will give longer lasting protection raised recently

Antivirals

Antivirals not recommended in otherwise healthy people (amantadine should not be used at all) - should ride it out

However when incidence reaches a certain level zanamivir and oseltamivir should be used in those considered high risk for the development of complications – PROVIDED THAT TREATMENT IS STARTED WITHIN 48 HOURS OF ONSET OF SYMPTOMS

Resistance is becoming an issue

Satellite phenomenon of Haemophilus influenzae around Staphilococcus aureus in blood agar

ANTIBIOTICS CHEAT SHEET :)

Also, REMEMBER!!!!

* Sulfonamides compete for albumin with:

Bilirrubin: given in 2°,3°T, high risk or indirect hyperBb and kernicterus in premies

Warfarin: increases toxicity: bleeding

* Beta-lactamase (penicinillase) Suceptible:

Natural Penicillins (G, V, F, K)

Aminopenicillins (Amoxicillin, Ampicillin)

Antipseudomonal Penicillins (Ticarcillin, Piperacillin)

* Beta-lactamase (penicinillase) Resistant:

Oxacillin, Nafcillin, Dicloxacillin

3°G, 4°G Cephalosporins

Carbapenems 

Monobactams

Beta-lactamase inhibitors

* Penicillins enhanced with:

Clavulanic acid & Sulbactam (both are suicide inhibitors, they inhibit beta-lactamase)

Aminoglycosides (against enterococcus and psedomonas)

* Aminoglycosides enhanced with Aztreonam

* Penicillins: renal clearance EXCEPT Oxacillin & Nafcillin (bile)

* Cephalosporines: renal clearance EXCEPT Cefoperazone & Cefrtriaxone (bile)

* Both inhibited by Probenecid during tubular secretion.

* 2°G Cephalosporines: none cross BBB except Cefuroxime

* 3°G Cephalosporines: all cross BBB except Cefoperazone bc is highly highly lipid soluble, so is protein bound in plasma, therefore it doesn’t cross BBB.

* Cephalosporines are "LAME“ bc they  do not cover this organisms 

L  isteria monocytogenes

A  typicals (Mycoplasma, Chlamydia)

M RSA (except Ceftaroline, 5°G)

E  nterococci

* Disulfiram-like effect: Cefotetan & Cefoperazone (mnemonic)

* Cefoperanzone: all the exceptions!!!

All 3°G cephalosporins cross the BBB except Cefoperazone.

All cephalosporins are renal cleared, except Cefoperazone.

Disulfiram-like effect

* Against Pseudomonas:

3°G Cef taz idime (taz taz taz taz)

4°G Cefepime, Cefpirome (not available in the USA)

Antipseudomonal penicillins

Aminoglycosides (synergy with beta-lactams)

Aztreonam (pseudomonal sepsis)

* Covers MRSA: Ceftaroline (rhymes w/ Caroline, Caroline the 5°G Ceph), Vancomycin, Daptomycin, Linezolid, Tigecycline.

* Covers VRSA: Linezolid, Dalfopristin/Quinupristin

* Aminoglycosides: decrease release of ACh in synapse and act as a Neuromuscular blocker, this is why it enhances effects of muscle relaxants.

* DEMECLOCYCLINE: tetracycline that’s not used as an AB, it is used as tx of SIADH to cause Nephrogenic Diabetes Insipidus (inhibits the V2 receptor in collecting ducts)

* Phototoxicity: Q ue S T  ion?

Q uinolones

Sulfonamides

T etracyclines

* p450 inhibitors: Cloramphenicol, Macrolides (except Azithromycin), Sulfonamides

* Macrolides SE: Motilin stimulation, QT prolongation, reversible deafness, eosinophilia, cholestatic hepatitis

* Bactericidal: beta-lactams (penicillins, cephalosporins, monobactams, carbapenems), aminoglycosides, fluorquinolones, metronidazole.

* Baceriostatic: tetracyclins, streptogramins, chloramphenicol, lincosamides, oxazolidonones, macrolides, sulfonamides, DHFR inhibitors.

* Pseudomembranous colitis: Ampicillin, Amoxicillin, Clindamycin, Lincomycin.

* QT prolongation: macrolides, sometimes fluoroquinolones

hey! could you do a study tips post on studying w friends who aren't doing the same subjects? like, how to make good flashcards/questions and answers etc so they can quiz you and give you hints etc even if they don't know the content?

How to Effectively Study with Friends

Using Flash Cards

Oh easy peasy! Simply write examination style questions on your flashcards - that way when your friends read the questions out to you, you’ll be testing yourself in a way that might show up on the easier exam questions. Reason being that in order to cover all the topics, your questions will tend to be somewhat simple e.g. describe the different components of x, explaining how they related to y. Obviously, flash cards aren’t the best way to study more complex interrelationships between ideas/concepts, which should be explored more in a mind map fashion. For tips on mind maps, you can check out my briefing here. 

Using Your Existing Study Notes

Other than flash cards, if you intend to study in groups for most subjects, one of the best ways to do that is to use the Cornell Notetaking System (which you can read about with my personal tips here). Writing the questions out as you study saves you the trouble of writing out questions for your friends to test you on, and as well as that, means you can test yourself almost as well without them for any times when you’re studying solitary. 

Using Essay or Long Response Questions

For long response essays, it’s better to use principles like the rubber duck method, i.e. explaining how concepts relate to each other as if the other person doesn’t know anything about it. So give your friends a list of essay questions and explain part by part in a logical sequential order how you would answer that question e.g. I would talk about the involvement of person A in event B, and explain their impact through examples C, D and E, etc. 

Choosing the Right Study Group 

Most of all, make sure you rally and encourage each other. Work with people who are like-minded, rotate between each other and have someone who will keep the others on task when you start getting too carried away when studying. Having a goal on what you intend to get finished during a group study session will make sure you always get more out of the session than studying alone!

Hope that helps! ^_^

13.02.18 Revision

I’ve always got my trusty reference book with me at work, but sometimes I like to read over a few topics just in case anything ever shows up :) and oml trying to write referral letter templates be like: …has been measuring … measured between 5-12 mmol/L … BGL measuring between 5-12 mmol/L  OTL

🎼 The Boots - Gugudan 구구단

Follow optomstudies for daily original posts and study masterposts! Links: all originals + langblr posts + 15-part college 101 series + web directory!

Hello everyone, welcome to my latest 4-part series to help you land that job after uni! This series will cover what to do before, during, and after a job interview to ensure you leave a positive impression on the interviewers and hopefully help you cinch opportunities! Enjoy!

How To Set Your Career On The Right Path Before You Even Graduate! (Link) Part 2: During The Interview (Link) Part 3: After The Interview (Link)

Research the job position and company values. 

It is critical to tackle all the requirements in your cover letter as well as your resume, and to be able to answer questions in the interview in a way that highlights you have those values the company is seeking. Even if the company doesn’t have a public ad, research similar positions at different companies and read those job descriptions. Have situations you’ve dealt with in your arsenal for answering situational questions. 

Make sure your resume is updated perfectly. 

It’ll save you a lot of time if you just update your resume every time you start something new! Standard stuff: Use ‘clean’ standard fonts, white A4 paper, single sided, 2 cohesive colours max. Include at least the minimum components or a combination of them: the rough order should be:

Career Objective

Education

Relevant Experience (include key responsibilities and noteworthy performance points)

Extra-Curricular Activities (if relevant)

Skills

Referees (usually just write “available on request”)

Cold call!

This is how I got my first relevant job as an optical assistant, which in a way, led to my current position today. Even whilst I was working as an optical assistant, occasionally we would get a new hire if their resume seemed good and they interviewed well. 

Prepare for common interview questions. 

Have scenarios ready illustrating how you dealt with a difficult situation 

nasty moodboard