T-b-a-blr-blog - Untitled

(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!

Antimicrobial Agents - Inhibition of DNA and Protein Synthesis

Bacterial chromosome replication

DNA replication

Bacterial Topoisomerases 

maintain DNA in appropriate state of supercoiling 

cut and reseal DNA

DNA gyrase (topoisomerase II) introduces negative supercoils 

Topoisomerase IV decatenates circular chromosomes 

these are the targets of the quinolone antibacterial agents 

Quinolones

bind to bacterial DNA gyrase and topoisomerase IV after DNA strand breakage 

prevent resealing of DNA 

disrupt DNA replication and repair 

bactericidal (kill bacteria)

Fluoroquinolone is particularly useful against

Gram +ves: Staphylococcus aureus, streptococci 

Gram -ves: Enterobacteriacea; Pseudomonas aeruginosa 

Anaerobes: e.g. Bacteroides fragilis 

many applications e.g. UTIs, prostatitis, gastroenteritis, STIs 

Adverse effects

Relatively well tolerated

GI upset in ~ 5% of patients 

allergic reactions (rash, photosensitivity) in 1 - 2% of patients 

Inhibition of Bacterial Protein Synthesis 

Macrolides 

in 1952: Erythromycin was isolated as the first macrolide (Streptomyces erythreus) 

Newer macrolides: clarithromycin, azithromycin 

Structurally they consist of a lactone ring (14- to 16-membered) + two attached deoxy sugars 

Mode of action 

bind reversibly to bacterial 50S ribosomal subunit 

causes growing peptide chain to dissociate from ribosome → inhibiting protein synthesis 

bacteriostatic (stops reproduction)

Macrolides’ spectrum of activity

good antistaphylococcal and antistreptococcal activity 

treatment of respiratory & soft tissue infections and sensitive intracellular pathogens • e.g. Chlamydia, Legionella 

Adverse effects

Generally well tolerated

nausea 

vomiting 

diarrhoea 

rash 

Aminoglycosides

large family of antibiotics produced by various species of Streptomyces (“mycin”) and Micromonospora (“micin”) 

include: streptomycin, neomycin, kanamycin, gentamicins, tobramycin 

Structure = linked ring system composed of aminosugars and an aminosubstituted cyclic polyalcohol 

Mode of action of aminoglycosides

Bind irreversibly to 30S ribosomal subunit 

disrupt elongation of nascent peptide chain 

translational inaccuracy → defective proteins 

bactericidal 

Spectrum of activity 

broad spectrum; mainly aerobic G-ve bacilli (e.g. P. aeruginosa) 

used to treat serious nosocomial infections (hospital acquired infections)

First TB antibiotic

Used for cystic fibrosis 

Adverse effects

all aminoglycosides have low Therapeutic Index (only a small amount needed to become toxic)

renal damage, ototoxicity, loss of balance, nausea 

Hi optom! I'm very new to the studyblr community and it's my first term of university. I was a straight A student in high school and i am not performing well in my classes. In fact... I'm doing terribly. About a B to B- average. I know I'm probably not the first to go through so I've been trying to find posts that help students cope with this. Resources. Helpful tips. Is there a tag you can recommend? Any posts that you've encountered/wrote that I could peruse? Thank you very much for any help!

Hey there, thanks for asking. This is actually a very common problem experienced by people as they progress from high school to university. 

The problem is that mediocre study techniques and a combination of natural ability may have gotten you straight As whilst in high school, but it’s just not going to cut it in university. Cracking down on yourself and sitting down for more hours isn’t going to make your grades much better; it’s just doing more of the same mediocre studying. 

So you basically need to read up on good studying techniques and actually apply them to your studies. 

Everything You Need to Cover To Succeed As A Student

I actually have a web directory of all my study tips which already lists all these links.

So because the problem you have at its base is most likely that you’re using high school level techniques to tackle university-level problems, you’ll need to find resources on all areas related to good studying. For some of these areas, I have a related post, but for the more generalised topics like procrastination, I haven’t yet put one out because if I do, I want to be certain that the post will be unique, useful and practical. 

Without further ado, here’s a list of all the tags/areas you should work through and evaluate whether you need to change your current study habits if you want to be a 4.0/HD student at university. 

Firstly, have a read of my recent answer about 20 Things You Can Do To Prepare for University, and click through to any of the parts of my 15-Part University 101 Series. 

Time management

Organisation (see Part 3 Studying and Part 8 Four Secrets from University and Part 11 Adapting to Uni Studying which covers how you can manage university workloads on the whole and specific changes to your studies you should make)

Motivation

Discipline / Staying Focused

Procrastination (see post by @samsstudygram​)

Study Methods (I’ve got one on the Blank Paper Method and the Cornell Method)

Exams (I’ve got a multi-part series in the works)

Study Materials (see Part 2 of my University Series for some tips)

Studying from Textbooks (see Part 12 How To Study From Textbooks in Uni which deals with this specifically)

Self Care (you can see my tag here of my own + useful curated posts)

Spaced Repetition (use Anki!)

Study Space (I have a masterpost with tips here)

Hope that helps! If you have a specific question about any areas then let me know! 

Neisseria gonorrhoeae

PMN filled with Neisseria gonorrhoeae => Gram- diplococci, glucose fermenter, non maltose fermenter, oxidase positive.

Very inflammatory response: exudate with high number of PMN. TX with ceftriaxone and always ALWAYS test for Chlamydia trachomatis (since is more common and exudate is similar)

How to tell them apart? 

N. gonorrhoeae’s exudate is more purulent than C. trachomatis.

N. gonorrhoeae’s exudate is “greenish-yellowish” but C. trachomatis’s is whiter.

N. gonorrhoeae is always inside a PMN while C. trachomatis is not 

Grows in Thayer-Martin medium (chocolote agar + antibiotics, is a selective medium)

What is Acute or Subacute Bacterial Endocarditis?

Acute or Subacute Bacterial Endocarditis is an infection of the heart’s endocardium. The endocardium is the inner lining of the heart muscle, which also covers the heart valves. Bacterial Endocarditis can damage or even destroy your heart valves. The difference between acute and subacute bacterial endocarditis is acute bacterial endocarditis is a sudden onset, whereas subacute bacterial endocarditis is a gradual onset.

Acute endocarditis most often occurs when an aggressive species of skin bacteria, especially a staphylococcus (staph), enters the bloodstream and attacks a normal, undamaged heart valve. Once staph bacteria begin to multiply inside the heart, they may send small clumps of bacteria called septic emboli into the bloodstream to spread the infection to other organs, especially to the kidneys, lungs and brain. Intravenous (IV) drug users are at very high risk of acute endocarditis, because numerous needle punctures give aggressive staph bacteria many opportunities to enter the blood.If untreated, this form of endocarditis can be fatal in less than six weeks.

Subacute endocarditis is caused by one of the viridans group of streptococci (Streptococcus sanguis, mutans, mitis or milleri) that normally live in the mouth and throat. Streptococcus bovis or Streptococcus equinus also can cause subacute endocarditis, typically in patients who have some form of gastrointestinal cancer, usually colon cancer. Subacute endocarditis tends to involve heart valves that already are damaged in some way, and it usually is less likely to cause septic emboli than acute endocarditis. If untreated, subacute bacterial endocarditis can worsen for as long as one year before it is fatal.

Micobacterium tuberculosis DX

Auramine-Rhodamine staining bacilli: fluorescent apple green (sensitive but not specific). If positive, do acid fast.

Acid Fast

Lowenstein-Jensen medium: aerobic, slow growing (2-3weeks)

PPD or Mantoux Test: measure 48-72h after. POSITIVE: >/= 5mm in VIH+ pts, >/=10mm in high risk population (IVDA, poverty, immigrants from high TB area, physicians, nurses), >/=15mm in low risk population

Positive indicates exposure, but not necessarily active disease.

Quantiferon-TB Gold Test: measures IF-gamma

Niacin producers

Catalase negative at 68° and catalase active at body T°

No serodiagnosis

Most Common facts about infectious diseases

1. Most common cause of septic arthritis in a person less than 40 years old = Gonococcus 2. Most common cause of osteomyelitis in general population = S. aureus 3. Most common cause of osteomyelitis in Sickle Cell patients = Salmonella 4. Most common cause of osteomyelitis due to nail-puncture wounds = Pseudomonas (V.Imp!) 5. Most common parasitic infection of the brain = Neurocysticercosis 6. Most common cause of Encephalitis in USA = Herpes Simplex Virus (HSV) 7. Most common cause of dysentry in the USA = C. jejuni (undercooked poultry) 8. Second most cause of dysentry in the USA = Shigella (daycare centers) 9. Most common cause of pneumonia in nursing home residents = S. pneumoniae 10. Most common cause of malignant otitis externa = P. aeruginosa 11. Most common risk for contracting HIV in USA= Intravenous Drug Use 12. Most common presenting Manifestation of AIDs = P. carinii pneumonia 13. Most common cause of Menigitis in adolescents = N. Gonorhhaea 14. Most common cause of Meningitis in the USA = Streptococcus pneumoniae 15. Most common Neurological Manifestation of Lyme Disease = Facial Nerve palsy! 16. Most common Cardiac manifestation of Lyme Disease = AV Heart Block 17. Most Common viral STD in the USA = HPV ! 18. Most Common Complication of Mumps in Pre-pubertal Children = Encephalitis 19. Most Common Complication of Mumps in Pubertal and Post-Pubertal Adults (and Males) = Orchitis

Cysteine Growth Requirements

MICROBIOLOGY MNEMONIC

BoyFriend Lost Penis

B rucella

F rancisella

L egionella

P asteurella

or….

The four sisters “Ella” worship in the “cystein” chapel

Brucella

Francisella

Legionella

Pasteurella

Antimicrobial Agents  - Cell wall inhibitors

Based on mode of action • divided into families based on chemical structure

 Modes of action Interference with: 

cell wall synthesis 

protein synthesis 

nucleic acid synthesis 

plasma membrane integrity 

metabolic pathway 

Inhibitors of Bacterial Cell Wall (peptidoglycan) Synthesis 

The Beta-lactam Family 

The Glycopeptides 

Peptidoglycan is composed of N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM) repeat units, and amino acids.  Each NAM is linked to peptide chain and the peptide chains are cross-linked.

β-lactams 

Includes penicillin derivatives (penams), cephalosporins (cephems), monobactams, and carbapenems.

class of broad-spectrum antibiotics containing a β-lactam ring

Bacterial transpeptidase enzymes are responsible for catalysing cross-linking of the peptide chains

β-lactam ring bind to these transpeptidases – this inhibits cross-linking between peptide chains and prevents synthesis of stable PG

Cell wall synthesis ceases and the bacterial cells eventually die due to osmotic instability or autolysis. 

Glycopeptides 

Polypeptide agents - basic structural elements amino acids 

Vancomycin: 

complexes with peptide portion of peptidoglycan’s precursor units 

vancomycin is a large hydrophilic molecule able to form hydrogen bonds with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides

preventing PG transglycosylation reaction – PG precursor subunits (NAG-NAM+peptide) cannot be inserted into peptidoglycan matrix;

Vancomycin also alters bacterial-cell-membrane permeability and RNA synthesis

Uses:  serious Gram positive infections e.g. MRSA wound infection

Adverse effects:

damage to auditory nerve 

hearing loss (ototoxicity) 

“Red man/neck” syndrome - rash on face, neck, upper torso