يالله 💙

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

This week’s infographic is a metabolic map showing the chemical reactions that happen inside our body. You can check out the full size version here.

http://www.youtube.com/embed/TS0zA6DSfvk?feature=oembed

الرقية الشرعية الشاملة فارس عباد 1 (by netter2cool)

A Basic Demonstration of Optical Cloaking (by UniversityRochester)

(via https://www.youtube.com/watch?v=TkdZ8k4VHZ4)

Frankenstein’s…bacteriophages?

A group of scientists have just published their work in CellPress on synthesising novel phages using common viral structures (Figure 1), to target a range of bacterial hosts. Anyone who frequently reads my posts will be fully aware of what bacteriophages are, however put simply phages are viruses that target bacteria (Figure 1). Currently a lot of research is going into these little guys to utilise them for both therapeutic and diagnostic purposes. 

Figure 1. Image depicts a transmission electron micrograph of a phage (left) and a diagrammatic representation of the phage on the (right) showing all the major components that make up the protein coat.

Phages have an elaborate protein coat that surrounds their DNA cargo (contained within the head, Figure 1). They scan their surrounding environment for potential ‘prey’ by using their tail fibres to interact with their cognate receptors. The diversity of receptors is immense and many still go unidentified even for well characterised phages. Once a target is found, the baseplate then irreversibly attaches to the cell wall of the bacteria and the DNA can be transferred into the cytoplasm of the cell. 

Unlike current therapeutics, the sheer diversity between phages means that they are highly specific with limited host ranges to the species or even strain level. As a result, for phage therapy to be effective, a cocktail of phages needs to be employed to target a wide range of potential bacterial hosts. To improve the host ranges of phage groups such as this one are trying to synthesis novel structures from existing phages - much like how Frankenstein stitched together a new human body from pre-existing parts (Figure 2). 

Figure 2. Simplified image showing how bacterial components can be shuffled between genomes of related phages with different host ranges. 

Innovatively, this group used a well characterised yeast-based (Saccharomyces cerevisiae) platform for capturing phage genomes to allow their genetic manipulation (Figure 3). Phage genomes could then be inserted into a yeast artificial chromosome (YAC) then manipulated. Yeast are fairly easy to genetically modify by homologous-recombingation, making this system far easier to employ than other methods. The YAC was then recovered and transformed into the normal host bacteria, allowing the generation of new phage particles. Unlike other methods phage generated via this method were relatively easy to reboot back into active viral particles.

Figure 3. Illustration of the genetic manipulation of phage DNA to generate hybrid phages with altered host ranges. 

The group managed to show that by swapping modular components such as tail fibres between phages, new host specificity could be generated. Thus illustrating that gene swapping can overcome strain or species barriers if the need arises. This work will hopefully lead way to further improve phage therapy and decrease the persistent need for the identification of novel phages. Further work needs to be done on increasing the scope of their work, but they have created a framework that will hopefully be able to reboot more synthetic phages.

“Our results show that common phage scaffolds can be re-targeted against new bacterial hosts by engineering single or multiple tail components. This capability enables the the construction of defined phage cocktails that only differ in their host range determinants and can be used to edit the compositions of microbial consortia and/or treat bacterial infections.” - Ando et al, 2015

Sources:

Engineering Modular Viral Scaffolds for Targeted Bacterial Population Editing, 2015. Ando, H., Lemire. S., Pires. D.P., Lu. T.K., Cell Systems , Volume 1 , Issue 3 , 187 - 196  

الشيخ عبد الباسط عبد الصمد(التكوير و سورة القدر)روعة (by theeslamcena)

Cone snails might not seem like deadly predators, especially when you consider how easily a fish could outswim them. However, these snails await the cover of darkness to prey on sleeping fish. They appear to release paralyzing chemicals before using a venomous barb to finally put the fish out of its misery. (Source)