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Pharmaforfun, Alexandria/, Alexandria (2026)

13/01/2026

✅As a clinical pharmacist delving into the IDSA guidelines for antimicrobial-resistant Gram-negative infections, the management of Carbapenem-Resistant Acinetobacter baumannii (CRAB) presents a particularly challenging puzzle.

After extensive review, one principle stands out: the antibiotic regimen must include a sulbactam-containing agent.

The current guidance is precise.

The preferred regimen is ✅✅sulbactam-durlobactam in combination with a carbapenem (e.g., imipenem-cilastatin or meropenem).

If this newer agent is unavailable, the alternative is high-dose ampicillin-sulbactam
(providing 9 grams of the sulbactam component daily) in combination with at least one other active agent,

the question is

🛑🛑🛑Where is the Antibiotic in Sulbactam-Durlobactam? ⁉️

In the familiar ampicillin-sulbactam duo, the roles seem clear: ampicillin is the beta-lactam antibiotic, and sulbactam is the beta-lactamase inhibitor. So, in the sulbactam-durlobactam combination,

🛑🛑🛑 where is the primary antibiotic if both components are classified as inhibitors?🤔👀⁉️

The answer is crucial and often surprising 😅

: Sulbactam is the antibiotic

Unlike other beta-lactamase inhibitors like clavulanate or tazobactam, which have minimal direct antibacterial activity,

✅sulbactam is a potent bactericidal agent against A. baumannii in its own right.

✅Its mechanism involves the direct inhibition of penicillin-binding proteins (PBP-1 and PBP-3), effectively disrupting cell wall synthesis. Therefore, in both regimens, sulbactam is the active therapeutic backbone.

So we can say that This dual capability positions sulbactam as a 'two-in-one' agent for Acinetobacter: a primary bactericidal antibiotic and at the same time a synergistic enzyme inhibitor."

24/11/2025

Today, we continue our journey to unravel the mysteries of the endless war between antibiotics and bacteria.

In previous posts, we've explored ✅Extended-Spectrum β-Lactamase-Producing Enterobacterales (ESBLs)

✅AmpC β-Lactamase-Producing Enterobacterales.

Now, we delve deeper into the realm of severe antibacterial resistance with ✅Carbapenem-Resistant Enterobacterales (CRE).

We'll examine the tips and tricks for managing each class.

First, let's categorize CRE infections outside the urinary tract into two main groups:

☑️Infections that are Not Carbapenemase-Producing

☑️Infections that are Carbapenemase-Producing

This article will focus on the second, more complex group. "Carbapenemase-producing CRE"

and it can be further divided into three critical classes based on the enzyme they produce.

🔴1. CRE with KPC Production

Management:
The preferred first-line treatment options for KPC-producing Enterobacterales infections are:

✔️Meropenem-vaborbactam

✔️Ceftazidime-avibactam

I✔️mipenem-cilastatin-relebactam

Cefiderocol serves as an excellent alternative option

🔴2. CRE with OXA-48-Like Production

Management:
For OXA-48-like-producing Enterobacterales,

✔️ ceftazidime-avibactam is the sole preferred treatment from the novel Beta-Lactam/Beta-Lactamase Inhibitor (BL/BLI) class.

But why only Ceftazidime-Avibactam?⁉️

The other novel BL/BLIs are not reliable against OXA-48 due to the specific inhibitor profiles:

✅Meropenem-Vaborbactam (M/V):

Vaborbactam is an excellent inhibitor of KPC but has poor activity against OXA-48-like enzymes.

✅Imipenem-Cilastatin-Relebactam (I/R):

Similarly, Relebactam powerfully inhibits KPC but has weak activity against OXA-48-like enzymes.

Therefore, only avibactam in the ceftazidime-avibactam combination effectively neutralizes the OXA-48 threat. Cefiderocol remains a valuable alternative treatment option.

🔴3. CRE with NDM or Other MBL Production

Management:
The preferred strategies for these formidable infections are:

✔️Ceftazidime-avibactam in combination with aztreonam

✔️Cefiderocol as monotherapy

Why is the "Triple Combination" of Ceftazidime-Avibactam + Aztreonam used? ⁉️

Why not as KPC and OXA 48 only Ceftazidime-avibactam without Aztreonam ⁉️

This is a brilliant pharmacological strategy:

✅Aztreonam's Role: Aztreonam is a unique monobactam beta-lactam that is stable against MBLs and is not hydrolyzed by them.

✅Avibactam's Role: MBL-producing bacteria almost always carry other beta-lactamases (like ESBLs, AmpCs). Avibactam in the ceftazidime-avibactam formulation protects aztreonam from these other enzymes.

☑️☑️In essence, this combination uses aztreonam to target the bacterium while using avibactam as a protector to shield it from all non-MBL enzymes.

This creates a powerful, synergistic effect against an otherwise pan-resistant pathogen.

13/11/2025

Today, we are continuing on exploring a critical paradox in clinical microbiology: why an antibiotic that appears "Susceptible" on a culture report may not be the best choice for the patient. ⁉️

Our focus is on infections caused by AmpC β-Lactamase-Producing Enterobacterales.

My own journey into understanding this paradox began with a culture growing Morganella morganii. It was our ( me and the physician) first time to know about this organism

So This unfamiliar organism sent us on a deep dive into the world of AmpC β-lactamases to unravel the mystery of the 'inoculum effect.'"

✅What are AmpC β-Lactamases?

AmpC β-lactamases are enzymes produced by certain gram-negative bacteria. While they are generated at low, basal levels by some organisms, the problem arises when production is amplified. These enzymes efficiently hydrolyze and inactivate a wide range of β-lactam antibiotics

✅The Usual Suspects: The "SCEAMP" Organisms

The primary members of the Enterobacterales family known for this inducible resistance are encapsulated by the helpful mnemonic "SCEAMP":

☑️Serratia

☑️Citrobacter freundii

☑️Enterobacter

☑️Aeromonas

☑️Morganella

☑️Providencia

✅The Two Tiers of Resistance

The clinical challenge of AmpC producers lies in two tiers of resistance:

✅Basal (Low-Level) Production:
The bacterium always produces a small, baseline amount of the AmpC enzyme. This is sufficient to hydrolyze "weaker" β-lactams as, rendering them ineffective from the start.

🔴Affected Drugs: Cefazolin, Ampicillin, Amoxicillin.

☑️Clinical Pearl: You would never use Cefazolin to treat a serious infection with a known AmpC producer.

✅Increased (High-Level) Production:
This is the heart of the paradox. The bacterium can significantly ramp up its production of the AmpC enzyme. This is often triggered by exposure to certain antibiotics themselves, a process known as induction.

🔴Affected Drugs: This includes "stronger" antibiotics like 3rd generation cephalosporins (Ceftriaxone, Cefotaxime, Ceftazidime) and Aztreonam. While they may withstand the basal enzyme levels, they are destroyed by the high-level surge.

☑️Clinical Pearl (The "Inoculum Effect"): A lab report may initially list the isolate as "Susceptible" to Ceftriaxone. However, during treatment, the antibiotic can select for pre-existing mutant bacteria that permanently overproduce AmpC (a state called "derepression"). This leads to treatment-emergent resistance, causing the therapy to fail even though it started with a seemingly appropriate drug

✅When selecting an antibiotic, we must consider two key properties: its potential to induce AmpC production and its ability to withstand hydrolysis by the enzyme.

☑️The Carbapenem Solution:

🔴Imipenem is a potent AmpC inducer, but it remains highly effective because it forms a stable, irreversible complex with the AmpC enzyme, jamming its active site. Meropenem and Ertapenem, while less studied for induction, share this superior stability against hydrolysis, making Carbapenems a reliable choice for serious infections.

☑️The Cefepime Advantage:

Cefepime, a 4th generation cephalosporin, is often the ideal agent for these infections. It possesses a dual advantage: it is a weak inducer of the AmpC gene, and its molecular structure is highly stable against hydrolysis by the AmpC enzyme. This is why guidelines suggest Cefepime for treating infections caused by organisms at moderate risk of significant AmpC production

✅✅Conclusion

Understanding AmpC β-lactamase producers is essential for preventing therapeutic failure. The key takeaway is to look beyond the initial susceptibility report for "SCEAMP" organisms. For serious infections, avoiding high-risk inducers like 3rd generation cephalosporins in favor of stable, low-inducing agents like Cefepime or the rock-solid Carbapenems is a cornerstone of effective antimicrobial stewardship

06/11/2025

"Susceptible" Antibiotic Is not all time the right Choice

Today our topic is about Extended-Spectrum β-Lactamase -Producing Enterobacterials ( ESBL- E)

Have you ever heard about an antibiotic that is sensitive in culture but we don't use it?! 😊

When I started my job this was a very strange point for me and it's still hard to be believed by many physicians. How can the antibiotic be sensitive in culture and we still can't use it? One of the secrets of this topic is going to be discovered today.

✅The ESBL Mechanism: A Master Key of Resistance

ESBLs are enzymes that inactivate most penicillins, cephalosporins, and aztreonam. This means that penicillins (ampicillin, amoxicillin) and 3rd generation cephalosporins (ceftriaxone, cefotaxime) are unequivocally destroyed by ESBL enzymes.

This leads to a critical rule: If a lab identifies an ESBL-E, you should consider ALL other penicillins and cephalosporins (except the specific caveats for piperacillin-tazobactam and cefepime) as
🛑UNACCEPTABLE choices, even if the lab report lists them as "Susceptible."

✅This is the heart of the paradox. The "Susceptible" result can be misleading because standard lab tests don't always replicate the complex environment of a real infection in the human body.

✅The Golden Exception and Non-Beta-Lactam Options

Fortunately, not all options are lost:
1. Carbapenems(e.g., meropenem, ertapenem)
are highly reliable and the gold standard for serious ESBL-E infections. They are not inactivated by ESBLs.

2. Non-β-lactam agents (e.g., ciprofloxacin, trimethoprim-sulfamethoxazole, gentamicin, doxycycline) are not inactivated by ESBLs. However, their use depends on confirmed susceptibility, as ESBL-E often carry co-resistance to these other classes.

🛑🛑🛑The "Therapeutic Gray Zone": Cefepime and Piperacillin-Tazobactam

This brings us to the core clinical dilemma involving two specific drugs: cefepime and piperacillin-tazobactam. These agents exist in a "therapeutic gray zone."

✅Piperacillin-Tazobactam: The tazobactam component can inhibit ESBLs, but it can be overwhelmed if there's a high bacterial load (e.g., in an abscess or the bloodstream).

This is known as the "inoculum effect" an isolate can test "Susceptible" in the lab but still lead to clinical failure in the patient.

✅Cefepime: This fourth-generation cephalosporin is more resistant to ESBL enzymes than 3rd-generation cephalosporins, but it is not completely stable.

Like piperacillin-tazobactam, it can test "Susceptible" in the lab but fail in practice, especially for serious infections, due to the inoculum effect.

This is why IDSA guidelines make nuanced, site-of-infection-based recommendations:

🛑For Piperacillin-Tazobactam:

1. Uncomplicated Cystitis: If it was started empirically and the patient is improving, no change is necessary.

2 .Pyelonephritis or cUTI: The panel suggests switching to TMP-SMX, a fluoroquinolone, or a carbapenem due to the risk of clinical failure.

3. Infections Outside the Urinary Tract: It is not suggested, even if susceptibility is demonstrated.

🛑For Cefepime:
1. Uncomplicated Cystitis: If the patient is improving on empiric therapy, no change is necessary. Its high urinary concentration is the only reason it's given a pass for simple cystitis.

2. Pyelonephritis, cUTI, or Any Non-Urinary
Infection: Avoid cefepime, even if susceptibility is demonstrated.

3. Infections outside of the urinary tract: Cefepime is also not suggested for the treatment even if susceptibility to cefepime is demonstrated

30/10/2025

A critical topic in antimicrobial therapy is the management of infections caused by Methicillin-Resistant Staphylococcus aureus (MRSA). This post outlines the key antibiotic classes and agents used for MRSA coverage.

1. Glycopeptides

This class is a cornerstone for treating serious MRSA infections.

✅Vancomycin (IV): Considered the gold standard for invasive MRSA infections, including bacteremia, pneumonia, endocarditis, meningitis, and osteomyelitis.
It is a bactericidal agent. Important considerations include the need for therapeutic drug monitoring to minimize the risks of nephrotoxicity and ototoxicity,
🔴 as well as the potential for Red Man Syndrome during infusion.

✅Teicoplanin: Widely approved in Europe and Asia, it is used for complicated skin and soft tissue infections (cSSTI) and bone and joint infections. Its advantages over vancomycin include a lower risk of nephrotoxicity and the absence of Red Man Syndrome.

2. Lipopeptides

✅Daptomycin (IV): This agent is a primary choice for MRSA bacteremia and right-sided endocarditis. It is also effective for complicated skin and soft tissue infections (cSSTI).
🔴A crucial contraindication is that it is ineffective for pneumonia, as pulmonary surfactant inactivates the drug.

3. Oxazolidinones

✅Linezolid (IV/PO): An excellent option for cSSTI and hospital-acquired/ventilator-associated pneumonia (HAP/VAP). Its excellent oral bioavailability makes it a key agent for IV-to-oral switch therapy.

🔴 It is bacteriostatic against staphylococci, which is why it is not a first-line agent for endocarditis, where a bactericidal effect is preferred.

4. Glycylcyclines

✅Tigecycline (IV): A broad-spectrum agent approved for cSSTI and intra-abdominal infections (IAI), typically used when other options are limited.

🔴 Its pharmacokinetics are characterized by a high volume of distribution, leading to extensive tissue pe*******on but low serum levels. Consequently, it should be avoided for bacteremia.

🔴 Furthermore, due to poor urinary excretion, it is not indicated for urinary tract infections (UTIs) and should be avoided for that purpose.

27/10/2025

Welcome back to our antibiotic series! In this second episode, we're focusing on a critical and often confusing area: antipseudomonal coverage. A common pitfall, especially early in one's career, is to assume all antibiotics within a class have identical coverage. I recall when starting my job treating every antibiotic in a class as interchangeable, overlooking the important exceptions. Today, we'll highlight those key exceptions across several major antibiotic classes.😊

Why Does Antipseudomonal Coverage Matter?

Pseudomonas aeruginosa is notoriously resistant to many drugs and is a major cause of severe healthcare-associated infections. Antipseudomonal coverage is essential for managing

✅Hospital-Acquired Infections: Especially in critically ill patients.

✅Ventilator-Associated Pneumonia (VAP) and Hospital-Acquired Pneumonia (HAP)

✅Catheter-Associated Urinary Tract Infections (CAUTI)

✅Central Line-Associated Bloodstream Infections (CLABSI)

✅Complex Skin and Soft Tissue Infections (e.g., in burn wounds or diabetic foot infections)

✅Bone Infections (Osteomyelitis), particularly in the spine or following trauma/surgery.

Now, let's look at which antibiotics provide this crucial coverage.

Antipseudomonal Coverage by Class:

1. Penicillins with β-Lactamase Inhibitors (BLI)

Within this group, only specific combinations
are effective.
✅Ticarcillin-clavulanate ( not in Egypt yet) a
✅Piperacillin-tazobactam
are the key players with reliable activity against Pseudomonas.

2. Cephalosporins
Out of the entire cephalosporin family, only three agents have significant antipseudomonal activity:

✅Ceftazidime

✅Cefepime

✅Cefoperazone

Among these, Cefepime is the most commonly used beta-lactam for targeting P. aeruginosa.

3. Fluoroquinolones

This class offers valuable oral options. Currently,
✅ciprofloxacin
✅levofloxacin
are the only oral agents used for quinolone-sensitive Pseudomonas. However, ciprofloxacin is generally preferred over levofloxacin due to a higher risk of emergent resistance with the latter.

🔴It is important to note that moxifloxacin does not have reliable antipseudomonal coverage.

4. Carbapenems
Most carbapenems are powerful weapons against Pseudomonas. This includes:

✅Meropenem

✅Imipenem

✅Doripenem

Meropenem is often preferred over imipenem because the latter has a higher propensity to induce resistance during treatment.

🔴A critical exception in this class is ertapenem, which has no antipseudomonal activity.

24/10/2025

As clinical pharmacists, we hold a significant responsibility in all matters related to antibiotics and infectious diseases. This field is dense with information and intricate details that can be challenging to memorize. Because we are consistently asked about antibiotic coverage and the most suitable agent for each case, I have decided to launch an antibiotic series. In each episode, we will demystify the spectrum of a different antibiotic.

Today's Episode: Atypical Bacterial Coverage in Community Acquired Pneumonia (CAP) ✨

We will focus on the "atypical" bacteria, key causative agents of Community Acquired Pneumonia (CAP). These pathogens include:

✅Mycoplasma pneumoniae

✅Chlamydia pneumoniae (now Chlamydophila pneumoniae)

✅Legionella pneumophila

A common clinical error in CAP management I always see during my job is neglecting this atypical coverage and relying solely on beta-lactam antibiotics.

To understand why this is a problem, let's review the common pathogens in CAP, which are broadly categorized as follows:

"Typical" Bacteria:

✅Streptococcus pneumoniae (the most common)

✅Haemophilus influenzae

✅Moraxella catarrhalis

And a typical Bacteria which I have mentioned earlier.
Here is the critical point: Beta-lactam antibiotics (e.g., penicillins like amoxicillin or cephalosporins like ceftriaxone) are excellent against typical bacteria. However, they have no reliable activity against atypical pathogens. This is because atypicals lack a traditional cell wall, the very target of beta-lactam drugs.

Therefore, ensuring empiric regimens have adequate atypical coverage is fundamental to effective CAP management ☺️

21/10/2025

As a junior clinical pharmacist, I
believe in self learning. To me, every drug holds a mystery waiting to be discovered, and every clinical case offers a new piece of information to add to my growing experience. I've decided to share my self learning journey, my quest to uncover every detail, no matter how simple or well known it might be to others. For me, each one is a discovery, and it's the first time I've ever heard of it! 😉"

"Today, we're going to talk about Nimodipine, a unique calcium channel blocker. (I only recently learned about it.)

Unlike its counterparts, Nimodipine is a highly cerebroselective, oral calcium-channel blocker. Due to its targeted action on cerebral arterioles, it is used to treat subarachnoid hemorrhage (SAH) rather than hypertension, which is the common indication for other dihydropyridines.

This preferential effect on the central nervous system's vasculature with minimal impact on peripheral arteries is attributed to Nimodipine's high lipophilicity. This unique property is the basis for its use in preventing neurologic deficits following SAH, which are often caused by cerebral vasospasm. It also explains its role in managing migraines."

20/01/2024

النهاردة هنتكلم شوية عن الكاربيمازول من أهم الأدوية اللى بتعالج فرط نشاط الغدة الدرقية و كمان فيه أزمة كبيرة دلوقتى في توفيره لأنه ناقص، كتير من الروشتات اللى بيبقي مكتوب فيها كاربيمازول بيبقي مكتوب ممكن بال 8 أو 10 حبة في اليوم وممكن توصل 12 حبة كمان ودا لأنه التركيز الوحيد المتوفر في السوق هو ال 5 mg بس ف دا يخلينا نسأل نفسنا ليه مفيش أدوية فيها تركيز أكبر من الكاربيمازول في السوق عشان مشكلة ال adherence و ال compliance للمريض خصوصا انى دورت ولقيت أنه مفيش اي سبب علمي أو صيدلانى يمنع وجود حاجة زى كده
لو حد عنده إجابة ياريت يشاركنا بيها فى الكومنتات.

Today's post is about a question that always confuses me regarding carbimazole, but first here is some information about carbimazole
Carbimazole is a medicine used to treat an overactive thyroid (hyperthyroidism).
dosage:
Adult: Initially, 15-60 mg daily in 2-3 divided doses, titrate dose against thyroid function until euthyroidism is achieved. Maintenance: 5-15 mg daily (may be given as a single dose), adjust dose as needed to maintain euthyroid state. Blocking-replacement regimen: Initially, 20-60 mg daily in combination with levothyroxine. Treatment duration: 6-18 months.
Child: 3-17 years Initially, 15 mg daily adjusted according to response
so after we knew the dose of carbimazole, i didn't find any product in the Egyptian market containing carbimazole higher than 5 mg per tablet so according to the dose, patients may need to take up to 12 tablets per day which is a real problem for patient adherence and compliance.
I saw many prescriptions containing this number of tablets and I searched very much for the reason why there's no drug containing higher dose of carbimazole and if it related to any Pharmaceutical cause but I didn't find any answer so if any one have any answer, you can share it with me and for the pharmacist from the other countries can you tell me if there's drugs containing crabimazole other than 5mg.

09/01/2024

دايمًا في الصيدلية بشوف روشتات كتيرة من دكاترة النسا مكتوب فيها المنيوريل أكياس اللى مادته الفعالة مضاد حيوي وهو الفوسفومايسن و استغربت كمان أنه بيتعطي دايما كجرعة واحدة بس وكمان مفيش أقراص خالص عندنا في الصيدلية فيها الفوسفومايسن ك مادة فعالة والطريقة الوحيدة اللى بيتاخد بيها أورال بتكون عن طريق الأكياس ف عشان كده قولت لازم نتكلم عليه النهاردة. 😉
As a new community pharmacist I always see doctors prescribing Monoril sachets to their female patients, and the dosage is always one sachet as a single dose, so i woundred why doctors may write monuril as a single dose and i noticed that i have never seen any tablets or capsules containing fosfomycin which is the active constituent of monuril so i decided to google it to find answers to all my questions about monuril and i I will share it with you in this post

first of all Monuril sachets contain the active ingredient "fosfomycin trometamol" which is an antibiotic used to treat bladder infections (such as acute cystitis or lower urinary tract infections) in women.

the commercially available formulations for oral fosfomycin treatment are fosfomycin trometamol and fosfomycin calcium.

Fosfomycin trometamol, which is a phosphonic acid derivative of fosfomycin, Its commercially available oral formulation consists of a single-dose sachet that contains white granules.

Fosfomycin calcium salt is the second commercially available formulation for oral fosfomycin treatment. It consists of a white tablet of 500 mg of fosfomycin

fosfomycin trometamol is now the preferred oral formulation due to its improved properties compared to fosfomycin calcium, including higher bioavailability (F) which ranges from 33% to 44% (compared to 12–37% for the calcium salt.

If you like the post, please share it with your pharmacist friends and for any questions or suggestions for the upcoming posters write them in the comments.

24/12/2023

If you as a pharmacist used to Mark classes of drugs by their suffixes after this post, you should be careful,
the last post was about two drugs that end with the same suffix but are not from the same class, rabeprazole ( a proton pump inhibitor (PPI)) and Aripeprazole (functional antagonist in the mesolimbic dopamine pathway and reduces the extent of dopaminergic pathway activity) today's poster about another two drugs Atorvastatin and cilastatin

If you like the post, please share it with your pharmacist friends and if you have any questions or suggestions for the upcoming posters, write them in the comments.

Pharmaforfun

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