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Azifast (Zithromax)

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Azalides are a class of macrolide antibiotics which contain a nitrogen in the macrolide ring. This imparts different pharmacokinetic properties and is associated with greater stability of the molecule. One such Azalide is the antibiotic Azifast. This medication is a macrolide antibiotic used for various bacterial infections such as infections of the middle ear, throat, bronchus, sinuses, skin and soft tissue. It is also useful in treating pneumonia, typhoid, gonorrhoea, granuloma inguinale and chancroid. It prevents bacterial growth.

Other names for this medication:
Azatril, Azenil, Azibiot, Azicip, Azigram, Azilide, Azimac, Azimax, Azimed, Azinix, Azithral, Azithromycin, Azitro, Azitrobac, Azitrocin, Azitrom, Azitromicina, Azitrox, Aziwok, Azomax, Aztrin, Azycyna, Azyth, Binozyt, Hemomycin, Koptin, Macrozit, Mezatrin, Misultina, Sumamed, Tritab, Tromix, Zertalin, Zibramax, Zimax, Zistic, Zithrin, Zithromax, Zithrox, Zitrocin, Zival, Zocin, Zomax, Zycin

Similar Products:
Biaxin, Chloromycetin, Cipro, Tetracycline, Omnicef


Also known as:  Zithromax.


Azifast is a semi-synthetic macrolide antibiotic of the azalide class. Like other macrolide antibiotics, Azifast inhibits bacterial protein synthesis by binding to the 50S ribosomal subunit of the bacterial 70S ribosome. Binding inhibits peptidyl transferase activity and interferes with amino acid translocation during the process of translation. Its effects may be bacteriostatic or bactericidal depending of the organism and the drug concentration. Its long half life, which enables once daily dosing and shorter administration durations, is a property distinct from other macrolides.

Azifast is the local analog (generic) of more famous drug Azifast that has the same active substance (ingredient) and in result the same therapeutic effect. The main difference is that Azifast is registered by a small local pharmaceutical company. The presence of the same active substance guarantees an identical pharmaceutical (therapeutic) effect on the body.

It is possible to buy Azifast only in the pharmacies of the country where it is produced. With us, you can buy its more famous analog Azifast, which is approved by the FDA and is sold worldwide. The same active substance guarantees the identity of the drugs and the identity of the pharmaceutical properties (they have only different names and packaging, in which they are sold).


It is important that your child completes the course of antibiotic. This means that they must take the medicine for the number of days that the doctor has told you to, or until all the medicine has been taken. If you stop giving the antibiotic too soon, the troublesome bacteria that are left will start to multiply again, and may cause another infection. There is also a risk that these bacteria will be resistant to (no longer be killed by) the first antibiotic. This means that it might not work next time, and your child might need a different antibiotic, which might not work as well or cause more side-effects.

Children are sometimes sick (vomit) or get diarrhoea when taking antibiotics. Encourage them to drink water to replace the fluid they have lost. If it is severe or your child is drowsy, contact your doctor.

Do not give your child any medicine to stop the diarrhoea unless your doctor has told you to, as this can make things worse.

Try to give the medicine at about the same times each day, to help you remember, and to make sure that there is the right amount of medicine in your child’s body to kill the bacteria.

Only give this medicine to your child for their current infection.

Never save medicine for future illnesses. Give old or unused antibiotics to your pharmacist to dispose of.

Only give the antibiotic to the child for whom it was prescribed. Never give it to anyone else, even if their condition appears to be the same, as this could do harm.


If you overdose Azifast and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Azifast overdosage: discomfort feeling in stomach, diarrhea, retching, nausea.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of reach of children in a container that small children cannot open.

Side effects

The most common side effects associated with Azifast are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Abnormal liver function, hepatitis, cholestatic jaundice, hepatic necrosis, and hepatic failure have been reported, some of which have resulted in death. Discontinue Azifast immediately if signs and symptoms of hepatitis occur.

The presence of other medical problems may affect the use of Azifast. Make sure you tell your doctor if you have any other medical problems, especially: allergy to any macrolide and ketolide antibiotic or liver disease with prior Azifast use or bacteremia (blood infection) or cystic fibrosis or infections, nosocomial or hospital-acquired or weak immune system or bradycardia (slow heartbeat) or hypokalemia (low potassium in the blood) or hypomagnesemia (low magnesium in the blood)

Not recommended in patients with these conditions: congestive heart failure or diarrhea or heart disease or Heart rhythm problems (e.g., prolonged QT interval), history of or Myasthenia gravis (severe muscle weakness).

Use with caution. May make these conditions worse: kidney disease, severe or liver disease. The effects may be increased because of slower removal of the medicine from the body.

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Bacterial superinfection and associated lung immunopathology are major contributors to hospitalizations and mortality after influenza. However, the underlying mechanisms and effective intervention strategies remain poorly defined. By using a model of influenza and pneumococcal superinfection, we found that dual-infected animals experienced rapid weight loss and succumbed to infection. Bacterial outgrowth, dysregulated cytokines, including keratinocyte-derived chemokine and macrophage inflammatory protein 2, and severe lung neutrophilia and immunopathology were linked to the poor clinical outcome. In vivo neutralization of highly induced macrophage inflammatory protein 2 did not affect clinical outcome, bacterial loads, or lung immunopathology. On the other hand, in vivo neutrophil depletion did not alter the clinical outcome and bacterial burden, although it moderately improved lung immunopathology. Treatment with a bacteriostatic antibiotic, azithromycin, alone significantly improved clinical outcome and bacterial clearance, but failed to reduce lung immunopathology. In comparison, treatment with a global inflammation inhibitor, dexamethasone, alone failed to alter clinical outcome, bacterial infection, and immunopathology, despite its moderate reducing effects on neutrophilic and cytokine responses. In contrast, combined treatment with both azithromycin and dexamethasone best improved clinical outcome, bacterial clearance, lung cellular and cytokine responses, and immunopathology. Our study suggests that marked improvement of clinical outcome and lung immunopathology caused by bacterial superinfection requires the control of both bacterial infection and aberrant host immune responses. Our findings hold implications in clinical management for influenza-associated bacterial superinfections.

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Non-chlamydia pathogenic bacteria were recovered from conjunctiva of 438 (31%) participants before treatment. The isolated conjunctival bacteria were Staphylococcus aureus, coagulase-negative Staphylococci, Streptococcus group (A, C, F and G), Enterococci, Streptococcus pneumoniae, Moraxella spp., Escherichia coli, Citrobacter spp., Proteus spp., Klebsiella spp., Pseudomonas spp. and Enterobacter spp. Overall, resistance rates of 57.8% to azithromycin and 68.5% to chloramphenicol were found. However, 86-94.4% sensitivity was demonstrated to ciprofloxacin and norfloxacin. Moderate sensitivity rates (61.8-78.4%) were observed to ceftriaxone, tetracycline and cotrimoxazole.

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Parental consent was obtained for 2849 (86.9%) of the 3278 matriculated students in grades 7 through 12. Fifty-one parents (1.6%) returned consent forms refusing permission for their child to participate in this screening and treatment program. The remaining 378 (11.5%) could not be reached by mail or telephone. Among all students with consent, 1933 (67.8% of those consented and 59.0% of those matriculated) were tested. Girls were less likely to be tested than boys (861/1363 [63. 2%] vs 1072/1465 [73.2%]). The overall prevalence of C trachomatis was 6.5%, with rates among girls more than twice that of boys (9.7% vs 4.0%). Generally, rates of infection increased with age. The prevalence rates among boys were for 7th grade, 2/208 (1%); 8th grade, 2/196 (2%); 9th grade, 10/236 (4.2%); 10th grade, 12/185 (6. 5%); 11th grade, 8/146 (5.5%); and 12th grade, 9/101 (8.9%). For boys 15 to 19 year old, the prevalence of chlamydia was 5.7%. Among girls, the prevalence rates were 7th grade, 0/105 (0%); 8th grade, 11/166 (6.6%); 9th grade, 23/218 (10.6%); 10th grade 23/146 (15.8%); 11th grade, 13/118 (11%); and 12th grade, 13/107 (12.1%). Among girls 15 to 19 years old, 12.7% were infected. Of 126 infected students, treatment was provided to 111 (88%). For this project, the laboratory cost of LCR testing was $17.76 per test. Without considering clinical staff time to collect the specimens, the average laboratory cost per infected student identified was $272. For students 15 to 19 years of age, of whom 104 (8.9%) of 1170 were infected, the laboratory cost was $200 per case identified.

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Hu-BEC obtained from patients undergoing lung resections were transferred to air-liquid-interface (ALI) culture. These cultures were incubated with cefuroxime (CXM, 10-62.5 mg/l), azithromycin (AZM, 0.1-1.5 mg/l), levofloxacin (LVX, 1-8 mg/l) and moxifloxacin (MXF, 1-16 mg/l). The spontaneous and TNF-alpha (10 ng/ml) induced expression and release of IL-8 and GM-CSF were measured using PCR and ELISA in the absence or presence of these antibiotics.

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This randomized controlled trial compared short-course therapy of once-daily azithromycin (500 mg before the wound repair followed by 250 mg/day for 5 days) with cephalexin (1000 mg before wound repair followed by 250 mg every 6 hours for 5 days) in the treatment of patients with simple traumatic wounds. A total of 366 patients were randomly selected for the study and 303 were evaluated for the final analysis.

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Ureaplasma spp. infection has been associated with bronchopulmonary dysplasia (BPD) in preterm infants. Macrolides have been used for the treatment of Ureaplasma spp. infection, with an intention to prevent BPD. The objective of this meta-analysis is to evaluate the use of macrolides in the prevention of BPD in preterm infants.

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A series of novel 11,12-cyclic carbonate azithromycin 4''-O-carbamate derivatives were designed, synthesized and evaluated for their in vitro antibacterial activities. Compounds 7b and 7d were the most effective (0.5 and 0.5 microg ml(-1)) against two strains of erythromycin-resistant Streptococcus pneumoniae whose resistance was encoded by the erm gene and the erm and mef genes, respectively. Compounds 7a, 7e and 7g showed significantly potent activity against erythromycin-susceptible strains such as Staphylococcus aureus and S. pyogenes. These results suggest that the introduction of the prolonged arylalkylcarbamoyl group to the C-4'' position can dramatically enhance the activity against erythromycin-resistant bacteria encoded by the erm gene or the erm and mef genes.

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In this report, the use of polyamidoamine dendrimers as Gloclav 625 Antibiotic intracellular drug-delivery vehicles into chlamydial inclusions is investigated. This method results in efficient intracellular delivery of azithromycin to address chlamydia infection.

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Over 95% were resistant to macrolides, while 92.0% were resistant to tetracycline. We also found that all isolates were sensitive to penicillin, chloramphenicol, cefradine, and levofloxacin. Among the 173 erythromycin resistant strains, 171 (98.8%) were assigned to the cMLS phenotype, while the remaining 2 (1.2%) were assigned to the iMLS phenotype. Among the 171 cMLS isolates, 168 isolates Trogyl Syrup (98.2%) had the ermB gene accounting for 98.2%. Meanwhile, 2 iMLS isolates had the ermA gene. Macrolides were highly resistant to ermB positive strains (MIC(90) > 256 microg/ml). Neither the M-phenotype nor the mefA gene was detected. Meanwhile, our studies of multiple centers showed that consumption of macrolides from 2000 to 2006 was very high.

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