Types of Acne

Type 1 acne – Minimal inflammation, minimal affected area, not painful, irregular outbreaks.

Type 1 acne is the most mild form of acne and generally is the least damaging and easiest to treat form of the disease.  It is characterized by a lack of inflammation and is usually not particularly painful.  The area of the body affected by the acne is usually limited.  This type of acne is often transient and often resolves on its own after about a week.  Non-inflamed blackheads and small red bumps (papules) are common with this form of acne.  This form of acne appears to be particularly common in females and often affects the forehead, cheeks, nose and neck.  Over the counter topical treatments such as benzoyl peroxide and salicylic acid washes are often effective at resolving the problem.  Topical antibiotics such as clindamycin and erythromycin are also often effective, but may not be necessary.

Type 2 acne – Mild inflammation, some painful pimples, regular outbreaks.

Type 2 acne on forehead

A common manifestation of the disease, Type 2 acne is similar to Type 1 acne, but is characterized by increased levels of inflammation and redness.  Pimples can range from small red bumps to medium sized whiteheads.  Unlike Type 1 acne blemishes, the increased inflammation causes pimples that are often  painful to the touch.  Over the counter topical treatments are often partially effective at decreasing the severity and duration of outbreaks, but are frequently inadequate.  Topical antibiotics and topical retinoids (e.g. Retin-A) can be quite effective.  In some instances it may be necessary to explore oral antibiotics or oral retinoids, if the acne is not responsive to treatment.  In general, Type 2 acne is minimally scarring if allowed to resolve on its own.  However, it is important to practice good hygiene and avoid exacerbating the situation by “popping” pimples without cleaning and sterilizing the area before and after.

Type 3 acne – Large, painful pimples, nodular pimples, frequent outbreaks.

Type 3 acne is characterized by the presence of mid sized to large nodules and pustules that are frequently painful.  In Type 3 acne, pimples are often associated with significant amounts of inflammation.  Large whiteheads and large, painful red bumps are common.  Individual pimples can often take longer to resolve, up to 10-14 days.  In type 3 acne, much of the inflammation and infection originates deeper in the tissue than in Types 1 and 2, often localizing in the dermis and sub-cutaneous fatty tissue.  Because of this, type 3 acne is usually unresponsive to over the counter topical medications.  Likewise, the efficacy of topical antibiotics and topical retinoids is often limited.  In many cases, oral antibiotics and oral retinoids are the only effective treamtents for Type 3 acne.  The increased inflammation associated with Type 3 acne poses a significant risk of permanent scarring.  Deep seated nodules and postules can cause damage to the structural matrix that underlies the skin, causing pitting, discoloration and the accumulation of scar tissue.

Type 4 acne – Large and painful nodules, pustules and cysts, presistent outbreak.

The most severe form of the disease, Type 4 acne almost invariably causes permanent skin damage and scarring.  Like Type 3 acne, Type 4 acne is characterized by a deep seated infection and extensive inflammation.  Large cysts, which are essentially large, irregular nodules are a common feature in Type 4 acne. Type 4 acne is is usually completely non-responsive to over the counter medications.  Topical antibiotics and retinoids are minimally effective, in most cases.  Type 4 acne often requires aggressive oral antibiotic and/or oral retinoid treatments.  Type 4 acne is a serious medical condition that should be evaluated  immediately by a dermatologist, if at all possible.   Type 4 acne can cause extensive damage to the skin and underlying structure, causing heavy scarring.  Type 4 acne is often extremely painful, both physically and emotionally, and should be treated as aggressively as possible.

Related Posts @ The Science of Acne

What is Acne?
What Causes Acne?
Frequently Asked Acne Questions
The Science of Acne Homepage

Additional Online Resources

Acne – Wikipedia
Types of Acne – Acne.org
Blog Directory

Rose Petals

Source: The flowers from several species of rose, but the most common are the Damask Rose, Rosa damascena  and the Cabbage Rose (Rosa centifolia).  Do not confuse rose essential oil with rose hip, rose hip seed or rosewood essential oils and extracts.
Type of Treatment: Naturopathic Medicine: Essential Oil.
How it Works:  Rose essential oil is primarily used in aromatherapy applications.  It is also blended with other essential oils and other plant extracts for use as a topical treatment.

Background

Roses are among the most popular flowers and are cultivated around the world.  Most of the commonly domesticated roses are originally from the Middle East and Asia.  However, Europe, Africa and North America all have their own native species of roses.   Historical records indicate that roses have been cultivated for over 2,000 years, primarily in southern Europe, Northern Africa and central Asia.  The popularity of roses, and a long history of selective breeding, has led to a massive expansion in the number of species and hybrids.  There are currently over 100 different species of rose and thousands of recognized hybrids.

Beyond the decorative use of rose flowers, several parts of the plant have been used in culinary and medicinal applications.  Rose essential oil has a long history of use as an ingredient in perfumes.  Rose water extracts, which are a byproduct of essential oil production, are also used for flavoring certain foods.  Rose hips, which are the red fruits that follow the flowers, are very high in vitamin C and are used to make jellies and other preserves.

Roses are flowering bushes, and some species can grow up to 8 meters (25 feet) high.  They come in a range of shapes, from free-standing shrubs to climbing vines.  Roses are notable for their woody stems that are often covered in thorns (aka prickles).

Rose essential oil may also be known as: Rose otto, attar of rose and rose absolute.

Composition of Rose Essential Oil

Chemical Composition of Rose Flower Essential Oil

Rose essential oil is generally a light yellow color, mildy oily and highly pungent.  The primary component of rose essential oil is Citronellol.  Citronellol makes up 30-35% (by volume) of rose essential oil.  Two other compounds that are abundant in rose oil are Geraniol (15-25%) and Nonadecane (10-25%).    Many additional molecules are present in lower concentrations including phenylethyl alcohol, heptadecane, geranyl acetate, eugenol, alpha-pinene and nerol.  Much of pleasant smell of rose flowers comes from a group of molecules called Damascenones, which often make up less than 2% of rose essential oil.

Rose Essential Oil in Acne Treatment

Rose Blossom

Rose essential oil and rose water are used in a variety of skin care products.  There are claims that both products are beneficial for skin tone and for treating oily skin.  There is very little direct research or evidence about the benefits of rose essential oil for the treatment of acne vulgaris.  However, several of the compounds that are abundant in rose oil, like citronellol and geraniol, have been shown to be fairly toxic towards the bacteria most responsible for acne, Propionibacterium acnes.

Related Articles

An Overview of Naturopathic Medicine in Acne Treatment
An Overview of Essential Oils used in Acne Treatment
What causes acne?

Additional Information

Rose @ Wikipedia
Rose Oil @ Wikipedia

References

1. Young. 2011.Essential Oils Pocket Reference.
2. Lawless. 1995. The Illustrated Encyclopedia of Essential Oils: The Complete Guide to the Use of Oils in Aromatherapy & Herbalism.
3. Bremness. 1994. The Complete Book of Herbs: A Practical Guide to Growing and Using Herbs.
4. Babu, et al. 2002. Essential oil composition of Damask rose (Rosa damascena Mill.) distilled under different pressures and temperatures.
5. Ulusoy, et al. 2009. Tocopherol, Carotene, Phenolic Contents and Antibacterial Properties of Rose Essential Oil, Hydrosol and Absolute.
6. Bowles, et al. 2003. The A-Z of Essential Oils.
7. Loghmani-Khouzani, et al. 2007. Essential Oil Composition of Rosa Damascena Mill Cultivated in Central Iran.
8. Antonelli, et al. 1997. Characterization of 24 Old Garden Roses from Their Volatile Compositions.
9. Zu, et al. 2010. Activities of Ten Essential Oils towards Propionibacterium acnes and PC-3, A-549 and MCF-7 Cancer Cells.
10. Tsai, et al. 2009. In vitro antimicrobial and anti-inflammatory effects of herbs against Propionibacterium acnes.
11. Adorjan, et al. 2010. Biological properties of essential oils: an updated review.
12. Lertsatitthanakorn, et al. 2008. Antibacterial activity of citronella oil solid lipid particles in oleogel against Propionibacterium acnes and its chemical stability.
13. Lertsatitthanakorn, et al. 2010. Effect of Citronella Oil on Time Kill Profile, Leakage and Morphological Changes of Propionibacterium acnes.

There are Multiple Ways a Bacteria can be Resistant to an Antibiotic (Levy, et al)

The extensive use of a particular antibiotic and patients failing to complete treatments when they feel better do contribute to increased antibiotic resistance, but are not necessarily the primary cause of the increasing frequency of antibiotic resistance.  This post discusses the many ways that antibiotic resistance may occur, as well as the conditions and environments that promote the development of antibiotic resistant bacteria.

What is Antibiotic Resistance?

Antibiotics work by targeting bacteria and either killing them, or inhibiting their growth. Generally speaking, antibiotics are small molecules that disrupt essential biological processes that are unique to bacteria. There are many types of antibiotics, and there are many types of bacteria. Some bacteria are naturally resistant to certain antibiotics. Depending on the type of bacteria, different types of antibiotics are more (and less) effective. Antibiotic resistance refers to a situation where a bacteria becomes less sensitive to a particular antibiotic (or class of antibiotics). Antibiotic resistance occurs because the resistant bacteria has developed or acquired an ability to prevent the normal function of the antibiotic.

Adaptation and Evolution of Antibiotic Resistance

Epigenetic Adaptation (No Genetic Mutation)

Bacteria that consistently encounter sub-inhibitory levels of an antibiotic (concentrations of the antibiotic that are too low to kill it) can develop a temporary resistance to that antibiotic. This type of resistance is called Epigenetic Adaptation, and produces no genetic changes that can be permanently inherited by subsequent generations of bacteria. This is roughly equivalent to an athlete who develops large muscles from weight lifting and physical training. Bacteria exposed to sub-inhibitory levels of an antibiotic can mobilize defenses such as pumps to expel the antibiotics, enzymes to break them down, or they can simply decrease the permeability of their cell wall to decrease their exposure to the antibiotic molecules.

Genetic Adaptation (Genetic Mutation and Selection)

UV Light can Cause Damage and Permanent DNA Changes (Friedberg)

Genetic mutations are small changes in the genetic code that occur randomly during DNA replication, or as a result of exposure to mutagens like ionizing radiation (UV light) or chemicals. Many genetic mutations happen in regions of the genome that are not essential for the organism and don’t significantly change how that organism functions. When a mutation does occur in something important, it is usually disruptive and weakens the organism. Mutations that improve the fitness of an organism are rare.

Some antibiotics are more likely than others to become less effective as the result of genetic mutations in the target bacteria. This is because resistance to some antibiotics can be acquired as a result of a single genetic mutation, while other antibiotics require a bacteria to develop multiple mutations in order to become resistant.  One example of a class of antibiotics that are susceptible to single mutation resistance are the fluoroquinolone class of antibiotics (ciprofloxacin, moxifloxacin, nadifloxacin). These antibiotics target a bacterial enzyme called DNA gyrase. The antibiotic binds this enzyme, which prevents the bacteria from properly accessing and replicating its DNA. A single mutation at a specific site in this enzyme can stop the antibiotic from binding, and allows the bacteria to become resistant to the antibiotic.  Because of this, some antibiotics (like ciprofloxacin) are not recommended for long-term use, partly because of the increased probability that an infectious bacteria will become resistant.

Genetic Acquisition (Plasmids, Transposons, Viruses, Conjugation, Naked DNA)

Transfer of Antibiotic Resistance Genes Between Bacteria (Furuya, et al)

Bacteria can acquire large pieces of DNA from other bacteria, viruses and the environment. It is almost impossible for a bacteria to randomly evolve a brand new gene or enzyme that provides resistance against a particular antibiotic (at least within a time-frame of weeks, months and years). But what does happen is that bacteria acquire big chunks of foreign DNA that contain many genes. Bacteria have many ways to acquire these large pieces of DNA that often contain many complete genes.

• Plasmids are mobile pieces of DNA (often circular) that bacteria can easily trade and acquire from the environment. Many bacteria have multiple plasmids. Plasmids can contain genes that inactivate an antibiotic (for example the a particular gene, Beta Lactamase, is commonly spread via plasmid and provides resistance to Beta-Lactam antibiotics, like Penicillin).
• Transposons are sections of DNA that can jump from one place in the genetic code to another, or even to the genetic code of another organism.
• Viruses (Bacteriophages) can infect bacteria and these viruses can copy and paste genetic code into the genomes of the bacteria they infect.
• Conjugation is where two bacteria that are directly adjacent to one another create a direct connection and share DNA (think “conjugal visit”). Conjugation is probably the closest thing that bacteria have to sex.
• Naked DNA is DNA that bacteria find in the environment and internalize. This DNA can be from bacteria that have been killed, or part of a biofilm structure (some bacteria use DNA as a scaffold structure to anchor themselves to a surface).

Bacteria can utilize one, multiple or all of these techniques to acquire DNA and that can help a bacteria become resistant to a particular type and/or class of antibiotic.

Conditions That Cause Antibiotic Resistance

The Necessity of “Selective Pressure”

The average bacterial genome (all of the DNA in a cell) is approximately 1000 times smaller than the genome of an animal (including humans). This isn’t because bacteria are smaller than human cells (although they are), it is because of competition and a concept called “genomic streamlining”. A genome is not free. It takes energy and resources to maintain and replicate. The bigger the genome, the more energy it takes to keep it up and running, and to duplicate it during reproduction. At the same time, there is an incredible level of competition between bacteria for resources. Bacteria grow much faster, and in much larger numbers, than most other organisms. For example, in a single handful of dirt there are more bacteria than the entire human population of the world. The huge bacterial population and intense competition is like “survival of the fittest” on steroids; weak and inefficient bacteria are quickly squeezed out by stronger, more efficient bacteria. Excess DNA is “dead weight” in this competition and is quickly eliminated. If a section of DNA is not essential for survival or does not confer a selective advantage, it is rapidly mutated and removed from the genome by the quickly evolving bacterial population.

How Does Selective Pressure Impact Antibiotic Resistance?

In order for a gene to remain functional and a part of the bacteria’s genome over an extended period, it has to help improve the survival and/or competitiveness of the bacteria. If a gene stops being helpful it will eventually become non-functional and will be removed from the genome. This means that the development and maintenance of antibiotic resistance is usually dependent on the bacterial population being frequently exposed to non-lethal doses of the antibiotic (note: some bacteria are intrinsically resistant to particular antibiotics). This process eliminates those bacteria that have lost resistance, and increases the percentage of resistant bacteria. In real life, this means that antibiotic resistance is likely to emerge in environments where bacteria are frequently exposed to antibiotics. On an individual level, this means that a person is more likely to develop an antibiotic resistant infection from undergoing long-term or prophylactic antibiotic treatment, as opposed to short-term antibiotic treatments of acute infections.  This also means that bacteria may lose resistance to antibiotics that are no longer frequently used.

Environments that Facilitate the Development of Antibiotic Resistance

If you have read the above sections, you now know that infectious bacteria do not randomly become resistant to antibiotics. It requires an environment that provides a good source of hosts (people/animals to infect), consistent selective pressure (frequent antibiotic use) and ideally, lots of other bacteria with which to share antibiotic resistance genes (pieces of DNA that provide protection from the antibiotic). It is because of this combination of factors that antibiotic resistance is not simply about using antibiotics too much, but also about where and how antibiotics are used. That said, here are some environments which encourage the development of antibiotic resistance:

Hospitals

Hospitals are a Major Source of Antibiotic Resistant Bacteria

Hospitals often are the perfect environment for developing bacterial antibiotic resistance. They have a many of the features that are necessary for antibiotic resistance to emerge. including:

• A lot of sick people (lots of bacteria hanging around).
• A high density of potential hosts for bacteria infection (lots of new people to infect).
• The frequent and sustained use of antibiotics (consistent selective pressure).

It is because of these factors that hospital acquired infections (HAIs) are often the most difficult types of infection to treat, because they are often highly resistant to standard antibiotic treatments. Hospitals are a reservoir for antibiotic resistance, and in many cases are the primary source of antibiotic resistant bacteria in the surrounding population. In the US, and other highly developed countries, hospitals are reasonably sterile and there are a number of systems in place to prevent hospital acquired infections. In many other places, the conditions are not as sanitary and this encourages the transmission of disease from patient to patient in the hospital setting.  In hospitals that have a high rate of antibiotic use but poor sterility, the development of antibiotic resistant bacteria is accelerated. It is not a coincidence that outbreaks of highly antibiotic resistant bacteria, like drug resistant Staphylococcus aureus (MRSA and VRSA) and Mycobacterium tuberculosis (XDR-TB), often originate in hospitals in countries like South Africa and Russia. In these places and others like them, high patient density, poor sterility, HIV/AIDs (see below) and high antibiotic usage combine to drive the rapid evolution of drug resistant bacteria.

Feedlots and Industrial Animal Farms

Industrial Animal Husbandry Uses More Antibiotics Than Human Medicine

Many people may do not realize that industrial animal farming operations are among the largest consumers of antibiotics. Industrial operations involve large amounts of animals, packed densely into enclosed spaces. In this type of environment, disease transmission is a major problem. To prevent disease outbreaks, many operations treat their animals prophylactically with antibiotics. In fact, animal farming consumes the majority of all antibiotics used in the United States ( more antibiotics than are used in human medicine).

Like highly unsanitary and overcrowded hospitals, the high level of antibiotic use in industrial animal farming drives the evolution of antibiotic resistance in bacteria.  In addition, the sewage produced by these operations can contain significant levels of un-metabolized antibiotics. These residual antibiotics combined with the huge and diverse population of bacteria living in the untreated sewage encourages the transfer of antibiotic resistance among different species of bacteria.  This can also cause the spread of antibiotic resistant bacteria to neighboring wildlife.  It also partly explains why detectable levels of antibiotics are found in many rivers, lakes and other waterways.

Nursing Homes, Sanitoriums and Other Residential Institutions

Nursing Homes Have High Rates of Antibiotic Usage and Immuno-Compromised People

Many countries around the world place people who are infirm or disabled into various institutions.  While the United States has largely moved away from large scale housing of disabled, diseased or infirm patients, the practice is still common in many places around the world.  In wealthier countries, these people are often placed into assisted living facilities, retirement homes and hospices.

In these environments there are dense populations of people who often have weakened immune systems.  The combination of these people with high levels of antibiotic use can contribute to the emergence of antibiotic resistant bacteria.  Elderly and disabled people often have compromised immune systems and this encourages more frequent and longer lasting infections. Prophylactic antibiotic use is common in these environments.

HIV and AIDS

HIV Patients in South Africa

HIV and AIDS lead to higher rates of antibiotic resistance for two closely related reasons. First, because people who suffer from HIV and AIDS have an impaired immune system they are often highly susceptible to bacterial infection. As a result, many physicians place these patients on a permanent course of antibiotics to prevent infection. (Note: This is becoming less of a factor in places where effective anti-retrovirals are available, because they mitigate the need for prophylactic antibiotic treatment.)

The second reason HIV and AIDS foster antibiotic resistant bacteria is that they cause more infections to happen and they make antibiotics less effective (indirectly). Even in a person with a healthy immune system, a bacterial infection may not be completely eliminated by a course of antibiotics. However, in most cases the antibiotic weakens and kills most of the bacteria and the immune system is able to target and eliminate the surviving bacteria.   But in a person with HIV, this small population of bacteria that remain after antibiotic treatment are not cleared by the immune system. This process selects for those bacteria that are slightly more resistant to the antibiotic treatment than the majority.

Regions with High Levels of Antibiotic Use

Correlation Between Penicillin Use and Penicillin Resistant Bacteria in Different Countries (Furuya, et al)

In the last ten years numerous studies have been done profiling the antibiotic susceptibility of the acne causing bacteria, P. acnes. The results tell a fascinating story. In countries that prescribe patients antibiotics to treat acne at higher rates, there are higher rates of antibiotic resistant P. acnes. This means that in places like the United States and Europe, a significantly higher percentage of P. acnes bacteria are resistant than in places like Mexico, Chile and India. Additionally, the frequency of P. acnes bacteria resistant to a particular antibiotic varies from country to country, and reflects the differences in prescribing frequencies of different drugs between countries.

Related Posts from The Science of Acne

In Depth: What is Propionibacterium acnes?
In Depth: Antibiotic Susceptibility of Propionibacterium acnes
Overview: Oral antibiotics for Acne
Overview: Topical antibiotics for Acne

References and Sources

Books

Dyer. 2003. A Field Guide to Bacteria (Comstock Book)
Medigan, et al. 2008. Brock Biology of Microorganisms (12th Edition)
Willey. 2010. Prescott’s Microbiology
Aarestrup. 2005. Antimicrobial Resistance in Bacteria of Animal Origin
Dunn. 2011. The Wild Life of Our Bodies: Predators, Parasites, and Partners That Shape Who We Are Today
Coyne. 2009 Why Evolution Is True

Online Resources

Antibiotic Resistance of Propionibacterium acnes in Acne Vulgaris @ eMedicine
How Bacteria Become Resistant to Antibiotics @ Discovery Health

Research Articles

Levy, et al. 2004. Antibacterial resistance worldwide: causes, challenges and responses.
Furuya, et al. 2005. Antimicrobial-resistant bacteria in the community setting.
Friedberg. 2003. DNA damage and repair.
Oprica, et al. 2005. European surveillance study on the antibiotic susceptibility of Propionibacterium acnes.
Gould. 2006. Genetic basis of resistance in Propionibacterium acnes strains isolated from diverse types of infection in different European countries.
Silbergeld, et al. 2008. Industrial Food Animal Production, Antimicrobial Resistance, and Human Health.
Walsh. 2000. Molecular mechanisms that confer antibacterial drug resistance.
Rooney, et al. 2009. Nursing homes as a reservoir of extended-spectrum b-lactamase (ESBL)-producing ciprofloxacin-resistant Escherichia coli.
Gould. 2006. Costs of hospital-acquired methicillin-resistant Staphylococcus aureus (MRSA) and its control.
Davies, et al. 2010. Origins and Evolution of Antibiotic Resistance.
Grau, et al. 2009. Trends in mortality and antibiotic resistance among HIV infected patients with invasive pneumococcal disease.

Bloggers.com

Inflamed hair follicle and sebaceous gland

Most people can recognize acne when it presents on the face or body. Most people also have the vague understanding that acne is associated with oily skin and an excess production of sebum. But beyond that, few people really grasp what is actually happening at the microscopic level of a pimple. Understanding the physiological and pathological processes behind acne can help you sort out what treatments and advice can help you make positive changes in your acne, and which things have no basis in scientific reality and should be ignored.

Labelled hair follicle

At a very basic level, acne results from a combination of factors that result in blocked pores, an accumulation of sebum, bacterial growth and inflammation. Acne generally occurs within the hair follicle, when excess sebum is produced by the sebaceous glands and creates a plug that blocks the follicle.  This plug creates a micro-environment that favors the growth of certain types of bacteria, such as Propionibacterium acnes and Staphylococcus aureus. The presence of this bacteria triggers an immune response, which is characterized by inflammation, increased blood flow (redness) and the recruitment of white blood cells to the follicle.   Primary inflammation can often cause additional damage to the follicle and surrounding tissue, allowing proliferation of the bacterial infection and in turn inducing further swelling.  In some individuals, this process becomes a vicious cycle and leads to extensive acne and significant damage to the skin and the subcutaneous  tissue.   In these cases, antibiotic and retinoid therapies are often necessary to disrupt this cycle, resolve the infection and allow healing of the tissue.

Sebum and a Healthy Follicle

In a healthy follicle, the sebaceous gland produces the appropriate amount of sebum to maintain the health of the hair and surrounding tissue, and that sebum is efficiently extruded along with the hair.  In people that suffer from acne, several things can happen that disrupt this delicate balance.  Normally, the sebaceous glands are relatively small and produce a minimal amount of sebum.  However, in many cases of acne, the primary culprit is an overproduction of sebum.  In some cases, the sebaceous glands grow larger and produce greater amounts of sebum.  Excessive growth and proliferation of the sebaceous glands is known as sebaceous hyperplasia.  Sebaceous hyperplasia can be triggered by increases in androgen hormones, as happens during puberty.

Sebum itself is created by the breakdown of the cells that form the sebaceous gland.  Sebaceous cells replicate at the base of the gland and move up towards the hair follicle as the new cells proliferate.  As the maturing cells approach the hair follicle, they undergo apoptosis and die.  The cells are lipid rich (oil) and the byproducts left over as the cells dissolve composes the sebum that lubricates and protects the hair.  Proliferation of the sebaceous glands causes an increase in the production of sebum, which is often manifested as oily skin and hair.  The sebum can also serve as a nutrition source for bacteria that are capable of living in the hair follicle, such as P. acnes and S. aureus. Excess amounts of sebum can encourage bacterial growth and lead to inflammation, redness and an infiltration of white blood cells (pus).  If the plug in the hair shaft is located near the surface, this process can often lead to the formulation of a surface pustule (whitehead).  However, for many people who suffer with nodular and cystic acne, the pustules are often formed deep in the tissue and away from the surface.

In these cases, the result is often the formation of large painful nodules and cysts.  Since the pustule is surrounded by tissue, it is not easily possible to drain the pus and bacteria to the surface (lance the pimple).  Many times, continued sebum production, bacterial growth and inflammation within a plugged follicle can cause the follicle to rupture and drain into the surrounding tissue.  This process can lead to further inflammation, dissemination of the bacterial infection and progression of the disease.
For most of the pimples in type 1 and type 2 acne, the blockage and inflammation is relatively close to the surface.  As a result, OTC topical medications are reasonably effective at treating the disease.  However, it is also important to note that most topical preparations are not capable of penetrating deep enough into the tissue to treat nodular and cystic acne.  In these cases, it is often necessary to utilize oral antibiotics to control the bacterial infection and oral retinoids to slow down the growth of the sebaceous glands.

Related Posts @ The Science of Acne

What is Acne?
What Causes Acne?
Frequently Asked Acne Questions
The Science of Acne Homepage

Genetics

Genetics Play a Central Role in the Development of Acne

Bacteria

Propionibacterium acnes are the Bacteria Most Often Associated with Acne Vulgaris

Environment

Environmental conditions, like temperature, sun exposure, humidity and allergens can play a big role in acne outbreaks. Low temperatures may decrease the fluidity of the sebum passing through the follicle and increase the risk of developing a plug. Or low humidity levels can dry the skin, causing the body to upregulate sebum production in a bid to protect the skin. Sunlight can affect both the bacteria and the skin, causing physiological changes or damage to various structures. Allergic reactions may exacerbate skin problems, or cause new ones. Many people notice that their acne tends to improve or worsen depending on the weather, and this is because the environmental conditions can directly affect the way the body functions.

Stress

Stress is well known to disrupt normal hormonal balance and depress the immune system. Both of these changes can lead to a worsening of acne sypmtoms. Again, many people notice that they tend to break out especially bad after pulling an all-nighter, drug/alcohol consumption or other activities that put stress on the body. Inadequate sleep is a very common form of stress.

Diet

Excessive Consumption of High Glycemic Index Foods (e.g. French Fries) is Associated With Increased Incidence of Acne

While there isn’t much data linking specific foods to worsening acne symptoms (milk excluded), research has shown a strong connection between high glycemic index diets and increased incidence of acne. High glycemic diets are those that are high in sugar and simple carbohydrates. Excessive consumption of sugar and starch is the primary cause of high blood sugar levels, and blood sugar levels are the primary regulator of metabolic function. Consistently elevated blood sugar levels are a type of stress, and they appear to negatively affect the body in ways that are similar to other forms of stress. Besides increased acne symptoms, high blood sugar levels can lead to other problems, like type 2 diabetes.

References and Sources

Pathogenesis of Acne.
Toyoda, et al. 2001. For article abstract, click here.

Related Posts @ The Science of Acne

Frequently Asked Acne Questions
Overview: What is Acne?
The Science of Acne Homepage

The Basics

Propionibacterium acnes bacteria

Propionibacterium acnes (P. acnes) is a bacteria that grows deep inside of pores, where it feeds on the sebum that is produced by the sebaceous glands that surround the base of the hair shaft.  In most cases, P. acnes bacteria are partially responsible for acne symptoms.  Several studies have indicated that specific strains of P. acnes bacteria are more commonly associated with acne vulgaris.  However, other bacteria (e.g. Staphylococcus and Corynebacterium) can also reside in the follicle and on the surface of the skin.

Propionibacteria are members of the “gram-positive” classification of bacteria, which includes many other species of infectious bacteria.  Gram positive bacteria have thick cell walls that are rich in peptidoglycans and lippolysacharides, (sugar molecules attached to proteins and fatty acids).

P. acnes is an oxygen tolerant, anaerobic bacteria that prefers to grow in low oxygen environments (like deep within a plugged follicle).  P. acnes uses sebum as an energy source.  In a plugged follicle, the low oxygen levels and accumulating sebum create a prime environment for the growth of P. acnes bacteria.

P. acnes bacteria can form sticky clumps of bacteria known as biofilms that help to anchor and protect the bacteria at the site of infection.  In many cases, bacterial biofilms have been shown to contribute to long term infections, and may play a role in the persistence of P. acnes infection in some individuals.

The Relationship Between Sebum and Propionibacterium acnes

Propionibacterium acnes growing in pores produces a fluorescent orange glow when illuminated by ultraviolet light

P. acnes bacteria use sebum, which is produced in follicles, as a primary source of food. P. acnes bacteria use specialized enzymes that digest the fatty acids and triglycerides that are abundant in sebum. In an anaerobic environment, P. acnes ferments the fatty acids and triglycerides, and releases short chain fatty acids and propionic acid as metabolic byproducts (that’s why it’s called Propionibacterium).

P. acnes has several complementary metabolic pathways as well, designed to harvest energy from additional sources.  Research indicates that the digestion of sebum by the bacterial enzymes can create comedogenic byproducts, a potential contributing factor to the severity of acne symptoms.

There is also some evidence that sebum production may be stimulated by the presence of P. acnes bacteria.  If this is true, it is possible that the bacteria has adapted to the environment of the follicle, and part of this adaptation includes a mechanism to get more food (sebum) from the surrounding tissue.

Propionibacterium acnes, Inflammation and Acne vulgaris

White Blood Cells Mediate Inflammation

Propionibacterium does not directly cause significant damage to the skin.   Instead, most of the damage caused by acne is due to the inflammatory process of the immune system.

For most people who suffer from inflammatory acne, the immune system over-reacts to the bacteria and sends in lots of white blood cells.  The immune system of some people may be more sensitive to P. acnes bacteria and may respond strongly, which can lead to symptoms of inlammatory acne vulgaris (eg. Types 2,3 and 4).

Many of the individual components that make up the bacteria are easily recognized by the immune system as “enemy” molecules.  This material includes components of the bacterial cell wall, like peptidoglycans, lipopolysacharides and proteins.  Even the DNA from P. acnesbacteria is recognized as foreign by the immune system.

The bacteria doesn’t even have to be alive to trigger a powerful immune response, dead bacteria can also set off alarms with the immune system.

Dysfunctional Immune Responses and Acne vulgaris

Inflamed follicle full of white blood cells (blue)

In some people who suffer from acne (especially severe acne), the root of the problem can be traced back to a faulty immune response.  There are two main types of immune failure that can lead to acne symptoms.

The first is known as a hyper-sensitive response. In this situation an individual’s immune system reacts over-aggressively to the presence of the bacteria and produces large amounts of inflammatory cytokines. These inflammatory cytokines induce white blood cells to release destructive enzymes and free radicals into the site of infection and that causes unnecessary collateral damage to the surrounding tissue. This damage often stimulates the production of more inflammatory cytokines and this can become a vicious cycle. In some cases, this damage can actually make it easier for the bacteria to proliferate.

The other main type of dysfunctional immune response occurs when an individual’s white blood cells do not effectively destroy and process the bacteria that they encounter. In an ideal situation, white blood cells engulf (phagocytose) all of the bacteria that they come in contact with. Once engulfed, the white blood cell isolates the bactiera into an intracellular compartment called a phagosome, and pumps toxic molecules and enzymes into this compartment. These molecules and enzymes kill the bacteria and digest it into small pieces. These pieces are then presented to the immune system, which uses them to design specific antibodies (and several other things) that specifically target the bacteria. In people who suffer from chronic, inflammatory infections (like acne vulgaris), they often have white blood cells that have a defect in this processing pathway. In these individuals, their white blood cells ingest bacteria normally, but their cells have an unusually difficult time killing the bacteria after eating them. If this happens, the white blood cell will often continue to secrete lots of inflammatory cytokines till it exhausts itself and dies in a process called apoptosis.  After the cell dies, the bacteria isn’t necessarily dead, and can sometimes escape and keep proliferating.

Both of the above examples of immune system dysfunction are usually genetic in origin. The susceptibility to acne vulgaris is likely hereditary. Individuals whose parents experienced difficulty with acne vulgaris are at an increased risk of encountering acne symptoms.

How to Kill P. acnes Bacteria

Antibiotics and Other Antibacterial Compounds

Extensive screening has been done to test the susceptibility of P. acnes bacteria to different classes of antibiotics. In general, what researchers have found is that P. acnes is moderately susceptible, when directly exposed, to many classes of antibiotics.

Researchers have also found that P. acnes bacteria is becoming increasingly resistant to some of the common antibiotics used to treat acne, like erythromycin and tetracycline family drugs (tetracycline, doxycycline and minocycline).  Interestingly, numerous studies have shown that P. acnes bacteria is extremely sensitive to Penicillin G, which was one of the first antibiotics ever developed.

It is important to keep in mind that these tests are primarily done on a petri dish in a laboratory. When asking whether an antibiotic is effective when treating a clinical acne infection there are additional factors that need to be considered. The biggest question is whether the antibiotic makes it to the site of infection. Many antibiotics may be effective at killing P. acnes bacteria on a petri dish, but they do not accumulate in sufficient concentration in the follicle and sebaceous glands to be effective at treating active acne infections.

Several Over-The-Counter medications, like benzoyl peroxide and triclosan, are also directly toxic to P. acnes bacteria. However, these topically applied medications have difficulty penetrating to the base of the hair follicle, which is where the P. acnes bacteria are causing problems.

Topical Retinoids, Isotretinoin (Accutane) and Hormone Treatments

P. acnes bacteria use the fatty acids and triglycerides found in sebum as its primary food source. Limiting the amount of sebum production can suppress the growth of P. acnes bacteria by reducing its food supply.

Treatment with retinoids can decrease the production of sebum in the skin. This is true for both oral retinoids (isotretinoin, accutane) and topical retinoids (retin-A, Adapalene).  Hormonal treatments (like androgen inhibitors (Spironolactone, Cyproterone) and birth control) may also decrease sebum production.   Certain light and laser therapies (diode lasers) can also decrease the production of sebum.

Phototherapy and Other Light-Based Treatments

A few light and laser treatments (eg. blue light therapy, photodynamic therapy) can specifically target and kill the P. acnes bacteria.

These light-based therapies work by exciting a particular molecule called a porphyrin, which is produced in large quantities by P. acnes bacteria.  Excitation of porphyrins with blue light causes them to release free radicals into the bacteria and killing them.

P. acnes growing in pores on the human face produce a red fluorescence when illuminated by an ultraviolet (UV) light source.

Essential Oils and Other Naturopathic Treatments

There are several naturopathic treatments that may also be helpful in inhibiting or killing P. acnes bacteria.

Many essential oils are toxic to P. acnes bacteria, such as Tea Tree Oil and Thyme Essential Oil.

Other natural compounds, like aloe vera gel and natural honey, have also been shown to have antibacterial properties against P. acnes.

Certain metals (eg. silver and copper) and other elements (sulfur) are also toxic to bacteria in pure form.

References and Sources

Books

Habif, et al. 2011. Skin Disease: Diagnosis and Treatment, 3rd Edition
Bauman. 2011. Microbiology with Diseases by Body System, 3rd Edition
PDR Staff. 2011. Physicians’ Desk Reference, 66th Edition
Pizzorno, et al. 2007. The Clinician’s Handbook of Natural Medicine, 2nd Edition
Gladwin, et al. 2011. Clinical Microbiology Made Ridiculously Simple

Online Resources

Propionibacterium acnes infections @ eMedicine
Propionibacterium acnes @ MicrobeWiki
Propionibacterium acnes @ Wikipedia

Research Articles

Brüggemann, et al. 2004.The Complete Genome Sequence of Propionibacterium Acnes, a Commensal of Human Skin.
Kurokawa, et al. 2009. New developments in our understanding of acne pathogenesis and treatment.
Bayston, et al. 2006. Biofilm formation by Propionibacterium acnes on biomaterials in vitro and in vivo: impact on diagnosis and treatment.
Holmberg, et al. 2009. Biofilm formation by Propionibacterium acnes is a characteristic of invasive isolates.
Burkhart, et al. 2007. Expanding the microcomedone theory and acne therapeutics: Propionibacterium acnes biofilm produces biological glue that holds corneocytes together to form plug.
Zouboulis. 2009. Propionibacterium acnes and Sebaceous Lipogenesis: A Love–Hate Relationship?
Ashkenazi, et al. 2002. Eradication of Propionibacterium acnes by its endogenic porphyrins after illumination with high intensity blue light.
Seo, et al. 2000. Fluorescence spectroscopy for endogenous porphyrins in human facial skin.
Borelli, et al. 2006. In vivo Porphyrin Production by P. acnes in Untreated Acne
Patients and its Modulation by Acne Treatment.

Explore the Science of Acne

Boxcar Acne Scars on the Temple (Fabbrochini, et al)

The vast majority of acne scars result from persistent cases of inflammatory acne affecting the same area of skin. Individuals who suffer from consistent nodular and cystic acne lesions are at a very high risk of developing permanent acne scarring. This is particularly true when a region is affected by overlapping acne outbreaks, with no opportunity to completely heal in-between.

In cases of persistent inflammatory acne vulgaris, large areas of skin and underlying tissue are damaged, but the continuing infection and inflammation prevent the body from mobilizing the cells and materials necessary for repairing those structures. As a result, the original (healthy) tissue is replaced by scar tissue.

The Role of Inflammation in Acne Scarring

Development of Inflammatory Acne (Pawin, et al)

What many people may not realize is that acne scarring is primarily due to the body’s own immune response to infection, and not the infection itself. A major component of inflammatory acne is the migration of white blood cells to the hair follicle, sebaceous gland and surrounding tissue. These white blood cells compose much of the “pus” or edema fluid that comes out when you pop a zit.

The white blood cells that make up the pus in a whitehead are not uniform, but rather are composed of many different sub-types of white blood cells, such as macrophages, neutrophils, dendritic cells, T cells, granulocytes, mast cells and others. Many of these cells produce powerful degradative enzymes, inflammatory molecules, super-oxides and free radicals. While these weapons are designed to help neutralize pathogens and foreign invaders, they can cause damage to the surrounding cells and tissue. In inflammatory acne the damage caused by these white blood cells actually causes the infection to spread, leading to more inflammation and damage, creating a vicious, self-fulfilling cycle.

Inflammatory acne causes white blood cells to secrete powerful enzymes that damage the tissue underneath the skin

When it comes to scarring, perhaps the most important type of white blood cell is the neutrophil. The neutrophil is one of the first responders to the infected follicle, and can accumulate in great numbers. Neutrophils are kind of like the suicide bombers of the cellular world. When they reach the site of infection they often undergo apoptosis (controlled suicide) and degranulation, which releases many anti-microbial molecules, DNA and proteases into environment. In particular it is these proteases that can cause tremendous damage to the surrounding tissue and ulimately lead to scarring. These proteases digest the elastin and collagen matrix that provides support and elasticity to the skin.

These powerful enzymes also damage many other proteins that are essential for the holding the matrix (aka: scaffolding) that provides the foundation for healthy skin tissue. Without this matrix to guide healing, the body has a very difficult time properly repairing and re-creating the damaged tissue. In cases of persistent infection and inflammation, the body is not able to repair the matrix fast enough to keep up with the damage. In these cases, the body begins to build scar tissue, which is simple and tough, in place of the more complex and delicate matrix. This process underlies not only the formation of acne scars, but of other diseases marked by chronic inflammation, such as chronic obstructive pulmonary disorder (emphysema) and rheumatoid arthritis.

The Formation of Scar Tissue

Inflamed Follicle Filled with White Blood Cells (Pus) (Hongcharu, et al)

Scar tissue is composed largely of collagen, which is the same material that comprises a healthy sub-cutaneous matrix. However, unlike the healthy matrix – which is a complex, spacious and interconnected web of collagen and other proteins – the collagen in scar tissue is much different. In scar tissue, the collagen becomes tightly bundled and tends to line up in a single direction, instead of the original random web pattern.

In scar tissue, many of the essential accessory proteins and molecules are excluded and there is much less open space. This alignment of the collagen fibers and their closely packed arrangement creates a denser, less elastic tissue. In addition, scar tissue becomes impermeable to migration by many cell types, preventing the formation of blood vessels and a regrowth of complex structures, such as hair follicles and sweat glands. This is why scar tissue is generally monotone, feels tough and dense to the touch, and is hairless. It also explains why the body has such a difficult time replacing scar tissue with healthy tissue.

Repairing Scar Tissue

Fractional C02 Laser Skin Resurfacing

Once scar tissue has been generated at a site of injury, it is relatively permanent. In some cases, the body will gradually replace some scar tissue with the proper tissue type, but this process is so slow that is largely irrelevant. The single best treatment for acne scarring, is to prevent it in the first place. This means aggressively attacking the infection and treating the inflammation as it arises. Treatment after the fact generally involves either surgically removing the scar tissue, or damaging it with laser, heat or surgical treatments. The damage stimulates the healing process and creates space for new, functional tissue to form.

Related Articles @ The Science of Acne

Collagen Matrix (stained blue) in Cutaneous Tissue (Lee, et al)

Overview: Acne Scar Treatment
Overview: Light and Laser Therapies for Acne
The Science of Acne Homepage
In Depth: What Causes Acne?

References and Sources

Research Articles

Physiopathology of acne vulgaris: recent data, new understanding of the treatments.
Pawin, et al. 2004. For article abstract, click here.
Topical ALA Photodynamic Therapy for the Treatment of Acne Vulgaris.
Hongcharu, et al. 2000. For article abstract, click here.
Human b Defensin-1 and -2 Expression in Human Pilosebaceous Units: Upregulation in Acne Vulgaris Lesions.
Chronnell, et al. 2001. For article abstract, click here.
A prospective, randomized, placebo-controlled, double-blinded, and split-face clinical study on LED phototherapy for skin rejuvenation: Clinical, profilometric, histologic, ultrastructural, and biochemical evaluations and comparison of three different treatment settings.
Lee, et al. 2007. For article abstract, click here.

Additional Online Resources

Scar @ Wikipedia
Inflammation @ Wikipedia
Neutrophil @ Wikipedia

This section contains all of the individual user reviews and antibiotic susceptibilty rankings for Silver Sulfadiazine (Silvadene).

If you have used Silver Sulfadiazine as a treatment for acne vulgaris, please share your experience and opinions.

Type of Treatment: Rx Medication – Antibiotic (Topical) - Sulfa Family

How It Works: Silver Sulfadiazine is an antibiotic. Antibiotics can improve acne symptoms by limiting the growth of bacteria that contribute to Acne Vulgaris.

When is this medication used? Silver Sulfadiazine is a topical antibiotic from the Sulfa Family.  Silver Sulfadiazine is a medication that is used to treat a range of bacterial skin infections.  Although, silver sulfadiazine is rarely used as a treatment for acne, there is some anecdotal evidence that this medication can be an effective treatment for acne symptoms. Silver sulfadiazine can be used as a treatment for all types of acne vulgaris (Acne Types: 1-4), although it is likely to be most effective for the treatment of mild to moderate acne (Acne Types: 1-2).   For the treatment of moderate to severe acne  (Acne Types: 3-4), topical Silver Sulfadiazine will likely need to be used in combination with a complementary treatment (eg. oral antibiotic, oral retinoid, androgen inhibitor or light/laser therapy).

Frequency of Silver Sulfadiazine Resistant P. acnes Bacteria: Rare. (What does this mean?)

Official Name: Silver Sulfadiazine.
Popular Brand Names: Flamazine, Silvadene, Silverex, Silvazine and Thermazene.
Related Medications: Co-Trimoxazole, Dapsone, Mafenide and Sulfacetamide.

Important Note: The information provided on this site is intended for informational purposes only and is not intended to diagnose or treat any diseases. The Science of Acne strongly encourages you to consult a qualified medical professional before making any treatment decisions. For the complete disclaimer, click here.

Overall (Composite) Ranking for Silver Sulfadiazine

Silver Sulfadiazine (Silvadene) Overall Score – Scale: 1 (WORST) to 5 (BEST)

The COMPOSITE ranking is calculated from a combination of all of the individual rankings for this medication (EFFECTIVENESS, ADVERSE EFFECTS and ANTIBIOTIC SUSCEPTIBILITY).

This ranking is scored on a scale of 1 (WORST) to 5 (BEST).

Share Your Experience with Silver Sulfadiazine – Rate This Medication

Effectiveness Ranking for Silver Sulfadiazine

Silver Sulfadiazine (Silvadene) Effectiveness Score – Scale: 1 (NOT EFFECTIVE) to 5 (VERY EFFECTIVE)

Silver Sulfadiazine is a topical medication that is infrequently used to treat acne vulgaris.  Silver Sulfadiazine may be used alone for the treatment of mild to moderate acne (Acne Types: 1-3).    Silver Sulfadiazine is generally used in addition to an oral antibiotic, oral retinoid or light-based treatment for the treatment of moderate to severe acne (Acne Types: 3-4).

The EFFECTIVENESS ranking is based on patient reports of how effective this medication was at improving their acne symptoms.

This ranking is scored on a scale of 1 (NOT EFFECTIVE) to 5 (VERY EFFECTIVE).

Share Your Experience with Silver Sulfadiazine – Rate This Medication

Adverse Effects Ranking for Silver Sulfadiazine

Silver Sulfadiazine (Silvadene) Side Effects Score – Scale: 1 (NONE) to 5 (SEVERE)

Topical silver sulfadiazine tends to have minimal side effects, most of which are mild.  Allergic reactions are the most common problem associated with this medication.

The ADVERSE EFFECTS ranking is based on patient reports about the adverse effects and side effects that they experienced with this medication.

This ranking is scored on a scale of 1 (NO SIDE EFFECTS) to 5 (SEVERE SIDE EFFECTS).

Share Your Experience with Silver Sulfadiazine – Rate This Medication

Antibiotic Susceptibility Ranking for Silver Sulfadiazine

Silver Sulfadiazine (Silvadene) Antibiotic Susceptibility Score – Scale: 1 (NOT SUSCEPTIBLE) to 5 (VERY SUSCEPTIBLE)

The ANTIBIOTIC SUSCEPTIBILITY ranking is based on scientific research reports about the antibiotic sensitivity of Propionibacterium acnes (P. acnes), which is a bacterium that is a primary cause of acne symptoms. Our antibiotic susceptibility data is generated from the combined results of over 50 independent scientific studies. For more information about which antibiotics are most effective against P. acnes bacteria, visit the Antibiotic Susceptibility of Propionibacterium acnes page.

Frequency of Silver Sulfadiazine Resistant P. acnes Bacteria: Rare. (What does this mean?)

This ranking is scored on a scale of 1 (NOT SUSCEPTIBLE) to 5 (VERY SUSCEPTIBLE).

Share Your Experience with Silver Sulfadiazine – Rate This Medication

User Recommendations for Silver Sulfadiazine

Do Acne Patients Recommend Silver Sulfadiazine (Silvadene) as a Treatment?

The USER RECOMMENDATIONS chart indicates how many reviewers recommended this medication as a treatment for Acne Vulgaris. These recommendations are only from The Science of Acne users. For additional reviews of this medication from outside sources, refer to the section below.

There are four options available for this ranking:

YES (definitely recommended)
MAYBE (conditionally recommended)
NO (not recommended)
DON’T KNOW (no opinion)

Share Your Experience with Silver Sulfadiazine – Rate This Medication

Outside Reviews of Silver Sulfadiazine

The following is a list of links to pages that review or discuss the use of this medication. Note: Some of these reviews are not specific to the use of this medication in the treatment of Acne Vulgaris.

Additional Patient Reviews of Silver Sulfadiazine: Acne.org, WebMD, Drugs.com, DailyStrength.org, RxList.com, EveryDayHealth.com, Treato.com, UserMeds.com, DrugsInfo.com, RateADrug.com.

Silver Sulfadiazine Background

Silver Sulfadiazine (Silvadene) Molecule

Silver sulfadiazine is a topical antibiotic cream that is commonly used to prevent secondary skin infections in burn patients.  Silver sulfadiazine is an antibiotic salt that inhibits the growth of bacteria in two different ways.  First, sulfadiazine is a sulfa family antibiotic.  This family of antibiotics kills bacteria by preventing them from synthesizing folic acid, which is an essential B-vitamin.  Second, silver sulfadiazine releases silver ions into the tissue where it is applied.  Silver itself is toxic to most types of bacteria.  The combined action of these two mechanisms contribute to the overall antibacterial activity of silver sulfadiazine.

Additional Names for Silver Sulfadiazine: Adiazine, Argedin, Bacternil, Bactrazine, Brandiazin, Burnazin, Dermazin Ditrim (Sulfadiazine and Trimethoprim), Flammazine, Geben, Labdiazina, Sanaderm, Sedoflame, Sicazine, Silbecor, Silvadex, Silvadiazin, Silvadin, Silvadina, Silvamed, Silvazine, Silvederma, Silver Sulphadiazene, Silverdin, Silverin, Silverol, Silvertone, Sliverex, SSD, SSDee, Sulfadiazin, Sulfadiazina, Sulfadiazinum argentum, Sulfasil, Sulfatral, Sulphargin, Theradia, Urgotül, Zilversulfadiazine and Zitep.

Important Note: The information provided on this site is intended for informational purposes only and is not intended to diagnose or treat any diseases. The Science of Acne strongly encourages you to consult a qualified medical professional before making any treatment decisions. For the complete disclaimer, click here.

Cost and Availability of Silver Sulfadiazine

Pharmaceutical products that contain silver sulfadiazine are available both as prescriptions and over the counter (OTC) medications.  When possible, prescription silver sulfadiazine should be obtained through consultation of a physician. Many physicians and dermatologists are familiar with this medication, although it is not widely used for the treatment of acne vulgaris.  Both generic forms and brand name formulations of this medication are widely available. Generic silver sulfadiazine tends to be inexpensive and brand name formulations tend to be moderately expensive.

Important Note: The information provided above is not intended as a recommendation or endorsement. The Science of Acne encourages you to adhere to all applicable legal regulations in your jurisdiction. Before ordering pharmaceutical medications online, please read our overview: A Guide to Buying Prescription Medications on the Internet.

Related Articles from The Science of Acne

In Depth: Silver Sulfadiazine (Silvadene) and Acne Vulgaris
Avoiding Negative Drug Interactions
A Guide to Buying Prescription Medications on the Internet
Prescription Medications Used in Acne Treatment
What causes acne?

References and Sources

Books

PDR Staff Writers. 2011. 2011 Physicians’ Desk Reference
Gallagher. 2011. Antibiotics Simplified, Second Edition
Habif. 2009. Clinical Dermatology
Goodheart. 2006. Acne For Dummies
Bartlett. 2012. Johns Hopkins Antibiotics Guide 2012 (Johns Hopkins Medicine)

Online Resources

PubMed Health – The National Institute of Health (US)
Silver Sulfadiazine @ Wikipedia
Physician’s Insert for Silver Sulfadiazine

Scientific Research Articles

1. Carr, et al. 1973. Silver Sulfadiazine: In Vitro Antibacterial Activity.
2. Elston. 2009. Topical Antibiotics in Dermatology: Emerging Patterns of Resistance.
3. Fox. 1968. Silver Sulfadiazine—A New Topical Therapy for Pseudomonas in Burns.
4. Fuller, et al. 1994. A Review of the Dosimetry of 1% Silver Sulfadiazine Cream in Burn Wound Treatment.
5. Atiyeh, et al. 2007. Effect of silver on burn wound infection control and healing: Review of the literature.

This section contains all of the individual user reviews and antibiotic susceptibilty rankings for Retapamulin (Altabax).

If you have used Retapamulin as a treatment for acne vulgaris, please share your experience and opinions.

Type of Treatment: Rx Medication – Antibiotic (Topical) - Pleuromutilin Family

How It Works: Retapamulin is an antibiotic. Antibiotics can improve acne symptoms by limiting the growth of bacteria that contribute to Acne Vulgaris.

When is this medication used? Retapamulin is a new antibiotic that was developed, in part, for the treatment of acne vulgaris.  Retapamulin is a topical antibiotic that can be used as a treatment for all types of acne vulgaris (Acne Types: 1-4).   For the treatment of moderate to severe acne  (Acne Types: 3-4), topical retapamulin may be combined with a complementary treatment (eg. oral antibiotic, oral retinoid, androgen inhibitor or light/laser therapy).

Frequency of Retapamulin Resistant P. acnes Bacteria: Rare. (What does this mean?)

Official Name: Retapamulin.
Popular Brand Names: Altabax, Altargo.
Related Medications: N/A.

Important Note: The information provided on this site is intended for informational purposes only and is not intended to diagnose or treat any diseases. The Science of Acne strongly encourages you to consult a qualified medical professional before making any treatment decisions. For the complete disclaimer, click here.

Overall (Composite) Ranking for Retapamulin

Retapamulin (Altabax) Overall Score – Scale: 1 (WORST) to 5 (BEST)

The COMPOSITE ranking is calculated from a combination of all of the individual rankings for this medication (EFFECTIVENESS, ADVERSE EFFECTS and ANTIBIOTIC SUSCEPTIBILITY).

This ranking is scored on a scale of 1 (WORST) to 5 (BEST).

Share Your Experience with Retapamulin – Rate This Medication

Effectiveness Ranking for Retapamulin

Retapamulin (Altabax) Effectiveness Score – Scale: 1 (NOT EFFECTIVE) to 5 (VERY EFFECTIVE)

Retapamulin is a topical medication that can be used to treat acne vulgaris.  Research indicates that retapamulin appears to be very effective for treatment of acne vulgaris.  Retapamulin may be used alone for the treatment of mild to moderate acne (Acne Types: 1-3).    Retapamulin is often used in combination with an oral antibiotic, oral retinoid or light-based treatment for the treatment of moderate to severe acne (Acne Types: 3-4).

The EFFECTIVENESS ranking is based on patient reports of how effective this medication was at improving their acne symptoms.

This ranking is scored on a scale of 1 (NOT EFFECTIVE) to 5 (VERY EFFECTIVE).

Share Your Experience with Retapamulin – Rate This Medication

Adverse Effects Ranking for Retapamulin

Retapamulin (Altabax) Side Effects Score – Scale: 1 (NONE) to 5 (SEVERE)

Topical retapumulin tends to have minimal side effects, most of which are mild.  Allergic reactions are the most common problem associated with this medication.

The ADVERSE EFFECTS ranking is based on patient reports about the adverse effects and side effects that they experienced with this medication.

This ranking is scored on a scale of 1 (NO SIDE EFFECTS) to 5 (SEVERE SIDE EFFECTS).

Share Your Experience with Retapamulin – Rate This Medication

Antibiotic Susceptibility Ranking for Retapamulin

Retapamulin (Altabax) Antibiotic Susceptibility Score – Scale: 1 (NOT SUSCEPTIBLE) to 5 (VERY SUSCEPTIBLE)

The ANTIBIOTIC SUSCEPTIBILITY ranking is based on scientific research reports about the antibiotic sensitivity of Propionibacterium acnes (P. acnes), which is a bacterium that is a primary cause of acne symptoms. Our antibiotic susceptibility data is generated from the combined results of over 50 independent scientific studies. For more information about which antibiotics are most effective against P. acnes bacteria, visit the Antibiotic Susceptibility of Propionibacterium acnes page.

Frequency of Retapamulin Resistant P. acnes Bacteria: Rare. (What does this mean?)

This ranking is scored on a scale of 1 (NOT SUSCEPTIBLE) to 5 (VERY SUSCEPTIBLE).

Share Your Experience with Retapamulin – Rate This Medication

User Recommendations for Retapamulin

Do Acne Patients Recommend Retapamulin (Altabax) as a Treatment?

The USER RECOMMENDATIONS chart indicates how many reviewers recommended this medication as a treatment for Acne Vulgaris. These recommendations are only from The Science of Acne users. For additional reviews of this medication from outside sources, refer to the section below.

There are four options available for this ranking:

YES (definitely recommended)
MAYBE (conditionally recommended)
NO (not recommended)
DON’T KNOW (no opinion)

Share Your Experience with Retapamulin – Rate This Medication

Outside Reviews of Retapamulin

The following is a list of links to pages that review or discuss the use of this medication. Note: Some of these reviews are not specific to the use of this medication in the treatment of Acne Vulgaris.

Additional Patient Reviews of Retapamulin: Drugs.com, WebMD, RxList.com, Acne.org, EveryDayHealth.com, Treato.com, Drugsinfo.com.

Retapamulin Background

Retapamulin (Altabax) Molecule

Retapamulin is part of a newly available class of antibiotics called Pleuromutilins.  Pleuromutilin antibiotics were discovered over 50 years ago, but were only recently approved for human use. Pleuromutilin antibiotics inhibit the growth of susceptible bacteria by preventing them from synthesizing new proteins.  They do this by inhibiting the function of an enzyme called Peptidyl Transferase, which is necessary for the translation of bacterial genes into proteins.

Because topical retapamulin is a newly available medication, it has a minimal history of use as an acne treatment.  Currently, the primary use of retapamulin is for the treatment of  Impetigo, which is a chronic skin disease. However, several research reports have indicated that retapamulin is highly active against most strains of the acne-causing bacterium, Propionibacterium acnes. The research also suggest that retapamulin may even be effective against strains of P. acnes bacteria that are resistant to other antibiotics.

Additional Names for Retapamulin: Retapamulina, Retapamuline and Retapamulinum.

Important Note: The information provided on this site is intended for informational purposes only and is not intended to diagnose or treat any diseases. The Science of Acne strongly encourages you to consult a qualified medical professional before making any treatment decisions. For the complete disclaimer, click here.

Cost and Availability of Retapamulin

Retapamulin is a newly approved medication and is only available in brand name formulations. Because it is new, many physicians and dermatologists may be unfamiliar with this medication. Retapamulin (Altabax) tends to be very expensive.

Related Articles from The Science of Acne

In Depth: Retapamulin (Altabax) and Acne
Overview: Avoiding Negative Drug Interactions
A Guide to Buying Prescription Medications on the Internet
Overview: Prescription Medications Used in Acne Treatment
In Depth: Antibiotic Susceptibility of Propionibacterium acnes

References and Sources

Books

PDR Staff Writers. 2011. 2011 Physicians’ Desk Reference
Gallagher. 2011. Antibiotics Simplified, Second Edition
Habif. 2009. Clinical Dermatology
Goodheart. 2006. Acne For Dummies
Bartlett. 2012. Johns Hopkins Antibiotics Guide 2012 (Johns Hopkins Medicine)

Online Resources

Nadifloxacin @ Wikipedia
Physician’s Insert for Nadifloxacin

Scientific Research Articles

1. Goldstein, et al. 2006. Comparative In Vitro Activities of Retapamulin (SB-275833) against 141 Clinical Isolates of Propionibacterium spp., Including 117 P. acnes Isolates.
2. Odou, et al. 2007.  In vitro activity against anaerobes of retapamulin, a new topical antibiotic for treatment of skin infections.
3. Jacobs. 2007.  Retapamulin: a semisynthetic pleuromutilin compound for topical treatment of skin infections in adults and children.
4. Scangarella-Oman, et al. 2009.  Microbiological profile of a new topical antibacterial: retapamulin ointment 1%.
5. Boyd, et al. 2006.  Retapamulin. Pleuromutilin antibiotic.
6. Yang, et al. 2008.  Retapamulin: A Review of its Use in the Management of Impetigo and Other Uncomplicated Superficial Skin Infections.
7. Nagabushan. 2010.  Retapamulin: A novel topical antibiotic.