Appearance, Causes, Symptoms & Treatment

Overview

What is folliculitis?

Folliculitis is a common skin condition that’s often caused by an infected or inflamed hair follicle. It can look similar to acne and be uncomfortable or itchy. Folliculitis often has a psychosocial impact because of its appearance. There are many different types of folliculitis — each one unique based on the cause, the infectious organism and its impact on the skin. Folliculitis can happen as a result of daily activities like shaving, getting in a hot tub, and excess sweating from exercise or outdoor work.

You can have folliculitis anywhere on the body that has hair. Common places include your:

• Face.
• Arms.
• Upper back.
• Lower legs.

You have hair almost everywhere on your body. Some hairs are so fine that you may not notice they are there, while others are very prominent. Your hair has a larger purpose than appearance — it acts like an insulator, keeping you warm. It’s part of your body’s protection system. The spot where an individual hair enters your skin is called a follicle. The follicle holds the thin hair in place and is home to oil glands.

Unfortunately, follicles can gather bacteria and other materials from the outside world that could cause inflammation or infection. When something is inflamed, it’s swollen. A swollen hair follicle will bulge up and make a bump on the skin. If you have an infected hair follicle, you may experience:

• Redness.
• Irritation.
• Itching.
• Bumps on the skin.

What are the types of folliculitis?

There are actually many different types of folliculitis. Think of folliculitis like a blanket term — it’s the family that each of these specific types of skin conditions lives under. Each type of folliculitis can have its own appearance, symptoms and cause. Often, the thing that causes the condition is one of the biggest factors that sets each type of folliculitis apart. Location can also play a role — where you experience this condition on your body can change depending on what type of folliculitis you have.

The types of folliculitis include:

• Staphylococcus aureus folliculitis: Infection of the hair follicle with Staphylococcus aureus bacteria is one of the most common causes of folliculitis. Small red or white pus-filled pimples can be seen on the skin. The affected area often gets better (resolves) within a few days and can be cared for at home. In severe and persistent cases, however, folliculitis should be treated by your healthcare provider.
• Pseudomonas aeruginosa (“hot tub”) folliculitis: Pseudomonas aeruginosa is a bacteria that thrives in heated, moving water (hot tubs, whirlpools, water slides). It can infect the hair follicle and cause a rash that looks a lot like the one caused by the staphylococcal species. Sometimes the rash is itchy. Hot tub folliculitis occurs one to two days after exposure to the water source and typically fades on its own within a few days. Rarely, some people may need medical treatment.
• Malassezia folliculitis: Malassezia are a family of yeast that can normally be found on the skin. Sometimes, when Malassezia gets into the hair follicles, it can cause an itchy condition that looks like an acne breakout. It usually occurs on the upper chest and back. This form of folliculitis is made worse (aggravated) by sweat. Using an antidandruff shampoo every day to wash the affected areas of skin is often helpful.
• Pseudofolliculitis barbae: Also called “razor bumps,” pseudofolliculitis barbae usually occurs in the beard area. After beard hairs are cut with a razor, sharply trimmed edges can turn back into the skin, causing irritation. Pseudofolliculitis barbae is more common in people with curly hair, particularly Black men. Avoidance of shaving or using trimmers can help. If the problem is persistent, you should see a dermatologist as this can lead to scarring.
• Sycosis barbae: Sycosis barbae is a severe, potentially scarring form of shaving-related folliculitis. The entire hair follicle is infected, resulting in large red pustules. Shaving should be avoided and you should see a dermatologist for discussion of treatment options.
• Gram-negative folliculitis: Gram-negative folliculitis can happen after prolonged antibiotic use to treat acne. Over time, resistant bacteria grow and multiply. This can lead to your acne actually getting worse. This condition requires treatment from a dermatologist or another healthcare provider.
• Boils (furuncles): Boils, or furuncles, occur when the hair follicle becomes deeply infected. The boil is often red, tender and painful. It will come to a head after several days and may leave a scar behind. In certain cases, oral medications or procedures are needed to resolve the lesion.
• Carbuncles: A carbuncle forms when several boils appear in one spot. Carbuncles are usually larger and are the combination of multiple infected hair follicles. As with boils, in certain cases, oral medications or procedures are needed to resolve the lesion.
• Eosinophilic folliculitis: This condition is usually seen in patients who are immunosuppressed (the immune system is not fully functioning). There’s also a form that’s seen in babies. Eosinophilic folliculitis is not infectious. It is characterized by itchy pustules, most often on the shoulders, upper arms, neck and forehead. They often resolve on their own, but can come back (recur).

How common is folliculitis?

Folliculitis is a very common skin condition that many people will experience throughout their lives. It can happen to men, women, children and infants. Certain types of folliculitis are more likely to happen in particular groups of people. Pseudofolliculitis barbae and sycosis barbae, for example, are two types of folliculitis are closely linked to shaving. These conditions are much more common in men who are frequently cutting beard hairs.

Symptoms and Causes

What are the symptoms of folliculitis?

In most cases, the main symptom of folliculitis is red bumps that look like pimples on your skin. These could also look like they’re white-filled bumps or they could be filled with pus (pustules). Folliculitis can feel itchy and uncomfortable. Many people feel the need to scratch when they have folliculitis. It’s best to try and not scratch at the spots because you don’t want to open them up (this could possibly cause a worse infection of the hair follicle).

What causes folliculitis?

In general, folliculitis is caused when a hair follicle is inflamed (swollen) and infected. This causes the follicle to swell under the skin, creating uncomfortable bumps on the surface of your skin. For many of the specific types of folliculitis, the cause isn’t always known. However, there are certain factors that can increase your risk of developing folliculitis. A few risks can include:

• If you shave often.
• If you have been using an oral antibiotic for a long period of time.
• If you are overweight or obese.
• If you have a history of diabetes.
• If you do activities that make you sweat a lot and don’t fully clean off afterwards.
• If you spend time in a hot tub or sauna that isn’t properly cleaned.

Diagnosis and Tests

How is folliculitis diagnosed?

Folliculitis is usually diagnosed during a physical exam with your healthcare provider. This can be done during an appointment and in most cases, you do not need to see a skincare specialist. Your primary care physician is usually able to diagnose folliculitis and provide a treatment plan. In certain, severe or persistent cases, an appointment with a dermatologist is recommended.

Your healthcare provider will go over your medical history and ask you about your habits. Some questions might include:

• Have you been sweating more than normal lately or doing activities that cause you to sweat a lot?
• Have you been in a hot tub or sauna?
• Do you shave every day?
• Are you currently taking any medications, including acne treatments?

The answers to these questions often confirm a diagnosis of folliculitis and help your provider determine which type it might be.

In some more severe cases, your provider may refer you to a dermatologist for additional tests to make sure your folliculitis isn’t another medical condition. One test that can be done is a biopsy. This is a test where a small sample of your skin is removed and then taken to a lab where it’s studied.

Management and Treatment

How is folliculitis treated?

Treatment options for folliculitis depend on the type of folliculitis you have and it’s severity. Certain types may need more aggressive types of care, while others may go away with little to no treatment. If your folliculitis is mild, it can sometimes be treated at home. There are several ways you can care for your irritated skin, including:

• Using antibacterial cleansers to clean the skin. This will limit the amount of bacteria on your skin.
• Applying warm towels to your irritated skin to sooth the discomfort.
• Using anti-itch creams.

In less severe types of folliculitis, like Pseudomonas folliculitis (hot tub rash), your symptoms will typically fade within a few days without treatment. If they don’t, reach out to your healthcare provider. When you have a more severe case of folliculitis, oral antibiotics may be needed to treat the condition. Deeper infections, like boils and carbuncles, may have to be drained by your healthcare provider. This will remove the build-up of pus and allow the area to heal. Because Pseudofolliculitis barbae and Sycosis barbae heavily affect the beard area, you can manage these conditions by changing your shaving habits. These changes can include:

• Softening the hair with hot water before shaving.
• Shaving with the grain of the hair, not against it.
• Using a shaving gel or cream.
• Shaving every other day, rather than daily.
• Using an electric razor or hair removal product instead of a traditional razor blade.
• Avoiding pulling the skin while shaving.

Prevention

Can folliculitis be prevented?

In many cases, you can work to prevent folliculitis or manage it by changing your lifestyle habits. Folliculitis infections usually involve bacteria and yeast entering your hair follicles. By changing some parts of your normal self-care routine, you can limit the amount of infectious material in your hair follicles.

A few tips for preventing folliculitis include:

• Keeping your skin clean.
• Limiting shaving.
• Checking the chemical disinfectant levels of hot tubs and heated pools before using them. The warmer a pool or hot tub, the faster the chemicals will fade away — making them less effective against bacteria.
• Washing off and removing your swimsuit when you get out of a hot tub or pool.
• Wearing breathable clothing to keep sweat from getting trapped between your clothes and skin.

Outlook / Prognosis

Will folliculitis come back?

Folliculitis can come back again after treatment if you don’t change your hygiene practices and self-care habits. Keeping your skin clean is an important part of its health. It’s also good to know what triggers your folliculitis so you can avoid those things in the future. For example, if you know that you get folliculitis after going in a hot tub, then you might want to make sure the chemicals are at full-strength before getting in.

If you are aware of what caused your folliculitis in the past and change your habits to correct those causes, the chance of it happening over and over is small.

Living With

When should I call my doctor about folliculitis?

Even though many cases of folliculitis can be cared for at home and go away after a short period of time, do not hesitate to call your healthcare provider if you are concerned. In most cases, a quick exam by your provider will tell you if you need treatment for folliculitis or if it will go away on its own. Severe cases of folliculitis do need to be treated and may require an oral medication or small procedure. If you experience any of the following, call your healthcare provider right away:

• Folliculitis that spreads from the original area to other parts of your skin.
• Spots that are firm or painful.
• Any bumps that are draining a fluid.
• Fevers, chills, fatigue or any other systemic symptoms.

A note from Cleveland Clinic

Folliculitis is a very common condition that many people experience throughout their lifetime. If you notice small red bumps on your arms, legs, face or back and start to experience uncomfortable symptoms (pain, fluid drainage, fever), reach out to your healthcare provider. Folliculitis can often be cared for at home and doesn’t require a trip to your healthcare provider’s office, but if you do have any concerns it’s best to call your provider.

Penile appearance, lumps and bumps

Vinita Rane

Tim Read

Background

Even after a thorough examination it can be difficult to distinguish a normal penile anatomical variant from pathology needing treatment.

Objective/s

This article aims to assist diagnosis by outlining a series of common penile anatomical variants and comparing them to common pathological conditions.

Discussion

The problems considered include pearly penile papules, penile sebaceous glands (Fordyce spots), Tyson glands, angiokeratomas of the scrotum, lymphocoele, penile warts, molluscum contagiosum, folliculitis and scabies.

‘More is missed from not looking than not knowing.’
Professor Thomas Macrae

Even after a thorough examination it can be difficult to distinguish a normal penile anatomical variant from pathology needing treatment. The common practice of treating any penile lump as a wart is no longer useful in the era of human papillomavirus (HPV) vaccination.

Since the introduction of the National Human Papillomavirus Vaccination Program for young women in 2007, the incidence of genital warts has fallen dramatically in young Australian heterosexuals.¹ With the extension of this vaccination program to young men, it is expected that the incidence of genital warts will fall further and will also decline in homosexual men: genital lumps in young adults are now less likely to be warts. This article aims to assist diagnosis by outlining some common anatomical variants and comparing them to a few pathological conditions. There are other conditions that may cause genital pathology that are not covered, and treatment is not discussed in detail.

Most anatomical variants share characteristic features that help with recognition, such as symmetry, a smooth surface and well circumscribed border. Normal variants should not produce any symptoms of pain or be associated with inguinal lymphadenopathy. Table 1 outlines some typical features that are suggestive of genital warts. Despite these features, it can sometimes still be difficult to be sure, especially if the appearance is atypical. Having access to a bank of images, such as those on the Melbourne Sexual Health Centre website (www.stiatlas.org), is very useful. These images can also be used to reassure patients and educate them on the differences between normal anatomy and conditions that would require treatment.

Normal variants

Pearly penile papules

Pearly penile papules (PPPs) are tiny lumps seen in neat rows around the corona of the glans penis (Figure 1). They can occur as a single row, or in multiple orderly rings encircling the corona. PPPs are numerous, uniform, symmetrical and dome shaped, and vary from 1 to 3 mm in length. PPPs occur in up to 20% of men and are frequently mistaken for warts, but bear no relationship to them.^2,3 In difficult cases dermoscopy can be useful, as PPPs will have delicate, regular vessels that are distinct from genital warts. Histologically, PPPs resemble angiokeratomas.

Figure 1. Pearly penile papules

Fordyce spots

Fordyce spots are visible sebaceous glands and occur along the shaft of the penis (Figure 2).⁴ They often appear in adolescence. Fordyce spots are more easily visible when the skin is stretched, and many patients may describe them as a lump that appears during an erection. Spots may also appear on the scrotum. Some patients may be able to express a thick, chalky discharge by squeezing the lump. Fordyce spots may also appear in other areas such as at the vermillion border of the lips when, if seen, can help reassure the patient that they are a normal anatomical variant that does not require any treatment.

Figure 2. Fordyce spots (penile sebaceous glands)

Tyson glands

Tyson glands are ectopic sebaceous glands that appear in pairs as openings on either side of the frenulum (Figure 3). As they are normal structures, treatment is not required.⁵

Figure 3. Tyson glands

Angiokeratomas

Angiokeratomas can occur alone or in multiples and appear as deep-red or purple papules, usually over the scrotum. They can also appear on the penis (Figure 4). Angiokeratomas advance with age and represent a collection of enlarged capillaries.⁶ Treatment is only required if they bleed frequently.

Figure 4. Angiokeratomas of the scrotum

Lymphocoeles

Lymphocoeles present as a palpable cord-like structure that can occur vertically or horizontally at the shaft of the penis (Figure 5). They are associated with friction and increased sexual activity. Lymphocoeles are probably due to sclerosing lymphangitis, an inflammatory process caused by a thrombosed vessel. ⁷ Sclerosing lymphangitis can also occur in the presence of some sexually transmissible infections (STIs) such as Neisseria gonorrhoea or syphilis, and appropriate STI screening may be necessary. The thrombosed vessel will usually spontaneously recanalise and therefore the condition itself requires no treatment.

Figure 5. Lymphocoele. Also note small pearly penile papules

Skin tags

Also known as acrochordons, skin tags are common in the skin creases of the groin in middle aged men. They typically have the size and shape of a grain of rice. They are often also present in the axillae and on the lateral skin of the neck. Skin tags have a fibrovascular centre and normal overlying epidermis.

Penile lumps that may require treatment

Warts

Penile warts(Condylomata acuminata) are irregular, rough lesions that can occur anywhere along the penile shaft, glans and prepuce; they can also arise from the meatus. Warts vary in size from a millimetre to a few centimetres. Warts on the shaft of the penis or pubic area tend to be more indurated and dome shaped, whereas those under the prepuce or emerging from the urethra are softer and fronded (Figure 6). A smooth-looking wart may be difficult to distinguish from an acrochordon (skin tag) or other normal structure, but using a bright light and magnification will reveal fine dots or a cobblestone pattern. Warts are most commonly due to strains 6 and 11 of HPV.⁸ There are a number of options for treatment including cryotherapy, podophyllotoxin and imiquimod. All of these therapeutic options typically require multiple treatments over a number of weeks. As the natural history of HPV in immunocompetent hosts is spontaneous recovery over 12–24 months, patients may also opt to have no treatment.^9,10

Figure 6. Penile warts

Molluscum contagiosum

Molluscum contagiosum appear as small papules with a central depression or umbilication. They are caused by a member of the poxvirus family, molluscum contagiosum virus (MCV). Molluscum contagiosum are commonly acquired by children from non-sexual skin contact, often during bathing or swimming with other infected children. In adults however, sexually transmitted molluscum may be seen on or near the genitals (Figure 7). The virus has a self limiting course over a period of months, but treatment with cryotherapy is often recommended to prevent the spread of MCV to others.^11,12

Figure 7. Molluscum contagiosum

Folliculitis

Folliculitis is an inflammation of the hair follicles, frequently seen at the base of the penis (Figure 8). Folliculitis presents as a pustule around the hair follicle, which is frequently itchy and sometimes painful. Patients are often concerned that genital herpes simplex virus (HSV) is the cause, but the association with a hair follicle and the quality of the pain helps distinguish folliculitis from HSV. If a lesion is aspirated, thick purulent material (which may be blood stained), is often seen, whereas, vesicles due to HSV express a clear or straw coloured fluid. Herpes simplex virus may also be associated with a prodrome of malaise, fatigue and paraesthesia of the affected area. Molluscum contagiosum lesions is another casue occasionally confused with folliculitis, but there is sometimes a red halo. Folliculitis is often successfully managed with topical treatments and genital hygiene measures, but may need appropriate antimicrobial therapy if there is a surrounding cellulitis or a large number of lesions.

Figure 8. Folliculitis

Primary syphilis

An early syphilis chancre may present as a non-ulcerated, button shaped lump on the penile skin. Chancres are often indurated and there is usually some sign of epidermal breakdown or inguinal lymphadenopathy. Syphilis serology may be negative for the first few days of a chancre and should be repeated 2–4 weeks later if syphilis is suspected. In very early syphilis, treponemal polymerase chain reaction (PCR), using a dry cotton swab vigorously rubbed on the lesion at the time of the initial consultation, may be more likely to yield a positive result. While only some specialist laboratories perform this, most can forward the specimen on for appropriate testing.

Scabies

Genital scabies presents as intensely itchy, pink nodules (Figure 9). Patients usually have some sign of scabies elsewhere, such as the wrists, fingers and lower abdominal skin, which may include typical linear burrows.

Figure 9. Scabies

Subcutaneous lumps

Lumps beneath the skin are uncommon on the penis and are more likely to represent pathology. An important diagnosis to consider is Peyronie disease, which can present as a plaque attached to the tunica albuginea, usually in the proximal half of the penis. The skin moves freely over this, and patients may have noticed curvature of the erect penis. In some cultures there is a practice of inserting steel, plastic or glass beads under the penile skin. A small lump near the hair bearing skin of the proximal penis may represent a healed furuncle.

Summary

While lumps on the penis are frequently a source of great anxiety for the patient, if it is unclear whether the lesion is a normal variant or not, there is usually no harm in asking the patient to return for review. In some cases, it is necessary to refer to a more experienced colleague, a sexual health service or dermatologist to assist with diagnosis. A second opinion is often more efficient and preferable to the patient than a biopsy or a trial of treatment.

Key points

• Genital warts are becoming less common.
• Normal variants can cause significant anxiety, but have no sequelae, do not represent an STI, cannot be passed to others, and do not require treatment.
• If the diagnosis is unclear, it may be useful to review the patient in a few weeks. A normal variant does not usually progress, and for most conditions that require treatment, there is no harm to the patient if treatment is delayed for a few weeks.

Competing interests: Tim Read has received payment from GlaxoSmithKline and Merck Sharp & Dohme for work as Site Principal Investigator for an antiretroviral trial (GSK) and HPV vaccine study (MSD).
Provenance and peer review: Commissioned; externally peer reviewed.

Acknowledgements

The authors gratefully acknowledge Ian Denham for his review of the manuscript and for contributing images. We also acknowledge the assistance of Afrizal Afrizal for the technical support of images.

References

1. Read TR, Hocking JS, Chen MY, Donovan B, Bradshaw CS, Fairley CK. The near disappearance of genital warts in young women 4 years after commencing a national human papillomavirus (HPV) vaccination programme. Sex Transm Infect 2011;87:544–77.
2. Watanabe T, Yoshida Y, Yamamoto O. Differential diagnosis of pearly penile papules and penile condyloma acuminatum by dermoscopy. Eur J Dermatol 2010;20:414–5.
3. Agrawal SK, Bhattacharya SN, Singh N. Pearly penile papules: a review. Int J Dermatol 2004;43:199–201.
4. O’Mahony C. Genital lumps and bumps: what is normal? Trends in Urology Gynaecology & Sexual Health 2007;12:25–7.
5. Hyman AB, Brownstein MH. Tyson’s “glands”. Ectopic sebaceous glands and papillomatosis penis. Arch Dermatol 1969;99:31–6.
6. Machan M, Tonkovic-Capin V. Images in clinical medicine. Fordyce’s angiokeratomas. N Engl J Med 2012;366:1240.
7. McMillan A. Lymphocoele and localized lymphoedema of the penis. Br J Vener Dis 1976;52:409–11.
8. Yanofsky VR, Patel RV, Goldenberg G. Genital warts: a comprehensive review. J Clin Aesth Dermatol 2012;5:25–36.
9. Russell D, Bradford D, Fairley CK. Sexual Health Medicine. 2nd edn. Melbourne: IP Communications Ltd, 2011.
10. Hathaway JK. HPV: diagnosis, prevention, and treatment. Clin Obstet Gynecol 2012;55:671–80.
11. Bikowski JB Jr. Molluscum contagiosum: the need for physician intervention and new treatment options. Cutis 2004;73:202–6.
12. Tyring SK. Molluscum contagiosum: the importance of early diagnosis and treatment. Am J Obstet Gynecol 2003;189:S12–6.

Correspondence [email protected]

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Causes, Diagnosis, Treatment and Care at Home

Folliculitis (foh LICK you LIE tiss) is a common inflammation of the hair follicles. Follicles are the openings in the skin where the hair grows (Picture 1). The rash appears as small red bumps or pus bumps that can itch or be mildly painful.

Folliculitis is common on the buttocks, arms and legs – especially the thighs. Most improve in 7 to 10 days. Sometimes after the rash is gone, dark marks can be left behind. These are not scars, and the dark marks will go away with time.

Causes

There are several reasons why hair follicles might become inflamed (red or irritated):

• Bacterial infections. An infection by common or normal bacteria on the skin surface is the most common cause of folliculitis. It can also come from bacteria that grow in hot tubs.
• Ingrown hairs. This may occur after shaving the hair anywhere on the body. As the hair regrows, it can curl into the skin, causing irritation.
• Friction (rubbing) from tight clothing or sports equipment.
• Blocked follicles. Thick moisturizers, medicines, tight bandages, sports equipment, casts or braces can plug hair follicles.
• Excessive sweating.

Diagnosis and Treatment

A doctor can diagnose folliculitis by physical examination. If there is concern that it might be caused by bacteria, the doctor may swab a pus bump to be tested by the lab.

For folliculitis caused by a bacterial infection, the doctor may suggest or prescribe:

• Topical antibiotics. This is a cream or ointment that is put on the skin.
• Bleach baths. Add ¼ cup of bleach to ½ of tub of warm water. Soak in a bleach bath twice a week for 10 to 15 minutes. This may help keep bacterial folliculitis from coming back.

What to Do at Home

Folliculitis may be avoided by following these strategies:

• Shaving: Shave with care. Use an electric razor or a new blade every time you shave. Keep the shaved area clean and try to avoid cuts and nicks. Apply a moisturizing lotion after you shave.
• Clothing: Avoid constrictive clothing. Tight clothes, especially jeans and athletic wear, can cause chafing and irritation of the hair follicle.
• Hot Tubs: Avoid hot tubs that are not well-maintained. If you own a hot tub, keep the chlorine levels and pH as recommended.
• Antibacterial soap: Use antibacterial bar soaps such as Dial® or Cetaphil®. Use skin washes that contain benzoyl peroxide.

When to Call the Doctor

• If these bumps are bothersome or painful.
• If they are not improving or continue to appear.
• If there is a large, painful, red area of skin that feels hard or has a lot of drainage.

Folliculitis (PDF)

HH- I-395 3/16 Copyright 2016, Nationwide Children’s Hospital

Is it skin cancer? 38 photos that could save your life (PICTURES)

Dermatologists take a close look at pigmented lesions like this one because in rare instances they turn out to be melanoma – the most dangerous kind of skin cancer. But the raised lesion shown here is actually a basal cell carcinoma.

skincancer.org

(CBS) What’s the secret to avoiding skin cancer? There’s no surefire strategy, but experts say it’s vital to avoid tanning booths and to minimize your exposure to harsh sunlight (with sunscreen, wraparound sunglasses, protective clothing, etc.).

In addition, periodically checking your skin can help you spot skin cancer at its earliest stages – when treatment is most likely to be effective. The Skin Cancer Foundation recommends monthly self-exams in which you check all of your skin, including between your fingers and toes, on your scalp, on your back and buttocks, etc.

Just what are you looking for? According to the American Melanoma Foundation, any mole or pigmented area that shows any of the four warning signs of melanoma, the deadliest form of skin cancer:

• A is for asymmetry – half of the mole doesn’t match the other half;
• B is for an irregular border – often notched uneven, or blurred;
• C is for varied color – shades of brown and black are present;
• D is for diameter – a mole that spans more than 6 mm (about the size of a pencil eraser – is more likely to be a melanoma.

Even if you can recite the skin cancer ABCD’s, it’s helpful to be able to eyeball photos of the various forms skin cancers and “precancers” can take. Here’s our quick-read photo guide.

38 photos that could save your life

skincancer.org

Actinic keratoses: These precancerous lesions (like the ones shown above on the back of a hand) can turn cancerous. They’re common in older golfers and others who have spent a lot of time in sunlight.

skincancer.org

Basal cell carcinomas: This lesion might look like a hive or pimple, but it’s actually a basal cell carcinoma. This form of skin cancer is considered less serious than others but should be removed anyway.

skincancer.org

Melanomas. The deadliest form of skin cancer, melanoma (like the one shown above) is characterized by dark pigmentation, often with different shades of color, and irregular, asymmetric shapes.

Click below for the next 35 slides.

Is it skin cancer?

38 photos

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Trichomycoses

Int J Trichology. 2009 Jul-Dec; 1(2): 100–107.

G Sentamilselvi

Department of Dermatology, Madras Medical College (Retd.), Chennai – 600 003, India

C Janaki

Department of Dermatology, Madras Medical College (Retd. ), Chennai – 600 003, India

Sundaram Murugusundram

¹Department of Consultant Dermatologist, Chennai – 600 010, India

Department of Dermatology, Madras Medical College (Retd.), Chennai – 600 003, India

¹Department of Consultant Dermatologist, Chennai – 600 010, India

Address for correspondence: Dr. G Sentamilselvi, No.8, 78^th Street, Sector 12, K. K. Nagar, Chennai – 600 078, India. Email: moc.oohay@rdivleslimatnesCopyright © International Journal of Trichology

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

This article has been cited by other articles in PMC.

Abstract

Hair infection by fungal agents, also called trichomycoses, is one of the common concerns in human beings. The common agents causing hair infections are dermatophytes, Malassezia species and those causing piedra. The former two can give rise to considerable discomfort and also cause immune-mediated reactions in the form of kerion and dermatophytids. The etiopathogenesis of trichomycoses, along with its clinical aspects and the management, are briefed here.

Keywords: Malassezia folliculitis, piedra, tinea capitis, trichomycoses

INTRODUCTION

Trichomycoses by definition are diseases of the hair caused by fungi. This field of trichology is gaining importance because of the following facts. Human trichomycoses cause great concern due to the cosmetic problem of loss of hair. The antigens of these fungi can induce severe inflammation, which may disable the persons. Vellus hair infection in sites other than the scalp may also give rise to recurrent episodes of infection and may maintain chronicity. There may be infection of the siblings and schoolmates in residential schools, especially with tinea capitis, and endemicity of the infection in Chennai has also been reported. [1‐3] Finally, hair infection has been suggested to be the portal of entry for deep mycosis due to dermatophytes.[4,5] Trichomycosis of the animals, although not described here, is also important because of the spread of infection to human and other animals and because the infected hide could be one of the causes for considerable economic loss in leather industries.

PATHOMECHANISM OF TRICHOMYCOSIS BY VARIOUS FUNGI

The pathogenic fungi affecting the follicular units are mostly dermatophytes, agents causing piedra and Malassezia spp [Tables –]. Dermatophytes and piedra directly invade the hair.

Table 1

Dermatophytes frequently causing trichomycosis

Table 3

Causative agents of piedra

The dermatophytes causing trichomycosis may be anthropophilic (human), zoophilic (animal) or geophilic (soil). The ability of the dermatophytes to grow on the hair can easily be demonstrated by the hair bait technique,[6] which involves placing the sterile (acetone treated and dried) hair in a Petriplate containing soil. The dermatophytes present in the soil start invading the hair and produce colonies using hair as the substrate, showing their affinity for the hair. Some of the dermatophyte species can also produce perforating organs in the hair shaft.

The dermatophytes causing trichomycosis are listed in . Trichophyton violaceum has been observed as the most common agent causing tinea capitis in India.[7] Infection of the hair can occur on any hair-bearing area on the body surface.

In human infection, the spores that get deposited on the stratum corneum invade the hair cortex, elongate, multiply and enter into the hair cortex as intrapilary hyphae. These hyphae cannot pass beyond the keratogenous zone and remain there in the form of a fringe called the Adomson’s fringe []. Then, the hyphae start producing spores within the hair cortex (endothrix) [] or on the surface of the hair cortex (ectothrix) [], depending on the species involved in the infection. Majority of the anthropophilic spp. induce no inflammation, while the zoophilic species and occasionally few anthropophilic spp. can mediate an inflammatory reaction, producing boggy nodular swelling called kerion or crusted plaque-like lesions called favus. The inflammatory type involves only few hairs whereas more hairs are involved in the non-inflammatory type. Therefore, the infectivity is higher with the latter type. Histologically, the non-inf lammatory types show very little or no cell infiltrate in the dermis and the inflammatory types show polymorphous infiltrate due to the cell-mediated immune reaction through their antigens. The destruction of hair follicular wall and sparse hair structures along with foreign body and Langhan’s type of giant cells may also be observed in the dermis in the inflammatory types. Ultimately, fibrosis may occur with some of the inflammatory types like favus and kerion if not identified and treated early. Women having tinea pedis due to Trichophyton rubrum are prone to develop a foreign body granuloma that rarely occurs in their legs, where the hair is repeatedly shaven. This condition is called Majocchi’s granuloma, clinically evidenced by discrete follicular papulonodules on the legs.

Intrapilary hyphae invading the hair cortex-schematic depiction

Endothrix spores-schematic depiction

Ectothrix spores-schematic depiction

Malassezia spp. are gaining more importance in trichology because of their pathogenic role in the etiology of pityriasis capitis simplex (Dandruff) through their immune-mediated reaction. They survive in sebum-rich areas such as scalp, face and upper trunk. Evidences support the fact that Malassezia acts upon the surface lipids to release oleic acid and other free fatty acids, which lead to not only a breach in the barrier function of the scalp but also a direct irritant effect on the scalp, contributing to the pathogenesis of scalp seborrheic dermatitis.[8] It is also hypothesized that Malassezia can induce keratinocytes to release pro-inflammatory cytokines such as interleukin-1 alfa and tumor necrosis factor-alfa. These agents also induce folliculitis (Malassezia folliculitis) due to the rupture of the follicular wall and the yeast escaping down from the infundibulum, giving rise to a foreign body granuloma in the dermis.

TRICHOMYCOSIS DUE TO DERMATOPHYTES

Tinea capitis is the most common infection, which is usually seen in children in the age group of 5-10 years.[7] Male children are more commonly affected.[7] The infection usually occurs through the use of contaminated blades in the pilgrimage centers where ritual head shaves are carried out in large numbers, mostly in unhygienic and overcrowded surroundings. Infection also occurs through fomites like towels, combs, hair brushes and theater seats.[9]

The inflammatory types of tinea capitis include kerion, favus, abscess and pustular (agminate folliculitis) types. The non-inflammatory types are the grey patch, black dot, seborrhoeic, smooth patch of baldness and the glabrous type (also called the adult type) [] of tinea capitis. In the latter type, extension of infection from the less-hairy skin to the scalp occurs, which is seen more in adults. Occasionally, one may see a mixture of all these types of tinea capitis in the same patient. Kerion is characterized by a boggy nodular swelling with follicular pustules [] and, if left untreated, might give rise to scarring. The condition is painful and tender. Abscess type presents itself as a smooth erythematous boggy swelling without follicular pustules. The pustular type of tinea capitis is characterized by discrete or grouped follicular pustules. Favus is a special type of tinea capitis caused by T. schoenleinii and, less frequently, by T. violaceum and M. gypseum and manifests as initial yellow-red perifollicular papules with scaling and, eventually, with coalescence, producing a yellow cup-shaped concretion of mycelia along with cellular debris called scutula, with one or more long hairs seen projecting through the center. Scarring is always a sequel of favus infection.

Glabrous type of tinea capitis, extension of infection from the forehead to the frontal region

The grey patch type of tinea capitis caused exclusively by anthropophilic agents is characterized by surface skin and hair infection with white scales along with broken bits of hair, a mixture of black and white resulting in the grey colour []. The black dot type of tinea capitis caused by T. violaceum and T. tonsurans shows minimal surface infection and hairs are predominantly involved and the broken stubs of hair on the scalp give the appearance of black dots []. Seborrhoeic type of tinea capitis is similar to seborrhoeic dermatitis in adults. Smooth patch of baldness resembling alopecia areata with minimal scaling also occurs in tinea capitis and hence all suspected cases of alopecia areata in children should be subjected for investigations to exclude tinea capitis.

Black dot type with Tinea facei involving the pinna

In all types of tinea capitis, regional lymph nodes are enlarged in the cervical and occipital regions, which are painful and tender, especially in the inflammatory type of tinea capitis. Inflammatory tinea capitis is more often associated with ‘id’ reactions, which occur due to dissemination of fungal antigens in the blood stream tackled by the local immune mechanism in the skin. Although ‘dermatophytids’ can occur with any type of inflammatory dermatophytosis, it should be remembered to be observed in children with inflammatory type of tinea capitis, which might occur as papular eruptions on the trunk.

Tinea facei is also more frequently encountered in children, where the eyelashes and eyebrows may be involved []. Tinea barbae, the infection of beard region in adult men, also causes considerable concern because of the cosmetic disability of loss of hair []. Inflammatory lesions like kerion and favus can also occur in this region. Vellus hair infection should be looked for in the body sites other than scalp, which may appear as small papules within the lesion []. It is difficult to visualize hair infection on the body sites in inflammatory lesions, which should be confirmed only through wet mount preparation in potassium hydroxide (KOH) solution.

Tinea facei with involvement of the eyebrow and eyelashes

Tinea barbae with loss of hair

Tinea corporis with intra lesional papules suggestive of hair invasion

The varied presentation of trichomycosis due to dermatophytes depends on factors like the virulence and the type of the infecting organisms, the site of involvement, the type of hair infected, the immune status of the patient and the immune status of different sites in the same patient.

Trichomycosis due to dermatophytes could easily be diagnosed by an experienced dermatologist and investigations are necessary only for doubtful cases. Sampling of hairs in trichomycoses is important to confirm the diagnosis. Affected hairs easily come out from a kerion like a pin out of the cushion. In other types of tinea capitis, scraping the affected area with a blunt scalpel that yields affected hairs, broken-off hair stubs and scalp scales is preferable to plucking, which may yield uninvolved hairs. Alternatively, rubbing with a wet gauze or a sterile toothbrush also could yield the right specimen for culture.[10,11] The conventional 40% KOH wet mount under light microscopy, although not always positive, is confirmatory, which shows endothrix [] or ectothrix spores, depending on the agents involved.

Endothrix spores in wet mount (KOH X400)

Cultures may be time consuming but offer accurate identification of the infecting agent, which may very often alter the course of treatment. Cultures are carried out in modified Sabouraud’s dextrose agar medium to isolate the organisms. T. violaceum being the most common agent causing tinea capitis, produces violet waxy colonies [] and the microscopic morphology shows plenty of chlamydospores [].

Trichophyton violaceum culture showing violet waxy colonies in culture

Microscopic colony morphology showing chlamydospores (LCB X1,000)

Polymerase chain reaction (PCR) using nested primers targeting the dermatophyte-specific sequence of chitin synthase 1 (CHS1) gene and modified PCR techniques have enabled rapid and specific diagnosis of trichomycosis.[12,13] Mycopathology and immunological investigations are rarely needed and are important only for academic purposes. Mycopathology of the infected hair reveals endothrix [] or ectothrix spores in the infected hair. The inflammatory reaction in the dermis depends on the presence or absence of inflammation. Wood’s lamp examination is not necessary in our part (Southern India) of the country, where the infecting agents are mostly non-fluorescent.

Endothrix spores within the hair cortex (H and E,× 400)

Management of dermatophytic trichomycosis is both topical and systemic. Topical application of antifungal lotions in the hairy sites of the body and shampoos like azoles, selenium sulfide, povidone iodine and zinc pyrithione (ZPT) in tinea capitis could reduce the spore load.[14] The topical agents that are useful in the hairy sites are the various azoles, ung. whitfield, tolnaftate, ciclopiroxolamine, terbinafine and buteneafine. Topical treatment alone is not sufficient and also not recommended.[15,16] But 2% ketoconazole shampoo as a monotherapy daily for 8 weeks has been reported to be successful in treating tinea capitis in children with clinical and mycological cure up to 1 year after treatment.[17]

Systemic antifungal therapy is often required to achieve a clinical and mycological cure rate as early as possible.[16] Griseofulvin in the dosage of 10-20 mg/kg body weight given at least for 8-10 weeks has remained as the licensed drug, economical and easily available, also as a syrup for children. Issues like prolonged treatment, long-term side effects, contraindications in pregnancy and liver disease, various drug interactions and the advent of newer relatively safer agents have limited the use of griseofulvin currently by many.

Terbinafine given in the dosage of 5 mg/kg body weight is effective against all dermatophytes. This could be considered as the systemic drug of choice for trichomycoses because this drug is fungicidal and therefore requires shorter duration of therapy with very minimal side-effects. Fluconazole 6 mg/kg and Itraconazole 6 mg/ kg could also be instituted, and the treatment duration is shorter with these latter drugs (4 weeks). Ketoconazole 4 mg/ kg for a period of 2-3 months may be used in adults but is not recommended in children because of the potential hepatotoxicity of the drug. Of these, griseofulvin alone is the licensed drug for the management of tinea capitis in children.[16]

MALASSEZIA INFECTIONS

Malassezia spp. are lipophilic yeasts present as commensal microorganisms accounting for 40% of the scalp flora in normal individuals and found to play an important pathogenetic role in the pathogenesis of pityriasis capitis simplex, a mild form of seborrhoeic dermatitis of the scalp, accounting for 75-85% in seborrheic individuals. Malassezia derive their name from their discoverer, Malassez, who isolated them from dandruff scales in 1874 and implicated them as a causative agent of dandruff in 1889, renamed as Pityrosporum malassez by Sabouraud in 1904, again renamed as P. ovale and P. orbiculare based on culture morphology and in 1984 regained their original genus name Malassezia.[18]

Currently, 12 species of Malassezia have been identified,[19‐24] of which one (M. pachydermatis) is non-lipid dependent and all the others are lipid dependent []. M. globosa seems to be the most common pathogen responsible for pityriasis capitis simplex, as shown by molecular techniques.[25] M. furfur, which was once thought to be the predominant causative agent based on culture techniques is now not present in vivo.

Table 2

M. globosa plays a pivotal role in damaging the scalp skin barrier, corneocytes hyperproliferation and scalp irritation through the release of oleic acid. The pro-inflammatory reaction triggered by this leads to subclinical scalp and hair follicle microinflammation,[26] which progresses to perifollicular fibrosis,[27] contributing to the etiopathogenesis of androgenetic alopecia. Dandruff scalps lose two to three times more hair than non-dandruff scalps, correlating with increased scalp hair shedding associated with carriage of M. globosa.[28] Scalp squamometry index shows a positive correlation between the percentage of hairs in the late telogen and the severity of dandruff.[29]

Malassezia folliculitis is relatively rare in the tropics and tends to occur more commonly in the temperate regions. Clinically, it resembles acneiform eruptions on the upper trunk and arms, which may occur along with the classical lesions of pityriasis versicolor.[30] The typical lesion is a molluscoid comedo papule with a central dell representing the follicle. Malassezia folliculitis tends to occur frequently in immunosuppressed individuals.[31] Eosinophilic folliculitis of human immunodeficiency virus and acquired immunodeficiency syndrome also shows marked colonization of Malassezia yeasts.[32]

Large numbers of Malassezia yeasts invade the dilated hair follicle, which is distended with keratinous material and is occluded.[33] Histopathological demonstration of spores in the dermis among the infiltrate is confirmatory, which are visualized by special stains such as Periodic acid Schiff’s or Gomari’s methane amine silver stains.

Treatment of pityriasis capitis simplex largely depends on antidandruff shampoos with active ingredients such as various azole antifungals, coal tar, sulfur, selenium sulfide or ZPT. Topical therapy apart from shampoos includes lotions, gels or mousses containing azoles, ciclopiroxolamine, terbinafine and butaneafine and, in resistant cases, systemic therapy is required for a longer duration. Systemic antifungal agents must be instituted with one of the various azoles like ketoconazole, fluconazole and itraconazole.

ZPT 1% in a shampoo base possessing cytostatic, antiproliferative and anti-inflammatory properties is believed to have direct inhibitory effects on M. globosa.[34] 1% ZPT was shown to have a comparable efficacy with 2% ketoconazole in dandruff.[35] Selenium sulfide is also reported to have anti-Malassezial effects[36] while coal tar and sulfur possess low anti-Mallasezial effects.[37]

Ketoconazole 2% shampoo with the maximum efficacy among azoles remains the mainstay of treatment in dandruff because it persists in the hair keratin up to 72 h after shampoo use and is safer in infants.[38] Combination of 2% ketoconazole with 1% ZPT has been shown to be very effective in pityriasis capitis simplex.[39,40] Ciclopirox olamine 1.5% has anti-Malassezial effects as effective as 2% ketoconazole.

PIEDRA

Piedra (meaning stone in Spanish) occurs on the hair shaft as asymptomatic multiple black [] and white nodules, with the hair breaking in bits at the level of the nodules. It was described in 1865 by Biegel[41] and was classified into two types, namely black piedra and white piedra by Horta[42] in 1911. Black piedra being the most common in tropical climates is caused by Piedraia hortae. White piedra being the most common in temperate and subtropical climates is caused by predominantly Trichosporon beigelli, which is now named as Trichospron asahii[42] and five other Trichosporon sp., listed in . Agents causing piedra involving hair shaft are in a state of saprophytic existence.

Application of plant oils on wet hair is implicated as a favorable factor for piedra infection in the tropics, assisted by the high humidity. The source of infection is mostly the soil. Black piedra mostly affects scalp hair with darkly pigmented stony hard nodules firmly attached around the hair shaft, able to create a metallic sound on combing. White piedra affects any hair-bearing site, mostly beard and pubic hair, with soft creamy white gelatinous nodules loosely attached to the hair shaft. Both types of piedra invade the hair shaft and lead to hair breakage, posing considerable cosmetic morbidity.

The disease can easily be diagnosed clinically and wet mount of the nodules in KOH is confirmatory, which shows organized brown spores in black piedra invading the hair. Matured nodules will show asci (sexual spores) containing eight ascopores, each showing a small flagellum at their tip, which is better seen when the ascus ruptures. Grouped hyaline spores of varying sizes invading the hair are seen in white piedra [‐].

Black piedra-black nodule arranged irregularly on the hair shaft

White hyaline spores of varying size of Trichosporon sp (white piedra)

Schematic depiction showing the organized spores of black piedra, ascus, ascospores with flagella and irregular spores of white piedra

Treatment of piedra consists of avoidance of moisture, clipping of the affected hair, topical application of high concentration of terbinafine, tolnaftate, azoles and 1 in 2,000 mercury bichloride solution. Oral terbinafine can be used to treat black piedra. Oral itraconazole has been found to be useful in treating white piedra.[43]

CONCLUSION

Dermatophytes and Malassezia spp. could be considered as common pathogens causing hair involvement compared to piedra, which is less frequent at least in our part of the country. With Malassezia, the involvement of the hair is secondary in the most commonly encountered pityriasis capitis simplex. Diagnosis of trichomycoses due to dermatophytes and piedra is simple, through wet mount of the skin scales and hair shaft in KOH. Pityriasis capitis is mostly a clinical diagnosis and Malassezia folliculitis needs histopathological confirmation. Response to therapy is total and complete in dermatophytic trichomycosis. Piedra takes a longer time to resolve while recurrence is most common with pityriasis capitis simplex, where other factors are also operative in addition to Malassezia spp., which colonize slowly following cessation of therapy.

Footnotes

Source of Support: Nil

Conflict of Interest: None declared

REFERENCES

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Focal and Generalized Folliculitis Following Smallpox Vaccination Among Vaccinia-Naive Recipients | Hair Disorders | JAMA

Context With the reintroduction of smallpox vaccination, detailed contemporary
descriptions of adverse reactions to the vaccine are needed to adequately
inform the public and clinicians. During a multicenter, randomized controlled
trial investigating the efficacy of various dilutions of smallpox vaccine,
we observed the appearance of a papulovesicular eruption (focal and generalized)
in study volunteers.

Objective To characterize the papulovesicular eruptions by clinical, virologic,
and histopathological characteristics.

Design, Setting, and Participants Prospective case series of papulovesicular eruptions following smallpox
vaccination in healthy, vaccinia-naive adult participants compared with noncases
conducted from October 2002 to March 2003. Variables potentially related to
these eruptions were collected retrospectively through chart review. Eruptions
were described based on viral culture, clinical examination, and histopathological
evaluation (1 biopsy specimen from 1 case).

Main Outcome Measure Cases of papulovesicular eruptions following vaccination.

Results During the trial, of 148 volunteers (56% women; mean age 23.6 years),
4 participants (2.7%) developed generalized eruptions and 11 (7.4%) noted
focal eruptions. Viral cultures of sample lesions were negative for vaccinia.
The result of a skin biopsy sample from 1 case of generalized rash revealed
suppurative folliculitis without evidence of viral infection. All lesions
resolved without scarring. In the cohort, cases and noncases did not show
significant differences in terms of sex, in the use of nonsteroidal anti-inflammatory
drugs or oral or depo contraceptives, in medication allergies, in the incidence
of fever or lymphadenopathy after vaccination, or in the dilution of vaccine
received.

Conclusions Folliculitis is a common and benign eruption observed in vaccinia-naive
adult volunteers following smallpox vaccination. This eruption may be seen
in volunteers receiving the vaccine in the newly instituted vaccination programs
and may be met with heightened anxiety, potentially being confused with generalized
vaccinia. This description of folliculitis using clinical, virologic, and
histopathological findings should allay these concerns and provide additional
insight into this eruption.

Adverse dermatologic reactions after smallpox vaccine administration,
including eczema vaccinatum and progressive vaccinia, were well described
when smallpox vaccination was routine practice.¹ While
these reactions were rare, they were associated with significant morbidity
and occasional mortality. Other less severe dermatologic reactions to smallpox
vaccine also were reported, including generalized vaccinia² and
erythema multiforme.³

During a clinical trial investigating the efficacy and safety of vaccinia
immunization in healthy, vaccinia-naive adult volunteers, (ie, those not previously
vaccinated) we observed a papulovesicular eruption following vaccination in
several volunteers that mirrored generalized vaccinia on initial inspection.
While cases were initially identified as generalized rashes, with a heightened
awareness to this eruption, cases of focal variants were noted as the trial
progressed. To further define the focal eruption to and contrast it with generalized
vaccinia, we reviewed the cases in our cohort and outlined the clinical, virologic,
and histopathological characteristics of this eruption.

After providing written informed consent, healthy, vaccinia-naive adult
participants aged 18 years to 32 years were enrolled in a multicenter, double-blind,
randomized controlled trial that was investigating the safety and efficacy
of 3 dilutions of smallpox vaccine (Aventis Pasteur Smallpox Vaccine, Swiftwater,
Pa). Exclusion criteria for eligibility to participate in this clinical trial
and to receive smallpox vaccine are noted in the Box. Approval for the trial was granted by the Vanderbilt
University institutional review board.

Box Section Ref IDBox. Exclusion Criteria for Eligibility to Participate in the Vaccine
Dilution Trial and Receive Smallpox Vaccination

History of autoimmune disease
Use of immunosuppressive medications
History
of human immunodeficiency virus infection
History of solid organ or
bone marrow transplantation
History of malignancy
History of or
current illegal injection drug use
Eczema (active or quiescent)
Current
exfoliative skin disorders
Presence of a typical vaccinia scar or history
of smallpox vaccination
Prior vaccination with any vaccinia-vectored
or other pox-vectored experimental vaccine
Presence of medical or psychiatric
conditions or occupational responsibilities that precluded subject compliance
with the protocol
Acute febrile illness (≥100.5°F [38°C])
on the day of vaccination
Allergies to components of the vaccine
Pregnant
or lactating women
Household or sexual contacts having any of the following
conditions: history of or concurrent eczema, a history of exfoliative skin
disorders, a history of the immunosuppressive conditions noted above, ongoing
pregnancy, or children younger than 12 months of age

Vaccination Methods and Follow-up

Eligible participants were randomized to receive 1 of 3 dilutions of
the vaccine (undiluted, n = 49; 1:5, n = 48; and 1:10, n = 51 dilutions).
Randomization was performed using an Internet-based program with fixed blocks
of 6 assignments per block. Vaccine dilutions were performed by the study
pharmacist, and vaccine doses were delivered to the study clinic in vials
labeled with a dilution group number (G1, G2, or G3). Both volunteers and
study personnel were blinded during the course of the study to the specific
vaccine dilution associated with each group number.

The frozen vaccine was reconstituted with diluent-containing glycerin,
phenol, and sterile water. The vaccine was administered to the deltoid region
via scarification by 15 punctures with a bifurcated needle, and the site was
covered with occlusive dressings, as described previously.⁴ Volunteers
were examined every 3 to 5 days for scheduled dressing changes, assessment
of response to the vaccine, and evaluation of adverse events. Volunteers were
counseled on routine self-assessment for new dermatologic lesions. Baseline
dermatologic examinations were performed at initial screening, but subsequent
examinations occurred only after volunteer report of a cutaneous eruption.
Bandages were changed until the site was deemed well-scabbed by study investigators,
usually several weeks after vaccination.

Culture Collection and Methods

Specimens from eruptions were cultured for vaccinia virus using methods
described previously.⁵ Briefly, specimens were
placed into viral transport media and frozen at −70°C for batch
processing. After thawing, 0.2 mL of each specimen was inoculated onto BSC-40
cells and incubated at 37°C. Uninfected BSC-40 cells were used as controls.
The presence of the distinctive cytopathic effect of vaccinia⁶ were
assessed every 48 to 72 hours for 10 days. Specimens considered positive for
vaccinia were those that developed cytopathic effect, while those without
cytopathic effect at 10 days were considered negative for vaccinia. Polymerase
chain reaction for vaccinia virus was not available for confirmation of culture
data.

Cases were prospectively defined as volunteers who developed a focal
or generalized papulovesicular rash distant from the vaccination site during
the month following vaccination. Noncases did not develop these findings.

Risk Factor Assessment and Analysis

Variables potentially related to a focal or generalized papulovesicular
rash were collected retrospectively for both cases and noncases via chart
review and included concurrent medications (oral or depo contraceptives, nonsteroidal
anti-inflammatory medications), medication allergies, the presence of fever
or lymphadenopathy after vaccination (surrogate markers of systemic and local
immune response), and vaccine dilution group number. Continuous variables
were compared between cases and noncases using the Fisher exact test; age
was compared using the Student t test with unequal
variances.

The statistical analysis was performed using STATA version 7.0 (Stata
Corp, College Station, Tex).

At the Vanderbilt site, 148 volunteers underwent smallpox vaccination.
The mean age of the cohort was 23.6 years; 56% of the group were women. All
participants completed follow-up. Four participants (2.7%) developed a generalized
papulovesicular reaction following vaccination with onset between 9 and 11
days postvaccination. The eruption was observed on several body sites, including
the face, torso, and extremities. The lesions began as follicular erythematous
papules that progressed into pustules, which eventually resolved without scarring.
Concurrent lesions were at different stages of development. All 4 participants
were afebrile at the time of the eruption.

In an additional 11 participants (7.4%), focal eruptions that were morphologically
similar to the generalized lesions were noted. These eruptions occurred on
various body sites away from the primary vaccination site, including the face,
neck, back, and extremities. Ten of these cases were afebrile throughout the
postvaccination course. One individual developed fever on day 6 postvaccination,
2 days before rash onset. All rashes resolved without scarring.

A 20-year-old man presented 10 days after vaccination with a 2-day history
of “worsening acne” and “ingrown hairs” on his leg. He noted an acneiform
rash along his beard line as well as several nontender, nonpruritic papules
on his legs. He denied fevers, chills, or other systemic symptoms. He denied
use of any new medications except ibuprofen and naproxen taken after vaccination.
He was afebrile (98.6°F [37°C]) and did not appear ill. His mucous
membranes were without abnormalities. His vaccination site measured 17mm in
diameter with 135 mm of surrounding skin showing erythema and associated induration.
Dermatologic examination revealed numerous follicular papules, macules, and
pustules in different stages of development on his chest, back, legs, face,
and right axilla (Figure 1). The
result of viral culture of 1 sample lesion was negative for vaccinia. Histopathological
findings of a skin biopsy sample taken from a lesion on the back revealed
a suppurative folliculitis with a neutrophil-predominant infiltrate involving
pilosebaceous structures (Figure 2).
The result of Gomori-Methenamine silver stain was negative for fungi. Histopathological
changes associated with viral infection (Guarnieri inclusion bodies, ballooning
keratinocyte degeneration, giant cells, dyskeratotic keratinocytes, ulceration,
and dermal edema) were absent. Treatment was given to ameliorate any symptoms
(eg, pain, itching), and the eruptions resolved during the next week without
scarring.

Vaccinia virus was not isolated from any of the 17 lesion samples from
7 of the volunteers available for culture (4 cases with generalized rash and
3 cases with focal rash).

Cases and noncases were not significantly different in terms of their
sex, in the use of nonsteroidal anti-inflammatory drug or oral or depo contraceptives,
in medication allergies, in vaccine dilution group, and in incidence of fever
or lymphadenopathy. Cases were significantly younger than noncases (mean age
22.2 years vs 23.7 years, P = .03).

Serious cutaneous adverse reactions after smallpox vaccination have
been described¹ and, while rare, are associated
with significant morbidity and some mortality. Vaccinia necrosum, usually
seen in patients who have immunodeficiencies, begins as a necrotic lesion
that relentlessly progresses to systemic infection and death. Eczema vaccinatum
occurs in individuals with eczema (active or quiescent) and may lead to disseminated
disease with extensive scarring and, rarely, death. Other less-severe, self-limited
cutaneous reactions due to smallpox vaccination also have been described,
including an erythematous urticarial reaction in primary vaccinees,⁷ mild forms of erythema multiforme,³ and
generalized vaccinia, which appears 6 to 9 days after vaccination and has
lesions similar in appearance to those at the vaccination site.²

We describe folliculitis following smallpox vaccination, another eruption
that should be added to this list of cutaneous complications. While benign
in our cohort, this eruption may be initially confused with generalized vaccinia,
because of morphological characteristics of the lesions and the generalized
distribution in some cases. Folliculitis following smallpox vaccination appears
distinct from earlier descriptions of generalized vaccinia. The lesions of
folliculitis exhibit neutrophil-predominant follicular inflammation without
histopathological evidence of viral infection, develop in different stages
(unlike generalized vaccinia), and do not scar after healing (Table 1). Mild forms of generalized vaccinia^1,2 have
been previously described and may represent the folliculitis observed in our
study, although the vaccine type administered in these cases may have differed
from the vaccine used in our study (Aventis Pasteur smallpox vaccine).

In this study, most cases of folliculitis following smallpox vaccination
occurred at the time of maximal viral replication and local inflammatory symptoms,
suggesting that the pathophysiology of this eruption may be explained by the
host response to vaccination and its accompanying inflammatory reaction. Similar
eruptions related to drug- and viral exposures have been reported. Acute generalized
exanthematous pustulosis, a generalized pustular rash associated with fever
and histopathological results showing leukocytosis and suppurative dermal
pustules, has been associated with drug and viral-induced T-cell activation
and an increase in IL-8 production.^14,15 Our
study cohort comprised healthy adults who could be expected to mount a robust
immune response to exposed antigens, and the substantial incidence of folliculitis
seen in our study may reflect a vigorous immune response to the vaccine. In
contrast to the children immunized with vaccinia virus when vaccination was
routine practice, the primary vaccinees in the current study are older and
may represent slightly different hosts. For example, prepubertal children
have limited hair follicles, and this might account for the difference in
rates of folliculitis in our cohort when compared with younger historical
controls. While cases were significantly younger than the noncases in this
study, the clinical significance of this finding is unclear given the limited
age range in our population.

The local inflammation around the sebaceous glands seen with folliculitis
following smallpox vaccination is curious. Targeting of the sebaceous glands
was described in natural smallpox disease with deep glandular involvement
leading to scarring.⁸ With smallpox, scarring
was much more common on the face, which has a greater distribution of sebaceous
glands compared with other body parts.⁸ Although
vaccinia virus was not isolated from eruptions in our study, it is interesting
to speculate whether the tropism of vaccinia virus for glandular tissue may
relate to the pathogenesis of this folliculitis.

Our characterization of folliculitis following smallpox vaccination
has limitations. Our study population consisted of young adults who could
be expected to have nonspecific dermatologic eruptions, such as acne. Although
this could lead to an overemphasis of routine eruptions, the cases were noted
to have follicular eruptions unlike any prior rashes, especially in severity
and distribution. A further limitation is that only 1 participant underwent
biopsy of the eruption. However, given the similar clinical picture in other
cases of follicular eruptions, they likely reflect the same process. While
we did not have the results of polymerase chain reaction to confirm our negative
viral culture results, culture data has been used as the criterion standard
for vaccinia in the past.⁵ We also have assumed
that the focal eruptions represent the same clinical and pathological process
as the generalized reaction. However, even if the local reactions are excluded,
4 participants (2.7%) of the vaccinia-naive cohort developed generalized folliculitis
following vaccination.

This high rate of presumed folliculitis after smallpox vaccine administration
has clinical importance, especially in the setting of larger-scale vaccination.
Early reports from the current military and civilian vaccination campaigns
have separately highlighted individuals who developed a pustular rash approximately
10 days after vaccination that was classified as “generalized vaccinia.”^16,17 These eruptions also may represent
folliculitis following smallpox vaccination. While these individuals received
a different formulation of vaccinia (New York City Board of Health strain,
Dryvax, Wyeth Laboratories, Marietta, Pa) than that administered in our trial,
it was derived from the same strain of vaccinia virus and might be expected
to have similar adverse events. In addition, a recent clinical trial investigating
the New York City Board of Health strain of smallpox vaccine noted the development
of a papular rash that appears very similar to folliculitis following smallpox
vaccination.¹⁸

While folliculitis following vaccination resolved fully in our volunteers,
required no specific interventions, and showed no apparent residual sequelae,
the concern caused by this eruption on the part of the participants and the
clinicians was substantial. The potential for misinformation and concern about
skin eruptions following smallpox vaccination are important issues. It is
hoped that this report will help educate clinicians, reduce anxiety, and provide
reassurance to the medical community.

1.

Neff JM. Vaccinia virus (cowpox). In: Mandell GL, Bennett JE, Dolin R, eds. Mandell,
Douglas, and Bennett’s Principles and Practice of Infectious Diseases.
5th ed. Philadelphia, Pa: Churchill Livingstone; 2000:1553-1554.

2.Centers for Disease Control and Prevention.  Smallpox vaccination and adverse reactions: guidance for clinicians.  MMWR Morb Mortal Wkly Rep.2003;52:1-29.Google Scholar3.Lane JM, Ruben FL, Neff JM, Millar JD. Complication of smallpox vaccination, 1968: results of ten statewide
surveys.  J Infect Dis.1970;122:303-309.http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&Dopt=r&uid=4396189Google Scholar4.Henderson DA, Ingelsby TV, Bartlett JG.
 et al.  Smallpox as a biological weapon: medical and public health management.  JAMA.1999;281:2127-2137.http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&Dopt=r&uid=10367824Google Scholar5.Graham BS, Belshe RB, Clements ML.
 et al.  Vaccination of vaccinia-naïve adults with a human immunodeficiency
virus type 1 gp160 recombinant vaccinia virus in a blinded, controlled, randomized
clinical trial.  J Infect Dis.1992;166:244-252.http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&Dopt=r&uid=1353102Google Scholar6.

Hsiung GD. Diagnostic Virology. New Haven, Conn: Yale University Press; 1982.

7.Neff JM, Drachman RH. Complications of smallpox vaccination, 1968: surveillance in a comprehensive
care clinic.  Pediatrics.1972;50:481-483.http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&Dopt=r&uid=5056427Google Scholar9.Lane JM, Rubin FL, Neff JM, Millar JD. Complications of smallpox vaccination, 1968—national surveillance
in the United States.  N Engl J Med.1969;281:1201-1208.http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&Dopt=r&uid=4186802Google Scholar10.Neff JM, Levine RH, Lane JM.
 et al.  Complications of smallpox vaccination, United States, 1963—results
obtained by four statewide surveys.  Pediatrics.1967;39:916-923.http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&Dopt=r&uid=4381735Google Scholar11.Neff JM, Lane JM, Pert JH, Moore R, Millar JD, Henderson DA. Complications of smallpox vaccination—national survey in the
United States, 1963.  N Engl J Med.1967;276:125-132.http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&Dopt=r&uid=4381041Google Scholar12.Ratner LH, Lane JM, Vicens CN. Complications of smallpox vaccination: surveillance during an island-wide
program in Puerto Rico, 1967-1968.  Am J Epidemiol.1970;91:278-285.http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&Dopt=r&uid=4391875Google Scholar13.Goldstein JA, Neff JM, Lane JM, Koplan JP. Smallpox vaccination reactions, prophylaxis, and therapy of complications.  Pediatrics.1975;55:342-347.http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&Dopt=r&uid=238178Google Scholar14.Sidoroff A, Halevy S, Bavinck JNB, Vaillant L, Roujeau J. Acute generalized exanthematous pustulosis (AGEP)—a clinical
reaction pattern.  J Cutan Pathol.2001;28:113-119.http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&Dopt=r&uid=11168761Google Scholar15.Schmid S, Kuechler PC, Britschgi M.
 et al.  Acute generalized exanthematous pustulosis: role of cytotoxic T cells
in pustule formation.  Am J Pathol2002;161:2079-2086.http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&Dopt=r&uid=12466124Google Scholar17.Centers for Disease Control and Prevention.  Smallpox vaccine adverse events among civilians—United States,
February 18-24, 2003.  MMWR Morb Mortal Wkly Rep.2003;52:156-157.http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&Dopt=r&uid=12625500Google Scholar18.Frey SE, Couch RB, Tacket CO.
 et al.  Clinical responses to undiluted and diluted smallpox vaccine.  N Engl J Med.2002;346:1265-1274.http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&Dopt=r&uid=11923490Google Scholar

Photo Gallery – Dermatologist Before and After Photos

Aglow Dermatology presents our dermatologist before and after procedure photo gallery. Our collection features real patients of Dr. Dina Strachan, MD, and the different procedures they went through. The photos on the left are how they looked before, and the photos on the right are the results after the specified time and amount of treatments have gone by.

Please feel free to browse the different procedures below, follow the links for further information on the specific topics, or contact us if you have any specific questions about any particular subject.

Before and After Acne

Before and After Chemical Peel

Before and After Vi Peel

Before and After Dark Circle Removal Treatment

Before and After Earlobe Filler

Before and After Juvederm UP

Under Eye Filler Before and After

Before and After For Smile Line Treatment

Before and After Female Pattern Hairloss

Before and After Scarring Alopecia

Before and After Folliculitis Decalvans

Before and After Kybella

Before and After Dermatosis Papulose Nirgra (DPN) Removal

Before and After Radiofrequency

Before and After Cuter Secret Micro-Needling

Before and After DEPIG

Before and After Acne

• Cystic acne before
• Cystic acne after isotretinoin

Aglow Dermatology Acne Services

Before and After Chemical Peel

• Before
• After

Modified Jessner’s peel

Aglow Dermatology Chemical Peel Services

Before and After Vi Peel

• Before
• After two weeks

Vi Peel for hyperpigmentation from acne.

1 month after 1 Vi peel for melasma

Aglow Dermatology Chemical Peel Services

Before and After Dark Circle Removal Treatment

• Before
• After

• Before
• After

Before and after with Enerpeel EL for dark eyelid circles.

Aglow Dermatology Chemical Peel Services

Before and After Earbobe Filler

• Before
• after

Before and after treatment of stretched earlobe.

Learn more about Juvederm here

Before and After Juvederm Ultra Plus

• Before
• After

Before and after for smile line treatment.

Learn more about Juvederm here

Under Eye Filler Before and After

• Before
• After

Mid-face and eyelid bag treatment.

Learn more about Juvederm here

Before and After for Smile Line Treatment

• Before
• After

We focus on natural looking results that people will notice but not necessarily know what was done.

Learn more about Juvederm here

Before and After Female Pattern Hairloss

• Before
• After

Female pattern baldness 3 months after medical treatment.

Learn more about hair loss here

Before and After Scarring Alopecia

• Before
• After

Results after four months of medical treatment of CCCA, a type of scaring alopecia.

Learn more about hair loss here

Before and After Folliculitis Decalvans

• Before
• After Accutane
• After 3 months

Significant regrowth of hair with isotretinoin.

Learn more about hair loss here

Before and After Double Chin Treatment with Kybella

• Before
• 2 Weeks After

Dermatologist before and after: Results from just one treatment of Kybella

Learn more about Kybella here

Before and After Dermatosis Papulosa Nigra (DPN) Removal

• Before
• Immediately After

Immediate results after DPN, aka facial “mole” removal.

Learn more about Dermatosis papulosa nigra (DPN) here

Before and After Facial Rejuvenation with Radiofrequency

• Before
• After 1 Month

Dramatic rejuvenation after just one treatment after radiofrequency.

Learn more about radiofrequency here

Before and After Cutera Secret RF Microneedling

• Before
• 1 month later

Successful Mommy make-over for stretch marks after just one treatment with RF microneedling.

• Before
• After

One month after one treatment of acne scars.

Before and After Depigmentation

• Before
• after

Dermatologist Before and After Conclusion

Shown here is just a small sample of all the work that we perform every day. If you have any questions or would like a consultation with Dr. Dina Strachan please feel free to contact us anytime.

90,000 photos, treatment, causes and symptoms

Folliculitis is a form of pyoderma, an infectious purulent disease that affects hair follicles. Typical manifestations of the disease: pustules (multiple or single) appear in the areas of germination of the hair follicle, through which the hair passes. When severely affected, the pustules form ulcers, leaving scars after healing.

Causes of folliculitis

In the photo, the manifestation of folliculitis on the face

The disease occurs for various reasons: virus, parasites, bacteria, fungus.Let’s consider the main ones:

• Fungal skin lesions can cause dermatophyte or candidiasis.
• Parasites, eg ticks, cause demodicosis.
• Virus – Herpes simplex or herpes zoster may develop.
• Pruritic dermatosis: eczema, allergic and atopic dermatitis.
• Increased sweating.
• Diseases that reduce immunity: HIV, diabetes.

One of the most common causes is skin microtrauma combined with inadequate hygiene.For example, socially disadvantaged groups of the population living in unsanitary conditions, as well as in hot countries, have a high risk of contracting folliculitis, since their climate contributes to the multiplication of infection.

Types of folliculitis

Photo of different types of folliculitis

• Staphylococcal folliculitis mainly affects men due to inaccurate shaving. Inflamed areas appear in the area of ​​hair growth: on the chin and around the mouth.See photos of staphylococcal folliculitis and how to treat it.
• Acne-like syphilis, appears against the background of syphilis, has a pale red color. Folliculitis treatment begins with the underlying pathology. The rash will not go away until the syphilis is cured.
• Inflammation causing dermatophytes. The inflammatory process begins with inflammation of the epidermis (the upper stratum corneum of the skin), after which the hair follicle (follicles and hair shaft) is affected. If folliculitis treatment is not started, the hair roots are deformed and skin folliculitis on the head begins to develop.
• Candidal folliculitis occurs with prolonged recumbency with the imposition of occlusive dressings and protracted fevers.
• Pseudomonas – occurs after taking a bath with insufficiently chlorinated water. Poor disinfection provokes the ingress of staphylococci and other pathogens into the body.
• Impetigo Bockhart – the disease causes hyperhidrosis when using warming compresses. Ulcers appear 2-5 mm.
• Professional – Affects people who come into contact with hazardous chemicals without skin protection.The disease forms on the back of the hand.
• Tick-borne is a dangerous species and does not respond well to treatment. Specific intensive care is required.
• Gonorrhea is a rare species. Inflammatory areas appear as insufficient treatment of gonorrhea or complications after it. When analyzed in the rash, a high level of gonococci is diagnosed. Ulcers are localized on the genitals of both sexes: in men in the foreskin area, in women – on the perineum.
• Eosinophilic folliculitis is a consequence of HIV infection.A rash is one of the symptoms of HIV. The results of blood tests revealed a high level of eosinophils. Pustules are localized on the face, limbs, trunk.
• Depilatory is a common disease among men who live in the tropics. Pustules with pus are symmetrically localized on the legs. Scars remain after treatment.
• Gram-negative – cause – weak immunity. It mainly occurs after taking antibiotics.
• Fungal – spreads in high temperature and humidity.Rashes occur on the shoulders, neck, face.

Folliculitis symptoms

Visually, folliculitis is manifested by red nodules on the skin, about 1 cm in diameter. The formation is localized in the hair growth zone. If the disease has affected the face, then pustules form on the forehead, nose, cheekbones. On the head, pustules form with a red rim. To determine the treatment of folliculitis, we find out the main characteristic symptoms of the disease:

• Skin redness.
• Purulent pimples of a spherical or conical shape.
• Itching.
• After opening the bubble and removing the pus, a red spot remains.

Rarely, lymph nodes near the affected area become inflamed. Scars and pigmentation may remain on the skin after folliculitis. During the bacterial process, the vesicles fill with bloody, yellow or white contents. Fungal folliculitis produces flat, bordered patches where white plaques accumulate.

The rash is painful, which provokes poor sleep in children, since contact with bed linen causes discomfort.Often, babies have a rise in body temperature. Crumbs are often affected: buttocks, groin and external genitalia. Less commonly, the neck, back and legs are affected.

Diagnosis of folliculitis

If you suspect the development of folliculitis, the dermatologist should:

• Establish the etiology of the disease.
• Examine the rash.
• Examine the hair follicle.
• Identify the pathogen.
• To detect concomitant diseases that may serve as the development of infection.
• Perform a dermatoscopy to determine the extent of the lesion.
• Send the patient to the analysis of the discharge from the pustules. It will be required for research on fungi, microsporia, bacteriological culture and research on treponema pallidum.
• To prevent follicles from being confused with syphilis and gonorrhea, prescribe an RPR test and an OCP.

If you have identified this skin infection, then go to the paragraph below “How to treat folliculitis.”

Folliculitis treatment

Treatment of folliculitis should be started as early as possible so that the disease does not turn into a chronic and acute inflammatory process.Therapy should be consistent with the etiology of the disease. When the first rash appears, treatment with solutions of aniline dyes is sufficient: greenery, fucarcinol, iodine, methylene blue. To prevent the rash from spreading, healthy areas of the skin are treated with salicylic / boric alcohol or other antiseptics. You cannot squeeze out pus with your nails, so as not to aggravate the disease.

How to treat folliculitis with pharmaceutical preparations. In case of fungal genesis, antifungal drugs (fungicidal creams) are prescribed, bacterial – ointments and antibiotic creams, herpes – Acyclovir.

In case of recurrence of the disease, UV irradiation is performed. With a deep relapse, the method of systemic therapy is used.

With staphylococcal infection, Cephalexin, Dicloxacillin or Erythromycin are prescribed orally, with pseudomonas, Ciprofloxacin is treated, with dermatophytic infection, Terbinafine is prescribed, with candidiasis, Itraconazole and Fluconazole are used.

Simultaneously with the treatment of folliculitis, therapy is carried out for concomitant diseases: diabetes mellitus, immunodeficiency.

Complications of folliculitis

Having determined the symptoms of folliculitis, it is necessary to start treatment on time, otherwise complications may develop:

• Skin abscesses (boils).
• Inflammation of the skin (carbuncle).
• Abscess.
• Infectious diseases of the scalp.
• Scarring at the site of the rash.

Prevention of folliculitis

For preventive purposes, it is recommended to follow the rules of personal hygiene and skin care. General recommendations are a healthy lifestyle, free meals and regular physical activity.

Video on what folliculitis is:

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Folliculitis in dogs – symptoms, diagnosis, treatment

Contents

1. Causes
2. Diagnostics
3. Treatment

Folliculitis in dogs is one of the most common types of superficial bacterial skin inflammation. Folliculitis is a symptom, it is always secondary to the underlying disease.

Causes

What root causes can be? The two most common causes of folliculitis are ectoparasites, allergies (allergic flea dermatitis, food allergies, atopic dermatitis).No sexual predisposition was identified, dogs of short-haired breeds often get sick.

How can folliculitis manifest in dogs? Clinical signs may vary. Most often, these are papules (a formation that occurs above the surface of the skin, does not have a cavity), pustules (a cavity filled with pus), alopecia (an area where there is no hair), crusts, darkening of the skin. A characteristic sign of folliculitis is the so-called “moth-eaten” hair. Itching may be mild to severe.

Diagnostics

In order to make the correct diagnosis and treatment of the pet, a number of diagnostic procedures are successfully carried out, namely, cytological examination of material taken from the lesions. To diagnose the root cause and exclude other possible diseases, it is necessary to take and study a deep scraping of the skin (to confirm or exclude ectoparasites), conduct an exclusionary diet (diagnosis of allergies), and take material for sowing (excluding lichen).

Treatment

Treatment is prescribed by the veterinarian depending on the clinical manifestation. Often this is a combination of systemic and local antibacterial drugs for at least 2-3 weeks. In addition to treating the folliculitis itself, treatment / elimination of the underlying causes is carried out in parallel.

veterinarian-dermatologist “MEDVET”

Many of us use the term “follicle” without fully understanding its true meaning.The follicle literally translates from Latin as “pouch”, meaning a rounded formation in the human body of various localization. In relation to the scalp, a follicle is a hair follicle, or hair root with surrounding tissues. The hair follicle is very complex in structure. In its life cycle, it goes through three periods of development: growth, transition and rest. The duration of these stages differs depending on the location of the hair.

Folliculitis is an infectious lesion of the middle and deep sections of the hair follicle, leading to its purulent inflammation.It manifests itself by the appearance of single or multiple pustules in the places of hair growth, along the center of which the hair passes. Opened pustules form ulcers, their healing with deep damage to the hair follicle is accompanied by scarring.

There are several types of folliculitis – depending on the cause.

1. Bacterial. The culprit is most often Staphylococcus aureus. It is followed by pseudomonas and gram-negative microflora.
2. Syphilitic.Of the causative agents of sexually transmitted diseases, in addition to pale treponema, gonococcus can cause folliculitis in advanced cases of gonorrhea.
3. Fungal or candidal. It occurs in bedridden patients, with febrile and immunodeficient conditions.
4. Viral. Herpes simplex and herpes zoster may play a role in the development of folliculitis. It manifests itself mainly in men, in the chin and nasolabial triangle.
5. Parasitic. The cause is a tick, which causes the common disease demodectic mange.
6. The latest variant of folliculitis is Bockhart’s impetigo. Interesting for its appearance on macerated skin. Maceration is a change in the skin caused by prolonged exposure to water. It is observed during the treatment with warming compresses, in bedridden patients.

Not only the above-mentioned organisms are capable of causing folliculitis – the causes of the disease lie much deeper. For the favorable development of infectious agents, conditions or factors predisposing to folliculitis are necessary.
Treatment of folliculitis should be started at an early stage of the disease. With a superficial form of the disease, conduct:

• Treatment of abscesses with salicylic or camphor alcohol (2% solution), brilliant green solution, fucorcin or other antiseptics.
• Application of creams or ointments containing salicylic acid.

If the folliculitis is deep, then it may be necessary to open the abscesses followed by treatment with antiseptic solutions.Also, the application of compresses with ichthyol ointment is used. It is strictly forbidden to squeeze out abscesses or put pressure on the affected area, since such actions can provoke the development of complications – a boil or phlegmon in a severe case.

In chronic folliculitis, antibiotics or sulfonamides are prescribed, as well as immunostimulating agents. AT THE HAIR HEALTH CENTER, our specialists will help you cope with any problem.

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Folliculitis – Humanitas

Folliculitis results from infection of hair follicles with Staphylococcus aureus or other bacteria.There are also known types of folliculitis such as pseudomonas folliculitis and common sycosis. Severe infections can lead to permanent hair loss and scarring, and even mild folliculitis can make the patient feel uncomfortable and embarrassed.

The infection usually appears as small white nodules that form around one or more wavy follicles – tiny indentations from which hair grows. The most common is superficial folliculitis, accompanied by itching and, in some cases, painful sensations.Superficial folliculitis usually resolves on its own within a few days, but deep or recurrent folliculitis may require treatment.

Symptoms

Folliculitis can manifest itself in different ways, depending on the type of infection.

For superficial folliculitis affecting the upper part of the hair follicle, the following is characteristic:

• Clusters of small red or pus-filled bumps around the hair follicle.
• Purulent blisters that open up with the formation of scabs
• Skin redness and inflammation
• Itching and soreness

Deep folliculitis begins in the lower skin around the follicle and completely affects the hair follicle. Signs and symptoms include:

• Large tumor node or mass
• Purulent water bursting with the formation of scabs and
• Pain
• Scars may form after infection has been cleared.

Forms of superficial folliculitis

The following forms of superficial folliculitis are distinguished:

Staphylococcal folliculitis. A common form characterized by the formation of itchy white ulcers anywhere on the body with hair follicles. The form of the disease that affects the area of ​​beard growth in men is called common sycosis. It develops when hair follicles are infected with Staphylococcus aureus. Despite the constant presence of Staphylococcus aureus on the skin, they can cause pathological changes when entering the body through cuts and other damaged skin areas.This can happen while shaving, scratching or other damage to the skin.
Pseudomonas folliculitis (hot bath folliculitis). This form of folliculitis is caused by pseudomonas bacteria that can multiply in almost any environment, including in a hot bath with inadequate chlorine and pH levels in the water. Between eight hours and five days after exposure to the bacteria, a rash appears on the skin in the form of red, round, itchy bumps, which can later develop pus-filled blisters (pustules).Typically, more intense rashes occur where the swimsuit touches the skin, where contaminated water accumulates.
Pseudofolliculitis of the beard growth zone Pseudofolliculitis of the beard growth zone – inflammation of the hair follicles in the beard growth zone – occurs in men as a result of hair ingrowth into the skin after shaving. This leads to inflammation and, in some cases, to dark, raised scars (keloids) on the face and neck.
Folliculitis caused by fungi of the genus Pityrosporum This form of folliculitis is especially common in adolescents and adult men as a result of infection with yeast-like fungi and is accompanied by the formation of red itchy pustules with a chronic course that occur in the back and chest, less often in the neck, shoulders and face.
Forms of deep folliculitis

The following forms of deep folliculitis are distinguished:

Sycosis vulgaris Occurs in men after shaving, accompanied by inflammation of the entire hair follicle. Small pustules appear first above the upper lip, on the chin and upper and lower jaw, then become more pronounced as you shave. After a severe form of ordinary sycosis, scars remain on the skin. Gram-negative folliculitis. This form of folliculitis develops with prolonged use of antibiotics to treat acne.Antibiotics interfere with the normal balance of microflora in the nasal cavity, which leads to the overgrowth of pathogens, namely gram-negative bacteria. In most cases, this does not lead to serious disorders: after stopping antibiotics, the microflora of the nasal cavity is restored. However, in some cases, the spread of gram-negative bacteria occurs, as a result of which new foci of acne appear, while in some cases the disease can become severe.
Boils and carbuncles . They arise with deep damage to the hair follicles with Staphylococcus aureus. The boil usually appears suddenly and is a painful pink or red bump. Redness and swelling may appear on the skin around the lump. As the pus fills, the tubercle increases in size, the pain syndrome grows, after opening the boil is freed from pus. Small boils, unlike large ones, usually do not leave scars. A carbuncle is a collection of boils, usually on the back of the neck, shoulders, back, and buttocks.Carbuncles cause deeper and more severe infections than boils. As a result, they develop and pass more slowly and often leave scars.
Eosinophilic folliculitis . This form of folliculitis is observed mainly in patients with AIDS and is characterized by the regular occurrence of foci of inflamed purulent ulcers, usually on the face, sometimes on the back and forearms. Ulcers tend to spread over the skin, can cause intense itching, and, when resolved, often leave dark spots on the skin (hyperpigmentation).The exact cause of eosinophilic folliculitis is unknown, but the same yeast-like fungi that provoke folliculitis caused by fungi of the genus Pityrosporum can act as a causative agent.
Conditions for which you need to see a doctor

For mild forms of folliculitis, as a rule, no treatment is required. However, if home treatment does not work, the infection spreads or recurs, you should see your doctor or dermatologist.Antibiotics and antifungal drugs are used to treat this disease.

Complications

Mild forms of folliculitis, as a rule, do not cause complications. Mild infections may have the following complications:

• Recurrent or generalized infection.
• Extensive itchy accumulations of Staphylococcus aureus lesions on the skin (plaques).

Severe forms of folliculitis include:

• Furunculosis.This condition is characterized by the appearance of a large number of boils under the skin. Furunculosis begins with the appearance of small red bumps, which, as they fill with pus, increase in size and become painful.
• Scarring. After severe forms of folliculitis, wide raised scars (hypertrophic or keloid) or darkening of the skin may remain.
• Destruction of the hair follicle. This leads to permanent hair loss.