Lesson 2

Theme: The main clinical features of staphylococcal–and streptococcal infection of the skin and mucous membranes. Psoriasis. Lichen planus. Diagnosis, clinical motion, treatment

 

 

NORMAL FLORA OF THE HUMAN BODY

1. http://ru.scribd.com/doc/2060199/Normal-Flora-of-the-Human-Body

2. http://www.dnatube.com/video/1365/Body-Normal-Flora

The mixture of organisms regularly found at any anatomical site is referred to as the normal flora.

The normal flora of humans is exceedingly complex and consists of more than 200 species of bacteria. The makeup of the normal flora depends upon various factors, including genetics, age, sex, stress, nutrition and diet of the individual. The normal flora of humans consists of a few eukaryotic fungi and protists, and some methanogenic Archaea that colonize the lower intestinal tract, but the Bacteria are the most numerous and obvious microbial components of the normal flora.

The normal flora derives from the host a supply of nutrients, a stable environment and constant temperature, protection, and transport. The host obtains from the normal flora certaiutritional benefits, stimulation of the immune system, and colonization strategies that exclude potential pathogens at the site.

The normal flora are obviously adapted to their host (tissues), most probably by biochemical interactions between bacterial surface components (ligands or adhesins) and host cell molecular receptors.

In general, there are three explanations for why the normal bacterial flora are located at particularanatomicalsites.

1.     The normal flora exhibit a tissue preference or predilection for colonization. This is referred to as tissue tropism . One explanation for tissue tropism is that the host provides an essential growth factor needed by the bacterium. Of course, to explain why bacteria are not at an alternative site, the host inherently provides an inhospitable environment for the bacterium by the production of such substances as stomach acids, bile salts and lysozyme.

2.     Many of the normal flora are able to specifically colonize a particular tissue or surface using their own surface components like capsules, fimbriae, cell wall components, as specific ligands for attachment to specific receptors located at the colonization site.

3. Some of the indigenous bacteria are able to construct bacterial biofilms on a tissue surface, or they are able to colonize a biofilm built by another bacterial species. Many biofilms are a mixture of microbes, although one member is responsible for maintaining the biofilm and may predominate.

THE COMPOSITION OF THE NORMAL FLORA

It has been calculated that the normal human is host to about 10¹² bacteria on the skin, 10¹⁰ in the mouth, and 10¹⁴ in the gastrointestinal tract.

Normal Flora of the Skin.

An adult is covered with approximately 2 square meters of skin. The density and composition of the normal flora of the skin vary with anatomical locale. The high moisture of content of the axilla, the groin, and the skin between the toes and near orifices supports the activity and growth of relatively high densities of bacterial cells, but at most other sites the bacterial population is fairly low, generally in 100s or 1000s per square cm.

The majority of skin microorganisms are found in the most superficial layers of the epidermis and the upper parts of the hair follicles. They consist largely of Staphylococcus epidermidis and Micrococcus spp and corynebacteria. These are generally nonpathogenic and considered to be commensal, although mutualistic and parasitic roles have been assigned to them. For example, skin bacteria or their metabolites may protect against colonization by dermatophytic fungi and/or bacterial metabolites on the skin may contribute to the development of certain skin cancers. Sometimes potentially pathogenic Staphylococcus aureus is found on the face and hands, particularly in individuals who are nasal carriers. Qualitatively, the bacteria on the skiear any body orifice may be similar to those in the orifice.

Bacterial skin infections

1.         http://dermnetnz.org/bacterial/

2.         http://video.about.com/dermatology/The-Most-Common-Bacterial-Skin-Infections.htm

 

 

 

 

Bacteria such as some Staphylococcus species, Corynebacterium spp., Brevibacterium spp and Acinetobacter live oormal skin and cause no harm. Propionibacteria live in the hair follicles of adult skin and contribute to acne.

Some bacteria invade normal skin, broken skin from eczema/dermatitis or wounds (causing wound infection). Bacteria, like viruses, may also sometimes result in exanthems (rashes). The most common bacteria to cause skin infections are:

• Staphylococcus aureus
• Folliculitis
• Furunculosis (boils)
• Impetigo (school sores)
• Methicillin (meticillin) resistant Staph. aureus
• Staphylococcal scalded skin syndrome
• Toxic shock syndrome
• Tropical pyomyositis
• Botryomycosis (pyoderma vegetans)
• Streptococcus pyogenes
• Cellulitis
• Erysipelas
• Impetigo
• Necrotising fasciitis
• Scarlet fever
• Rheumatic fever, erythema marginatum
• Overgrowth of Corynebacterium spp. (erythrasma, pitted keratolysis & trichomycosis axillaris)

Less commonly, other bacteria may also cause infection with skin signs.

 These include:

• Neisseria species, cause of gonorrhoea and meningococcal disease
• Erysipelothrix insidiosa, cause of erysipeloid (usually an animal infection)
• Haemophilus species, cause of chancroid and cellulitis in young children
• Helicobacter pylori, a stomach infection, which may be associated with some cases of chronic urticaria and rosacea
• Klebsiella rhinoscleromatis, cause of rhinoscleroma
• Mycoplasma pneumoniae, a cause of pneumonia, causes non-specific erythema, bullous eruptions, urticarial rashes, erythema multiforme, mucositis and rarely, SJS/TEN
• Pseudomonas aeruginosa causes wound infections, athlete’s foot, gram negative folliculitis, chronic paronychia, spa pool folliculitis and ecthyma gangrenosum
• Calymmatobacterium granulomatis, cause of granuloma inguinale
• Bacillus anthracis, cause of anthrax
• Clostridium perfringens and other species cause gas gangrene
• Treponema species cause syphilis, yaws and pinta
• Bartonella species cause cat scratch fever, bacillary angiomatosis and bartonellosis
• Mycobacterium species cause tuberculosis, leprosy and atypical mycobacterial infections including Buruli ulcer
• Leptospira, cause of leptospirosis, which may cause bleeding into the skin (purpura)
• Nocardia, cause of nocardiosis
• Yersinia pestis, cause of bubonic plague, which causes swollen lymph glands and pustules, ulcers and scabs on the skin
• Serratia marcescens, a facultative anaerobic gram-negative bacillus that may rarely cause skin infections such as cellulitis, abscesses and ulcers; usually in patients with immunodeficiency.
• Fusibacterium species, Bacillus fusiformis, Treponema vincenti and other bacteria may result in tropical ulcer
• Burkholderia species, cause of melioidosis and glanders, in which abscesses may be associated with systemic symptoms.
• Actinomcyes species, cause of actinomycosis, in which granular bacteriosis occurs i.e. abscesses and sinus tracts draining sulphur-yellow granules.
• Vibrio vulnificus, a cause of septic shock characterised by blood-filled blisters.
• Brucella species, cause of brucellosis, a febrile illness caught from unvaccinated animals or their unpasteurised milk.

Tick-borne bacterial infections include:

• Lyme disease, due to Borrelia burgdorferi
• Relapsing fever, due to Babesia microti
• Tularaemia, due to Francisella tularensis
• Rickettsial diseases.

 

 

BACTERIAL INFECTION OF THE SKIN (PYODERMA)

 

u              Pyoderma is a group name for pyococcal dermatoses which are generally purulent. In tropical countries, pyoderma is a common problem, particularly in the summer and the monsoon.

u              The two important pyogenic organisms are the Staphylococcus aureus and the Streptococcus pyogenes.

u              Follicular infections are mainly due to staphylococci; while erysipelas and cellulitis are caused by streptococci.

u              Besides these, other organisms which occasionally come across in pyodermas are Proteus, Pseudomonas and Coliform bacilli.

 

 

SKIN INFECTIONS

 

 

 

 

 

Staphylococcal skin infections

Staphylococci (‘staph’) are a common type of bacteria that live on the skin and mucous membranes (eg. iose) of humans. Staphylococcus aureus (S. aureus) is the most important of these bacteria in human diseases. Other staphylococci, including S. epidermidis, are considered commensals, or normal inhabitants of the skin surface.

About 15-40 per cent of healthy humans are carriers of S. aureus, that is, they have the bacteria on their skin without any active infection or disease (colonisation). The carrier sites are usually the nostrils and flexures, where the bacteria may be found intermittently or every time they are looked for.

 

Bacteriology

Staphylococcal aureus bacteria are classified as Gram-positive cocci based on their appearance under a microscope. They may occur singly or grouped in pairs, short chains or grape-like clusters. They are usually facultative anaerobes, that is, they are capable of surviving at various levels of oxygenation, and are generally very hardy organisms.

They are only able to invade via broken skin or mucous membranes, hence intact skin is an excellent human defence. Once they have invaded they have various ways to avoid host defences. They:

• Hide their antigens to avoid an immune response
• Kill infection-fighting cells (phagocytes)
• Survive within host infection-fighting cells.
• Develop resistance to antibiotics
• Release toxins (intoxication) – these do not require the presence of live bacteria to have an effect.

Types of skin disease

Staphylococcal skin infections include:

• Impetigo (school sores)
• Ecthyma (crusted ulcers)
• Cellulitis (more often due to streptococcus)
• Hair follicle infections including staphylococcal folliculitis, boils (furuncles & carbuncles) and sycosis (beard infection)
• Secondary skin infection of wounds, dermatitis, scabies, diabetic ulcers etc.
• Staphylococcal hypersensitivity reactions such as folliculitis decalvans (a cause of scarring hair loss) .

 

Streptococcal skin infections

http://www.dermnetnz.org/bacterial/streptococcal-disease.html

 

Streptococci (strep) are bacteria that are commonly found harmlessly living in the human respiratory, gut and genitourinary systems. Several species are capable of causing disease in humans, including skin diseases. Skin diseases due to direct infection with streptococcus include:

• Impetigo
• Ecthyma
• Cellulitis
• Erysipelas
• Necrotising fasciitis
• Secondary skin infection of wounds, dermatitis, scabies, diabetic ulcers etc.
• Tropical ulcers
• Blistering distal dactylitis
• Streptococcal perianal and/or vulval dermatitis

in addition, streptococci are capable of causing skin disease through means other than direct infection of the skin. For example:

• Scarlet fever is a reaction to a circulating toxin that is produced by some strains of streptococcus
• Streptococcal toxic shock-like syndrome (STSS)
• Allergic hypersensitivity to streptococcal bacteria may result in erythema nodosum or vasculitis.
• Psoriasis, especially guttate forms, may be provoked or aggravated by streptococcal infection.
• Pustulosis acuta generalisata: scattered sterile pustules on hands, feet and elsewhere following an streptococcal upper respiratory tract infection. May be associated with painful joints.

Bacteriology

Streptococci are classified as Gram-positive cocci based on their appearance under a microscope. They are spherical or ovoid in shape and tend to forms chains with each other.

Streptococci that cause human disease are usually facultative anaerobes, that is, they prefer lower levels of oxygen in their environment. Streptococci are further classified into subtypes based on sugar chains expressed on their outer shell (Lancefield group) and their behaviour when grown in the laboratory (alpha- or beta- haemolysis). Most streptococci important in skin infections belong to the Lancefield groups A, C and G, and are beta-haemolytic. Streptococci pneumoniae (pneumococci) are bacteria important in pneumonia and meningitis but rarely cause skin disease. Pneumococci are alpha-haemolytic and do not belong to the Lancefield group.

Lancefield Group A

This group consists of a single type of streptococcus called Streptococcus pyogenes. Up to one-fifth of the healthy population can carry Strep. pyogenes in the throat. Strep. pyogenes produces many toxins and enzymes that aid it in establishing infection. It is an important cause of pharyngitis, impetigo, cellulitis and necrotising fasciitis. It is capable of inducing scarlet fever, post-infectious glomerulonephritis (kidney disease) and rheumatic fever (heart disease).

Several of these products produce an antibody response in the patient’s blood that aids in detection of recent streptococcal infection (eg. anti-DNAase, anti-streptolysin). These can help in the diagnosis of rheumatic fever, post-streptococcal glomerulonephritis and erythema nodosum. Rapid-result throat swabs are also available but are not absolutely reliable and should be interpreted in the clinical context (remembering that asymptomatic carriage of streptococci in the throat is common).

References:

1. Fraser JD, Proft T. The bacterial superantigen and superantigen-like proteins. Immunol Rev. Oct 2008;225:226-43. [Medline].

2. National Center for Immunization and Respiratory Diseases: Division of Bacterial Diseases. Group A Streptococcal (GAS) Disease. April 3, 2008. [Full Text].

3. Shaikh N, Martin JM, Casey JR, Pichichero ME, Wald ER, Colborn DK, et al. Development of a patient-reported outcome measure for children with streptococcal pharyngitis. Pediatrics. Oct 2009;124(4):e557-63. [Medline].

4. [Guideline] Gerber MA, Baltimore RS, Eaton CB, Gewitz M, Rowley AH, Shulman ST, et al. Prevention of rheumatic fever and diagnosis and treatment of acute Streptococcal pharyngitis: a scientific statement from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young, the Interdisciplinary Council on Functional Genomics and Translational Biology, and the Interdisciplinary Council on Quality of Care and Outcomes Research: endorsed by the American Academy of Pediatrics. Circulation. Mar 24 2009;119(11):1541-51. [Medline].

5. Deutscher M, Lewis M, Zell ER, Taylor TH Jr, Van Beneden C, Schrag S. Incidence and severity of invasive Streptococcus pneumoniae, group A Streptococcus, and group B Streptococcus infections among pregnant and postpartum women. Clin Infect Dis. Jul 15 2011;53(2):114-23. [Medline].

6. Borek AL, Wilemska J, Izdebski R, Hryniewicz W, Sitkiewicz I. A new rapid and cost-effective method for detection of phages, ICEs and virulence factors encoded by Streptococcus pyogenes. Pol J Microbiol. 2011;60(3):187-201. [Medline].

 

 

IMPETIGO

 

http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/dermatology/common–skin–infections/

http://www.medclip.com/index.php?page=videos&section=view&vid_id=104267

Definition and Etiology

Impetigo is a superficial skin infection usually caused by S. aureus and occasionally by S. pyogenes.

Prevalence and Risk Factors

Impetigo affects approximately 1% of children.

Pathophysiology and Natural History

S. aureus produces a number of cellular and extracellular products, including exotoxins and coagulase, that contribute to the pathogenicity of impetigo, especially when coupled with preexisting tissue injury. Impetigo commonly occurs on the face (especially around the nares) or extremities after trauma.

Signs and Symptoms

 

Two clinical types of impetigo exist: nonbullous and bullous.

The nonbullous type is more common and typically occurs on the face and extremities, initially with vesicles or pustules on reddened skin. The vesicles or pustules eventually rupture to leave the characteristic honey-colored (yellow-brown) crust Bullous impetigo, almost exclusively caused by S. aureus, exhibits flaccid bullae with clear yellow fluid that rupture and leave a golden-yellow crust.

1. Non-bullous impetigo

 

    Staph. aureus or gp A stretp. (GAS) or both “mixed infections”.

    May arise as 1ry inf. or as 2ry inf. of pre-existing dermatoses, e.g. pediculosis, scabies & eczemas.

    An intact st. corneum is probably the most important defense against invasion of pathogenic bacteria.

 

 

 

 

 

 

 

•         A thin-walled vesicle on erythematous base, that soon ruptures & the exuding serum dries to form yellowish-brown (honey-color) crusts that dry & separate leaving erythema which fades without scarring.

•         Regional adenitis with fever may occur in severe cases.

 

 

 

 

 

 

 

 

 

 

Varieties

•         Circinate impetigo: with peripheral extension of lesion & healing in the center.

 

 

 

 

 

 

}       Crusted impetigo: on the scalp complicating pediculosis. Occipital & cervical LNs are usually enlarged & tender.

 

 

 

 

 

 

•         Ecthyma (ulcerative impetigo): adherent crusts, beneath which purulent irregular ulcers occur. Healing occurs after few wks, with scarring.

 

 

 

 

 

 

Site: more on distal extremities (thighs & legs).

 

 

 

 

 

 

  

 

2. Bullous impetigo

 

}       Age: all ages, but commoner in childhood & newborn (impetigo neonatorum).

}       Site: face is often affected, but the lesions may occur anywhere, including palms & soles.

 

 

 

    

 

 

 

The bullae are less rapidly ruptured (persist for 2-3 days) & become much larger. The contents are at first clear, later cloudy. After rupture, thin, brownish crusts are formed.

 

 

Diagnosis

Diagnosis is by clinical presentation and confirmation by culture.

Treatment

For most patients with impetigo, topical treatment is adequate, either with bacitracin (Polysporin) or mupirocin (Bactroban), applied twice daily for 7 to 10 days. Systemic therapy may be necessary for patients with extensive disease.

 

 

Treatment of impetigo

 

Topical	Systemic	Dosing
First-Line Treatment
Mupirocin bid for 7-10 days	Dicloxacillin	250-500 mg PO qid for 5-7 days
	Amoxicillin plus clavulanic acid; cephalexin	25 mg/kg PO tid; 250-500 mg PO qid for 10 days
	Clavulanic acid
Second-Line Treatment (Penicillin allergy)
	Azithromycin	500 mg PO × 1, then 250 my PO daily for 4 days
	Clindamycin	15 mg/kg/day PO tid for 10 days
	Erythromycin	250-500 mg PO qid for 5-7 days

 

 

 

FOLLICULITIS

 

1. https://www.clinicalkey.com/topics/dermatology/folliculitis.html

2. http://www.youtube.com/watch?v=W9JMNjzu8mE

 

What is folliculitis?

Folliculitis is an infection in the hair follicles. Each hair on your body grows out of a tiny pouch called a follicle. You can have folliculitis on any part of your body that has hair. But it is most common on the face and scalp and areas rubbed by clothing, such as the thighs and groin.

 

What causes folliculitis?

It usually is caused by bacteria. It also can be caused by yeast or another type of fungus.

You may get folliculitis if you have damaged hair follicles. Shaving or wearing clothes that rub the skin can irritate the follicles, which can lead to folliculitis. They also can become blocked or irritated by sweat, machine oils, or makeup. When the follicles are injured, they are more likely to become infected.

You are more likely to get folliculitis if you:

• Use a hot tub, whirlpool, or swimming pool that is not properly treated with chlorine.
• Wear tight clothes.
• Use antibiotics or steroid creams for long periods.
• Use or work with substances that can irritate or block the follicles. Examples include makeup, cocoa butter, motor oil, tar, and creosote.
• Have an infected cut, scrape, or surgical wound. The bacteria or fungi can spread to nearby hair follicles.
• Have a disease such as diabetes or HIV that lowers your ability to fight infection.

What are the symptoms?

Folliculitis usually looks like red pimples with a hair in the center of each one. The pimples may have pus in them, and they may itch or burn. When the pimples break open, they may drain pus, blood, or both.

“Hot tub folliculitis” most often appears about 72 hours after you’ve been in a hot tub or spa. Many small pimples appear on your stomach and sometimes on your arms and legs. You might have a mild fever and have an upset stomach. Most of the time, this kind of folliculitis goes away on its own in 7 to 10 days.

How is folliculitis diagnosed?

Your doctor will check your skin and ask about your health and activities. He or she may do tests to find out what is causing your folliculitis and to make sure you don’t have a different problem, such as impetigo or heat rash. Testing a sample of the fluid in the pimples or a sample of tissue can help your doctor learn what is causing the infection.

How is it treated?

Mild folliculitis usually heals on its own in about 2 weeks. You can take care of yourself at home with:

• Warm compresses made with white vinegar or Burow’s solution. These may ease itching and help healing.
• Medicated shampoo. It can be used to treat folliculitis on the scalp or beard.

 

           

 

 

 

 

 

 

References:

1. Habif TM. Principles of diagnosis and anatomy. In: Habif TP, ed. Clinical Dermatology. 5th ed. Philadelphia, Pa: Mosby Elsevier; 2009:chap 1.

2. Habif TM. Bacterial infections. In: Habif TP, ed. Clinical Dermatology. 5th ed. Philadelphia, Pa: Mosby Elsevier; 2009:chap 9.

3. Pasternack MS, Swartz MN. Cellulitis, necrotizing faciitis, and subcutaneous tissue infections. In: Mandell GL, Bennett JE, Dolin R, eds. Principles and Practice of Infectious Diseases. 7th ed. Philadelphia, Pa: Elsevier Churchill Livingstone; 2009:chap 90.

 

FURUNCLE

1. http://www.mdguidelines.com/furuncle

2. http://emuaid.com/furuncle-treatment.html

 

 

Definition

 

 

 

 

 

 

 

 

A furuncle is a pocket of infection that occurs when the entire hair follicle and the underlying tissue become infected, usually from Staphylococcus aureus, and fill with pus. Often it is preceded by a superficial or deep infection and inflammation of hair follicles (folliculitis). Furuncles can be multiple and recurrent. They may occur anywhere where hair follicles are present, but they are most common in areas subject to friction, perspiration, and rubbing from clothing or athletic equipment (e.g., the neck, face, armpits, and buttocks). The condition is more common in people who are overweight or obese, diabetic, do not practice good hygiene, or use intravenous drugs (West). Other predisposing factors include treatment with corticosteroids or cytotoxic agents (e.g., anticancer medications), immunodeficiency conditions, mite infestation (scabies), chronic nasal carriage of Staphylococcus aureus, dermatitis with scratches and cracks (excoriations), and malnutrition. Individuals with oily skin, dark complexion, acne, and dandruff (acne-seborrhea complex) or those undergoing hormonal changes (e.g., adolescents) are also at increased risk of developing furuncles. Risk: Men and women are equally affected. Incidence and Prevalence: Furuncles are very common; nearly everyone has one at some point.

Diagnosis

History: The individual may complain of a hard, tender, red, enlarged, and painful nodule on the skin or itching in the area before the furuncle develops. The furuncle may be swollen with pus. If the furuncle has ruptured, the discharge of pus may lead to decreased swelling, redness, and pain. Fever, fatigue, or general discomfort may be present. The individual may have a history of folliculitis or previous furuncles. Physical exam: The exam may reveal a reddened nodule that may be hard, tender, warm, and painful to the touch. The boils may be swollen, and discharge may occur. Tests: Bacterial culture of the pus can determine the offending organism and its antibiotic sensitivities. A complete blood count (CBC) may be done in patients who have fever or are acutely ill.

 

 

 

 

 

 

Treatment

Some furuncles may burst, drain, and resolve on their own. Warm, moist cloths can be applied to facilitate drainage. Deep or large furuncles may need to be lanced and drained (incision and drainage). If the infection has spread or the furuncle is on the face, oral antibiotics may be prescribed. General skin care should include use of antimicrobial soap solution, wearing a protective bandage, and avoidance of skin irritants (e.g., strong soaps, deodorants). Clothing should be loose, lightweight, and porous. Immunocompromised or febrile individuals, or those who have furuncles with surrounding skin inflammation (cellulitis), may require intravenous (IV) antibiotics.

Prognosis

The outcome is very good in most cases but depends on the severity of the infection, response to treatment, and the individual’s overall health and ability to resist infection. Furunculosis is often recurrent. Deep furuncles may result in scarring.

Complications

Complications may be local, such as skin inflammation (cellulitis), a walled-off focus of infection (abscess), or systemic, when the infection is spread via the bloodstream. A systemic infection is life-threatening because it may cause infection of the heart (endocarditis), inflammation of bone (osteomyelitis), or brain abscess. Squeezing of furuncles located about the lips, nose, or spine can spread the infection even more rapidly and lead to a brain or spinal abscess. Multiple furuncles can merge and form a mass of furuncles (carbuncle).

 

CARBUNCLE

 

1. http://www.webmd.com/skin-problems-and-treatments/guide/carbuncles-causes-treatments

 

2. http://www.goldbamboo.com/video-t9371.html

 

A carbuncle is a red, swollen, and painful cluster of boils that are connected to each other under the skin. A boil (or furuncle) is an infection of a hair follicle that has a small collection of pus (called an abscess) under the skin. Usually single, a carbuncle is most likely to occur on a hairy area of the body such as the back or nape of the neck. But a carbuncle also can develop in other areas of the body such as the buttocks, thighs, groin, and armpits.

 

Most carbuncles are caused by Staphylococcus aureus bacteria, which inhabit the skin surface, throat, and nasal passages. These bacteria can cause infection by entering the skin through a hair follicle, small scrape, or puncture, although sometimes there is no obvious point of entry.

Filled with pus — a mixture of old and white blood cells, bacteria, and dead skin cells — carbuncles must drain before they’re able to heal. Carbuncles are more likely than boils to leave scars.

An active boil or carbuncle is contagious: the infection can spread to other parts of the person’s body or to other people through skin-to-skin contact or the sharing of personal items. So it’s important to practice appropriate self-care measures, like keeping the area clean and covered, until the carbuncle drains and heals.

Carbuncles require medical treatment to prevent or manage complications, promote healing, and minimize scarring. Contact your doctor if you have a boil or boils that have persisted for more than a few days.

 

Risk Factors for Carbuncles

Older age, obesity, poor hygiene, and poor overall health are associated with carbuncles. Other risk factors for carbuncles include:

• Chronic skin conditions, which damage the skin’s protective barrier
• Diabetes
• Kidney disease
• Liver disease
• Any condition or treatment that weakens the immune system 

Carbuncles also can occur in otherwise healthy, fit, younger people, especially those who live together in group settings such as college dorms and share items such as bed linens, towels, or clothing. In addition, people of any age can develop carbuncles from irritations or abrasions to the skin surface caused by tight clothing, shaving, or insect bites, especially in body areas with heavy perspiration.

Symptoms of Carbuncles

The boils that collect to form carbuncles usually start as red, painful bumps. The carbuncle fills with pus and develops white or yellow tips that weep, ooze, or crust. Over a period of several days, many untreated carbuncles rupture, discharging a creamy white or pink fluid. 

Superficial carbuncles — which have multiple openings on the skin’s surface — are less likely to leave a deep scar. Deep carbuncles are more likely to cause significant scarring. 

Other carbuncle symptoms include fever, fatigue, and a feeling of general sickness. Swelling may occur iearby tissue and lymph nodes, especially lymph nodes in the neck, armpit, or groin.

 

 

 

Complications of Carbuncles

Sometimes, carbuncles are caused by methicillin-resistant Staphylococcus aureus (MRSA) bacteria, and require treatment with potent prescription antibiotics if the lesions are not drained properly.

In rare cases, bacteria from a carbuncle can escape into the bloodstream and cause serious complications, including sepsis and infections in other parts of the body such as the lung, bones, joints, heart, blood, and central nervous system. 

Sepsis is an overwhelming infection of the body that is a medical emergency and can be fatal if left untreated. Symptoms include chills, a spiking fever, rapid heart rate, and a feeling of being extremely ill.

 

 

 

 

Pyoderma Management

 

http://www.vet.utk.edu/dermvet/pyoderma.php

 

 

 

Management of pyoderma requires recognition of the type and depth of infection and, in many instances, identification of the pathogenic organism in order to make appropriate treatment recommendations. Treatment usually involves the use of systemic antibiotics, often accompanied by topical therapy. Treatment choices vary depending on whether the pyoderma is a first-time infection or whether it is recurrent iature. Treatment choices also depend on whether the infection is focal or generalized, surface, superficial or deep.

General principles of antibiotic usage apply in all cases of bacterial skin infection. Antibiotic dosage should be based on the body weight of the animal and the full dosage administered. Length of antibiotic administration should be 7 days past clinical remission in uncomplicated infections and 10-14 days past clinical remission in complicated infections such as recurrent or deep infections and those associated with immunosuppression. This usually results in 3 to 5 weeks of antibiotics for superficial infections and 6 or more weeks for deep infections. Concurrent steroid use is contraindicated when treating skin infections. Corticosteroids will mask the clinical response, making the lesions look resolved when they are not. This may result in discontinuation of the antibiotic too soon, encouraging the development of recurrent infections. It will also interfere with diagnostic procedures. Last, many cases of pyoderma have an underlying cause such as allergy or endocrinopathy. Remember to look for an underlying cause for all cases of recurrent pyoderma.

Factors to consider when choosing an antibiotic

Choice of antibiotics will depend on many factors. These include the type of infection, depth of infection, the cost of the antibiotic, route and frequency of administration. Potential side effects of the drug need to be taken into account. In addition, the impact that the antibiotic may have on the normal flora may also need to be considered.

Empirical antibiotic selection

Antibiotics may be chosen without prior culture and susceptibility in a number of situations. Specifically, antibiotics may be empirically chosen in uncomplicated superficial skin infections, in recurrent infections when the previous antibiotic choice successfully cleared the infection, and in deep infections pending culture and susceptibility results.

Because Staphylococcus pseudintermedius (formerly known as S. intermedius) is the most frequent organism isolated in canine skin infections, antibiotics chosen should have a known spectrum of activity against Staphylococcus spp. Antibiotics that should be avoided for empirical treatment of pyoderma include penicillin, ampicillin, amoxicillin, and tetracycline.

Antibiotic selection based on culture and susceptibility testing

Cultures should be obtained from all cases of deep pyoderma, skin infections that fail to respond to empirical treatment, infections in dogs on immunosuppressive medications, infections in dogs with prior exposure to many classes of antibiotics (eg. recurrent pyodermas), and lesions in which intracellular rod bacteria are identified cytologically.

Antibiotic choices

First-line antibiotics are those antibiotics that may be chosen empirically or based on culture and susceptibility that target Staphylococcus spp. primarily with minimal impact on other bacteria. Antibiotics included here are erythromycin, lincomycin, and clindamycin. These antibiotics have a narrow spectrum of action and are considered bacteriostatic for most bacteria. They are generally effective when chosen empirically to treat first-time skin infections; however, repeat exposure to these antibiotics results in the development of resistance. In addition, cross-resistance occurs among these three antibiotics. Therefore, use of these antibiotics to treat recurrent infections should be based on culture and susceptibility results.

Potentiated sulfonamide antibiotics (trimethoprim-sulfonamide; ormetoprim-sulfamethoxine) may also be considered as first-line antibiotic choices but their use should be avoided when long-term administration is required. Potentiated sulfonamides are bactericidal and demonstrate good efficacy against Gram-positive bacteria. Bacterial resistance to this class of antibiotics is quite variable, ranging from 0 to 33%; therefore, use of this antibiotic based on culture and susceptibility results may be more appropriate. Side effects in dogs associated with potentiated sulfonamides include hypothyroidism, keratoconjunctivitis sicca, neutropenia, hepatopathy and polyarthritis.

High levels of resistance to tetracyclines exist in S. pseudintermedius; therefore, this class of antibiotics cannot be regarded as a good empirical choice. Yet, doxycycline has been used effectively to treat bacterial skin infections caused by susceptible strains. Therefore, because of its narrow spectrum of action, doxycycline would be a good first-line antibiotic choice based on culture and susceptibility results.

Many people use first-generation cephalosporins (cephalexin, cefadroxil) as first-line antibiotics. These antibiotics are bactericidal and have a broad spectrum of action but primarily target gram positive bacteria. Resistance to this class of antibiotics is only now being identified. Ideally, use of these antibiotics should be reserved for those cases in which culture and susceptibility indicate they are the antibiotic of choice. For cases in which there have been multiple antibiotic exposures (e.g. recurrent infections) and success of other antibiotics is questioned, then first-generation cephalosporins can be used empirically.

Two third-generation cephalosporins, cefovecin and cefpodoxime proxetil, have recently been registered in the USA and Europe. Cefovecin is a long-acting injectable antibiotic which lasts 14 days and cefpodoxime proxetil is an oral antibiotic that can be administered once daily. While both drugs offer good activity against staphylococci, their activity against S. pseudintermedius is not superior to first-generation cephalosporins. In addition, they are active against a wide range of Gram-negative bacteria. Therefore, their use has the potential for selection of both methicllin resistance in staphylococci and multi-resistant E. coli. In spite of their convenient dosing, these drugs should only be used as first-line antibiotics if compliance is anticipated to be a problem.

Amoxicillin with clavulanate is also a broad-spectrum bactericidal antibiotic that primarily targets Gram-positive bacteria. It, too, should be reserved for those cases of pyoderma in which culture and susceptibility indicate it is the preferred antibiotic. In addition, it can be used empirically similar to first-generation cephalosporins.

Second-line antibiotics should be based solely on culture and susceptibility results. Antibiotics included here include chloramphenicol, rifampin, and amikacin. Chloramphenicol is a bacteriostatic, narrow spectrum antibiotic. While it meets the criteria to be a first-line antibiotic, it is reserved for treatment of methicillin resistant S. pseudintermedius which are sometimes only susceptible to this antibiotic. Chloramphenicol is administered three times daily. In addition to this inconvenient frequency of administration, it often causes gastrointestinal disturbances, is associated with drug interactions, and may cause bone marrow suppression.

Rifampin is a bactericidal antibiotic with excellent tissue penetration. It has a broad spectrum of activity against many Gram-negative and most Gram-positive microorganisms and is the most active antibiotic known against staphylococci. Resistance to rifampin readily develops with monotherapy; therefore, it is best to use in combination with another antibiotic such as clindamycin or cephalexin. Rifampin is potentially hepatotoxic and this side effect appears to occur more commonly in dogs than in people. Mild increases in alkaline phosphatase activity occur frequently and appear to be benign; however, treatment should be discontinued if there are concurrent increases in other hepatic enzyme activities. Other rare signs associated with rifampin administration in dogs include thrombocytopenia, hemolytic anemia, anorexia, vomiting, diarrhea, and death.

Amikacin is an aminoglycoside that is not typically considered for treating dogs with skin infections. It is an injectable antibiotic and is nephrotoxic. Therefore, use of this antibiotic is only based on culture and susceptibility results wheo other antibiotic would be effective.

Third-line antibiotics should be chosen last because of the pressure they place on bacteria in terms of selecting for antimicrobial resistance. These include the third-generation cephalosporins (see above) and fluoroquinolones. While staphylococci often are susceptible to fluoroquinolones, resistance develops rapidly. In addition, fluoroquinolone use appears to select for methicillin resistance. Use of this class of antibiotics should be preserved for cases of deep infections associated with Gram-negative organisms.

Topical therapy

Topical therapy may be used as both an adjunct to systemic therapy or, in some cases, as the sole therapy for cutaneous skin infections. Topical therapy includes whirlpool baths, especially for dogs with deep pyodermas, and antibacterial shampoos. Chlorhexidine, benzoyl peroxide, and ethyl lactate containing shampoos all have demonstrated beneficial responses in dogs with infections. Bathing should be done two to three times per week with a 10 minute contact time. In a study using topical therapy alone to treat superficial pyodermas, 50% of the cases were treated effectively when bathed three times per week. In cases of recurrent or resistant infections, a topical chlorhexidine spray is very beneficial when used once to twice daily.

Duration of therapy

Length of therapy depends of the depth of infection and is determined by clinical cure. For superficial infections the average duration of therapy is 3 to 4 weeks with treatment continued 1 week past clinical cure. For recurrent superficial infections the average duration of therapy is a bit longer and is continued for 10 to 14 days past clinical cure. Deep infections require 6 to 12 weeks of antibiotics with treatment continued 2 weeks past clinical cure. If lesions recur within 1 week after discontinuing therapy, it is likely that treatment was not long enough.

In order to determine if clinical cure is achieved, the dog should be re-examined before the antibiotic course is completed. Discontinuation of therapy too soon leads to the selection of resistant bacteria. A common reason why pyodermas fail to respond to treatment or recur is if the length of therapy is too short.

Reasons for treatment failure

Pyoderma may fail to respond to treatment if the bacteria are resistant or develop resistance to the chosen antibiotic. This may occur because an inappropriate antibiotic was chosen initially (e.g. amoxicillin) or resistant bacteria were selected during the antibiotic course. As stated before, treatment failure also occurs if the antibiotic course was not long enough.

Management of methicillin resistant staphylococcal infections

An infection caused by methicillin resistant staphylococci is managed similar to management of any pyoderma. An antibiotic is chosen based on culture results. Staphylococci exhibiting resistance to methicillin or oxacillin are also resistant to other penicillins, cephalosporins, and amoxicillin/clavulanate despite apparent in vitro susceptibility. Not all methicillin resistant staphylococci are multi-drug resistant. Typical antibiotic choices may include clindamycin, chloramphenicol, doxycycline, minocycline, amikacin, and rifampin. Unfortunately, antibiotic choices are becoming limited for some of the methicillin resistant Staphylococcus pseudintermedius (MRSP). We have managed some cases with aggressive topical therapy as the sole treatment. Use of the antibiotics reserved for MRSA in people, such as vancomycin and linezolid, is ethically questionable.

Staphylococcus pseudintermedius has been shown to colonize people temporarily, yet human infections with this organism are rarely reported. Since Staphylococcus pseudintermedius is not a common human pathogen, the primary recommendation to owners involves frequent handwashing after handling their pets. There is a potential increased risk to immunocompromised members of the household, but this is not known.

It is likely that other pets in the household will be colonized with the same resistant bacteria; therefore, pets with infections from households with known MRSP should always be cultured rather than empirically treated.

Recurrent infections

Reasons for recurrence

Common reasons for recurrent pyodermas include too short a duration of therapy, inappropriate dose of antibiotics, and concurrent glucocorticoids. If lesions recur within 1 week after discontinuing therapy, it is likely that treatment was not long enough. If the skin infection recurs after 3 to 4 weeks of discontinuing therapy, then there is likely an underlying condition predisposing the patient to infections that needs to be addressed. Common causes of recurrent infections include allergies and endocrinopathies. Occasionally, an underlying cause is not identified.

Managing idiopathic recurrent infections

Management of idiopathic recurrent pyoderma will depend on the frequency and severity of the infections. If the infections only occur a few times per year, then each episode should be treated with antibiotics as described above.

In some cases aggressive topical therapy can increase the interval between pyoderma episodes. Owners can bath their dogs with antibacterial shampoos containing chlorhexidine, ethyl lactate, or benzoyl peroxide three times per week at the first sign of the infection returning. In addition, chlorhexidine spray can be applied to the infected areas.

In cases where the infection is severe, the goal may be to prevent recurrence of the infection. This can be attempted using pulse antibiotic therapy. The antibiotic is administered until the infection is cleared and then is given either at weekly intervals or every other day to prevent the infection from returning. Because of the increasing incidence of MRSP, pulse therapy is unlikely to be effective because it will select for resistant staphylococci.

Immune modulation with bacterins has been used to manage some cases of idiopathic recurrent pyodermas. Bacterins contain various cellular products of staphylococci or other bacteria and are available commercially as Staphage Lysate (Delmont Laboratories) and ImmunoRegulin (Neogen Vet). In addition, some microbiology laboratories will make autogenous bacterins from the patient’s staphylococci. Bacterins will not clear an existing infection and must be started concurrently with antibiotics. Once the infection is cleared, the antibiotics are discontinued while the bacterin is continued. If the infection recurs, then a complete course of antibiotics will again be needed.

 

References

 

1. Stevens DL, Bisno AL, Chambers HF, Everett ED, Dellinger P, Goldstein EJ. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. Nov 15 2005;41(10):1373-406. [Medline].

2. Lopez FA, Lartchenko S. Skin and soft tissue infections. Infect Dis Clin North Am. Dec 2006;20(4):759-72, v-vi. [Medline].

3. May AK. Skin and soft tissue infections. Surg Clin North Am. Apr 2009;89(2):403-20, viii. [Medline].

4. Napolitano LM. Severe soft tissue infections. Infect Dis Clin North Am. Sep 2009;23(3):571-91. [Medline].

5. Roberts JR, Hedges JR. Clinical Procedures in Emergency Medicine. 5^th ed. 2009.

6. Dryden MS. Complicated skin and soft tissue infection. J Antimicrob Chemother. Nov 2010;65 Suppl 3:iii35-44. [Medline].

7. De Waele JJ. Early source control in sepsis. Langenbecks Arch Surg. Jun 2010;395(5):489-94. [Medline].

 

ERYTHRASMA

1. http://emedicine.medscape.com/article/1052532-overview

2. http://www.youtube.com/watch?v=fwFG1M4ZXBg

 

Background

Erythrasma is a chronic superficial infection of the intertriginous areas of the skin. The incriminated organism is Corynebacterium minutissimum, which usually is present as a normal human skin inhabitant. In 1996, Corynebacterium afermentans was reported in one case.^[1]

Pathophysiology

Corynebacteria invade the upper third of the stratum corneum; under favorable conditions such as heat and humidity, these organisms proliferate. The stratum corneum is thickened. The organisms that cause erythrasma are seen in the intercellular spaces as well as within cells, dissolving keratin fibrils. The coral-red fluorescence of scales seen under Wood light is secondary to the production of porphyrin by these diphtheroids.

Clinical Presentation

The typical appearance of erythrasma is well-demarcated, brown-red macular patches. The skin has a wrinkled appearance with fine scales (see the image below).

 

 

 

 

 

Lichenification and hyperpigmentation are common. The skin occasionally has a wrinkled appearance with scales. KOH test results are negative. Courtesy of Michael Bryan, MD.

Infection commonly is located over inner thighs, crural region, scrotum, and toe webs. Axillae, submammary area, periumbilical region, and intergluteal fold are less commonly involved in erythrasma. Toe web lesions appear as maceration, with the fourth interdigital space most frequently affected.^]

Due to the association of erythrasma with other corynebacterial skin infections such as pitted keratolysis and trichomycosis axillaris, all body folds and feet should be screened.{{Ref16}

Causes

C minutissimum, a member of the normal skin flora, is the causative agent of erythrasma. The bacterium is a lipophilic, gram-positive, non–spore-forming, aerobic, and catalase-positive diphtheroid. C minutissimum ferments glucose, dextrose, sucrose, maltose, and mannitol.

Predisposing factors for erythrasma include the following:

       Excessive sweating/hyperhidrosis

       Delicate cutaneous barrier

       Obesity

       Diabetes mellitus

       Warm climate

       Poor hygiene

       Advanced age

       Other immunocompromised states

        

Differential Diagnoses

• Acanthosis Nigricans
• Candidiasis, Cutaneous
• Contact Dermatitis, Allergic
• Contact Dermatitis, Irritant
• Intertrigo
• Psoriasis, Plaque
• Seborrheic Dermatitis
• Tinea Corporis
• Tinea Cruris
• Tinea Pedis

Laboratory Studies

Wood light examination of erythrasma lesions reveals coral-red fluorescence of lesions. Results may be negative if the patient bathed prior to presentation.^[23] Note the image below. The cause of this color fluorescence has been attributed to excess coproporphyrin III synthesis by these organisms, which accumulates in cutaneous tissue and emits a coral-red fluorescence when exposed to a Wood light.

 

 

 

Under Wood lamp examination, the porphyrins produced by the bacteria fluoresce with a coral pink color. A small focus is visible on this photo. If the patient recently has bathed, the pigment may be washed away. In suspicious cases, a repeat examination the following day may be necessary. Courtesy of Michael Bryan, MD.

Gram staining reveals of erythrasma lesions gram-positive filamentous rods. In culture media composed of 20% fetal bovine serum, 2% agar, 78% tissue culture medium #199, and 0.05% tris, the organisms grow as nonhemolytic, 1- to 1.5-mm smooth colonies. Methylene blue stain may be used to highlight both the fungal spores of pityriasis versicolor and the curved or club-shaped bacterial rods of C minutissimum, the causative agent of erythrasma, in case both organisms coexist.

Medical Care

Photodynamic therapy using red light (broadband, peak at 635 nm) has been reported to clear erythrasma in 23% of 13 patients and to improve erythrasma in the remaining patients.

Antibacterial and/or antifungal agents are used to eradicate C minutissimum and possible concomitant infection. Erythromycin is the DOC. Infection may be treated with topical and/or oral agents. Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting. C minutissimum is generally susceptible to penicillins, first-generation cephalosporins, erythromycin, clindamycin, ciprofloxacin, tetracycline, and vancomycin. However, multiresistant strains have been isolated.

In a recent susceptibility study of 40 patients, several antibiotics were tested, including penicillin G, ampicillin, cefaclor, amoxicillin-clavulanate, ampicillin-sulbactam, tetracycline, erythromycin, ofloxacin, fusidic acid, levofloxacin, and azithromycin. The study revealed statistically significant resistance to erythromycin, azithromycin, penicillin, and ampicillin. Significant susceptibility was statistically found to amoxicillin-clavulanate, cefaclor, and fusidic acid.

Because culture and antibiogram are not performed routinely in daily clinical practice, the recommended initial treatment is topical fusidic acid. If this drug is not available, then topical tetracycline may be an alternative. In cases of treatment failure, amoxicillin-clavulanate should be chosen for the systemic treatment.

In a large double-blind, placebo-controlled, randomized trial, 151 patients older than 18 years were randomized into 5 groups and were given either erythromycin, single-dose clarithromycin, topical fusidic acid, placebo cream, or placebo tablets. Fusidic acid cream was significantly more effective than other therapies. Additionally, the group who received clarithromycin did better at 48 hours than did the group that received erythromycin. However, there was no statistical difference on day 7 and day 14.

    Erythromycin (E.E.S., E-Mycin, Ery-Tab)

    Clarithromycin (Biaxin)

    Fusidic acid (Zeta)

    Topical antibacterial that inhibits bacterial protein synthesis, causing bacterial death.

    Use 2% cream.

    Miconazole topical (Femazole, Lotrimin, Monistat)

    Use 2% cream.

    Benzoic acid 6%, salicylic acid 3% (Whitfield’s ointment)

    Clindamycin (Cleocin)

    Tetracycline (Achromycin)

 

Complications:

• Fatal septicemia in immunocompromised patients with erythrasma
• Infective endocarditis in valvular heart disease patients with erythrasma
• Postsurgical wound infection in erythrasma patients

 

References

1. Ahmad NM, Ahmad KM. Corynebacterium minutissimum pyelonephritis with associated bacteraemia: a case report and review of literature. J Infect. Dec 2005;51(5):e299-303. [Medline].

2. Aperis G, Moyssakis I. Corynebacterium minutissimum endocarditis: a case report and review. J Infect. Feb 2007;54(2):e79-81. [Medline].

3. Dalal A, Likhi R. Corynebacterium minutissimum bacteremia and meningitis: a case report and review of literature. J Infect. Jan 2008;56(1):77-9. [Medline].

4. Morales-Trujillo ML, Arenas R, Arroyo S. [Interdigital erythrasma: clinical, epidemiologic, and microbiologic findings]. Actas Dermosifiliogr. Jul-Aug 2008;99(6):469-73. [Medline].

5. Inci M, Serarslan G, Ozer B, et al. The prevalence of interdigital erythrasma in southern region of Turkey. J Eur Acad Dermatol Venereol. Oct 7 2011;[Medline].

 

6. Finch J. Case of trichomycosis axillaris and erythrasma. J Drugs Dermatol. Dec 2011;10(12):1472-3. [Medline].

 

7. Yasuma A, Ochiai T, Azuma M, et al. Exogenous coproporphyrin III production by Corynebacterium aurimucosum and Microbacterium oxydans in erythrasma lesions. J Med Microbiol. Jul 2011;60:1038-42. [Medline].

 

7. Turk BG, Turkmen M, Aytimur D. Antibiotic susceptibility of Corynebacterium minutissimum isolated from lesions of Turkish patients with erythrasma. J Am Acad Dermatol. Dec 2011;65(6):1230-1. [Medline].

8. Avci O, Tanyildizi T, Kusku E. A comparison between the effectiveness of erythromycin, single-dose clarithromycin and topical fusidic acid in the treatment of erythrasma. J Dermatolog Treat. Sep 18 2011;[Medline].

 

 

PSORIASIS

 

1. http://www.medicinenet.com/psoriasis/article.htm#what_is_psoriasis

2. http://www.youtube.com/watch?v=WRS9UJFKHMk

 

Psoriasis is a chronic disorder of the skin characterized by reddish, scaly patches of inflammation, most commonly affecting the elbows, knees, scalp, and/or groin. Psoriasis can be mild or severe. When it is severe, it can adversely affect functions of daily living including work and social activities.

Psoriasis has been reported to affect approximately 2% of the world’s population.

The treatment of psoriasis depends on its severity and location. Treatments range from local (cortisone cream application, emollients, coal tar, anthralin preparations, and sun exposure) to systemic (internal medications, including methotrexateand cyclosporine).

Psoriasis facts

• Psoriasis is a chronic inflammatory skin disease.
• Psoriasis has no known cause.
• The tendency toward developing psoriasis is inherited in genes.
• Psoriasis is not contagious.
• Psoriasis gets better and worse spontaneously and can have periodic remissions (clear skin).
• Psoriasis is controllable with medication.
• Psoriasis is currently not curable.
• There are many promising therapies, including newer biologic drugs.
• Future research for psoriasis is promising.

What is psoriasis?

Psoriasis is a noncontagious skin condition that produces red, dry plaques of thickened skin. The dry flakes and skin scales are thought to result from the rapid proliferation of skin cells that is triggered by abnormal lymphocytes from the blood . Psoriasis commonly affects the skin of the elbows, knees, and scalp.

Some people have such mild psoriasis (small, faint dry skin patches) that they may not even suspect that they have a medical skin condition. Others have very severe psoriasis where virtually their entire body is fully covered with thick, red, scaly skin.

Psoriasis is considered a non-curable, long-term (chronic) skin condition. It has a variable course, periodically improving and worsening. It is not unusual for psoriasis to spontaneously clear for years and stay in remission. Many people note a worsening of their symptoms in the colder winter months.

Psoriasis is seen worldwide, in all races, and both sexes. Although psoriasis can be seen in people of any age, from babies to seniors, most commonly patients are first diagnosed in their early adult years.

Patients with more severe psoriasis may have social embarrassment, job stress, emotional distress, and other personal issues because of the appearance of their skin.

 

 

Pathophysiology

Psoriasis is a complex, multifactorial disease that appears to be influenced by genetic and immune-mediated components. This is supported by the successful treatment of psoriasis with immune-mediating, biologic medications.

The pathogenesis of this disease is not completely understood. Multiple theories exist regarding triggers of the disease process including an infectious episode, traumatic insult, and stressful life event. In many patients, no obvious trigger exists at all. However, once triggered, there appears to be substantial leukocyte recruitment to the dermis and epidermis resulting in the characteristic psoriatic plaques.

Specifically, the epidermis is infiltrated by a large number of activated T cells, which appear to be capable of inducing keratinocyte proliferation. This is supported by histologic examination and immunohistochemical staining of psoriatic plaques revealing large populations of T cells within the psoriasis lesions. One report calculated that a patient with 20% body surface area affected with psoriasis lesions has around 8 billion blood circulating T cells compared with approximately 20 billion T cells located in the dermis and epidermis of psoriasis plaques.

Ultimately, a ramped-up, deregulated inflammatory process ensues with a large production of various cytokines (eg, tumor necrosis factor-α [TNF-α], interferon-gamma, interleukin-12). Many of the clinical features of psoriasis are explained by the large production of such mediators. Interestingly, elevated levels of TNF-α specifically are found to correlate with flares of psoriasis.

One study adds further support that T-cell hyperactivity and the resulting proinflammatory mediators (in this case IL-17/23) play a major role in the pathogenesis of psoriasis.

Key findings in the affected skin of patients with psoriasis include vascular engorgement due to superficial blood vessel dilation and altered epidermal cell cycle. Epidermal hyperplasia leads to an accelerated cell turnover rate (from 23 d to 3-5 d), leading to improper cell maturation.

Cells that normally lose their nuclei in the stratum granulosum retain their nuclei, a condition known as parakeratosis. In addition to parakeratosis, affected epidermal cells fail to release adequate levels of lipids, which normally cement adhesions of corneocytes. Subsequently, poorly adherent stratum corneum is formed leading to the flaking, scaly presentation of psoriasis lesions, the surface of which often resembles silver scales.

Conjunctival impression cytology demonstrated a higher incidence of squamous metaplasia, neutrophil clumping, and nuclear chromatin changes in patients with psoriasis.

 

 

 

 

Etiology

Psoriasis involves hyperproliferation of the keratinocytes in the epidermis, with an increase in the epidermal cell turnover rate. (See Pathophysiology.) The cause of the loss of control of keratinocyte turnover is unknown. However, environmental, genetic, and immunologic factors appear to play a role.

Environmental factors

Many factors besides stress have also been observed to trigger exacerbations, including cold, trauma, infections (eg, streptococcal, staphylococcal, human immunodeficiency virus), alcohol, and drugs (eg, iodides, steroid withdrawal, aspirin, lithium, beta-blockers, botulinum A, antimalarials). One study showed an increased incidence of psoriasis in patients with chronic gingivitis. Satisfactory treatment of the gingivitis led to improved control of the psoriasis but did not influence longterm incidence, highlighting the multifactorial and genetic influences of this disease.^[8]

Hot weather, sunlight, and pregnancy may be beneficial, although the latter is not universal. Perceived stress can exacerbate psoriasis. Some authors suggest that psoriasis is a stress-related disease and offer findings of increased concentrations of neurotransmitters in psoriatic plaques.

Genetic factors

Patients with psoriasis have a genetic predisposition for the disease. The gene locus is determined. The triggering event may be unknown in most cases, but it is likely immunologic. The first lesion commonly appears after an upper respiratory infection.

Psoriasis is associated with certain human leukocyte antigen (HLA) alleles, particularly human leukocyte antigen Cw6 (HLA-Cw6). In some families, psoriasis is an autosomal dominant trait.

A multicenter meta-analysis confirmed that deletion of 2 late cornified envelope (LCE) genes, LCE3C and LCE3B, is a common genetic factor for susceptibility to psoriasis in different populations.^[9]

Obesity is another factor associated with psoriasis. Whether it is related to weight alone, genetic predisposition to obesity, or a combination of the 2 is not certain. Onset or worsening of psoriasis with weight gain and/or improvement with weight loss is observed.

Immunologic factors

Evidence suggests that psoriasis is an autoimmune disease. Studies show high levels of dermal and circulating TNF-α. Treatment with TNF-α inhibitors is often successful. Psoriatic lesions are associated with increased activity of T cells in the underlying skin.

Psoriasis is related to excess T-cell activity. Experimental models can be induced by stimulation with streptococcal superantigen, which cross-reacts with dermal collagen. This small peptide has been shown to cause increased activity among T cells in patients with psoriasis but not in control groups. Some of the newer drugs used to treat severe psoriasis directly modify the function of lymphocytes.

Also of significance is that 2.5% of those with HIV develop worsening psoriasis with decreasing CD4 counts. This is paradoxical, in that the leading hypothesis on the pathogenesis of psoriasis supports T-cell hyperactivity and treatments geared to reduce T-cell counts help reduce psoriasis severity. This finding is possibly explained by a decrease in CD4 T cells, which leads to overactivity of CD8 T cells, which drives the worsening psoriasis. The HIV genome may drive keratinocyte proliferation directly.

HIV associated with opportunistic infections may see increased frequency of superantigen exposure leading to similar cascades as above mentioned.

Guttate psoriasis often appears following certain immunologically active events, such as streptococcal pharyngitis, cessation of steroid therapy, and use of antimalarial drugs.

 

Symptoms of psoriasis may include the following:

• Worsening of a long-term erythematous scaly area
• Sudden onset of many small areas of scaly redness
• Recent streptococcal throat infection, viral infection, immunization, use of antimalarial drug, or trauma
• Family history of similar skin condition
• Pain (especially in erythrodermic psoriasis and in some cases of traumatized plaques or in the joints affected by psoriatic arthritis)
• Pruritus (especially in eruptive, guttate psoriasis)
• Afebrile (except in pustular or erythrodermic psoriasis in which the patient may have high fever)
• Dystrophic nails
• Long-term rash with recent presentation of joint pain
• Joint pain without any visible skin findings

The skin almost always is affected before the eyes. Ocular findings occur in approximately 10% of patients. The most common ocular symptoms are redness and tearing due to conjunctivitis or blepharitis.

The nonocular symptoms are related to rash and psoriatic arthritis. The rash can be uncomfortable or even painful. Psoriatic arthritis can cause stiffness, pain, throbbing, swelling, or tenderness of the joints. The distal joints, such as the fingers, toes, wrists, knees, and ankles, are most often affected.

 

 

 

 

 

 

 

PSORIASIS VULGARIS

 

Common 0.5-3% of population; single or multiple plaques; age 15-40 (mean age 28yrs); extensor surfaces, back, sacrum, hairline, knees, elbows.

 

 

 

 

 

 

GUTTATE PSORIASIS

 

Multiple small lesions post infection; often spontaneously resolve in 2-3/12; respond poorly to topical agents; differential with pityriasis; (scale confined to edge of esions)

 

 

 

 

 

FLEXURAL PSORIASIS

 

Typical eczema distribution; often associated with psoriasis in the hair; differential with intertrigo.

 

 

 

 

 

 

 

ERYTHRODERMIC PSORIASIS

 

Results when 90% of body affected; precipitated by withdraw of steroids; Consequences: infection; dehydration; high out-put cardiac failure

 

 

 

 

 

 

PALMOPLANTAR  PSORIASIS

 

Vesicles on soles of hands & feet; painful rather than itchy; chronic condition

 

 

 

 

 

 

PSORIATIC  ARTHRITIS

 

5 main clinical subtypes:

 

    symmetrical polyarthritis;

    asymmetrical oligoarthritis (large joint);

    spondylitic (sero-negative);

    distal-interphalangeal (nail);

    severe mutilans.

 

 

 

 

 

 

NAIL  PSORIASIS

 

50% of patients with skin involvement; 90% of psoriatic arthritis; pitting; onycholysis of distal nail bed; subungal hyperkeratosis

 

 

 

         

 

 

Complications

Complications of psoriasis may include the following:

• Secondary infections
• Possible increased risk of lymphoma
• Possible increased risk of cardiovascular and ischemic heart disease
• Psoriatic arthritis
• Mitral valve prolapse

Lab Studies

Laboratory studies and findings for patients with psoriasis may include the following:

• Test result for rheumatoid factor (RF) is negative.
• Erythrocyte sedimentation rate (ESR) is usually normal (except in pustular and erythrodermic psoriasis).
• Uric acid level may be elevated in psoriasis (especially in pustular psoriasis), causing confusion with gout in psoriatic arthritis.
• Fluid from pustules is sterile with neutrophilic infiltrate.
• Perform fungal studies. (This is especially important in cases of hand and foot psoriasis that seem to be worsening with the use of topical steroids.)

If starting systemic therapies such as immunological inhibitors, consider obtaining baseline laboratory studies (ie, complete blood count [CBC], blood urea nitrogen [BUN]/creatinine, liver function tests [LFTs], hepatitis panel, tuberculosis [TB] screening).

Treatment

http://www.oprah.com/health/Dr-Oz-Discusses-Possible-Treatments-for-Psoriasis-Video

Treatment of Skin Lesions

Patients with guttate, erythrodermic, or pustular psoriasis may present to the emergency department. In each of these cases, restoration of the barrier function of the skin is of prime concern. This can be performed with cleaning and bandaging.

Plaque and scalp lesions are frequently encountered in patients seeking care for other problems, and initial treatment of the lesions should be offered.

The simplest treatment of psoriasis is daily sun exposure, sea bathing, topical moisturizers, and relaxation. Moisturizers, such as petrolatum jelly, are helpful. Daily application of moisturizing cream to the affected area is inexpensive and successful adjunct to psoriasis treatment. Application immediately after a bath or shower helps to minimize itching and tenderness. Section 3 (2009) of the AAD guideline discusses topical agents and recommends their use adjunctively but not as monotherapy if the disease is extensive or recalcitrant.

Nonprescription tar preparations are available and have therapeutic success, especially when used in conjunction with topical corticosteroids; the newer foams are less messy preparations than some of the older ones. Anthralin, topical corticosteroids, salicylic acid, phenolic compounds, and calcipotriene (a vitamin D analog) also may be effective. Systemic corticosteroids are generally ineffective, and they can significantly exacerbate the disease upon withdrawal. Combination therapy with a vitamin D analog (calcipotriol and calcipotriene) or a retinoid such as tazarotene and a topical corticosteroid is more effective than therapy with either agent alone. Oatmeal baths may be helpful.

Solar or ultraviolet radiation may be helpful. Various ultraviolet light treatments are used—most commonly, psoralen-ultraviolet A (PUVA) therapy. Among phototherapy options, Section 5 (2010) of the AAD guideline gives the highest recommendation to oral PUVA or a combination of PUVA and topical agents.Psoralen is a photosensitizer that is ingested prior to light exposure. PUVA treatment results in conjunctival hyperemia and dry eye, particularly if sun protection is not used. With proper eye protection, there does not appear to be a risk of cataract. Psoralens for either topical (bath) or systemic use may occasionally be difficult to obtain because of stocking shortages.

According to the AAD guidelines, PUVA can result in long remissions, but long-term use of PUVA in Caucasians may increase the risk of squamous cell carcinoma (SCC) and possibly malignant melanoma. A prospective study of 1,380 patients found a strong correlation betweeumber of PUVA treatments and risk of developing one or more SCC. According to the study, exposure to more than 350 PUVA treatments greatly increases the risk of SCC.

Narrow-band ultraviolet B (UVB) therapy has always been accepted as a good treatment modality of psoriasis and the AAD guidelines recommend it over broad-band (UVA), although both are less effective than PUVA. As with PUVA, the guidelines also recommend treatment with combinations of UVB and topic or systemic agents.However, a study by Keaney and Kirsner gives objective reasoning for the benefit of narrow-band UV therapy by showing decreases in T cells, dendritic cells, and interleukins within responsive psoriatic plaques compared with plaques that did not respond to therapy. Gutate psoriasis may prove especially responsive to phototherapy. Therapies such as UVB and PUVA have low efficacy for the treatment of nail psoriasis because of the blockage of the UV radiation by the intervening nail plate.

Patients with psoriasis should avoid injury to skin, including sunburn and other physical trauma, as these areas may develop psoriasis. The appearance of psoriatic lesions in previously uninvolved areas after irritation or trauma is known as the Köbner phenomenon. Patients with psoriasis should also avoid drugs known to worsen the problem (eg, chloroquine, beta-blockers, aspirin or other NSAIDs).

In severe cases, retinoids (acitretin), methotrexate, cyclosporine, 6-thioguanine, azathioprine, a biologic, or hydroxyurea may be used. Retinoids have been reported to cause dry eye, blepharitis, corneal opacities, cataracts, and decreased night vision. All of these may be associated with gastrointestinal intolerance, hepatic damage (acitretin, 6-thioguanine, azathioprine, methotrexate), marrow suppression (6-thioguanine, methotrexate, azathioprine, hydroxyurea) or renal damage (cyclosporine). The use of these systemic medications, with appropriate safety considerations, is supported by Section 4 (2009) of the AAD guidelines.

In addition, systemic retinoids and hydroxyurea may interfere with proper wound healing and elective procedures, including dental surgery, which are best performed before the start of the medications. Acitretin appears more effective than isotretinoin in psoriasis and does not require enrollment in the IPledge program. On the other hand, there is a 3-year pregnancy prohibition after its use, and many will not use this medication in any patient capable of ever becoming pregnant. Combination therapies, such as a biologic plus another immunosuppressive medication, have been used with good effect but data detailing the safest way to do this are scant. All of the systemic medications except acitretin may increase the risk of infection.

Abruptly stopping steroid therapy in psoriasis or adding known irritant drugs can result in the sudden worsening of psoriasis or appearance of a new form. Commonly, this new form is guttate psoriasis, which is much more severe and cosmetically problematic than the preexisting plaque type. It may also present with a more threatening pustular or erythrodermic psoriatic flare.

The use of biologic agents (proteins with pharmacologic activity) is discussed in Section 1 (2008) and reviewed, with updated safety information, in Section 6 of the AAD guidelines. The AAD recommends a set of baseline laboratory studies before starting treatment with a biologic agent to ensure any underlying conditions or risk factors are understood.

Many of the therapies for psoriasis manipulate the function of the immune system and expose the patient to risk of severe infections while blunting the body’s response. In these patients, findings suggestive of minor infections must be taken seriously, and the risk versus the benefit of continuing the drug in the face of the infection must be weighed.

Treatment of Ocular Complications

Keratoconjunctivitis sicca can be treated with ocular lubricants and punctal occlusion. Trichiasis and cicatricial ectropion usually require surgical treatment. Conjunctival, corneal, and anterior chamber inflammation can be treated with topical corticosteroids. Nonsteroidal anti-inflammatory agents or oral corticosteroids are occasionally necessary. Whether systemic immunosuppression is effective for ocular disease is not clear.

Corneal melting, inflammation, and vascularization can be difficult to treat. A bandage contact lens may retard the melting. Topical corticosteroids can control the infiltration and delay the vascularization. In some cases, progression can occur in spite of these treatments and can lead to the need for lamellar or penetrating keratoplasty.

 

References

 1. Pietrzak AT, Zalewska A, Chodorowska G, Krasowska D, Michalak-Stoma A, Nockowski P, et al. Cytokines and anticytokines in psoriasis. Clin Chim Acta. Aug 2008;394(1-2):7-21. [Medline].

2. Keaney TC, Kirsner RS. New insights into the mechanism of narrow-band UVB therapy for psoriasis. J Invest Dermatol. Nov 2010;130(11):2534. [Medline].

3. Kurd SK, Troxel AB, Crits-Christoph P, Gelfand JM. The risk of depression, anxiety, and suicidality in patients with psoriasis: a population-based cohort study. Arch Dermatol. Aug 2010;146(8):891-5. [Medline]. [Full Text].

4. Riveira-Munoz E, He SM, Escaramís G, et al. Meta-Analysis Confirms the LCE3C_LCE3B Deletion as a Risk Factor for Psoriasis in Several Ethnic Groups and Finds Interaction with HLA-Cw6. J Invest Dermatol. May 2011;131(5):1105-9. [Medline].

5. Patel RV, Shelling ML, Prodanovich S, Federman DG, Kirsner RS. Psoriasis and vascular disease-risk factors and outcomes: a systematic review of the literature. J Gen Intern Med. Sep 2011;26(9):1036-49. [Medline].

6. Stern DK, Creasey AA, Quijije J, Lebwohl MG. UV-A and UV-B Penetration of Normal Human Cadaveric Fingernail Plate. Arch Dermatol. Apr 2011;147(4):439-41. [Medline].

7. Keller JJ, Lin HC. The Effects of Chronic Periodontitis and Its Treatment on the Subsequent Risk of Psoriasis. Br J Dermatol. Jul 3 2012;[Medline].  

8. Li WQ, Han JL, Manson JE, Rimm EB, Rexrode KM, Curhan GC, et al. Psoriasis and risk of nonfatal cardiovascular disease in U.S. women: a cohort study. Br J Dermatol. Apr 2012;166(4):811-8. [Medline].

9. Oostveen AM, de Jager ME, van de Kerkhof PC, Donders AR, de Jong EM, Seyger MM. The influence of treatments in daily clinical practice on the Children’s Dermatology Life Quality Index in juvenile psoriasis: a longitudinal study from the Child-CAPTURE patient registry. Br J Dermatol. May 23 2012;[Medline].

10. Lucka TC, Pathirana D, Sammain A, Bachmann F, Rosumeck S, Erdmann R, et al. Efficacy of systemic therapies for moderate-to-severe psoriasis: a systematic review and meta-analysis of long-term treatment. J Eur Acad Dermatol Venereol. Mar 9 2012;[Medline].

11. Stern RS. The risk of squamous cell and basal cell cancer associated with psoralen and ultraviolet A therapy: A 30-year prospective study. J Am Acad Dermatol. Jan 18 2012;[Medline].

 

LICHEN PLANUS

 

1. http://emedicine.medscape.com/article/1123213-medication#5

2. http://freevideolectures.com/Course/118/Oral-Pathology/14

3. http://www.youtube.com/watch?v=iioBR_XCpJo

 

 

Lichen planus (LP) is a pruritic eruption commonly associated with hepatitis C. Lesions are characteristically papular, purple (violaceous color), polygonal, and peripherally located (eg. on the distal extremities). LP may also affect the genitalia or mucous membranes. It is most likely an immunologically mediated reaction, though the pathophysiology in unclear. See Oral Lichen Planus for more information on this variant of lichen planus.

Pathophysiology

Lichen planus is a cell-mediated immune response of unknown origin. It may be found with other diseases of altered immunity; these conditions include ulcerative colitis, alopecia areata, vitiligo, dermatomyositis, morphea, lichen sclerosis, and myasthenia gravis.

An association is noted between lichen planus and hepatitis C virus infection chronic active hepatitis, and primary biliary cirrhosis.In one meta-analysis, 16% of patients with LP had hepatitis C infection.This association has been shown to exist in all regions of the world, including North America.  A workup for hepatitis C should be considered in patients with widespread or unusual presentations of lichen planus. Onset or exacerbation of lichen planus has also been linked to stressful events.

Most cases of lichen planus (LP) are insidious.

• Lesions usually develop on flexural surfaces of the limbs, such as the wrists (see the image below). After a week or more, a generalized eruption develops with maximal spreading within 2-16 weeks.

 

• 

 

• Lichen planus on the flexor part of the wrist.
• Pruritus is common in lichen planus but varies in severity depending on the type of lesion and the extent of involvement. Hypertrophic lesions are extremely pruritic.
• Oral lesions may be asymptomatic or have a burning sensation, or they may even be painful if erosions are present.
• In more than 50% of patients with cutaneous disease, the lesions resolve within 6 months, and 85% of cases subside within 18 months. On the other hand, oral lichen planus had been reported to have a mean duration of 5 years. Large, annular, hypertrophic lesions and mucous membrane involvement are more likely to become chronic.

 

 

    

In addition to the cutaneous eruption, lichen planus (LP) can involve the mucous membranes, the genitalia, the nails, and the scalp. The clinical presentation of lichen planus has several forms: actinic (in sun-exposed areas), annular, atrophic, erosive, follicular, hypertrophic, linear, pigmented, and vesicular/bullous. The papules are violaceous, shiny, and polygonal; varying in size from 1 mm to greater than 1 cm in diameter (see the image below). They can be discrete or arranged in groups of lines or circles. Characteristic fine, white lines, called Wickham stria, are often found on the papules (see the image below).

 

Lichen planus shows Wickham striae (white, fine, reticular scales).

Mucous membrane involvement is common and may be found in patients who do not have skin involvement. Lesions are most commonly found on the tongue and the buccal mucosa; they are characterized by white or gray streaks forming a linear or reticular pattern on a violaceous background (see the image below). Oral lesions are classified as reticular, plaquelike, atrophic, papular, erosive, and bullous. Ulcerated oral lesions may have a higher incidence of malignant transformation in men, but this observation may be confounded by other factors, such as smoking and chewing tobacco. Lesions may also be found on the conjunctivae, the larynx, the esophagus, the tonsils, the bladder, the vulva, and the vaginal vault; throughout the gastrointestinal tract; and around the anus.

    

 

 

Lichen planus on the oral mucosa with ulceration in the center of the lesion appears with whitish papules and plaques in the periphery.

Genital involvement is common in lichen planus. Typically, men develop annular lesions on the glans. Wickham striae may also be observed on these lesions. Vulvar involvement can range from reticulate papules to severe erosions. Dyspareunia, a burning sensation, and pruritus are common in women. Vulvar and urethral stenosis may be a complication. It is estimated that more than 50% of women with oral lichen planus also had undiagnosed vulvar lichen planus. (Also see the clinical guideline summa

Nail findings are found in roughly 10% of patients with lichen planus. Thes findings are most commonly longitudinal grooving and ridging. Hyperpigmentation, subungual hyperkeratosis, onycholysis, and longitudinal melanonychia can result from lichen planus. Rarely, inflammation may result in permanent destruction of the nail matrix with subsequent pterygium formation. Lichen planus has been linked to childhood idiopathic nail atrophy and may overlap with twenty-nail dystrophy of childhood.

Cutaneous lesions may be accompanied by follicular and perifollicular lesions on the scalp, which may be violaceous, scaly, and pruritic papules. These lesions can progress to atrophic cicatricial alopecia, known as lichen planopilaris. This can appear even many weeks after the skin lesions have disappeared. Pseudopelade can be a final endpoint.

Variations in lichen planus include the following:

• Hypertrophic lichen planus: These extremely pruritic lesions are most often found on the extensor surfaces of the lower extremities, especially around the ankles. Hypertrophic lesions are often chronic; residual pigmentation and scarring can occur when the lesions eventually clear.
• Atrophic lichen planus: Atrophic lichen planus is characterized by a few lesions, which are often the resolution of annular or hypertrophic lesions.
• Erosive/ulcerative lichen planus: These lesions are found on the mucosal surfaces and evolve from sites of previous lichen planus involvement.
• Follicular lichen planus (aka Lichen planopilaris): This is characterized by keratotic papules that may coalesce into plaques. This condition is more common in women than in men, and ungual and erosive mucosal involvement is more likely to be present. A scarring alopecia may result.
• Annular lichen planus: Lichen planus papules that are purely annular are rare. Annular lesions with an atrophic center can be found on the buccal mucosa and the male genitalia.
• Linear lichen planus: Isolated linear lesions may form a zosteriform lesion, or they may develop as a Köebner effect.
• Vesicular and bullous lichen planus: Most commonly, these lesions develop on the lower limbs or in the mouth from preexisting lichen planus lesions. A rare condition, lichen planus pemphigoides, is a combination of both lichen planus and bullous pemphigoid.
• Actinic lichen planus: Subtropic or actinic lichen planus occurs in regions, such as Africa, the Middle East, and India. This mildly pruritic eruption usually spares the nails, the scalp, the mucous membranes, and covered areas. Lesions are characterized by nummular patches with a hypopigmented zone surrounding a hyperpigmented center.
• Lichen planus pigmentosus: This is a rare variant of lichen planus but can be more common in persons with darker-pigmented skin, such as Latinos or Asians. It usually appears on face and neck. Some believe it is similar to or the same as erythema dyschromicum perstans (ie, ashy dermatosis).
• Lichen planus pemphigoides: This is a rare form of lichen planus. Blisters subsequently develop on lichen planus lesions. Clinically, histopathologically and immunopathologically, it has features of lichen planus and bullous pemphigoid, it but carries a better prognosis than pemphigoid.

 

Nail changes in LP

 

 

 

  

 

 

Differential Diagnoses

• Graft Versus Host Disease
• Lichen Nitidus
• Lichen Simplex Chronicus
• Pityriasis Rosea
• Psoriasis, Guttate
• Psoriasis, Plaque
• Syphilis
• Tinea Corporis

 

Medication Summary

The first-line treatments of cutaneous lichen planus are topical steroids, particularly class I or II ointments. A second choice would be systemic steroids for symptom control and possibly more rapid resolution. Many practitioners prefer intramuscular triamcinolone 40-80 mg every 6-8 weeks. Oral metronidazole has been shown to be an effective therapy for some patients.Oral acitretin has been shown to be effective in published studies.Many other treatments, including mycophenolate mofetil at 1-1.5 g twice daily, are of uncertain efficacy because of the lack of randomized controlled trials. In a randomized double-blinded study, sulfasalazine at up to 2.5 g/day for 6 weeks showed improvement in lesions (>80%) and pruritus (>90%) in patients with generalized lichen planus.

For lichen planus of the oral mucosa, topical steroids are usually tried first. Topical and systemic cyclosporin have been tried with some success ; however, a randomized double-blind study indicated that topical cyclosporin was a less effective but much more costly regimen than clobetasol.Newer topical calcineurin inhibitors have replaced topical cyclosporin for the treatment of lichen planus. Other options include oral or topical retinoids. Even with these effective treatments, relapses are common.

Close monitoring of lipid levels is suggested for patients with lichen planus who are treated with oral retinoid agents because a case control study found that the risk of dyslipidemia in these patients is increased 2-3 fold.

Patients with widespread lichen planus may respond to narrow-band or broadband UV-B therapy. Psoralen with UV-A (PUVA) therapy for 8 weeks has been reported to be effective. Risks and benefits of this treatment should be considered. PUVA is carcinogenic. Long-term risks include dose-related actinic degeneration, squamous cell carcinoma, and cataracts. A phototoxic reaction with erythema, pruritus, phytophotodermatitis, and friction blisters could occur.

UV-A therapy combined with oral psoralen consists of oral psoralen (0.6 mg/kg), 1.5-2 hours before ultraviolet light, which usually starts at 0.5-1 J/cm² and is increased by 0.5 J/cm² per visit. Use of topical ointment at the time of receiving UV-A treatment may decrease the effectiveness of PUVA. Precaution should be taken for persons with a history of skin cancers or hepatic insufficiency.

Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body’s immune response to diverse stimuli. Topical steroids may be as effective as systemic steroids. Class I or II steroids in ointment form reduce pruritus in cutaneous lichen planus, but they have not been proven to induce remission.

     Prednisone

     Betamethasone topical (Diprolene, Celestone, Luxiq)

     Triamcinolone (Aristospan, Kenalog)

     Halobetasol (Ultravate, Halonate)

     Isotretinoin (Amnesteem, Claravis, Myorisan, Sotret)

     Tretinoin topical (Retin-A, Avita, Renova, Atralin, Tretin-X)

     Acitretin (Soriatane)

 

Immunosuppressants

Cyclosporine (Sandimmune, Neoral, Gengraf)

 

Antibiotics, Other

Metronidazole (Flagyl)

 

References

 

1. Pavlotsky F, Nathansohn N, Kriger G, Shpiro D, Trau H. Ultraviolet-B treatment for cutaneous lichen planus: our experience with 50 patients. Photodermatol Photoimmunol Photomed. Apr 2008;24(2):83-6. [Medline].

2. [Guideline] American College of Obstetricians and Gynecologists. Diagnosis and management of vulvar skin disorders. National Guideline Clearinghouse. May 2008.

3. Raslan HM, Ezzat WM, Abd El Hamid MF, Emam H, Amre KS. Skin manifestations of chronic hepatitis C virus infection in Cairo, Egypt. East Mediterr Health J. May-Jun 2009;15(3):692-700. [Medline].

4. [Best Evidence] Shengyuan L, Songpo Y, Wen W, Wenjing T, Haitao Z, Binyou W. Hepatitis C virus and lichen planus: a reciprocal association determined by a meta–analysis. Arch Dermatol. Sep 2009;145(9):1040-7. [Medline].

5. Bigby M. The relationship between lichen planus and hepatitis C clarified. Arch Dermatol. Sep 2009;145(9):1048-50. [Medline].

6. Rasi A, Behzadi AH, Davoudi S, Rafizadeh P, Honarbakhsh Y, Mehran M, et al. Efficacy of oral metronidazole in treatment of cutaneous and mucosal lichen planus. J Drugs Dermatol. Oct 2010;9(10):1186-90. [Medline].

7. Arias-Santiago S, Buendia-Eisman A, Aneiros-Fernandez J, et al. Cardiovascular risk factors in patients with lichen planus. Am J Med. Jun 2011;124(6):543-8. [Medline].

 

ORAL  lICHEN  PLANUS

1. http://emedicine.medscape.com/article/1078327-followup#a2649

2. http://www.youtube.com/watch?v=VRTOA8KTLvE

 

Background

Oral lichen planus (OLP) is a chronic inflammatory disease that causes bilateral white striations, papules, or plaques on the buccal mucosa, tongue, and gingivae. Erythema, erosions, and blisters may or may not be present. Note the images below.

 

 

Pathophysiology

Current data suggest that oral lichen planus is a T-cell–mediated autoimmune disease in which autocytotoxic CD8⁺ T cells trigger apoptosis of oral epithelial cells.

The dense sub-epithelial mononuclear infiltrate in oral lichen planus is composed of T cells and macrophages, and there are increased numbers of intra-epithelial T cells. Most T cells in the epithelium and adjacent to the damaged basal keratinocytes are activated CD8⁺ lymphocytes. Therefore, early in the formation of oral lichen planus lesions, CD8⁺ T cells may recognize an antigen associated with the major histocompatibility complex (MHC) class I on keratinocytes. After antigen recognition and activation, CD8⁺ cytotoxic T cells may trigger keratinocyte apoptosis. Activated CD8⁺ T cells (and possibly keratinocytes) may release cytokines that attract additional lymphocytes into the developing lesion.

Oral lichen planus lesions contain increased levels of the cytokine tumor necrosis factor (TNF)–alpha.Basal keratinocytes and T cells in the subepithelial infiltrate express TNF in situ.Keratinocytes and lymphocytes in cutaneous lichen planus express elevated levels of the p55 TNF receptor, TNF-RI.T cells in oral lichen planus contain mRNA for TNF and secrete TNF in vitro.Serum and salivary TNF levels are elevated in oral lichen planus patients.TNF polymorphisms have been identified in patients with oral lichen planus, and they may contribute to the development of additional cutaneous lesions.Oral lichen planus has been treated successfully with thalidomide, while thalidomide is known to suppress TNF production.Together, these data implicate TNF in the pathogenesis of oral lichen planus.

The lichen planus antigen is unknown, although it may be a self-peptide (or altered self-peptide), in which case lichen planus would be a true autoimmune disease. The role of autoimmunity in the pathogenesis is supported by many autoimmune features of oral lichen planus, including its chronicity, onset in adults, predilection for females, association with other autoimmune diseases, occasional tissue-type associations, depressed immune suppressor activity in patients with oral lichen planus, and the presence of autocytotoxic T-cell clones in lichen planus lesions. The expression or unmasking of the lichen planus antigen may be induced by drugs (lichenoid drug reaction), contact allergens in dental restorative materials or toothpastes (contact hypersensitivity reaction), mechanical trauma (Koebner phenomenon), viral infection, or other unidentified agents.

Clinical Presentation

Lichen planus may arise in patients with other immunologically mediated disorders, including alopecia areata, dermatomyositis, lichen sclerosis et atrophicus, morphea, myasthenia gravis, primary biliary cirrhosis, ulcerative colitis, and vitiligo.

In many patients, the onset of oral lichen planus is insidious, and patients are unaware of their oral condition. In such instances, the referring medical or dental practitioner identifies the clinical changes in the oral mucosa.

Some patients report a roughness of the lining of the mouth, sensitivity of the oral mucosa to hot or spicy foods or oral hygiene products, painful oral mucosa, sore gums, red or white patches on the oral mucosa, red gums, or oral ulcerations.

Approximately two thirds of patients with oral lichen planus report oral discomfort, especially in association with atrophic and erosive lesions. Erythematous and erosive lesions are often sensitive or painful. Symptoms vary from mucosal sensitivity to continuous debilitating pain.

Oral mucosal lichenoid lesions may occur after the administration of systemic drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs), sulfonylureas, antimalarials, beta-blockers, and some angiotensin-converting enzyme (ACE) inhibitors. The period between the commencement of the drug therapy and the clinical appearance of oral lichen planus–like disease varies.

In rare cases, oral mucosal lichenoid lesions occur after a dental restoration is performed or after the patient starts using a denture; the lag period varies. Patients with an associated allergy to metals or components of the appliance should be evaluated by means of patch testing.

Up to 44% of patients with oral lichen planus develop coincident skin lesions. Conversely, more that 70% of patients with cutaneous lichen planus develop coincident oral lichen planus.

The genitals are involved in as many as 25% of women with oral lichen planus, compared with only 2-4% of men with oral lichen planus. The features are similar to those of the oral lesions. Patients do not often complain of pain or pruritus, although on questioning, they may admit to such symptoms.

In patients with oral lichen planus, scalp involvement (lichen planopilaris) is rare.

Nail involvement in patients with oral lichen planus is uncommon.

In a small group of patients, lichen planus may involve the esophagus.

Differential Diagnoses

       Dermatitis Herpetiformis

       Graft Versus Host Disease

       Linear IgA Dermatosis

       Oral Manifestations of Autoimmune Blistering Diseases

       Pemphigus Vulgaris

       Squamous Cell Carcinoma

Laboratory Studies

The history, typical oral lesions, and skin involvement are usually sufficient to diagnose oral lichen planus (OLP), though laboratory studies and biopsy may be required (see Procedures).

Direct immunofluorescence testing can help in distinguishing erosive or the rare bullous oral lichen planus from pemphigus vulgaris, benign mucous membrane pemphigoid, dermatitis herpetiformis, and linear immunoglobulin A (IgA) disease. The most characteristic feature of oral lichen planus is shaggy linear fibrin distribution.

Some studies show an increased incidence of C albicans infection in patients with oral lichen planus. Periodic acid-Schiff (PAS) staining of biopsy specimens and candidal cultures or smears may be performed. However, these tests may be of limited clinical value because oral C albicans is present in more than 70% of the population. The presence of C albicans and the oral load of this organism do not aid either the diagnosis or the treatment of oral lichen planus.

Other Tests

Skin patch testing may be helpful in identifying a contact allergy in some patients with oral lichen planus. The current recommendation is to use a standard series; a dental prosthesis series; and a metal salt series that includes gold, mercury, and palladium salts as well as other salts of metals used in dental restorations. Late readings, or those obtained at 10 and 17 days after the application of the skin patch, may be required.

The most common allergy is related to mercury contained in amalgam restorations. Compared with patients with lesions in other locations, patients with lesions near the amalgam restoration have a higher rate of positive patch test results to mercury. When the amalgam restorations are removed, patients with a positive result have a higher remission rates (47-100% depending on the study) than that of patients without this positive result.

Although the assessment of hepatic function in the treatment of otherwise healthy southern European and Japanese patients with oral lichen planus may be warranted, similar screening in British and American patients appears to be of limited benefit. Formal studies are still ongoing. Consider hepatic biochemical testing only when patients have proven oral lichen planus and suspected liver disease.

Oral Lichen Planus Medication

Topical corticosteroids are the mainstay of medical treatment of oral lichen planus, although rarely, corticosteroids may be administered intralesionally or systemically. Some topical corticosteroid therapies may predispose the patient to oral pseudomembranous candidosis. However, this condition is rarely if ever symptomatic, and it generally does not complicate healing of the erosions related to oral lichen planus. Topical antimycotics (eg, nystatin, amphotericin) may be prescribed when an infection is present.

Erosive oral lichen planus that is recalcitrant to topical corticosteroids may respond to topical tacrolimus. Other potential therapies for recalcitrant oral lichen planus include hydroxychloroquine, azathioprine, mycophenolate, dapsone, systemic corticosteroids, and topical and systemic retinoids.

Corticosteroids

    Fluocinolone (Synalar, Synalar-HP, Fluonid)

     Clobetasol (Cormax, Olux, Temovate)

    Beclomethasone (Beclovent, Vanceril)

     Triamcinolone (Amcort, Aristocort, Aristospan)

     Prednisolone (Delta-Cortef, Prednisol TBA injection)

 

Immunosuppressants

Azathioprine (Imuran)

 

Further Outpatient Care

Re-examine patients with oral lichen planus (OLP) during active treatment, and monitor lesions for reduction in mucosal erythema and ulceration and alleviation of symptoms. Continue active treatment and try alternative therapies until erythema, ulceration, and symptoms are controlled. Follow up with patients with oral lichen planus at least every 6 months.

Advise patients with oral lichen planus to pay attention to when symptoms are exacerbated or when lesions change. Such changes generally indicate a phase of increased erythematous or erosive disease.

In view of the potential association of oral lichen planus with oral SCC, an appropriate specialist should follow up with the patients every 6-12 months. In addition, advise patients to regularly examine their mouths and seek the help of a specialist if persistent red or ulcerative oral mucosal lesions develop.

Candidal cultures or smears may be obtained periodically. Infections can be controlled with topical antimycotic preparations. These tests may be of limited clinical value because oral C albicans is present in at least 70% of all healthy persons.

Deterrence/Prevention

Patients with oral lichen planus may have a slightly increased risk of oral cancer, although the precise risk is unknown.

The risk of oral cancer in patients with oral lichen planus may be reduced by means of the following:

• Elimination of smoking and alcohol consumption
• Effective treatment of atrophic, erosive, and plaque oral lichen planus lesions
• Consumption of a nutritious diet including fresh fruit and vegetables
• Elimination of C albicans superinfection
• Clinical examination with any exacerbation of symptoms or change in lesion presentation
• Regular clinical examination and repeat biopsy as required. Oral brush biopsy can be used to limit the number of scalpel biopsies. The frequency of brush biopsy for oral lichen planus patient follow-up has not been established. However, if the clinical features of the lesions change, scalpel biopsy should be repeated.

Complications

Oral lichen planus and its treatment may predispose people to oral C albicans superinfection.

Patients with oral lichen planus may have a slightly increased risk of oral cancer, which they may be able to reduce (see Deterrence/Prevention).

Oral SCC in patients with oral lichen planus is a feared complication and a controversial issue. In retrospective studies, fewer than 5% of patients with oral lichen planus who were not using tobacco products developed oral SCC. Atrophic, erosive, and plaque lesions may be at greater risk of malignant change, although SCC may arise in the unaffected oral mucosa as well. The most important risk factors of oral SCC remain the concomitant use of alcohol and tobacco products. Any additive effect of oral lichen planus is difficult to detect in patients who use both.

Proposed reasons for the increased risk of oral SCC in patients with oral lichen planus include the following:

• Compared with healthy mucosa, the oral mucosa affected by oral lichen planus may be more sensitive to C albicans and to the exogenous mutagens found in tobacco, alcohol, and betel quid.
• In patients with oral lichen planus, the chronic inflammatory response and the simultaneous healing response of epithelial wounds may increase the likelihood of cancer-forming gene mutations.

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