Healthy human skin has many physiological barriers against microorganisms. The stratum corneum provides mechanical protection as a covering layer. Desquamation, resulting from the skin's continuous self-renewal, also ensures that colonising bacteria are shed. The acidic barrier formed by the secretions of the eccrine sweat glands (acid mantle) and the lipid mantle formed by sebum partly prevent bacteria from multiplying. The relative dryness of the skin surface also limits the growth of Gram-negative bacteria. Human skin harbours many saprophytic microorganisms that normally do not cause disease. These bacteria make up the skin flora and prevent pathogenic bacteria from multiplying.
A breakdown in any of the skin's protective mechanisms leads to the appearance of infections. Skin infections develop more frequently in certain metabolic and chronic systemic diseases. There is also a predisposition to bacterial infections in atopic dermatitis. Impairment of the cellular (neutropenia) or humoral (low Ig) immune response causes infections to follow a more severe and resistant course.
Bacterial skin infections caused by different agents have quite different morphological features and courses. These infections can be classified as infections caused by Gram-positive bacteria, Gram-negative bacteria and various other microorganisms (such as spirochaetes, rickettsiae, chlamydiae and mycoplasmas).
The great majority of bacterial skin infections are caused by the Gram-positive bacteria streptococci and staphylococci. These agents are known as pyococci, and their infections as pyoderma.
Most microorganisms cannot get past the stratum corneum of the skin. This is due to factors such as the acid mantle, the lipid mantle, physiological turnover (renewal), the low pH of the skin, bacterial interference, the inhibition of pathogens by the skin's resident flora and the relative dryness of the skin, which generally prevent bacteria from colonising and spreading. Although pyoderma can mean infectious skin diseases caused by any kind of bacteria, in practice it refers to diseases caused by staphylococci and streptococci. These cocci are present on intact skin and mucous membranes without causing disease; the acid mantle is important in keeping them from doing so. If pyoderma develops secondarily on top of any dermatosis, this is called pyodermisation or impetiginisation.
There are certain principles in the diagnosis and treatment of bacterial skin infections. It is important to identify the type of bacteria in the lesion: an appropriate sample must be taken from the lesion, the Gram stain must be evaluated well and a suitable medium must be chosen for culture.
Pyodermas caused by staphylococci: impetigo, furuncle, carbuncle, sycosis simplex, hordeolum (stye), acne keloidalis, hidradenitis, staphylococcal scalded skin syndrome (Ritter's disease), systemic infections caused by staphylococci, toxic shock syndrome.
Pyodermas caused by streptococci: impetigo, ecthyma, erysipelas, cellulitis, lymphangitis, systemic infections caused by streptococci, scarlet fever.
Pyodermas
Pyodermas are suppurative skin diseases caused by bacteria called streptococci and staphylococci. We will examine these diseases in two separate groups: the first group consists of pyodermas caused by streptococcal bacteria, and the second of pyodermas caused by staphylococcal bacteria. Pyodermas caused by streptococci are:
1) Erysipelas
2) Angular cheilitis (perlèche)
3) Impetigo
4) Pemphigus neonatorum
5) Ecthyma
6) Intertrigo
Pyodermas caused by staphylococci are:
1) Ostiofolliculitis
3) Furuncle
4) Anthrax (carbuncle)
5) Hidradenitis
6) Acne necrotica
7) Acne keloidalis
8) Pyogenic granuloma
9) Pyodermatitis vegetans
Impetigo Contagiosa
This is a highly contagious disease. It is most common in late summer and early autumn, and is seen particularly in pre-school children. In most cases the responsible agent is group A streptococcus. Rarely it may be caused by S. aureus. Streptococci other than group A can very rarely be responsible; among these, group B streptococci have been isolated as the cause, particularly in newborns.
Ecthyma
Ecthyma (contagious ecthyma) is a viral dermatitis zoonosis seen particularly in sheep and goats, and can cause economic losses in livestock farming. In herds where the disease appears, morbidity is usually 100% and mortality around 1%. However, in suckling animals the death rate can rise to 50%.
Ecthyma (orf) can also be transmitted to people who come into contact with animals. The disease is characterised by lesions on hairless areas of skin, especially the gums and lips, the genitals and between the claws. In this disease, which has an incubation period of 8–10 days, the lesions form papules and crusts. This article attempted to examine observations on the effect of genotype in a case of ecthyma (ecthyma contagiosum) occurring in Gökçeada, Maltese and Turkish Saanen goats.
Erysipelas
Erysipelas, also known in Turkish as "yılancık", is a skin infection that presents with pain, redness, swelling and warmth of the skin and is seen most often on the legs. If treatment is delayed, the infection can spread through the body. It should therefore not be neglected, and a doctor should be consulted early for treatment. Erysipelas is a bacterial skin infection accompanied by redness, swelling, warmth and pain of the skin. It can occur at any age and can affect any part of the body. It is seen most often between the ages of 60 and 80 and on the legs.
What else should be considered in the treatment of erysipelas?
Bed rest should be taken, and the area affected by erysipelas should not be left hanging down but kept raised if possible. Compression stockings can be used to prevent oedema in the legs. Drinking plenty of fluids is recommended to help prevent possible side effects of the medicines used in treatment and to make up for fluid loss due to the infection. Possible entry points for the infection and the underlying cause should also be assessed and, if found, treated. In recurrent cases, long-term antibiotic treatment can be used to prevent erysipelas from developing.
Cellulite
Cellulite is the name given to the orange-peel-like appearance of the skin. It is also called lipodystrophy. Cellulite develops when lymph fluid accumulates between cells, particularly as a result of the lymph circulation in our tissues slowing down for any reason.
The fibrous bands beneath the skin that attach perpendicular to it are responsible for the orange-peel appearance. Because these fibrous bands differ between women and men, cellulite hardly forms in men, also owing to the effect of their hormones.
How Does Cellulite Form?
It is an enlargement of the fatty tissue beneath the skin (subcutaneous). This enlargement:
- Disrupts the microcirculation,
- Disrupts the lymphatic circulation,
- As a result of disrupted lymphatic and blood circulation, pressure in the spaces between cells increases and fluid and toxins begin to leak out,
- With the disruption of lymphatic circulation, fat also begins to accumulate in the spaces between cells in the tissues. This accumulation, i.e. oedema, also impairs cell function.
The gradual enlargement of fat cells further disrupts the flow and increases the accumulation of fat cells. - As the subcutaneous thickness increases and the fibrous bands cannot expand, the fat deposits cause the skin to bulge outwards in places. These bulges are responsible for the orange-peel appearance of the skin.
- With the added accumulation of fat, cellulite becomes harder to treat with each passing day.
- This accumulation begins to affect the person's psychosocial wellbeing as well, leading to reduced muscle and joint function, back and lower back pain, tiring easily, varicose veins and skin deformities, sagging tissue and stretch marks.
Acute Lymphangitis
This is characterised by thin red streaks spreading in the arm from the epitrochlear lymph nodes towards the axillary lymph nodes, and in the leg from the popliteal lymph nodes towards the inguinal lymph nodes. Redness appears as a result of the inflammatory reaction. Widespread redness, fever, tenderness and oedema are usually seen in the area. Body temperature rises to 39–40 degrees. Movement of the limb makes it easier for bacteria to spread along the lymph channels. The local lymph nodes swell within 12–24 hours of the first signs of infection. Recovery from acute lymphangitis is usually complete. However, because circulation becomes impaired after recurrent infections, the likelihood of recurrence increases due to stasis. Chronic or recurrent infections of the vessels in this way damage the lymphatic structures, the late result of which is lymphoedema.
Treatment
The infection should be treated by immobilisation and elevation of the limb, local warm, moist antiseptic dressings and appropriate broad-spectrum antibiotics. Any accompanying fungal infection should also be treated.
Acute Paronychia
Paronychia is the name given to an infection of the area around the nail caused by certain bacteria or fungi. It can be acute or chronic. Depending on the underlying cause it may appear suddenly or, in some cases, develop over weeks. It is commonly known in Turkish as "dolama". It is easy to diagnose and can be treated successfully with care.
Acute paronychia is usually bacterial in origin and appears suddenly after traumatic events such as biting or a puncture. Chronic paronychia, on the other hand, starts slowly and gradually worsens, and the person is aware of it. It is more likely in people exposed to moist environments.
Who Gets Acute Paronychia?
- People and children who habitually bite their nails
- Babies who suck their fingers
- After procedures such as manicures
- After certain situations such as having a plaster cast
- After certain other injuries
Blistering Distal Dactylitis
This is a local infection caused by group A streptococci, often developing in young adults and children at the tips of the fingers and toes, characterised by the formation of a tense bulla filled with seropurulent fluid. Staphylococci and group B streptococci are also responsible for the development of this condition. The microorganism can be grown in cultures taken from the blister fluid.
Penicillins, beta-lactamase inhibitors and, in patients allergic to penicillin, erythromycin can be used in treatment.
Elephantiasis (Elephantiasis Nostras Verrucosa)
It is popularly known as "elephant disease". Elephantiasis is the disproportionate enlargement of various parts of the body. The exact cause of this rare disease is not known. According to Dr Michael Cohen, there are about 200 people with this condition.
Why does it occur?
This condition, passed to humans when larvae released by reproducing worms are carried by mosquitoes, blocks the lymph vessels and causes inflammation. As a result, excessive swelling is seen, especially in the feet and legs.
Elephantiasis can also occur when cancerous tissue blocks the lymph channels or when the lymph channels are damaged during surgery. As the fluid increases, or fails to enter the circulation and spreads beneath the skin and into the tissue spaces, it causes swelling in the areas mentioned, as well as in the arms and face.
How is it diagnosed?
The pit left by a finger when the swelling is pressed is a diagnostic sign of the disease. Over time the skin thickens, changes colour and takes on a shape resembling an elephant's skin. In addition, a cough and mild fever are also among the signs of the disease. The definitive diagnosis is made by seeing microfilariae in blood samples taken at night.
Symptoms
The first sign that may be seen is painful swelling appearing between three months and two years after being bitten.
The finger leaving a pit when the swelling is pressed is important for diagnosis. When the genital area is affected, urination becomes difficult. Over time, as a result of the blockage, the skin thickens, becomes rough
and changes colour. The underlying tissue also coarsens and hardens, and the skin comes to resemble an elephant's skin.
Staphylococcus
Staphylococcal infections are caused by staphylococcus bacteria, a type of germ commonly found on the skin and even inside the nose of healthy people. Most of the time these bacteria cause no problems, or they may cause relatively minor skin infections.
But if the bacteria get into your body, enter the bloodstream and affect your joints, bones, lungs or heart, staphylococcal infections can have fatal consequences.
In the past, a fatal staphylococcal infection could occur in people who were hospitalised, had a chronic illness or had a weakened immune system. Now, by contrast, life-threatening staphylococcal infections are being seen in an increasing number of healthy people. Many staphylococcal infections no longer respond to commonly used antibiotics.
Causes
Many people carry staphylococcus bacteria but never develop a staphylococcal infection. If you do have a staphylococcal infection, it is likely to be caused by bacteria you have been carrying for some time.
These bacteria can also be passed from person to person. Because staphylococcus bacteria are very hardy, they can live on inanimate objects such as pillows or towels long enough to pass to the next person who touches them.
Bullous Impetigo
Bullous impetigo is always caused by S. aureus, phage group II, type 71; the blisters are secondary to bacterial toxins that target desmoglein 1 in the granular layer. Bullous impetigo can develop on intact skin.
Bullous impetigo may begin as small vesicles and progress to superficial, flaccid bullae. Systemic symptoms are common in bullous impetigo but rare in non-bullous impetigo.
Staphylococcal Scalded Skin Syndrome
Staphylococcal scalded skin syndrome (SSSS) (Ritter's disease) is a severe infection usually caused by staphylococcal exfoliative toxins. It is seen more often in newborns and children than in adults. It is characterised by fever, widespread erythema that can involve the whole skin, and Nikolsky-positive flaccid bullae that rupture quickly, leaving large erosions. Skin peeling appears 2–5 days after the widespread erythema. The bullae, usually seen in flexural areas, gradually enlarge and tear easily, leaving a moist erythematous base. Without an appropriate treatment approach, it can also lead to serious clinical conditions such as fluid and electrolyte imbalance and sepsis.
The diagnosis is usually made clinically; a definitive diagnosis is made by skin biopsy. With early diagnosis and early antibiotic treatment, SSSS is a reversible condition that improves clinically within 7–10 days. In patients in whom it is recognised late, appropriate treatment is not started and measures to protect against infection are not taken, it can be fatal.
It is important that patients with haemodynamic instability and/or respiratory distress are monitored in a paediatric intensive care unit.
Folliculitis
Folliculitis is a bacterial infection of the hair follicle. Bacteria on the skin affect the hair root for various reasons. Although folliculitis is commonly caused by Staphylococcus aureus, Gram-negative bacilli, fungi and viruses can also cause the disease.
It surrounds the hair follicle as an erythematous lesion averaging 2–5 mm in diameter. Systemic symptoms are not often seen in this disease. The lesions burst on their own and can heal without scarring. However, cases that do not resolve definitely require examination and treatment by a dermatologist.
Among the factors involved in folliculitis, irregular use of medicines and antibiotics weakens the body's resistance and can lead to certain diseases. Folliculitis can develop due to causes such as immune system disorders, metabolic diseases, corticosteroid use, bowel diseases, diabetes, liver diseases, pools, jacuzzis, increased humidity and close contact with someone who has the condition.
Although folliculitis can be seen at any age, it is usually seen in young adults. In children, folliculitis may usually be caused by fungi. Use of medicines, such as irregular or indiscriminate antibiotic use, also plays a considerable part in the development of folliculitis. Folliculitis can cause loss of hair and beard. It can occur not only in the hair and beard but in any hair-bearing area of the body.
What is a furuncle?
A furuncle usually arises when folliculitis (inflammation of the hair root) progresses to form a deep, inflamed lump ranging from the size of a chickpea to that of an orange. A furuncle is popularly known as a boil. The causative bacterium is usually Staphylococcus aureus.
Symptoms of a furuncle
Furuncles appear in areas containing hair roots that are exposed to sweating and friction (such as the neck, face, armpits and buttocks). Signs include a pink or red tender swelling on the skin, gradual spreading of the swelling and redness, and pain in the skin. These infections can spread through contact with other parts of the body or with another person.
What is a carbuncle?
A carbuncle forms when several furuncles become abscessed and spread beneath the skin. It usually occurs on the neck, back and buttocks.
Symptoms of a carbuncle
Sometimes, in the early stages, the boil disappears on its own after itching and mild pain. Usually, however, the boil grows very quickly within 1–2 days. As pus builds up in the boil, pressure and pain increase, accompanied by symptoms such as fever, chills and fatigue. The lump forms a white or yellow head and bursts. Carbuncles occur more often in men than in women. The boil can recur repeatedly.
Sycosis Barbae (Sycosis Simplex)
This is a chronic disease of the beard and moustache area caused by staphylococci and characterised by pustules. It is seen in men (those who shave). The causative agent is mostly Staph. aureus, which reaches the skin from the nasal cavity via nasal discharge and causes disease. The disease usually begins in the moustache area. Erythema develops in this area together with sensations such as burning and stinging. Then pinhead-sized pustules appear, each with a hair in the centre. Through shaving and scratching, the disease jumps from one follicle to another and spreads to the surrounding area and the beard area; as it becomes chronic, pustule formation decreases and is replaced by inflammatory papules. The hairs do not come out easily when pulled with tweezers.
Differential diagnosis: this should be made from tinea barbae. In tinea barbae the hairs come out easily when pulled, the inflammatory signs are more pronounced and the course is acute. They are distinguished by direct microscopy.
Treatment: the hairs should be epilated. Antiseptic dressings or antibiotic ointments are used on both the lesions and the nostrils (preferably mupirocin, Bactroban). Systemic antibiotics are given by mouth.
Folliculitis Decalvans
Painful pustular folliculitis, oedematous, swollen-looking scarring and, on dermatoscopy, follicles forming tufts are seen. Histopathologically, neutrophils predominate at first, followed later by a mixture of neutrophils, lymphocytes and plasma cells. Its pathogenesis is thought to involve a hypersensitivity reaction to Staphylococcus aureus (S. aureus) and its superantigens, and a defect in the patient's cell-mediated immune response.
Treatment
Before starting treatment, cultures are taken from both the nose and the pustules. The patient's items such as hats, scarves, headbands or wigs should be disinfected frequently, as they can act as a focus for S. aureus colonisation. Treatment is planned according to staphylococcal sensitivity and may include tetracycline, doxycycline, cephalosporins, erythromycin or fusidic acid. Topical antibiotics (erythromycin, fusidic acid, clindamycin) are helpful; nadifloxacin in particular is successful. Success has been achieved with a combination of oral fusidic acid (1500 mg/day, 3 weeks), zinc sulphate (400 mg/day, 6 months) and topical fusidic acid. In resistant cases, a combination of rifampicin (300 mg x2) and clindamycin (300 mg x2) is beneficial. Ciprofloxacin or clarithromycin may be given instead of clindamycin. Dapsone can be effective, given at 75–100 mg for the first 6 months and 25 mg for maintenance.
Acne Keloidalis
There are hard, dome-shaped follicular papules and pustules on the nape of the neck and the occipital area. They merge and leave keloid scars. Trauma and mechanical irritation should be avoided. Potent topical steroids and intralesional triamcinolone acetonide (ILTA) injections are the first step of treatment. In more severe cases these treatments can be combined with tetracycline. Where tetracycline is insufficient, the condition can be controlled with isotretinoin, given initially at a high dose (1–1.5 mg/day) and at 10 mg/day or every other day for maintenance. Favourable results have been reported with surgical treatment, and some patients benefit from laser hair removal.
Anthrax (malignant pustule)
The causative agent is Bacillus anthracis. The disease is mostly seen in people who handle animals and their by-products. Two to three days after the microorganism enters the skin, an inflammatory papule develops. Within a short time this papule turns into a bulla filled with serohaemorrhagic fluid, surrounded by erythema and oedema. The base of the bulla becomes necrotic; this is called the anthrax pustule. The lesion is painless and may be single or several. A crust then forms over it, and after the crust falls off a deep ulcer develops in its place. Patients have swollen regional lymph nodes, with general fever and malaise. There is another, rare clinical form of anthrax called malignant oedema, in which a soft oedematous swelling develops where the bacillus entered. Shortly afterwards, necrotic bullae form over this area, followed by the formation of a necrotic crust. This clinical form follows a more severe course than malignant pustule, and septicaemia and death may occur.
Diagnosis is made by the clinical appearance, by seeing Gram-positive anthrax bacilli in material taken from the lesions, and by special culture methods.
Treatment: patients should be given high-dose intravenous or intramuscular penicillin, oral tetracycline and, in case of severe oedema, IV steroids. Local wound care is carried out.
Erythrasma
This is a disease caused by Corynebacterium minutissimum. The main predisposing factors are diabetes, obesity and excessive sweating. The disease settles in intertriginous areas, especially the groin, the armpits and between the 3rd and 4th toes. Between the toes it presents with maceration. In the groin and armpits it appears as sharply demarcated, brown, slightly scaly areas with no difference between the centre and the edges. There is no weeping, and it rarely causes itching. Under Wood's light it shows coral-red fluorescence due to the porphyrins (coproporphyrin) produced by the causative agent.
Differential diagnosis: this should be made from tinea inguinalis. In tinea inguinalis the centre of the lesions has receded and the edges are active, and vesicles are also noticeable at the edges. They are distinguished by direct microscopy and Wood's light examination. The disease should also be distinguished from intertrigo, in which weeping is prominent.
Treatment: systemic (erythromycin) and topical antibiotics (or imidazole antifungal creams) are given. Sweating should be prevented or reduced.
Pitted Keratolysis
This is a disease of the soles of people who sweat excessively, especially soldiers, caused by Micrococcus sedentarius and characterised by painful, foul-smelling (stale cheese odour), macerated skin with very small pits. Preventing sweating and topical antiseptics (1/10,000 potassium permanganate solution, povidone-iodine) are sufficient.
Trichomycosis Axillaris
Trichomycosis axillaris is a tropical infection caused by bacteria of the genus Corynebacterium, involving the axillary hairs and, more rarely, the pubic hairs. Because it is a bacterial infection, the term trichobacteriosis is recommended instead of trichomycosis. On light microscopy it is characterised by nodular, reddish, yellow or blackish deposits adhering to the hair along the hair shaft.
Ecthyma Gangrenosum
Ecthyma gangrenosum is a disease that tends to occur in people with predisposing conditions such as immunosuppression, malignancy, diabetes and neutropenia, and in damaged tissue such as burns.
The causative agent is Pseudomonas aeruginosa. Pseudomonas species can cause dermatological conditions such as folliculitis, toe-web infection, green nail syndrome, otitis externa and ecthyma gangrenosum. Ecthyma gangrenosum can arise in Pseudomonas sepsis or primarily in the skin. It can be located anywhere, especially the anogenital area and the armpits. It begins as tense, grouped vesicles. The vesicles soon become haemorrhagic and rupture, forming a round, painless, indurated ulcer with a black, necrotic base. There may be erythema around the ulcer.
Rickettsiae
Rickettsiae are obligate intracellular Gram-negative coccobacilli and short bacilli of the Rickettsiaceae family that cause disease in humans and animals; they multiply within the cytosol of endothelial cells. Although they are found worldwide, different genera occur in different geographical regions. They are transmitted to humans by arthropods such as lice, fleas, ticks and mites, in whose digestive systems they live as parasites. For rickettsioses other than epidemic typhus, humans are only a secondary, mostly incidental, host.
Microorganisms of the Rickettsiaceae family were originally thought to be viruses because they are small, do not stain well with Gram stain and can survive in the cytoplasm of eukaryotic cells. However, because they structurally resemble Gram-negative bacilli, contain DNA, RNA, enzymes and ribosomes, and are inhibited by antibiotics, they have been classed as bacteria.
As a result of 16S rRNA sequence-based studies over the last 20 years, the genera Rickettsia, Orientia, Neorickettsia, Wolbachia, Anaplasma and Ehrlichia have been placed within the order Rickettsiales, while Coxiella burnetii has been placed in the gamma group of the proteobacteria.
Rocky Mountain Spotted Fever
Rocky Mountain spotted fever (RMSF) is a condition whose causative agent is Rickettsia rickettsii, and it is the most severe of the rickettsial diseases. It is carried by ticks of the Dermacentor and Amblyomma genera. Its prevalence is highest in the USA, particularly in the south and south-east. Although it is passed transovarially in ticks, uninfected ticks can sometimes acquire the bacterium by feeding on the blood of rickettsaemic small mammals. The host becomes infected in the season when the vector tick is active. The disease is seen most often in children aged 5–9, and the mortality rate is 3–5%. After R. rickettsii is inoculated into the dermis via the secretions of the ticks' salivary glands, it spreads throughout the body by the lymphohaematogenous route. Clinical signs appear after an incubation period of about 1 week (2–14 days). In the early stage of the disease, RMSF presents with a picture that is confused with many viral illnesses. The most common symptoms in the first 3 days are fever (38–40°C), headache, malaise, muscle pain, joint pain, nausea, vomiting and loss of appetite.