Streptococcal intertrigo

• caused - group A streptococci is an under-recognized entity that usually affects young children.

• Infants are particularly vulnerable due to irritation and friction in moist, deep skin folds of the
neck, axillae, antecubital and popliteal fossae, and inguinal region. Sharply demarcated,
intensely erythematous patches or thin plaques are observed in an intertriginous site, often
accompanied by a foul odor.

• In contrast to intertriginous candidiasis, satellite lesions are uncommon.

• Treatment - 10-day course of oral penicillin is usually effective (?) .

Erysipelas
• C ause - group A streptococci - groups G, B, C and D

Occasionally

• S. aureus,   Pneumococcus spp., Klebsiella pneumoniae, Yersinia enterocolitica and Haemophilus

influenzae type b

• Affects - face, lower extremity is now the most common location.

• After an incubation period of 2 to 5 days, there is an abrupt onset of fever, chills, malaise and
nausea.

• A few hours to a day later, a sharply marginated erythematous plaque with a ridge-like border
develops and progressively enlarges.

• It is clearly demarcated from the surrounding skin hot, tense and indurated with non-pitting
edema.

• The affected area is painful to palpation and may burn.

• Regional lymphadenopathy is usually present, with or without lymphangitis. Pustules, vesicles,

bullae and small areas of hemorrhagic necrosis may also form.

• Treatment - A 10- to 14-day course of Penicillin is the treatment of choice for erysipelas
caused by streptococci.
• Although Macrolides such as erythromycin may be used in penicillin-allergic patients, some
strains of Str. pyogenes are macrolide-resistant.

• Erysipelas may recur in patients with abnormal local circulation (e.g. lymphedema), and
penicillin prophylaxis is occasionally required .

• The future development of an effective vaccine against Streptococcus spp. could dramatically

change the epidemiology of the infections caused by this microorganism 3.

Cellulitis
• Cellulitis is an infection of the deep dermis and subcutaneous tissue that manifests as areas of
erythema, swelling, warmth and tenderness

• Caused - group A streptococci or S. aureus

• Clinical features - four of the cardinal signs of inflammation: rubor (erythema), calor (warmth),
dolor (pain), and tumor (swelling). The borders are usually ill-defined and non-palpable.

• In severe infections, vesicles, pustules or necrotic tissue may be present.

• Ascending lymphangitis and regional lymph node involvement may occur. In children, cellulitis
most often affects the head and neck, whereas in adults it tends to involve the extremities.

• Intravenous drug users typically develop cellulitis of the upper extremities (the usual sites of
drug injection).

• Complications are uncommon, potentially including acute glomerulonephritis (if caused by a

nephritogenic strain of streptococcus), lymphadenitis, subacute bacterial endocarditis, and
recurrences related to abnormal lymphatic damage
 • Treatment - typically targeted against group A streptococci and S. aureus. For uncomplicated
cases, a 10-day course of an oral antibiotic that covers these organisms (e.g. dicloxacillin,
cephalexin or clindamycin) is appropriate

Erythrasma
• Caused - Corynebacterium minutissimum

• Lesions- pink to red, well-defined patches

• covered with fine scales and have associated wrinkling

• With time, the red color fades to brown

• The condition is asymptomatic or mildly pruritic. A “disciform” variant can occur in a more
widespread distribution outside the usual intertriginous locations

• Treatment - topical erythromycin, clindamycin, mupirocin, tetracycline and azole antifungals

have all been reported to lead to a rapid resolution of pitted keratolysis.

- Oral erythromycin is occasionally indicated for extensive involvement. Aluminum chloride 20%
solution or (in recalcitrant cases) botulinum toxin can be used to treat the associated hyperhidrosis.
 Pitted keratolysis
Pitted keratolysis is a non-inflammatory bacterial infection of palmoplantar skin

Small (1–7 mm), crater-like depressions are present within the stratum corneum on weight-
bearing regions of the soles and (rarely) the palms.

These pits may coalesce into large craters or rings of craters.

There is usually no associated erythema, and the condition often goes unnoticed by the patient.
Hyperhidrosis and malodor are common associated findings

Treatment - topical erythromycin, clindamycin, mupirocin, tetracycline and azole antifungals have all
been reported to lead to a rapid resolution of pitted keratolysis. Oral erythromycin is occasionally
indicated for extensive involvement.

Aluminum chloride 20% solution or (in recalcitrant cases) Botulinum toxin can be used to treat the
associated hyperhidrosis.

Botriomycosis
• Botryomycosis (named for its characteristic groups of granules that resemble grapes) is a rare,
chronic, purulent and granulomatous bacterial infection that primarily affects the skin . . Caused
- S. aureus

• Biopsy specimens reveal a chronic inflammatory reaction with fibrosis and foreign body giant
cells.

• The (histo) is 1–3 mm granular bodies (grains) that represent bacteria, cells and debris.
 • Treatment - typically treated surgically with debridement or excision in conjunction with
antibiotic therapy. The CO2 laser has also been used successfully.

Cutaneus Tb
Etiology: Mycobacterium tuberculosis complex; Transmission: airborne spread of droplet nuclei from
those with infectious pulmonary Tb. Up to 10% of those infected with MTb will develop active Tb in their
lifetime Incidence of Tb highest in late adolescence and early adulthood One-third of global population
infected. Predisposing factors (exogenous factor) for acquiring MTb infection: poverty, crowding,
HIV/AIDS. Factors for developing tuberculous disease (endogenous):Age, malnutrition, diabetes
mellitus ...

Forms of skin Tb

Verrucosa - Initial papule with violaceous halo. Evolves to hyperkeratotic, warty, firm plaque. Initial
papule ill defined and soft and evolves into well-defined, irregular plaque.
Tb Lupuis Vulgaris - reddish-brown: diascopy (i.e., use of glass slide pressed against skin) reveals an (i.e.,
yellowish-brown) color.

Scrofuloderma - Firm subcutaneous nodule that initially is freely movable; lesion then becomes doughy
and evolves into irregular, deep-seated node or plaque that liquefies and perforates.

Exanthema - Disseminated lesions are minute macules and papules or purpuric lesions. Sometimes
vesicular and crusted.
Laboratory diagnosis

• Dermatopathology PIT: initially nonspecific inflammation; after 3–6 weeks, it becomes more
specific

• Culture Yields mycobacteria (also from lesions of LV and TVC: positive)

• Skin Testing PIT: Patient converts from intradermal skin test negative to positive

• PCR - Can be used to identify M. tuberculosis DNA in tissue specimens

Skin Tb Therapy
Standard antituberculous therapy:

• Isoniazid (5 mg/kg daily) plus

• Rifampin (600 mg/kg daily)

Supplemented in initial phases with:

• Ethambutol (25 mg/kg daily) and/or

• Streptomycin (10–15 mg/kg daily) and/or

• Pyrazinamide (15–30 mg/kg daily)

Leprosy
Leprosy is a chronic infection caused by the acid-fast, rod-shaped bacillus Mycobacterium leprae.
Leprosy can be considered 2 connected diseases that primarily affect superficial tissues, especially the
skin and peripheral nerves. The social and psychological effects of leprosy, as well as its highly visible
debilities and have resulted in a historical stigma associated with leprosy.

It is also known as Hansen disease. This mycobacterium grows extremely slowly and has not been
successfully cultured in vitro.
The incubation period of leprosy is long, ranging from a few months to 20-50 years. The mean
incubation time is estimated to be 10 years for lepromatous leprosy and 4 years for tuberculoid leprosy.

Individuals who have a vigorous cellular immune response to M leprae have the tuberculoid form of
the disease that usually involves the skin and peripheral nerves.

Individuals with minimal cellular immune response have the lepromatous form of the disease, which is
characterized by extensive skin involvement.
Tuberculoid form - Painless skin patch accompanied by loss of sensation but not itchiness (Loss of
sensation is a feature of tuberculoid leprosy, unlike lepromatous leprosy, in which sensation is
preserved.)

Loss of sensation or paresthesias where the affected peripheral nerves are distributed. Wasting
(atrophy) and muscle weakness Foot drop or clawed hands (may result from neuritic pain and rapid
peripheral nerve damage;

Laboratory tests
• Skin biopsy, nasal smears, or both are used to assess for acid-fast bacilli using Fite stain.

• Serologic assays can be used to detect phenolic glycolipid-1 (specific for M leprae) and
lipoarabinomannan (commonly seen in mycobacteria). 
 • Molecular probes detect 40-50% of cases missed on prior histologic evaluation.

• Polymerase chain reaction (PCR): PCR and recombinant DNA technology have allowed for the
development of gene probes with M leprae–specific sequences.

• Lymphocyte migration inhibition test (LMIT): As determined by a lymphocyte transformation

and LMIT, cell-mediated immunity to M leprae is absent in patients with lepromatous leprosy
but present in those with tuberculoid leprosy.

• Contact or family screening for history of leprosy

Management
In response to the increased incidence of dapsone resistance, the WHO introduced a multidrug regimen
in 1981 that includes rifampicin, dapsone, and clofazimine.

WHO still recommends the use of the long-term multidrug regimens whenever possible because they
have been found to be more efficacious.

The goals of surgical treatment in patients with leprosy are to prevent further deterioration, to improve
motor function, and, in some cases, to improve sensation.

Lyme disease
Lyme disease - is a multisystem illness usually caused by infection with the spirochete Borrelia
burgdorferi and the body's immune response to the infection.  The disease is transmitted to humans via
tick bites, from infected ticks of the Genus Ixodes.

Signs and symptoms of Lyme disease vary by disease stage. Physical findings in patients with early
disease are as follows: Flulike illness - Fever, chills,  malaise, myalgias, arthralgia, headache

Tender local adenopathy (local, not diffuse) Erythema migrans (EM) – Rash. With later disseminated
form clinical findings are as follows: EM (single or multiple lesions), Headache; Fever; Tender
adenopathy (regional or generalized); Conjunctivitis (uncommon, never prominent); Carditis (usually
manifests as heart block); Meningismus as a sign of aseptic meningitis; Cranioneuropathy, especially
damage of cranial nerve.
Diagnostic tests
• In endemic areas, patients with probable erythema migrans and a recent source of tick exposure
should be started on treatment without blood tests.

• For serologic testing, the CDC recommends a two-tier testing procedure, as follows:

• Step 1: enzyme immunoassay (EIA) or immunofluorescence assay (IFA) - Total Lyme titer or IgG
and IgM titers

• Step 2: Western blot testing

Management (skin manifestations)

Adult patients with early localized or early disseminated Lyme disease associated with erythema
migrans: Doxycycline, amoxicillin, or cefuroxime axetil

Children under 8 years and pregnant or nursing women with early localized or early disseminated Lyme
disease: Amoxicillin or cefuroxime axetil

Neurologic Lyme disease: IV penicillin, ceftriaxone, or cefotaxime; oral doxycycline, when not
contraindicated, in patients with Lyme-associated meningitis, facial nerve palsy, or radiculitis