1

Pyoderma
ICD-10 L08.0
ICD-9 686.0

Pyoderma means any skin disease that is pyogenic. These include superficial
bacterial infections such as impetigo, impetigo contagiosa, ecthyma, folliculitis,
Bockhart's impetigo, furuncle, carbuncle, tropical ulcer, etc.[1][2] Autoimmune
conditions include pyoderma gangrenosum.[citation needed] Pyoderma affects more than
111 million children worldwide, making it one of the three most common skin
disorders in children along with scabies and tinea.[1]

References

1. Andrews RM, McCarthy J, Carapetis JR, Currie BJ (December 2009). "Skin

disorders, including pyoderma, scabies, and tinea infections". Pediatr. Clin.
North Am. 56 (6): 1421–40. doi:10.1016/j.pcl.2009.09.002.
PMID 19962029.
2. Page 348 in: Fisher, Bruce; Harvey, Richard P.; Champe, Pamela C.
Lippincott's Illustrated Reviews: Microbiology (Lippincott's Illustrated
Reviews Series). Hagerstown, MD: Lippincott Williams & Wilkins. ISBN 0-
7817-8215-5.

Infectious skin disease: Bacterial skin disease (L00–L08, 680–686)

 Staphylococcus
o Staphylococcal scalded skin syndrome
o Impetigo
o Toxic shock syndrome
 Streptococcus
o Impetigo
Gram + Firmicutes o Cutaneous group B streptococcal
infection
o Streptococcal intertrigo
o Cutaneous Streptococcus iniae infection
o Erysipelas / Chronic recurrent erysipelas
o Scarlet fever
 Corynebacterium
 2

o Erythrasma

 Listeriosis

 Clostridium
o Gas gangrene
o Dermatitis gangrenosa
 Mycoplasma infection
 Erysipeloid of Rosenbach

 Mycobacterium-related: Aquarium granuloma

 Borderline lepromatous leprosy
 Borderline leprosy
 Borderline tuberculoid leprosy
 Buruli ulcer
 Erythema induratum
 Histoid leprosy
 Lepromatous leprosy
 Leprosy
 Lichen scrofulosorum
 Lupus vulgaris
 Miliary tuberculosis
 Mycobacterium avium-intracellulare complex
infection
 Mycobacterium haemophilum infection
Actinobacteria
 Mycobacterium kansasii infection
 Papulonecrotic tuberculid
 Primary inoculation tuberculosis
 Rapid growing mycobacterium infection
 Scrofuloderma
 Tuberculosis cutis orificialis
 Tuberculosis verrucosa cutis
 Tuberculous cellulitis
 Tuberculous gumma
 Tuberculoid leprosy

 Cutaneous actinomycosis
 Nocardiosis
 Cutaneous diphtheria infection
 Arcanobacterium haemolyticum infection
 3

 Group JK corynebacterium sepsis

 α: Endemic typhus
 Epidemic typhus
 Scrub typhus
 North Asian tick typhus
 Queensland tick typhus
 Flying squirrel typhus
 Trench fever
 Bacillary angiomatosis
 African tick bite fever
 American tick bite fever
 Rickettsia aeschlimannii infection
 Rickettsialpox
 Rocky Mountain spotted fever
 Human granulocytotropic anaplasmosis
 Human monocytotropic ehrlichiosis
 Flea-borne spotted fever
 Japanese spotted fever
 Mediterranean spotted fever
Gram - Proteobacteria  Flinders Island spotted fever
 Verruga peruana
 Brill–Zinsser disease
 Brucellosis
 Cat scratch disease
 Oroya fever
 Ehrlichiosis ewingii infection

 β: Gonococcemia/Gonorrhea/Primary
gonococcal dermatitis
 Melioidosis
 Cutaneous Pasteurella hemolytica infection
 Meningococcemia
 Glanders
 Chromobacteriosis infection

 γ: Pasteurellosis
 Tularemia
 Vibrio vulnificus infection
 4

 Rhinoscleroma
 Haemophilus influenzae cellulitis
 Pseudomonal pyoderma / Pseudomonas hot-
foot syndrome / Hot tub folliculitis / Ecthyma
gangrenosum / Green nail syndrome
 Q fever
 Salmonellosis
 Shigellosis
 Plague
 Granuloma inguinale
 Chancroid
 Aeromonas infection

 ε: Helicobacter cellulitis

 Syphilid
 Syphilis
 Chancre
 Yaws
 Pinta
 Bejel
Other
 Chlamydial infection
 Leptospirosis
 Rat-bite fever
 Lyme disease
 Lymphogranuloma venereum

 Abscess
o Periapical abscess
 Boil/furuncle
o Hospital furunculosis
 Carbuncle
Unspecified  Cellulitis
pathogen o Paronychia / Pyogenic paronychia
o Perianal cellulitis
 Acute lymphadenitis
 Pilonidal cyst
 Pyoderma
 5

 Folliculitis
o Superficial pustular folliculitis
o Sycosis vulgaris
 Pimple
 Ecthyma
 Pitted keratolysis
 Trichomycosis axillaris
 Necrotizing fascitis
 Gangrene
o Chronic undermining burrowing ulcers
o Fournier gangrene
 Elephantiasis nostras
 Blistering distal dactylitis
 Botryomycosis
 Malakoplakia
 Gram-negative folliculitis
 Gram-negative toe web infection
 Pyomyositis
 Blastomycosis-like pyoderma
 Bullous impetigo
 Chronic lymphangitis
 Recurrent toxin-mediated perineal erythema
 Tick-borne lymphadenopathy
 Tropical ulcer

This page was last modified on 29 January 2014 at 0

 6

Impetigo

Facial impetigo
ICD-10 L01
ICD-9 684
DiseasesDB 6753
MedlinePlus 000860
MeSH D007169

Impetigo /ɪmpɨˈtaɪɡoʊ/ is a highly contagious bacterial skin infection most

common among pre-school children.[1] People who play close contact sports such
as rugby, American football and wrestling are also susceptible, regardless of age.

Antibiotic creams or pills are often used.

Globally impetigo affected approximately 140 million people (2% of the

population) in 2010.[2] Impetigo is not as common in adults. The name derives
from the Latin impetere ("assail"). It is also known as school sores.[3]
 7

Classification

Impetigo on the neck

Impetigo contagiosa

This most common form of impetigo, also called nonbullous impetigo, most often
begins as a red sore near the nose or mouth which soon breaks, leaking pus or
fluid, and forms a honey-colored scab, followed by a red mark which heals without
leaving a scar. Sores are not painful, but may be itchy. Lymph nodes in the
affected area may be swollen, but fever is rare. Touching or scratching the sores
may easily spread the infection to other parts of the body.[4] Ulcerations with
erythema and scarring also may result from scratching or abrading of the skin.

Bullous impetigo

Bullous impetigo
 8

Bullous impetigo, mainly seen in children younger than 2 years, involves painless,
fluid-filled blisters, mostly on the arms, legs and trunk, surrounded by red and
itchy (but not sore) skin. The blisters may be large or small. After they break, they
form yellow scabs.[4]

Ecthyma

In this form of impetigo, painful fluid- or pus-filled sores with redness of skin,
usually on the arms and legs, become ulcers that penetrate deeper into the dermis.
After they break open, they form hard, thick, gray-yellow scabs, which sometimes
leave scars. Ecthyma may be accompanied by swollen lymph nodes in the affected
area.[4]

Causes

It is primarily caused by Staphylococcus aureus, and sometimes by Streptococcus

pyogenes.[5] According to the American Academy of Family Physicians, both
bullous and nonbullous are primarily caused by Staphylococcus aureus, with
Streptococcus also commonly being involved in the nonbullous form."[6]

Transmission

The infection is spread by direct contact with lesions or with nasal carriers. The
incubation period is 1–3 days after exposure to Streptococcus and 4–10 days for
Staphylococcus.[7] Dried streptococci in the air are not infectious to intact skin.
Scratching may spread the lesions.

Diagnosis

Impetigo generally appears as honey-colored scabs formed from dried serum, and
is often found on the arms, legs, or face.[5]

Treatment

For generations, the disease was treated with an application of the antiseptic
gentian violet.[8] Today, topical or oral antibiotics are usually prescribed.
Treatment may involve washing with soap and water and letting the impetigo dry
in the air. Mild cases may be treated with bactericidal ointment, such as mupirocin,
which in some countries may be available over-the-counter. More severe cases
require oral antibiotics, such as dicloxacillin, flucloxacillin or erythromycin.
 9

Alternatively amoxicillin combined with clavulanate potassium, cephalosporins

(1st generation) and many others may also be used as an antibiotic treatment.

Epidemiology

Globally impetigo affected approximately 140 million people (2% of the

population) in 2010.[2]

References

Notes

1. NHS Impetigo
2. Vos, T (Dec 15, 2012). "Years lived with disability (YLDs) for 1160
sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for
the Global Burden of Disease Study 2010.". Lancet 380 (9859): 2163–96.
doi:10.1016/S0140-6736(12)61729-2. PMID 23245607.
3. Impetigo — school sores — Better Health Channel
4. Mayo Clinic staff (5 October 2010). "Impetigo". Mayo Clinic Health
Information. Mayo Clinic. Retrieved 25 August 2012.
5. Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; & Mitchell, Richard N.
(2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier. pp. 843 ISBN
978-1-4160-2973-1
6. Stulberg DL, Penrod MA, Blatny RA (2002). "Common bacterial skin
infections.". American Family Physician 66 (1): 119–24. PMID 12126026.
7. http://www.state.in.us/isdh/23303.htm
8. MacDonald RS (October 2004). "Treatment of impetigo: Paint it blue". BMJ
329 (7472): 979. doi:10.1136/bmj.329.7472.979. PMC 524121.
PMID 15499130.

This page was last modified on 16 May 2014 at 16:27.

 10

Ecthyma
From Wikipedia, the free encyclopedia
Ecthyma
Classification and external resources

Ecthyma
ICD-10 L08.3 (ILDS L08.830)
ICD-9 686.8
DiseasesDB 30731
MedlinePlus 000864
MeSH D004473

Ecthyma is an ulcerative pyoderma of the skin caused by bacteria such as

Pseudomonas (the most common isolate), Streptococcus pyogenes, and
Staphylococcus aureus. Because ecthyma extends into the dermis, it is often
referred to as a deeper form of impetigo.

Causes include insect bites and an ignored minor trauma. Wound cultures usually
reveal that the lesions are teeming with bacteria.

Ecthyma describes ulcers forming under a crusted surface infection. The site may
have been that of an insect bite or of neglected minor trauma. It is treated by
antibiotics like cloxacillin, erythromycin, and cephalexin. Pseudomonas infections
are often treated with two antibiotics due to frequent resistance.

Ecthyma has a predilection for children and elderly individuals. Outbreaks have
also been reported in young military trainees

Ecthyma usually arises on the lower extremities of children, persons with diabetes,
and neglected elderly patients.
 11

During wartime in tropical climates, ecthymatous ulcers are commonly found on

the ankles and dorsa of the feet.

Etiology

Ecthyma can be seen in areas of previously sustained tissue injury (e.g.,

excoriations, insect bites, dermatitis). Ecthyma can be seen in patients who are
immunocompromised (e.g., diabetes, neutropenia, HIV infection). Important
factors contribute to the development of streptococcal pyodermas or ecthyma: ♦
High temperature and humidity ♦ Crowded living conditions ♦ Poor hygiene

Untreated impetigo that progresses to ecthyma most frequently occurs in patients

with poor hygiene.

Some strains of Streptococcus pyogenes have a high affinity for both pharyngeal
mucosa and skin. Pharyngeal colonization of S. pyogenes has been documented in
patients with ecthyma.

Pathophysiology

Ecthyma begins similarly to superficial impetigo. Group A beta-hemolytic

streptococci may initiate the lesion or may secondarily infect preexisting wounds.
Preexisting tissue damage (e.g., excoriations, insect bites, dermatitis) and
immunocompromised states (e.g., diabetes, neutropenia) predispose patients to the
development of ecthyma. Spread of skin streptococci is augmented by crowding
and poor hygiene.

The difference between ecthyma and impetigo is that in impetigo the erosion is at
the stratum corneum, while in ecthyma the ulcer is full thickness and thus heals
with scarring.

There is no racial or sexual dominance in Ecthyma.

Morbidity/Mortality

Ecthyma rarely leads to systemic symptoms or bacteremia. Lesions are painful and
can have associated lymphadenopathy. Secondary lymphangitis and cellulitis can
occur. Ecthyma does heal with scarring. The rate of poststreptococcal
glomerulonephritis is approximately 1%.
 12

References
eMedicine http://emedicine.medscape.com/article/1052279-overview

Infectious skin disease: Bacterial skin disease (L00–L08, 680–686)

 Staphylococcus
o Staphylococcal scalded skin syndrome
o Impetigo
o Toxic shock syndrome
 Streptococcus
o Impetigo
o Cutaneous group B streptococcal infection
o Streptococcal intertrigo
o Cutaneous Streptococcus iniae infection
o Erysipelas / Chronic recurrent erysipelas
o Scarlet fever
Firmicutes
 Corynebacterium
o Erythrasma

 Listeriosis

 Clostridium
o Gas gangrene
o Dermatitis gangrenosa
Gram +  Mycoplasma infection
 Erysipeloid of Rosenbach

 Mycobacterium-related: Aquarium granuloma

 Borderline lepromatous leprosy
 Borderline leprosy
 Borderline tuberculoid leprosy
 Buruli ulcer
 Erythema induratum
 Histoid leprosy
 Lepromatous leprosy
Actinobacteria  Leprosy
 Lichen scrofulosorum
 Lupus vulgaris
 Miliary tuberculosis
 Mycobacterium avium-intracellulare complex infection
 Mycobacterium haemophilum infection
 Mycobacterium kansasii infection
 Papulonecrotic tuberculid
 Primary inoculation tuberculosis
 13

 Rapid growing mycobacterium infection

 Scrofuloderma
 Tuberculosis cutis orificialis
 Tuberculosis verrucosa cutis
 Tuberculous cellulitis
 Tuberculous gumma
 Tuberculoid leprosy

 Cutaneous actinomycosis
 Nocardiosis
 Cutaneous diphtheria infection
 Arcanobacterium haemolyticum infection
 Group JK corynebacterium sepsis

 α: Endemic typhus
 Epidemic typhus
 Scrub typhus
 North Asian tick typhus
 Queensland tick typhus
 Flying squirrel typhus
 Trench fever
 Bacillary angiomatosis
 African tick bite fever
 American tick bite fever
 Rickettsia aeschlimannii infection
 Rickettsialpox
 Rocky Mountain spotted fever
 Human granulocytotropic anaplasmosis
 Human monocytotropic ehrlichiosis
Gram - Proteobacteria  Flea-borne spotted fever
 Japanese spotted fever
 Mediterranean spotted fever
 Flinders Island spotted fever
 Verruga peruana
 Brill–Zinsser disease
 Brucellosis
 Cat scratch disease
 Oroya fever
 Ehrlichiosis ewingii infection

 β: Gonococcemia/Gonorrhea/Primary gonococcal dermatitis

 Melioidosis
 Cutaneous Pasteurella hemolytica infection
 Meningococcemia
 Glanders
 14

 Chromobacteriosis infection

 γ: Pasteurellosis
 Tularemia
 Vibrio vulnificus infection
 Rhinoscleroma
 Haemophilus influenzae cellulitis
 Pseudomonal pyoderma / Pseudomonas hot-foot syndrome /
Hot tub folliculitis / Ecthyma gangrenosum / Green nail
syndrome
 Q fever
 Salmonellosis
 Shigellosis
 Plague
 Granuloma inguinale
 Chancroid
 Aeromonas infection

 ε: Helicobacter cellulitis

 Syphilid
 Syphilis
 Chancre
 Yaws
 Pinta
 Bejel
Other
 Chlamydial infection
 Leptospirosis
 Rat-bite fever
 Lyme disease
 Lymphogranuloma venereum

 Abscess
o Periapical abscess
 Boil/furuncle
o Hospital furunculosis
 Carbuncle
 Cellulitis
Unspecified
o Paronychia / Pyogenic paronychia
pathogen
o Perianal cellulitis
 Acute lymphadenitis
 Pilonidal cyst
 Pyoderma

 Folliculitis
 15

o Superficial pustular folliculitis

o Sycosis vulgaris
 Pimple
 Ecthyma
 Pitted keratolysis
 Trichomycosis axillaris
 Necrotizing fascitis
 Gangrene
o Chronic undermining burrowing ulcers
o Fournier gangrene
 Elephantiasis nostras
 Blistering distal dactylitis
 Botryomycosis
 Malakoplakia
 Gram-negative folliculitis
 Gram-negative toe web infection
 Pyomyositis
 Blastomycosis-like pyoderma
 Bullous impetigo
 Chronic lymphangitis
 Recurrent toxin-mediated perineal erythema
 Tick-borne lymphadenopathy
 Tropical ulcer

This page was last modified on 12 March 2014 at 08:24.

Folliculitis
Classification and external resources
ICD-10 L73.9 (ILDS L73.91)
ICD-9 704.8
DiseasesDB 31367
MedlinePlus 000823
MeSH D005499

Folliculitis (also known as hot tub rash) is the infection and inflammation of one
or more hair follicles. The condition may occur anywhere on the skin with the
exception of the palms of the hands and soles of the feet. They may appear as red
dots that come to white tips on the chest, back, arms, legs, and head.
 16

Causes

Most carbuncles, furuncles, and other cases of folliculitis develop from

Staphylococcus aureus and Pseudomonas aeruginosa.

Folliculitis starts when hair follicles are damaged by friction from clothing, an
insect bite,[1] blockage of the follicle, shaving, or braids too tight and too close to
the scalp. In most cases of folliculitis, the damaged follicles are then infected with
the bacterium Staphylococcus. Folliculitis usually affects those in their early adult
life, and may persist till their early 30s. Warmer weather may worsen the
condition.

Iron deficiency anemia is sometimes associated with chronic cases.

Fungal

 Tinea barbae is similar to barber's itch, but the infection is caused by the
fungus T. rubrum.
 Malassezia folliculitis, formerly known as Pityrosporum folliculitis, is
caused by yeasts (fungi) of the genus Malassezia.

Bacterial

 Hot-tub folliculitis is caused by the bacterium Pseudomonas aeruginosa.[2]

The folliculitis usually occurs after sitting in a hot tub that was not properly
cleaned before use. Symptoms are found around the body parts that sit in the
hot tub—typically the legs, hips, buttocks, and surrounding areas. Symptoms
are typically amplified around regions that were covered by wet clothing,
such as bathing suits.
 Sycosis vulgaris, Sycosis barbae or Barber's itch is a staphylococcus
infection of the hair follicles in the bearded area of the face, usually the
upper lip. Shaving aggravates the condition.
 Gram-negative folliculitis may appear after prolonged acne treatment with
antibiotics.[3]

Viral

 Herpetic folliculitis may occur when Herpes Simplex Virus infection

spreads to nearby hair follicles - mostly around the mouth.

Non-infectious
 17

 Pseudofolliculitis barbae is a disorder occurring when hair curves back into

the skin and causes inflammation.
 Eosinophilic folliculitis may appear in persons with impaired immune
systems.
 Folliculitis decalvans or tufted folliculitis usually affects scalp. Several
hairs arise from the same hair follicle. Scarring and permanent hair loss may
follow. The cause is unknown.
 Folliculitis keloidalis scarring on the nape of the neck, most common among
males of curly hair.
 Oil folliculitis is inflammation of hair follicles due to exposure to various
oils and typically occurs on forearms or thighs. It is common in refinery
workers, road workers, mechanics, and sheep shearers. Even makeup may
cause it.
 Malignancy may also be represented by recalcitrant cases.[4]

Symptoms

 rash (reddened skin area)

 itching skin
 pimples or pustules located around a hair follicle
o may crust over
o typically occur on neck, armpit, or groin area
o may present as genital lesions
 spreading from leg to arm to body through improper treatment of antibiotics

Treatment

1. Topical antiseptic treatment is adequate for most cases

2. Topical antibiotics such as mupirocin or neomycin containing ointment
3. Some patients may benefit from systemic narrow-spectrum penicillinase-
resistant penicillins (such as dicloxacillin in US, or flucloxacillin in UK)
4. Fungal folliculitis can worsen with antibiotics and may require an oral
antifungal such as Fluconazole. Topical antifungals such as Econazole
Nitrate may also be effective.

Folliculitis may reoccur even after symptoms have gone away.

References
1. "NHS Direct".
2. MedlinePlus Encyclopedia Hot tub folliculitis
 18

3. "Severe Acne: 4 types". American Academy of Dermatology. Archived from the original
on December 15, 2010. Retrieved December 15, 2010.
4. Folliculitis, follicular mucinosis, and papular mucinosis as a presentation of chronic
myelomonocytic leukemia. Rashid R, Hymes S. Dermatol Online J. 2009 May
15;15(5):16.

Diseases of the skin and appendages by morphology

Disorders of skin appendages (L60–L75, 703–706)
Inflammation
Categories:

 Conditions of the skin appendages

 Bacterium-related cutaneous conditions

This page was last modified on 16 April 2014 at 20:43.

Superficial pustular folliculitis

Classification and external resources
ICD-10 L01.0

Superficial pustular folliculitis (also known as "Impetigo of Bockhart"[1] and

"Superficial folliculitis"[1]) is a superifical folliculitis with thin-walled pustules at
the follicular openings.[2]:252

References
1. Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume
Set. St. Louis: Mosby. p. 518. ISBN 1-4160-2999-0.
2. James, William D.; Berger, Timothy G.; et al. (2006). Andrews' Diseases of the Skin:
clinical Dermatology. Saunders Elsevier. ISBN 0-7216-2921-0.

Infectious skin disease: Bacterial skin disease (L00–L08, 680–686)

Disorders of skin appendages (L60–L75, 703–706)

This page was last modified on 5 November 2013 at 14:57.

 19

Boil
Classification and external resources

Furuncle
ICD-10 L02
ICD-9 680.9
DiseasesDB 29434
MedlinePlus 001474 000825
MeSH D005667

A boil, also called a furuncle, is a deep folliculitis, infection of the hair follicle. It
is most commonly caused by infection by the bacterium Staphylococcus aureus,
resulting in a painful swollen area on the skin caused by an accumulation of pus
and dead tissue.[1] Individual boils clustered together are called carbuncles.[2] Most
human infections are caused by coagulase-positive S. aureus strains, notable for
the bacteria's ability to produce coagulase, an enzyme that can clot blood. Almost
any organ system can be infected by S. aureus.

Signs and issues

Boils are bumpy, red, pus-filled lumps around a hair follicle that are tender, warm,
and very painful. They range from pea-sized to golf ball-sized. A yellow or white
point at the center of the lump can be seen when the boil is ready to drain or
discharge pus. In a severe infection, an individual may experience fever, swollen
lymph nodes, and fatigue. A recurring boil is called chronic furunculosis.[1][3][4][5]
Skin infections tend to be recurrent in many patients and often spread to other
family members. Systemic factors that lower resistance commonly are detectable,
including: diabetes, obesity, and hematologic disorders.[6]
 20

Causes
Usually, the cause is bacteria such as staphylococci that are present on the skin.
Bacterial colonization begins in the hair follicles and can cause local cellulitis and
inflammation.[1][4][5] Additionally, myiasis caused by the Tumbu fly in Africa
usually presents with cutaneous furuncles.[7] Risk factors for furunculosis include
bacterial carriage in the nostrils, diabetes mellitus, obesity, lymphoproliferative
neoplasms, malnutrition, and use of immunosuppressive drugs.[8] Patients with
recurrent boils are as well more likely to have a positive family history, take
antibiotics, and to have been hospitalized, anemic, or diabetic; they are also more
likely to have associated skin diseases and multiple lesions.[9]

Complications
The most common complications of boils are scarring and infection or abscess of
the skin, spinal cord, brain, kidneys, or other organs. Infections may also spread to
the bloodstream (bacteremia) and become life-threatening.[4][5] S. aureus strains
first infect the skin and its structures (for example, sebaceous glands, hair follicles)
or invade damaged skin (cuts, abrasions). Sometimes the infections are relatively
limited (such as a stye, boil, furuncle, or carbuncle), but other times they may
spread to other skin areas (causing cellulitis, folliculitis, or impetigo).
Unfortunately, these bacteria can reach the bloodstream (bacteremia) and end up in
many different body sites, causing infections (wound infections, abscesses,
osteomyelitis, endocarditis, pneumonia)[10] that may severely harm or kill the
infected person. S. aureus strains also produce enzymes and exotoxins that likely
cause or increase the severity of certain diseases. Such diseases include food
poisoning, septic shock, toxic shock syndrome, and scalded skin syndrome.[11]
Almost any organ system can be infected by S. aureus.

Treatment
A small boil may burst and drain on its own without any assistance.[12]

Furuncles at risk of leading to serious complications should be incised and drained.

These include furuncles that are unusually large, last longer than two weeks, or are
located in the middle of the face or near the spine.[1][5] Fever and chills are signs of
sepsis that require immediate treatment. [13]

Antibiotic therapy is advisable for large or recurrent boils or those that occur in
sensitive areas (such as around or in the nostrils or in the ear).[1][3][4][5]
 21

Staphylococcus aureus has the ability to acquire antimicrobial resistance easily,

making treatment difficult. Knowledge of the antimicrobial resistance of S. aureus
is important in the selection of antimicrobials for treatment.[14] Poor personal
hygiene being common, the role of nasal S. aureus carrier may differ from
communities with good hygienic practices. Staphylococcus aureus re-infection
may result from contact with infected family members, contaminated fomites, or
from other extra-nasal sites. This raises a suggestion to treat household contacts
and close contacts if recurrence persists, because it is likely that one or more
contacts are asymptomatic carriers of S. aureus. In addition to the increase in the
cost of treatment in poor countries, the possibility of developing drug resistance
must be considered. The most important independent predictor of recurrence is a
positive family history. Boils are spread among individuals by touching or bursting
a boil. The role of iron deficiency anemia in recurrent furunculosis was
demonstrated, all patients were free from recurrence during the six months follow-
up period after iron supplementation.[15] A variety of host factors, such as abnormal
neutrophil chemotaxis, deficient intra-cellular killing, and immuno-deficient states
are of importance in a minority of patients with recurrent furunculosis. [16] Health
education about sound personal hygiene and correction of anemia should be
mandatory in management of furunculosis.[9] It was found that recurrence was
significantly associated with poor personal hygiene.[17] A previous study reported
that MRSA infection was significantly associated with poor personal hygiene.[citation
needed]
It was reported that frequent hand and body washing with water and
antimicrobial soap solution[citation needed] decreases staphylococcus skin colonization.
Previous use of antibiotics is associated with a high risk of recurrence. This may be
due to the development of resistance to the antibiotics used.[18] An associated skin
disease favors recurrence. This may be attributed to the persistent colonization of
abnormal skin with S. aureus strains, such as is the case in patients with atopic
dermatitis.[18]

References
1. MedlinePlus Encyclopedia Furuncle
2. MedlinePlus Encyclopedia Carbuncle
3. Blume JE, Levine EG, Heymann WR (2003). "Bacterial diseases". In Bolognia JL,
Jorizzo JL, Rapini RP. Dermatology. Mosby. p. 1126. ISBN 0-323-02409-2.
4. Habif, TP (2004). "Furuncles and carbuncles". Clinical Dermatology: A Color Guide to
Diagnosis and Therapy (4th ed.). Philadelphia PA: Mosby.
5. Wolf K, et al. (2005). "Section 22. Bacterial infections involving the skin". Fitzpatrick's
Color Atlas & Synopsis of Clinical Dermatology (5th ed.). McGraw-Hill.
 22

6. Steele RW, Laner SA, Graves MH (February 1980). "Recurrent staphylococcal infection
in families". Arch Dermatol 116 (2): 189–90. doi:10.1001/archderm.116.2.189.
PMID 7356349.
7. Tamir J, Haik J, Schwartz E (2003). "Myiasis with Lund's fly (Cordylobia rodhaini) in
travelers". J Travel Med 10 (5): 293–5. PMID 14531984.
8. Scheinfeld NS (2007). "Furunculosis". Consultant 47 (2).
9. El-Gilany AH, Fathy H (January 2009). "Risk factors of recurrent furunculosis".
Dermatol Online J 15 (1): 16. PMID 19281721.
10. Lina G, Piémont Y, Godail-Gamot F, Bes M, Peter MO, Gauduchon V, Vandenesch F,
Etienne J (November 1999). "Involvement of Panton-Valentine leukocidin-producing
Staphylococcus aureus in primary skin infections and pneumonia". Clin Infect Dis 29 (5):
1128–32. doi:10.1086/313461. PMID 10524952.
11. http://www.emedicinehealth.com/staphylococcus/page4_em.htm
12. Mayo Clinic
13. ref=http://www.mayoclinic.com/health/boils-and-
carbuncles/DS00466/DSECTION=complications
14. Nagaraju U, Bhat G, Kuruvila M, Pai GS, Babu RP (2004). "Methicillin-resistant
staphylococcus aureus in community-acquired pyoderma". Int J Dermatol 43 (6): 412–4.
doi:10.1111/j.1365-4632.2004.02138.x. PMID 15186220.
15. Demircay Z, Eksioglu-Demiralp E, Ergun T, et al. (1998). "Phagocytosis and oxidative
burst by neutrophils in patients with recurrent furunculosis". Br J Dermatol 138 (6):
1036–8. doi:10.1046/j.1365-2133.1998.02274.x. PMID 9747369.
16. Fitzpatrick JE (1996). "Bacterial infection". In Fitzpatrick JE, Aeling JL. Dermatology
secrets. Hanley and Belfus. p. 174.
17. Shah KS, Hansotia MF (2005). "Personal hygiene". In Iliyas M. Community medicine
and public health. p. 557.
18. Laube S, Farrell M (2002). "Bacterial skin infection in the elderly: diagnosis and
treatment". Drugs and Aging 19 (5): 331–42. doi:10.2165/00002512-200219050-00002.
PMID 12093320.

Diseases of the skin and appendages by morphology

Infectious skin disease: Bacterial skin disease (L00–L08, 680–686)

This page was last modified on 10 May 2014 at 05:19.

 23

Carbuncle

A carbuncle (/ˈkɑːbʌŋkəl/ or /ˈkɑrbʌŋkəl/) is an abscess larger than a boil, usually

with one or more openings draining pus onto the skin. It is usually caused by
bacterial infection, most commonly Staphylococcus aureus, or Streptococcus
pyogenes, which can turn lethal. However, the presence of carbuncles is actually a
sign that the immune system is working.[1] The infection is contagious and may
spread to other areas of the body, or other people; those living in the same
residence may develop carbuncles at the same time.

Presentation
A carbuncle is made up of several skin boils. The infected mass is filled with fluid,
pus and dead tissue. Fluid may drain out of the carbuncle, but sometimes the mass
is so deep that it cannot drain on its own. Carbuncles may develop anywhere, but
they are most common on the back and the nape of the neck.

The carbuncle may be the size of a pea or as large as a golf ball. It may be red and
irritated, and might hurt when touched. It may also grow very fast and have a white
or yellow center. It may crust or spread to other skin areas. Sometimes other
symptoms may occur, such as fatigue, fever and a general discomfort or sick
feeling. Itching may occur before the carbuncle develops.

Causes
Often, the initial cause of a carbuncle cannot be determined. Triggers that make
carbuncle infections more likely include rashes such as folliculitis; friction from
clothing or shaving; having the hair pulled out, such as sites where clothing or
furniture grab at hairs; generally poor hygiene; poor nutrition; or weakening of
immunity. Poor nutrition may be an important factor. For example, persons with
diabetes and immune system diseases are more likely to develop infections
(especially bacterial infections of the leg or foot).
 24

Society and culture

Etymology

The word is believed to have originated from the Latin: carbunculus, originally a
small coal; diminutive of carbon-, carbo: charcoal or ember, but also a carbuncle
stone, "precious stones of a red or fiery colour", usually garnets.[2]

Monstrous carbuncle

In 1984 Charles, Prince of Wales famously described the proposed Sainsbury

Wing extension to the National Gallery in London as a "monstrous carbuncle on
the face of a much-loved and elegant friend",[3] a term now widely used to describe
architecture, particularly modernist architecture, unsympathetic to its
surroundings.[4][5]

References
1. "Carbuncle - PubMed Health". National Institute of Health. 2007-04-12. Retrieved 2011-
05-10.
2. OED, "Carbuncle": 1) stone, 3) medical
3. "A speech by HRH The Prince of Wales at the 150th anniversary of the Royal Institute of
British Architects (RIBA), Royal Gala Evening at Hampton Court Palace". Retrieved
2007-06-16.
4. "Prince's new architecture blast". BBC News. 2005-02-21. Retrieved 2007-06-16.
5. "No cash for 'highest slum'". BBC News. 2001-02-09. Retrieved 2007-06-16.

Infectious skin disease: Bacterial skin disease (L00–L08, 680–686)

 Staphylococcus
o Staphylococcal scalded skin syndrome
o Impetigo
o Toxic shock syndrome
 Streptococcus
o Impetigo
o Cutaneous group B streptococcal infection
Gram + Firmicutes
o Streptococcal intertrigo
o Cutaneous Streptococcus iniae infection
o Erysipelas / Chronic recurrent erysipelas
o Scarlet fever
 Corynebacterium
o Erythrasma
 25

 Listeriosis

 Clostridium
o Gas gangrene
o Dermatitis gangrenosa
 Mycoplasma infection
 Erysipeloid of Rosenbach

 Mycobacterium-related: Aquarium granuloma

 Borderline lepromatous leprosy
 Borderline leprosy
 Borderline tuberculoid leprosy
 Buruli ulcer
 Erythema induratum
 Histoid leprosy
 Lepromatous leprosy
 Leprosy
 Lichen scrofulosorum
 Lupus vulgaris
 Miliary tuberculosis
 Mycobacterium avium-intracellulare complex infection
 Mycobacterium haemophilum infection
 Mycobacterium kansasii infection
Actinobacteria  Papulonecrotic tuberculid
 Primary inoculation tuberculosis
 Rapid growing mycobacterium infection
 Scrofuloderma
 Tuberculosis cutis orificialis
 Tuberculosis verrucosa cutis
 Tuberculous cellulitis
 Tuberculous gumma
 Tuberculoid leprosy

 Cutaneous actinomycosis
 Nocardiosis
 Cutaneous diphtheria infection
 Arcanobacterium haemolyticum infection
 Group JK corynebacterium sepsis

 α: Endemic typhus
 Epidemic typhus
 Scrub typhus
Gram - Proteobacteria
 North Asian tick typhus
 Queensland tick typhus
 Flying squirrel typhus
 26

 Trench fever
 Bacillary angiomatosis
 African tick bite fever
 American tick bite fever
 Rickettsia aeschlimannii infection
 Rickettsialpox
 Rocky Mountain spotted fever
 Human granulocytotropic anaplasmosis
 Human monocytotropic ehrlichiosis
 Flea-borne spotted fever
 Japanese spotted fever
 Mediterranean spotted fever
 Flinders Island spotted fever
 Verruga peruana
 Brill–Zinsser disease
 Brucellosis
 Cat scratch disease
 Oroya fever
 Ehrlichiosis ewingii infection

 β: Gonococcemia/Gonorrhea/Primary gonococcal dermatitis

 Melioidosis
 Cutaneous Pasteurella hemolytica infection
 Meningococcemia
 Glanders
 Chromobacteriosis infection

 γ: Pasteurellosis
 Tularemia
 Vibrio vulnificus infection
 Rhinoscleroma
 Haemophilus influenzae cellulitis
 Pseudomonal pyoderma / Pseudomonas hot-foot syndrome /
Hot tub folliculitis / Ecthyma gangrenosum / Green nail
syndrome
 Q fever
 Salmonellosis
 Shigellosis
 Plague
 Granuloma inguinale
 Chancroid
 Aeromonas infection

 ε: Helicobacter cellulitis

Other  Syphilid
 27

 Syphilis
 Chancre
 Yaws
 Pinta
 Bejel
 Chlamydial infection
 Leptospirosis
 Rat-bite fever
 Lyme disease
 Lymphogranuloma venereum

 Abscess
o Periapical abscess
 Boil/furuncle
o Hospital furunculosis
 Carbuncle
 Cellulitis
o Paronychia / Pyogenic paronychia
o Perianal cellulitis
 Acute lymphadenitis
 Pilonidal cyst
 Pyoderma

 Folliculitis
o Superficial pustular folliculitis
o Sycosis vulgaris
 Pimple
 Ecthyma
Unspecified
 Pitted keratolysis
pathogen
 Trichomycosis axillaris
 Necrotizing fascitis
 Gangrene
o Chronic undermining burrowing ulcers
o Fournier gangrene
 Elephantiasis nostras
 Blistering distal dactylitis
 Botryomycosis
 Malakoplakia
 Gram-negative folliculitis
 Gram-negative toe web infection
 Pyomyositis
 Blastomycosis-like pyoderma
 Bullous impetigo
 Chronic lymphangitis
 Recurrent toxin-mediated perineal erythema
 Tick-borne lymphadenopathy
 28

 Tropical ulcer

This page was last modified on 12 May 2014 at 15:13.

Tropical ulcer
Classification and external resources
ICD-10 L98.4 (ILDS L98.440)

Tropical ulcer (also known as Aden ulcer, Jungle rot, Malabar ulcer, and
Tropical phagedena)[1] is a lesion occurring in cutaneous leishmaniasis. It is
caused by a variety of microorganisms, including mycobacteria. It is common in
tropical climates.[2]

Ulcers occur on exposed parts of the body, primarily on anterolateral aspect of the
lower limbs and may erode muscles and tendons, and sometimes, the bones.[3]
These lesions may frequently develop on preexisting abrasions or sores sometimes
beginning from a mere scratch.[1]

Clinical features

This image depicted the left foot of a patient, which displayed this acute tropical ulcer upon his
admission to toborra Goroka Hospital, in Goroka, New Guinea.

The vast majority of the tropical ulcers occur below the knee, usually around the
ankle. They may also occur on arms. They are often initiated by minor trauma, and
subjects with poor nutrition are at higher risk. Once developed, the ulcer may
become chronic and stable, but also it can run a destructive course with deep tissue
invasion, osteitis, and risk of amputation. Unlike Buruli ulcer, tropical ulcers are
very painful.[4] Lesions begin with inflammatory papules that progress into vesicles
 29

and rupture with the formation of an ulcer.[1] Chronic ulcers involve larger area and
may eventually develop into squamous epithelioma after 10 years or more [5]

Microbiology

There is now considerable evidence to suggest that this disease is an infection. F.

ulcerans has recently been isolated from lesions and is unique to tropical ulcers. [5]
Early lesions may be colonized or infected by, Bacillus fusiformis (Vincent's
organism), anaerobes and spirochaetes. Later, tropical ulcer may become infected
with a variety of organisms, notably, staphylococci and/or streptococci.[4] The
condition has been shown to be transmissible by inoculation of material from
affected patients. [5]

Epidemiology

Tropical ulcer has been described as a disease of the 'poor and hungry'; it may be
that slowly improving socioeconomic conditions and nutrition account for its
decline[citation needed]. Urbanization of populations could be another factor, as tropical
ulcer is usually a rural problem. More widespread use of shoes and socks also
provides protection from initiating trauma[citation needed]. Despite this, susceptible
individuals still develop tropical ulcers. Sometimes outbreaks can occur; one was
recorded in Tanzania in sugarcane workers cutting the crops while barefoot.
Tropical ulcers can also occur to the visitors of tropics.[4] The disease is most
common in native laborers and in schoolchildren of the tropics and subtropics
during the rainy season and is caused in many instances by the bites of insects,
poor hygiene, and pyogenic infections.[1] Males are more commonly infected than
females.[5]

Geographic distribution

Tropical ulcer is seen throughout the tropics and subtropics. In some of these
countries, such as northern Papua New Guinea, it is the most common skin disease.
It is also a frequent problem amongst the homeless in tropical countries, as both the
exposure to the elements and their unhygienic lifestyle make them a high-risk
population. Open skin from intravenous drug use often exacerbates the
problem.[citation needed]

Treatment

 Antibiotics: In early stages, penicillin or metronidazole are used in

combination with topical antiseptic.[5]
 30

 Improved nutrition and vitamins.[5]

 Non-adherent dressings and elevation of limbs.[5]
 Large infected ulcers may require debridement under anesthesia.
 Skin grafting may be helpful in advanced cases to ensure the lesion does not
progress to chronic stage.[5]
 In extreme cases, amputation is necessary.

Prevention

Adequate footwear is important to prevent trauma. General good health and

nutrition also reduce ulcer risk. Adequate and prompt cleansing and treatment of
ankle and leg skin breaks is also important.[citation needed] Improving hygiene and
nutrition may help to prevent tropical ulcers.[1]

Complications

 Skin color: Rarely, Jungle rot will result in complications with skin
pigmentation. It has been known to leave the victim with different colors
such as bright red, blue, green, and a rare color change of orange.
 Deep tissue invasion: Often with bone involvement, and potentially leading
to amputation.[citation needed]
 Chronic ulceration.[citation needed]
 Recurrent ulceration.[citation needed]
 Squamous cell carcinoma may occasionally develop, usually in chronic
cases, and at the edge of ulcer.[citation needed]
 Tetanus: by entry of tetanus bacilli through the ulcer.[citation needed]

References
1. Odom, Richard B.; Davidsohn, Israel; James, William D.; Henry, John Bernard; Berger,
Timothy G.; Clinical diagnosis by laboratory methods; Dirk M. Elston (2006). Andrews'
diseases of the skin: clinical dermatology. Saunders Elsevier. pp. 276–267. ISBN 0-7216-
2921-0.
2. Stedman's Electronic Medical Dictionary
3. Medcyclopedia-Tropical ulcer
4. Gill, Geoffrey V.; Geoff Gill; Beeching, N. (2004). Lecture notes on tropical medicine.
Oxford: Blackwell Science. ISBN 0-632-06496-X.
5. Tropical dermatology. 2001. pp. 310–313. ISBN 9781570594939.

Sources
 31

 Adriaans B, Hay R, Drasar B, Robinson D (January 1987). "The infectious aetiology of

tropical ulcer--a study of the role of anaerobic bacteria". Br. J. Dermatol. 116 (1): 31–7.
doi:10.1111/j.1365-2133.1987.tb05788.x. PMID 3814513.
 Aribi M, Poirriez J, Breuillard F (June 1999). "Guess what! Tropical phagedenic ulcer".
Eur J Dermatol 9 (4): 321–2. PMID 10465620.
 MacDonald P (March 2003). "Tropical ulcers: a condition still hidden from the western
world". J Wound Care 12 (3): 85–90. PMID 12677870.

This page was last modified on 31 January 2014 at 02:50.

Pyoderma gangrenosum

Pyoderma gangrenosum on the leg of a patient with Crohn's disease.

ICD-10 L88
ICD-9 686.01
DiseasesDB 11064
MeSH D017511

Pyoderma gangrenosum is a condition that causes tissue to become necrotic,

causing deep ulcers that usually occur on the legs. When they occur, they can lead
to chronic wounds. Ulcers usually initially look like small bug bites or papules, and
they progress to larger ulcers. Though the wounds rarely lead to death, they can
cause pain and scarring.

The disease was identified in 1930. It affects approximately 1 person in 100,000 in

the population. Though it can affect people of any age, it mostly affects people in
their 40s and 50s.[1]

Types
 32

Pyoderma gangrenosum

There are two main types of pyoderma gangrenosum:[1]

 the 'typical' ulcerative form, which occurs in the legs

 an 'atypical' form that is more superficial and occurs in the hands and other
parts of the body

Other variations are:[2]

 Peristomal pyoderma gangrenosum is 15% of all cases of pyoderma

 Bullous pyoderma gangrenosum
 Pustular pyoderma gangrenosum[3]
 Vegetative pyoderma gangrenosum[4]

Causes

Though the etiology is not well understood, the disease is thought to be due to
immune system dysfunction, and particularly improper functioning of neutrophils.
At least half of all pyoderma gangrenosum patients also suffer from illnesses that
affect their systemic function.[1] For instance, ulcerative colitis, rheumatoid
arthritis, and multiple myeloma (MM) sufferers have the condition. It can also be
part of a syndrome, for instance in PAPA syndrome. Major and minor trauma are
also believed to play a role.[5]

Associations

The common conditions associated with pyoderma gangrenosum are:[6]

 Inflammatory bowel disease:

o Ulcerative colitis
o Crohn's Disease
 Arthritides:
o Rheumatoid arthritis
 33

o Seronegative arthritis
 Haematological disease:
[7]
o Myelocytic leukemia
o Hairy cell leukemia
o Myelofibrosis
o Myeloid metaplasia
o Monoclonal gammopathy
 Autoinflammatory Disease:
o Pyogenic sterile arthritis, pyoderma gangrenosum, and acne syndrome
(PAPA syndrome)

Also Wegener's Granulomatosis[8]

Treatment

First-line therapy for disseminated or localized instances of pyoderma

gangrenosum is systemic treatment by corticosteroids and cyclosporine. Topical
application of Clobetasol, Mupirocin, and Gentamicin alternated with Tacrolimus
can be effective.

Papules that begin as small "spouts" can be treated with Dakins Solution to prevent
infection and entire wounds cluster also benefit from this disinfectant. Wet to dry
applications of Dakins can defeat spread of interior infection. Heavy drainage can
be offset with Coban dressings. Grafting is not recommended due to tissue
necrosis.

If ineffective, alternative therapeutic procedures include systemic treatment with

corticosteroids and mycophenolate mofetil; mycophenolate mofetil and
cyclosporine; tacrolimus; thalidomide; infliximab; or plasmapheresis.[9]

References
1. Jackson, J Mark; Callen, Jeffrey P (April 23, 2012). "Pyoderma Gangrenosum". In
Elston, Dirk M. Emedicine.
2. Brooklyn, T.; Dunnill, G; Probert, C (2006). "Diagnosis and treatment of pyoderma
gangrenosum". BMJ 333 (7560): 181–4. doi:10.1136/bmj.333.7560.181. PMC 1513476.
PMID 16858047.
3. Shankar, S.; Sterling, J. C.; Rytina, E. (2003). "Pustular pyoderma gangrenosum".
Clinical and Experimental Dermatology 28 (6): 600–3. doi:10.1046/j.1365-
2230.2003.01418.x. PMID 14616824.
 34

4. Langan, Sinead M.; Powell, Frank C. (2005). "Vegetative pyoderma gangrenosum: A

report of two new cases and a review of the literature". International Journal of
Dermatology 44 (8): 623–9. doi:10.1111/j.1365-4632.2005.02591.x. PMID 16101860.
5. Rashid, RM (2008). "Seat belt pyoderma gangrenosum: Minor pressure as a causative
factor". Journal of the European Academy of Dermatology and Venereology 22 (10):
1273–4. doi:10.1111/j.1468-3083.2008.02626.x. PMID 18837131.
6. Brooklyn, Trevor; Giles Dunnill, Chris Probert (2006). "Diagnosis and treatment of
pyoderma gangrenosum". British Medical Journal 333: 181–184.
doi:10.1136/bmj.333.7560.181. PMC 1513476. PMID 16858047. Retrieved 31 December
2013.

Tendas, Andrea; Niscola P, Barbati R, Abruzzese E, Cuppelli L, Giovannini M, Scaramucci

L, Fratoni S, Ales M, Neri B, Morino L, Dentamaro T, De Fabritiis P. (May 2011). "Tattoo
related pyoderma/ectyma gangrenous as presenting feature of relapsed acute myeloid
leukaemia: an exceptionally rare observation.". Injury 42 (5): 546–7.
doi:10.1016/j.injury.2010.08.014.

Ponniah, I.; Shaheen, Ahmed; Shankar, K.A.; Kumaran, M.G. (2005). "Wegener's
granulomatosis: The current understanding". Oral Surgery, Oral Medicine, Oral Pathology,
Oral Radiology, and Endodontology 100 (3): 265–70. doi:10.1016/j.tripleo.2005.04.018.
PMID 16122651.

7. Reichrath, Jörg; Bens, Guido; Bonowitz, Anette; Tilgen, Wolfgang (2005). "Treatment
recommendations for pyoderma gangrenosum: An evidence-based review of the literature
based on more than 350 patients". Journal of the American Academy of Dermatology 53
(2): 273–83. doi:10.1016/j.jaad.2004.10.006. PMID 16021123.

Neutrophilic and eosinophilic dermatoses (L98.2-3)

[Cutaneous keratosis, ulcer, atrophy, and necrobiosis (L82–L94, 700–701.5)
Paraneoplastic syndromes

 This page was last modified on 2 February 2014 at 08:03.

 35

Scabies

A photomicrograph of an itch mite (Sarcoptes scabiei)

ICD-10 B86
ICD-9 133.0
DiseasesDB 11841
MedlinePlus 000830
MeSH D012532

Scabies (from Latin: scabere, "to scratch"),[1] also known colloquially as the
seven-year itch,[2] is a contagious skin infection caused by the mite Sarcoptes
scabiei. The mite is a tiny, and usually not directly visible, parasite which burrows
under the host's skin, causing intense allergic itching. The infection in animals
other than humans is caused by a different but related mite species, and is called
sarcoptic mange.

Scabies is classified by the World Health Organization as a water-related disease.[3]

The disease may be transmitted from objects, but is most often transmitted by
direct skin-to-skin contact, with a higher risk with prolonged contact. Initial
infections require four to six weeks to become symptomatic. Reinfection, however,
may manifest symptoms within as few as 24 hours. Because the symptoms are
allergic, their delay in onset is often mirrored by a significant delay in relief after
the parasites have been eradicated. Crusted scabies, formerly known as Norwegian
scabies, is a more severe form of the infection often associated with
immunosuppression.
 36

Scabies is one of the three most common skin disorders in children, along with
tinea and pyoderma.[4] As of 2010 it affects approximately 100 million people
(1.5% of the population) and is equally common in both genders.[5]

Signs and symptoms

The characteristic symptoms of a scabies infection include intense itching and

superficial burrows.[6] The burrow tracks are often linear, to the point that a neat
"line" of four or more closely placed and equally developed mosquito-like "bites"
is almost diagnostic of the disease.

Itching

In the classic scenario, the itch is made worse by warmth, and is usually
experienced as being worse at night, possibly because there are fewer
distractions.[6] As a symptom, it is less common in the elderly.[6]

Rash

Commonly involved sites of rashes of scabies[7]

The superficial burrows of scabies usually occur in the area of the hands, feet,
wrists, elbows, back, buttocks, and external genitals.[6] Except in infants and the
immunosuppressed, infection generally does not occur in the skin of the face or
scalp. The burrows are created by excavation of the adult mite in the epidermis.[6]

In most people, the trails of the burrowing mites are linear or s-shaped tracks in the
skin often accompanied by rows of small, pimple-like mosquito or insect bites.
These signs are often found in crevices of the body, such as on the webs of fingers
and toes, around the genital area, and under the breasts of women.[8]
 37

Symptoms typically appear two to six weeks after infestation for individuals never
before exposed to scabies. For those having been previously exposed, the
symptoms can appear within several days after infestation. However, it is not
unknown for symptoms to appear after several months or years.[9] Acropustulosis,
or blisters and pustules on the palms and soles of the feet, are characteristic
symptoms of scabies in infants.[8]

Scabies of the foot

Scabies of the arm

Scabies of the hand

Scabies of the finger

Crusted scabies
 38

Crusted scabies in a person with AIDS

The elderly and people with an impaired immune system, such as HIV, cancer, or
those on immunosuppressive medications, are susceptible to crusted scabies
(formerly called Norwegian scabies).[6][9][10] On those with weaker immune
systems, the host becomes a more fertile breeding ground for the mites, which
spread over the host's body, except the face. Sufferers of crusted scabies exhibit
scaly rashes, slight itching, and thick crusts of skin that contain thousands of
mites.[11] Such areas make eradication of mites particularly difficult, as the crusts
protect the mites from topical miticides, necessitating prolonged treatment of these
areas.

Cause

Main article: Sarcoptes scabiei

Video of the Sarcoptes scabiei mite

 39

Life cycle of scabies[7]

In the 18th century, Italian biologist Diacinto Cestoni (1637–1718) described the
mite now called Sarcoptes scabiei, variety hominis, as the cause of scabies.
Sarcoptes is a genus of skin parasites and part of the larger family of mites
collectively known as scab mites. These organisms have eight legs as adults, and
are placed in the same phylogenetic class (Arachnida) as spiders and ticks.

Sarcoptes scabiei mites are microscopic, but sometimes are visible as pinpoints of
white. Pregnant females tunnel into the dead, outermost layer (stratum corneum) of
a host's skin and deposit eggs in the shallow burrows. The eggs hatch into larvae in
three to ten days. These young mites move about on the skin and molt into a
"nymphal" stage, before maturing as adults, which live three to four weeks in the
host's skin. Males roam on top of the skin, occasionally burrowing into the skin. In
general, few mites usually occur on a healthy hygienic person infested with
noncrusted scabies; about 11 females in burrows can be found on such a person.[12]

The movement of mites within and on the skin produces an intense itch, which has
the characteristics of a delayed cell-mediated inflammatory response to allergens.
IgE antibodies are present in the serum and the site of infection, which react to
multiple protein allergens in the body of the mite. Some of these cross-react to
allergens from house-dust mites. Immediate antibody-mediated allergic reactions
(wheals) have been elicited in infected persons, but not in healthy persons;
immediate hypersensitivity of this type is thought to explain the observed far more
rapid allergic skin response to reinfection seen in persons having been previously
infected (especially having been infected within the previous year or two).[13]
Because the host develops the symptoms as a reaction to the mites' presence over
time, usually a four– to six-week incubation period after the onset of infestation is
found. As noted, those previously infected with scabies and cured may exhibit the
symptoms of a new infection in a much shorter period, as little as one to four
days.[14]

Scabies is contagious and can be spread by scratching an infected area, thereby

picking up the mites under the fingernails, or through physical contact with a
scabies-infected person for a prolonged period of time.[15] Scabies is usually
transmitted by direct skin-to-skin contact. It can also be spread through contact
with other objects, such as clothing, bedding, furniture, or surfaces with which a
person infected with scabies might have come in contact.[16] Scabies mites can
survive without a human host for 24 to 36 hours.[17] As with lice, scabies can be
 40

transmitted through sexual intercourse even if a latex condom is used, because it is

transmitted from skin-to-skin at sites other than sex organs.[18]

Pathophysiology

The symptoms are caused by an allergic reaction of the host's body to mite
proteins, though exactly which proteins remains a topic of study. The mite proteins
are also present from the gut, in mite feces, which are deposited under the skin.
The allergic reaction is both of the delayed (cell-mediated) and immediate
(antibody-mediated) type, and involves IgE (antibodies, it is presumed, mediate the
very rapid symptoms on reinfection).[12] The allergy-type symptoms (itching)
continue for some days, and even several weeks, after all mites are killed. New
lesions may appear for a few days after mites are eradicated. Nodular lesions from
scabies may continue to be symptomatic for weeks after the mites have been
killed.[12]

Diagnosis

Magnified view of a burrowing trail of the scabies mite: The scaly patch on the left
was caused by the scratching and marks the mite's entry point into the skin. The
mite has burrowed to the top-right, where it can be seen as a dark spot at the end.

Scabies may be diagnosed clinically in geographical areas where it is common

when diffuse itching presents along with either lesions in two typical spots or there
is itchiness of another household member.[4] The classical sign of scabies is the
burrows made by the mites within the skin.[4] To detect the burrow, the suspected
area is rubbed with ink from a fountain pen or a topical tetracycline solution, which
glows under a special light. The skin is then wiped with an alcohol pad. If the
person is infected with scabies, the characteristic zigzag or S pattern of the burrow
will appear across the skin; however, interpreting this test may be difficult, as the
burrows are scarce and may be obscured by scratch marks.[4] A definitive diagnosis
 41

is made by finding either the scabies mites or their eggs and fecal pellets. [4]
Searches for these signs involve either scraping a suspected area, mounting the
sample in potassium hydroxide and examining it under a microscope, or using
dermoscopy to examine the skin directly.[6]

Differential diagnosis

Symptoms of early scabies infestation mirror other skin diseases, including

dermatitis, syphilis, various urticaria-related syndromes, allergic reactions, and
other ectoparasites such as lice and fleas.[19]

Prevention

Mass treatment programs that use topical permethrin or oral ivermectin have been
effective in reducing the prevalence of scabies in a number of populations. [4] No
vaccine is available for scabies. The simultaneous treatment of all close contacts is
recommended, even if they show no symptoms of infection (asymptomatic), to
reduce rates of recurrence.[4][4] Since mites can only survive for two to three days
without a host, objects in the environment pose little risk of transmission except in
the case of crusted scabies, thus cleaning is of little importance.[4] Rooms used by
those with crusted scabies require thorough cleaning.[20]

Management

A number of medications are effective in treating scabies; however, treatment must

often involve the entire household or community to prevent reinfection.[4] Options
to control itchiness include antihistamines.[21]

Permethrin

Permethrin is the most effective treatment for scabies,[22] and is the treatment of
choice.[4][23] It is applied from the neck down, usually before bedtime, and left on
for about eight to 14 hours, then showered off in the morning.[4] One application is
normally sufficient for mild infections. For moderate to severe cases, another dose
is applied seven to 14 days later.[4][23][24] Permethrin causes slight irritation of the
skin, but the sensation is tolerable.[6] The medication, however, is the most costly
of topical treatments.[6]
 42

Ivermectin

Ivermectin is an oral medication shown by many clinical studies to be effective in

eradicating scabies, often in a single dose.[3][4] It is the treatment of choice for
crusted scabies, and is often used in combination with a topical agent.[6][4] It has not
been tested on infants and is not recommended for children under six years of
age.[6]

Topical ivermectin preparations have been found to be effective for scabies in

adults, and are attractive due to their low cost, ease of preparation, and low
toxicity.[25] It has also been useful for sarcoptic mange (the veterinary analog of
human scabies).[26]

Others

Other treatments include lindane, benzyl benzoate, crotamiton, malathion, and

sulfur preparations.[6][4] Lindane is effective, but concerns over potential
neurotoxicity has limited its availability in many countries.[6] It is approved in the
United States for use as a second-line treatment.[27] Sulfur ointments or benzyl
benzoate are often used in the developing world due to their low cost; [6] 10% sulfur
solutions have been shown to be effective,[28] and sulfur ointments are typically
used for at least a week.[6] Crotamiton has been found to be less effective than
permethrin in limited studies.[6] Crotamiton or a sulfur preparation is often
recommended instead of permethrin for children, due to concerns over dermal
absorption of permethrin.[4]

Day 4

Day 8 (treatment begins)

 43

Day 12 (under treatment)

Healed

Communities

Scabies is endemic in many developing countries,[29] where it tends to be

particularly problematic in rural and remote areas. In such settings community
wide control strategies are required to reduce the rate of disease, as treatment of
only individuals is ineffective due to the high rate of reinfection. Large-scale mass
drug administration strategies may be required where coordinated interventions
aim to treat whole communities in one concerted effort.[30] Although such
strategies have shown to be able to reduce the burden of scabies in these kinds of
communities, debate remains about the best strategy to adopt, including the choice
of drug.[30][31]

The resources required to implement such large-scale interventions in a cost-

effective and sustainable way are significant. Furthermore, since endemic scabies
is largely restricted to poor and remote areas, it is a public health issue that has not
attracted much attention from policy makers and international donors.[30][31]

Epidemiology

Scabies is one of the three most common skin disorders in children, along with
tinea and pyoderma.[4] As of 2010 it affects approximately 100 million people
(1.5% of the population) and is equally common in both genders.[5] The mites are
distributed around the world and equally infect all ages, races, and socioeconomic
classes in different climates.[11] Scabies is more often seen in crowded areas with
unhygienic living conditions.[32] Globally as of 2009, an estimated 300 million
cases of scabies occur each year, although various parties claim the figure is either
 44

over- or underestimated.[9][33] About 1–10% of the global population is estimated to

be infected with scabies, but in certain populations, the infection rate may be as
high as 50–80%.[4]

History

Wax figurine of a man with Norwegian scabies

Scabies is an ancient disease. Archeological evidence from Egypt and the Middle
East suggests scabies was present as early as 494 BC.[14][34] The first recorded
reference to scabies is believed to be from the Bible (Leviticus, the third book of
Moses) circa 1200 BC.[35] Later, in the fourth century BC, the ancient Greek
philosopher and naturalist Aristotle reported on "lice" that "escape from little
pimples if they are pricked";[36] scholars believe this was actually a reference to
scabies.[who?]

Nevertheless, Greek physician Celsus is credited with naming the disease "scabies"
and describing its characteristic features.[36] The parasitic etiology of scabies was
later documented by the Italian physician Giovanni Cosimo Bonomo (1663–
99 AD) in his famous 1687 letter, "Observations concerning the fleshworms of the
human body".[36] With this discovery, scabies became one of the first diseases with
a known cause.[14][34]

Society and culture

The International Alliance for the Control of Scabies was started in 2012,[31][37][38]
and brings together over 70 researchers, clinicians and public health experts from
more than 15 different countries. It has managed to bring the global health
implications of scabies to the attention of the World Health Organization.[31]
Consequently, the WHO has included scabies on its official list of neglected
tropical diseases and other neglected conditions.[39]
 45

A street dog in Bali, Indonesia, suffers from sarcoptic mange.

Scabies may occur in a number of domestic and wild animals; the mites that cause
these infestations are of different subspecies.[6] These subspecies can infest animals
or humans that are not their usual hosts, but such infections do not last long. [6]
Scabies-infected animals suffer severe itching and secondary skin infections. They
often lose weight and become frail.[12]

The most frequently diagnosed form of scabies in domestic animals is sarcoptic

mange, which is found on dogs. This disease is caused by the subspecies Sarcoptes
scabiei canis. Scabies-infected domestic fowl suffer what is known as "scaly leg".
Domestic animals that have gone feral and have no veterinary care are frequently
afflicted with scabies and a host of other ailments.[40] Nondomestic animals have
also been observed to suffer from scabies. Gorillas, for instance, are known to be
susceptible to infection via contact with items used by humans.[41]

References

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Mosby-Year Book Inc., 1994, p. 1395
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BJ (December 2009). "Skin disorders, including pyoderma, scabies, and
tinea infections". Pediatr. Clin. North Am. 56 (6): 1421–40.
doi:10.1016/j.pcl.2009.09.002. PMID 19962029.
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sequelae of 289 diseases and injuries 1990–2010: a systematic analysis for
the Global Burden of Disease Study 2010.". Lancet 380 (9859): 2163–96.
doi:10.1016/S0140-6736(12)61729-2. PMID 23245607.
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6. ^ a b c d e f g h i j k l m n o p q r Hay RJ (2009). "Scabies and pyodermas—

diagnosis and treatment". Dermatol Ther 22 (6): 466–74.
doi:10.1111/j.1529-8019.2009.01270.x. PMID 19889132.
7. ^ a b CDC web site > DPDx - Laboratory Identification of Parasites of Public
Health Concern > Scabies [1]
8. ^ a b "Scabies". DermNet NZ. New Zealand Dermatological Society
Incorporated.
9. ^ a b c Bouvresse, S.; Chosidow, O. (Apr 2010). "Scabies in healthcare
settings". Curr Opin Infect Dis 23 (2): 111–8.
doi:10.1097/QCO.0b013e328336821b. PMID 20075729.
10.^ Hicks MI, Elston DM (2009). "Scabies". Dermatol Ther 22 (4): 279–92.
doi:10.1111/j.1529-8019.2009.01243.x. PMID 19580575.
11.^ a b "DPDx—Scabies". Laboratory Identification of Parasites of Public
Health Concern. CDC.
12.^ a b c d Walton, SF; Currie, BJ (April 2007). "Problems in Diagnosing
Scabies, a Global Disease in Human and Animal Populations". Clinical
Microbiology Reviews 20 (2): 268–79. doi:10.1128/CMR.00042-06.
PMC 1865595. PMID 17428886.
13.^ Clinical Microbiology Reviews, April 2007, p. 268-279, Vol. 20, No. 2
0893-8512/07/$08.00+0 doi:10.1128/CMR.00042-06 Problems in
Diagnosing Scabies, a Global Disease in Human and Animal Populations
online reference PMID 17428886
14.^ a b c Markell, Edward K.; John, David C.; Petri, William H. (2006).
Markell and Voge's medical parasitology (9th ed.). St. Louis, Mo: Elsevier
Saunders. ISBN 0-7216-4793-6.
15.^ Carol Turkington and Jeffrey S. Dover, M.D. (2006). The Encyclopedia of
Skin and Skin Disorders. New York: Facts on File inc. ISBN 978-0-8160-
6403-8.
16.^ Causes "Scabies Causes". WebMD. October 2010. Retrieved 2010-10-09.
17.^ Chosidow O (April 2006). "Clinical practices. Scabies". N. Engl. J. Med.
354 (16): 1718–27. doi:10.1056/NEJMcp052784. PMID 16625010.
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2010-10-09.
19.^ Arlian, LG (1989). "Biology, host relations, and epidemiology of
Sarcoptes scabiei". Annual review of entomology 34: 139–61.
doi:10.1146/annurev.en.34.010189.001035. PMID 2494934.
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and Prevention. Retrieved 2010-10-09.
 47

21.^ Vañó-Galván, S; Moreno-Martin, P (2008). "Generalized pruritus after a

beach vacation. Diagnosis: scabies". Cleveland Clinic journal of medicine
75 (7): 474, 478. doi:10.3949/ccjm.75.7.474. PMID 18646583.
22.^ Strong M, Johnstone PW (2007). "Interventions for treating scabies". In
Strong, Mark. Cochrane Database Syst Rev (3): CD000320.
doi:10.1002/14651858.CD000320.pub2. PMID 17636630.
23.^ a b "Scabies". Illinois Department of Public Health. January 2008.
Retrieved 2010-10-07.
24.^ The Pill Book. Bantam Books. 2010. pp. 867–869. ISBN 978-0-553-
59340-2.
25.^ Victoria J, Trujillo R (2001). "Topical ivermectin: a new successful
treatment for scabies". Pediatr Dermatol 18 (1): 63–5. doi:10.1046/j.1525-
1470.2001.018001063.x. PMID 11207977.
26.^ "Parasitology Research, Volume 78, Number 2". SpringerLink. Retrieved
2010-11-14.
27.^ "FDA Public Health Advisory: Safety of Topical Lindane Products for the
Treatment of Scabies and Lice". Fda.gov. 2009-04-30. Retrieved 2010-11-
14.
28.^ Jin-Gang A, Sheng-Xiang X, Sheng-Bin X, et al. (March 2010). "Quality
of life of patients with scabies". J Eur Acad Dermatol Venereol 24 (10):
1187. doi:10.1111/j.1468-3083.2010.03618.x. PMID 20236379.
29.^ Andrews, RM; McCarthy, J; Carapetis, JR; Currie, BJ (Dec 2009). "Skin
disorders, including pyoderma, scabies, and tinea infections.". Pediatric
clinics of North America 56 (6): 1421–40. doi:10.1016/j.pcl.2009.09.002.
PMID 19962029.
30.^ a b c Hay, RJ; Steer, AC; Chosidow, O; Currie, BJ (Apr 2013). "Scabies: a
suitable case for a global control initiative.". Current opinion in infectious
diseases 26 (2): 107–9. doi:10.1097/QCO.0b013e32835e085b.
PMID 23302759.
31.^ a b c d Engelman, D; Kiang, K; Chosidow, O; McCarthy, J; Fuller, C;
Lammie, P; Hay, R; Steer, A; Members Of The International Alliance For
The Control Of, Scabies (2013). "Toward the global control of human
scabies: introducing the International Alliance for the Control of Scabies.".
PLoS neglected tropical diseases 7 (8): e2167.
doi:10.1371/journal.pntd.0002167. PMID 23951369.
32.^ Green MS (1989). "Epidemiology of scabies". Epidemiol Rev 11 (1): 126–
50. PMID 2509232.
33.^ Hicks, MI; Elston, DM (Jul–Aug 2009). "Scabies". Dermatologic therapy
22 (4): 279–92. doi:10.1111/j.1529-8019.2009.01243.x. PMID 19580575.
34.^ a b "Scabies homepage". Stanford University. Retrieved 2010-10-09.
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35.^ Leviticus 13:29-13:37

36.^ a b c Roncalli RA (July 1987). "The history of scabies in veterinary and
human medicine from biblical to modern times". Vet. Parasitol. 25 (2): 193–
8. doi:10.1016/0304-4017(87)90104-X. PMID 3307123.
37.^ "Scabies". Neglected tropical diseases. World Health Organization.
Retrieved 1 February 2014.
38.^ "International Alliance for the Control of Scabies". International Alliance
for the Control of Scabies. Retrieved 1 February 2014.
39.^ "The 17 neglected tropical diseases". Neglected tropical diseases. World
Health Organization. Retrieved 1 February 2014.
40.^ "Bali Animal Welfare Association". Retrieved 2009-07-28.
41.^ "Uganda: Out of the Wild". Frontline. PBS. Retrieved Nov 4, 2013.

Diseases of the skin and appendages by morphology

 wart
 callus
 seborrheic keratosis
 acrochordon
 molluscum contagiosum
 actinic keratosis
Epidermal
 squamous cell carcinoma
 basal cell carcinoma
 merkel cell carcinoma
 nevus sebaceous
 trichoepithelioma

 Freckles
Growths  lentigo
 melasma
Pigmented
 nevus
 melanoma

 epidermal inclusion cyst

 hemangioma
 dermatofibroma
 keloid
Dermal and
 lipoma
subcutaneous
 neurofibroma
 xanthoma
 Kaposi's sarcoma
 infantile digital fibromatosis
 49

 granular cell tumor

 leiomyoma
 lymphangioma circumscriptum
 myxoid cyst

 contact dermatitis
 atopic dermatitis
 seborrheic dermatitis
 stasis dermatitis
 lichen simplex chronicus
 Darier's disease
Eczematous  glucagonoma syndrome
 langerhans cell histiocytosis
 lichen sclerosus
 pemphigus foliaceus
 Wiskott-Aldrich syndrome
 Zinc deficiency

 psoriasis
 tinea (corporis
 cruris
 pedis
 manuum
 faciei)
With  pityriasis rosea
Rashes epidermal Scaling
 secondary syphilis
involvement  mycosis fungoides
 systemic lupus erythematosus
 pityriasis rubra pilaris
 parapsoriasis
 ichthyosis

 herpes simplex
 herpes zoster
 varicella
 bullous impetigo
 acute contact dermatitis
Blistering  pemphigus vulgaris
 bullous pemphigoid
 dermatitis herpetiformis
 porphyria cutanea tarda
 epidermolysis bullosa simplex

 scabies
Papular
 insect bite reactions
 50

 lichen planus
 miliaria
 keratosis pilaris
 lichen spinulosus
 transient acantholytic dermatosis
 lichen nitidus
 pityriasis lichenoides et varioliformis acuta

 acne vulgaris
 acne rosacea
 folliculitis
 impetigo
 candidiasis
Pustular
 gonococcemia
 dermatophyte
 coccidioidomycosis
 subcorneal pustular dermatosis

 tinea versicolor
 vitiligo
 pityriasis alba
 postinflammatory hyperpigmentation
Hypopigmented  tuberous sclerosis
 idiopathic guttate hypomelanosis
 leprosy
 hypopigmented mycosis fungoides

 drug eruptions
 viral exanthems
 toxic erythema
Generalized
 systemic lupus
erythematosus

 cellulitis
Without  abscess
Blanchable
epidermal Red  boil
Erythema
involvement  erythema nodosum
Localized
 carcinoid
syndrome
 fixed drug eruption

 urticaria
Specialized  erythema
(multiforme
 51

 migrans
 gyratum repens
 annulare
centrifugum
 ab igne)

 thrombocytopenic
purpura
Macular
 actinic purpura
Nonblanchable
 disseminated
Purpura
intravascular
Papular coagulation
 vasculitis

 scleroderma/morphea
 granuloma annulare
Indurated  lichen sclerosis et atrophicus
 necrobiosis lipoidica

Ulcers
 telogen effluvium
 androgenic alopecia
 trichotillomania
 alopecia areata
 systemic lupus erythematosus
Hair  tinea capitis
 loose anagen syndrome
 lichen planopilaris
 folliculitis decalvans
 acne keloidalis nuchae
Miscellaneous
disorders
 onychomycosis
 psoriasis
Nail  paronychia
 ingrown nail

 aphthous stomatitis
 oral candidiasis
Mucous  lichen planus
membrane  leukoplakia
 pemphigus vulgaris
 mucous membrane pemphigoid
 52

 cicatricial pemphigoid
 herpesvirus
 coxsackievirus
 syphilis
 systemic histoplasmosis
 squamous cell carcinoma

Infectious diseases – Parasitic disease: ectoparasitic infestation / arthropod (B85–

B89, 132–134)

 Body louse / Head louse

 Pediculosis
 Head lice infestation
 Pediculosis corporis
Louse
 Crab louse
 Phthiriasis
Insecta
 Bed bug (Cimicosis)
Hemiptera

 Dermatobia hominis / Cordylobia anthropophaga (Myiasis)

Fly

 Chigoe flea
Flea  Tungiasis

 Trombidiformes: Trombicula
 Trombiculosis
 Chigger bite
 Demodex brevis / Demodex folliculorum
 Demodicosis
 Demodex mite bite
Acariasis  Pyemotes herfsi
/ mange  Cheyletiella
Arachnida mites)  Cheyletiellosis
 Sarcoptiformes: Sarcoptes scabiei
 Scabies

 Dermanyssus gallinae
 Liponyssoides sanguineus

 Tick infestation
Ticks

Crustacea Pentastomida  Linguatula serrata

 53

 Linguatulosis
 Porocephalus crotali / Armillifer armillatus
 Porocephaliasis

Tinea
Classification and external resources
DiseasesDB 17492
MedlinePlus 001439
MeSH D014005

Tinea (often called ringworm) is any of a variety of skin mycoses.[1] Tinea is a

very common fungal infection of the skin. Tinea is often called "ringworm"
because it is circular, and has a "ring-like" appearance.

It is sometimes equated with dermatophytosis, and, while most conditions

identified as "tinea" are members of the imperfect fungi that make up the
dermatophytes, conditions such as tinea nigra and tinea versicolor are not caused
by dermatophytes.

Signs and causes

 Itching and stinging
 Red scaly rash that is shaped like a ring
 Cracking, splitting and peeling on toes
 Blisters
 Yellow or white discoloration the finger nails
 Spots with no hair on scalp

The cause of tinea are dermatophytes that grow on the dead keratin cells skin.
These cells multiply in warm, damp environments on the body and can be
transmitted by touch from human or animal.
 54

Types of tinea
Tinea capitis: Tinea of the scalp

Tinea pedis: Athlete’s foot

Tinea manuum: Tinea of the hands

Tinea unguium (also known as onychomycosis): Nail infection

Tinea barbae: Tinea of the beard area

Tinea cruris: Jock itch

Tinea corporis: Tinea of the body

Treatment
Antifungal creams or medication can be prescribed by a physician or even bought
over-the-counter.

These steps should be taken to treat tinea.

 Wash and then dry the area.

 Apply the antifungal cream, powder, or spray as directed on the label.
 Continue this treatment for 2 weeks, even if symptoms disappear, to prevent
the infection from coming back tolerant.

Prevention of tinea
 Keeping body clean.
 Change underwear every day.
 Wearing shower shoes, shoes, or socks in public showering areas and locker
rooms.
 Alternate shoes or sneakers to prevent moisture buildup and fungus growth.
 Avoid socks that trap moisture.
 Select shoes that are well ventilated with small holes to keep the feet dry.
 Not sharing clothes, brushes, combs, socks and underwear.
 55

References
http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Tinea
http://www.patient.co.uk/doctor/dermatophytosis-tinea-infections#
http://www.medicinenet.com/ringworm/page6.htm
http://kidshealth.org/parent/infections/fungal/ringworm.html#

1. "tinea". medical-dictionary.thefreedictionary.com. Retrieved 2012-07-25.

Infectious diseases

 Mycoses and Mesomycetozoea (B35–B49, 110–118)

 Tinea barbae/Tinea capitis

o Kerion
 Tinea corporis
o Ringworm
o Dermatophytid
 Tinea cruris
 Tinea manuum
 Tinea pedis (Athlete's foot)
 Tinea
Superficial and unguium/Onychomycosis
cutaneous By o (White superficial
(dermatomyco location onychomycosis
sis): Dermatophyte o Distal subungual
Tinea = skin; Ascomycota (Dermatophytos onychomycosis
Piedra is) o Proximal subungual
(exothrix/ onychomycosis
endothrix) =  Tinea corporis gladiatorum
hair  Tinea faciei
 Tinea imbricata
 Tinea incognito
 Favus

 Epidermophyton floccosum
By  Microsporum canis
organis  Microsporum audouinii
m  Trichophyton
interdigitale/mentagrophytes
 56

 Trichophyton tonsurans
 Trichophyton schoenleini
 Trichophyton rubrum

 Hortaea werneckii
o Tinea nigra
Other  Piedraia hortae
o Black piedra

 Malassezia furfur
o Tinea versicolor
Basidiomyco o Pityrosporum folliculitis
ta  Trichosporon spp
o White piedra

 Coccidioides
immitis/Coccidioides posadasii
o Coccidioidomycosis
o Disseminated
coccidioidomycosis
o Primary cutaneous
coccidioidomycosis.
Primary pulmonary
coccidioidomycosis
 Histoplasma capsulatum
o Histoplasmosis
Onygena o Primary cutaneous
les histoplasmosis
Subcutaneous, Dimorphi o Primary pulmonary
systemic, c histoplasmosis
Ascomycota
and (yeast+mo o Progressive disseminated
opportunistic ld) histoplasmosis
 Histoplasma duboisii
o African histoplasmosis
 Lacazia loboi
o Lobomycosis
 Paracoccidioides brasiliensis
o Paracoccidioidomycosis

 Blastomyces dermatitidis
o Blastomycosis
Other o North American
blastomycosis
o South American
 57

blastomycosis
 Sporothrix schenckii
o Sporotrichosis
 Penicillium marneffei
o Penicilliosis

 Candida albicans
o Candidiasis
o Oral
o Esophageal
o Vulvovaginal
o Chronic mucocutaneous
o Antibiotic candidiasis
o Candidal intertrigo
o Candidal onychomycosis
o Candidal paronychia
o Candidid
Yeast-like o Diaper candidiasis
o Congenital cutaneous candidiasis
o Perianal candidiasis
o Systemic candidiasis
o Erosio interdigitalis blastomycetica
 C. glabrata
 C. tropicalis
 C. lusitaniae
 Pneumocystis jirovecii
o Pneumocystosis
o Pneumocystis pneumonia

 Aspergillus
o Aspergillosis
o Aspergilloma
o Allergic bronchopulmonary
aspergillosis
o Primary cutaneous aspergillosis
 Exophiala jeanselmei
o Eumycetoma
Mold-like
 Fonsecaea pedrosoi/Fonsecaea
compacta/Phialophora verrucosa
o Chromoblastomycosis
 Geotrichum candidum
o Geotrichosis
 Pseudallescheria boydii
o Allescheriasis
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 Cryptococcus neoformans
o Cryptococcosis
Basidiomycota o Trichosporon spp
o Trichosporonosis

 Rhizopus oryzae
 Mucor indicus
Mucorales  Lichtheimia corymbifera
(Mucormycosis)  Syncephalastrum racemosum
 Apophysomyces variabilis
Zygomycota
 Basidiobolus ranarum
(Zygomycosis)
o Basidiobolomycosis
Entomophthorales  Conidiobolus
(Entomophthoramyc coronatus/Conidiobolus
osis) incongruus
o Conidiobolomycosis

Microsporidia
 Enterocytozoon bieneusi/Encephalitozoon intestinalis
(Microsporidi
osis)
 Rhinosporidium seeberi
Mesomycetozo
o Rhinosporidiosis
ea

 Alternariosis
 Fungal folliculitis
 Fusarium
o Fusariosis
Ungrouped  Granuloma gluteale infantum
 Hyalohyphomycosis
 Otomycosis
 Phaeohyphomycosis

This page was last modified on 21 May 2014 at 22:40.