Control of this parasite should be directed against reducing the level of

environmental contamination. Treatment of heavily infected individuals is one

way to reduce the source of contamination (one study has estimated that 60% of

the total worm burden resides in less than 10% of the population). Other

obvious methods are to improve access to sanitation, e.g. toilets, but also

convincing people to maintaining them in a clean, functional state, thereby making

them conducive to use.

The clinical aspects of ancylostomiasis were first described in Europe as "miner's anaemia". During the construction of the Gotthard Tunnel in Switzerland (1871–1881), a large number of miners suffered from severe anaemia of unknown cause. Medical investigations let to the understanding that it was caused by "Ancylostoma duodenale" (favoured by high temperatures and humidity) and to "major advances in parasitology, by way of research into the aetiology, epidemiology and treatment of ancylostomiasis".

Hookworms still account for high proportion of debilitating disease in the tropics and 50-60,000 deaths per year can be attributed to this disease.

CLM can be treated in a number of different ways:

- Systemic (oral) agents include albendazole (trade name "Albenza") and ivermectin (trade name "Stromectol")).

- Another agent which can be applied either topically "or" taken by mouth is thiabendazole (trade name "Mintezol")), an anti-helminthic.

- Topical freezing agents, such as ethylene chloride or liquid nitrogen, applied locally can freeze and kill the larvae, but this method has a high failure rate because the larvae are usually located away from the site of the visible skin trails. Additionally, this is a painful method which can cause blistering and/or ulceration of the skin and it is therefore not recommended.

- It is recommended to use Benadryl or some anti-itch cream (i.e. Cortizone or Calamine lotion). This will help relieve some of the itch.

- Wearing shoes in areas where these parasites are known to be endemic offers protection from infection. In general, avoiding exposure of skin to contaminated soil or sand offers the best protection. In some areas dogs have been banned from beaches in an attempt to control human infection.

Cutaneous larva migrans (abbreviated CLM) is a skin disease in humans, caused by the larvae of various nematode parasites of the hookworm family (Ancylostomatidae). The most common species causing this disease in the Americas is "Ancylostoma braziliense". These parasites live in the intestines of dogs, cats, and wild animals and should not be confused with other members of the hookworm family for which humans are definitive hosts, namely "Ancylostoma duodenale" and "Necator americanus".

Colloquially called creeping eruption due to its presentation, the disease is also somewhat ambiguously known as "ground itch" or (in some parts of the Southern USA) "sandworms", as the larvae like to live in sandy soil. Another vernacular name is plumber's itch. The medical term CLM literally means "wandering larvae in the skin".

Seabather's eruption is a pruritic dermatitis caused by a hypersensitivity reaction to the immature nematocysts of larval-stage Thimble Jellyfish ("Linuche unguiculata"), sea anemones ("Edwardsiella lineata") and other larval cnidarians.

It should not be confused with Swimmer's itch. However, the term "sea lice" is also sometimes used to describe Seabather's eruption.

This reaction occurs mainly in the tropics and in Florida, due to the proximity of the Gulf Stream to the U.S. state. It has been identified in other locations as well.

An "Arcanobacterium haemolyticum" infection is any of several types of infection with the gram-positive bacillus "Arcanobacterium haemolyticum". It can cause an acute pharyngitis, and it may cause an exanthem characterized by an erythematous, morbilliform or scarlatiniform eruption involving the trunk and extremities.

Alphavirus infection may be caused by a Sindbis virus infection, and result in a cutaneous eruption of multiple, erythematous, 4- to 4-mm papules.

Red thread disease is a fungal infection found on lawns and other turfed areas. It is caused by the corticioid fungus "Laetisaria fuciformis" and has two separate stages. The stage that gives the infection its name is characterised by very thin, red, needle-like strands extending from the grass blade. These are stromata, which can remain viable in soil for two years. After germinating, the stromata infect grass leaf blades through their stomata. The other stage is visible as small, pink, cotton wool-like mycelium, found where the blades meet. It is common when both warmth and humidity are high.

Environment

"Laetisaria fuciformis", the fungus that causes red thread disease develops more often in cool (59-77°F) and wet conditions. These conditions are more present in the spring and fall when rainfall is higher and temperatures are slightly lower. Turf grass that is poor in nutrition and are slow growing are areas that are more susceptible to red thread disease. The fungus grows from the thread like red webbing structures called sclerotia. The sclerotia can survive in leaf blades, thatch, and soil for months to years. These areas that have been infected spread the disease by water, wind, and contaminated equipment. Since this fungus can survive for long periods of time it is essential to cure the infected area so further spreading of the disease does not occur.

Management

Managing red thread disease first starts by providing conditions that are not favorable for the fungal disease to develop. Having a balanced and adequate nitrogen fertilization program helps suppress the disease. This includes applying mild to substantial amounts of phosphorus and potassium to the turf. Other than properly fertilizing the turf, it is very important to maintain a soil pH between 6.5 and 7. Having a more basic pH creates less favorable conditions for a fungus to form. Reducing shade on turf areas also reduces chances of the fungal disease to form because shaded areas create a higher humidity near the turfs surface. Another technique to suppressing red thread disease is top dressing with compost. Suppression of the disease increases with the increase of compost used on the turf. Fungicides are not recommended to control red thread because the cost of chemical control is expensive and turf grasses usually recover from the disease quickly. If the use of fungicides is necessary, products containing strobilurins can be applied and can be very effective if applied before symptoms occur.

Hosts and symptoms

The hosts of the red thread disease only include turf grass. Turf grass is primarily present on home lawns and athletic fields. Some of these turf grass species include annual bluegrass, creeping bentgrass, Kentucky bluegrass, pereninial ryegrass, fine fescue, and bermudagrass. These species of grass are not the only types of turf that can be diagnosed with red thread disease but are the most common hosts. Noticeable symptoms of red thread disease are irregular yellow patches on the turf that are 2 to 24 inches in diameter. Affected areas are diagnosed with faintly pinkish web like sclerotia on the leaf blades. This sclerotia is the fungus growing on the leaf blades. This sclerotia has a reddish to pink spider web look to it.

Lichen scrofulosorum (also known as "Tuberculosis cutis lichenoides") is a rare tuberculid that presents as a lichenoid eruption of minute papules in children and adolescents with tuberculosis. The lesions are usually asymptomatic, closely grouped, skin-colored to reddish-brown papules, often perifollicular and are mainly found on the abdomen, chest, back, and proximal parts of the limbs. The eruption is usually associated with a strongly positive tuberculin reaction.

Of the three tuberculids, the incidence of lichen scrofulosorum was found to be the lowest (2%) in a large study conducted in Hong Kong. This highlights its rarity and significance as an important marker of undetected tuberculosis.

Bacterial wilt of turfgrass is the only known bacterial disease of turf. The causal agent is the Gram negative bacterium Xanthomonas campestris pv. graminis. The first case of bacterial wilt of turf was reported in a cultivar of creeping bentgrass known as Toronto or C-15, which is found throughout the midwestern United States. Until the causal agent was identified in 1984, the disease was referred to simply as C-15 decline. This disease is almost exclusively found on putting greens at golf courses where extensive mowing creates wounds in the grass which the pathogen uses in order to enter the host and cause disease.

General biocides such as copper, Junction, or ZeroTol offer a potential solution to bacterial wilt of turf grass, however such chemical control ages must be applied after every mowing which may be economically impractical and ultimately phytotoxic. If bacterial wilt is present of the golf course, the best option may be to designate a mower for use on infected greens only in order to prevent the spread of the pathogen to other greens. Other viable methods include simply limiting the number of wounds the plant incurs, thereby limiting entry sites for the pathogen. A simple example would be less frequent mowing. It has also been proven that the disease is most devastating in grass cut to a length of between 1/8 and 3/16 of an inch, but less so in grass over 1/4 of an inch in length or longer, which presents an additional argument for limiting mowing. Another example is limiting sand topdressing as this is also a very abrasive technique which can create small wounds which allow entry of bacteria into the plant.

A major factor complicating the control of Xanthomonas campestris pv. graminis is weather. While it is not possible to control the weather per se, a study found great decreases in pathogen efficacy at temperatures below 20 °C, suggesting that cooling measures may be effective in combating this pathogen.

Ideally, resistant strains of the host plant should be used to control such a plant pathogen, however no resistant cultivars of turf grass have been identified to date. While no completely resistant cultivars exist, golf course owners can find solace in the fact that certain cultivars such as Penncross and Penneagle are more resistant to bacterial wilt and may thus reduce the need for frequent chemical applications and other cultural controls. Researchers are making gains towards the identification of resistant cultivars as evidenced by the finding that variation in genetic linkage groups 1, 4, and 6 accounted for over 43% of resistance among Italian rye grass.

A 1987 study found evidence of a possible biocontrol strategy for bacterial wilt of turf grass. The researchers found that antiserum to Pseudomonas fluorescens or Erwinia herbicola from hosts which have survived infections by the corresponding pathogens is capable of reducing wilt symptoms in turf grass caused by Xanthomonas campestris pv. graminis. The researchers did note, however, that while it is important to ensure the presence of a higher number of competing bacterial cells in order to reduce symptoms, one should take care to avoid over-infecting the host with a new bacterial pathogen.

Further gains towards host resistance were made in 2001 when researchers found that inoculation of meadow fescue during breeding with a single aggressive strain of the bacterial wilt pathogen greatly increased resistance in offspring, thereby demonstrating the potential of selective breeding to reduce bacterial wilt pathogenesis on turf and rye grasses.

http://www.lawnandmower.com/red-thread-disease.aspx

http://www.grassclippings.co.uk/RedThread.pdf

Generalized vaccinia is a cutaneous condition that occurs 6–9 days after vaccination, characterized by a generalized eruption of skin lesions, and caused by the vaccinia virus.

Infantile acropustulosis (also known as "Acropustulosis of infancy") is an intensely itchy vesicopustular eruption of the hands and feet.

Involvement of scabies has been suggested.

infantile acropustulosis is characterized by itchy papules and vesicles that are similar to those found in scabies "mosquito like bites" but there is absence of the typical burrowing with S like burrows on the skin and can occur in small babies as opposed to scabies mostly found on children and young adults.

It can be treated with systemic antiviral drugs, such as aciclovir or valganciclovir. Foscarnet may also be used for immunocompromised host with Herpes simplex and acyclovir-resistant Herpes simplex.

Eczema herpeticum is a rare but severe disseminated infection that generally occurs at sites of skin damage produced by, for example, atopic dermatitis, burns, long term usage of topical steroids or eczema. It is also known as Kaposi varicelliform eruption, Pustulosis varioliformis acute and Kaposi-Juliusberg dermatitis.

Some sources reserve the term "eczema herpeticum" when the cause is due to human herpes simplex virus, and the term "Kaposi varicelliform eruption" to describe the general presentation without specifying the virus.

This condition is most commonly caused by herpes simplex virus type 1 or 2, but may also be caused by coxsackievirus A16, or vaccinia virus. It appears as numerous umbilicated vesicles superimposed on healing atopic dermatitis. it is often accompanied by fever and lymphadenopathy. Eczema herpeticum can be life-threatening in babies.

Photoleukomelanodermatitis of Kobori is a cutaneous condition, a dyschromic drug eruption that occurs after ingestion of afloqualone, thiazides or tetracyclines, followed by exposure to sunlight.

Parasitic infestations, stings, and bites in humans are caused by several groups of organisms belonging to the following phyla: Annelida, Arthropoda, Bryozoa, Chordata, Cnidaria, Cyanobacteria, Echinodermata, Nemathelminthes, Platyhelminthes, and Protozoa.

- "Acanthamoeba" infection

- Amebiasis cutis

- Ant sting

- Arachnidism

- Baker's itch

- "Balamuthia" infection

- Bedbug infestation (bedbug bite, cimicosis)

- Bee and wasp stings

- Blister beetle dermatitis

- Bombardier beetle burn

- Bristleworm sting

- Centipede bite

- Cheyletiella dermatitis

- Chigger bite

- Coolie itch

- Copra itch

- Coral dermatitis

- Creeping eruption (cutaneous larva migrans)

- Cutaneous leishmaniasis (Aleppo boil, Baghdad boil, bay sore, Biskra button, Chiclero ulcer, Delhi boil, Kandahar sore, Lahore sore, leishmaniasis tropica, oriental sore, "pian bois, uta")

- "Cysticercosis" cutis

- Demodex mite bite

- Dogger Bank itch

- Dracunculiasis (dracontiasis, guinea worm disease, Medina worm)

- Echinococcosis (hydatid disease)

- Elephantiasis tropica (elephantiasis arabum)

- Elephant skin

- Enterobiasis (oxyuriasis, pinworm infection, seatworm infection)

- "Erisipela de la costa"

- Feather pillow dermatitis

- Funnel web spider bite

- Gamasoidosis

- Gnathostomiasis (larva migrans profundus)

- Grain itch (barley itch, mattress itch, prairie itch, straw itch)

- Grocer's itch

- Head lice infestation (cooties, pediculosis capitis)

- Hookworm disease (ancylostomiasis, ground itch, necatoriasis, uncinariasis)

- Human trypanosomiasis

- Hydroid dermatitis

- Irukandji syndrome

- Jellyfish dermatitis

- Ked itch

- Larva currens

- Latrodectism (widow spider bite)

- Leech bite

- Leopard skin

- Lepidopterism (Caripito itch, caterpillar dermatitis, moth dermatitis)

- Lizard bite

- Lizard skin

- Loaiasis (Calabar swelling, fugitive swelling, "loa loa", tropical swelling)

- Loxoscelism (brown recluse spider bite, necrotic cutaneous loxoscelism)

- "Mal morando"

- Millipede burn

- Mosquito bite

- Mucocutaneous leishmaniasis (espundia, leishmaniasis americana)

- Myiasis

- Nairobi fly dermatitis (Kenya fly dermatitis, Nairobi eye)

- Nematode dermatitis

- Norwegian scabies (crusted scabies)

- Onchocerciasis

- Ophthalmia nodosa

- Paederus dermatitis

- Pediculosis corporis (pediculosis vestimenti, Vagabond's disease)

- Pediculosis pubis (crabs, phthirus pubis, pthirus pubis, pubic lice)

- Pneumocystosis (often classified as fungal)

- Portuguese man-of-war dermatitis

- Post-kala-azar dermal leishmaniasis (post-kala-azar dermatosis)

- Protothecosis

- Pulicosis (flea bites)

- Reduviid bite

- Scabies (itch mite infestation, seven-year itch)

- Scorpion sting

- Sea anemone dermatitis

- Seabather's eruption (sea lice)

- Sea urchin injury

- Seaweed dermatitis

- Snake bite

- Sowda

- Sparganosis

- Spider bite

- Stingray injury

- Swimmer's itch (cercarial dermatitis, schistosome cercarial dermatitis)

- Tarantula bite

- Tick bite

- Toxoplasmosis

- Trichinosis

- Trichomoniasis

- Tungiasis ("bicho de pie", chigoe flea bite, jigger bite, "nigua, pique")

- Visceral leishmaniasis (dumdum fever, "kala-azar")

- Visceral schistosomiasis (bilharziasis)

- Viscerotropic leishmaniasis

- Wheat warehouse itch

Prurigo is an itchy eruption of the skin.

Specific types include:

- Prurigo nodularis

- Actinic prurigo

- Besnier's prurigo (a specific type of atopic dermatitis).

Urticarial allergic eruption is a cutaneous condition characterized by annular or gyrate urticarial plaques that persist for greater than 24 hours.

Lichen striatus (also known as blaschko linear acquired inflammatory skin eruption and linear lichenoid dermatosis) is a rare skin condition that is seen primarily in children, most frequently appearing ages 5–15. It consists of a self-limiting eruption of small, scaly papules.

Acne aestivalis (also known as Mallorca acne) is a special form of mono-morphic light eruption. It is a monomorphous eruption consisting of multiple, uniform, red, papular lesions, reported to occur after sun exposure.

The cause of erythema toxicum is thought to be an activation of the immune system. Some neonates are more sensitive than others and develop erythematous spots all over the body. Another theory is hypersensitivity to detergents in bedsheets and clothing is sometimes suspected, but the connection remains unproven.

It is thought to be a benign condition that causes no discomfort to the infant. The rash will generally disappear spontaneously in about 2 weeks.

The cause for actinic prurigo is unknown, however researchers believe that protein in our bodies may be a cause to the condition also:

•UV-A and UV-B light seem to be the main provoking agents. This observation is supported by the fact that most patients live at high altitudes (>1000 m above sea level), and the condition improves in many patients when they move to lower altitudes. However, some patients who are affected already live at sea level.18,19,27 •Some authors are considering a food photosensitizer or a nutritional selective deficiency as a cause; however, no evidence proves this theory.27