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.

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.

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.

The infection causes a red, intensely pruritic (itchy) eruption. The itching can become very painful and if scratched may allow a secondary bacterial infection to develop. Cutaneous larva migrans usually heals spontaneously over weeks to months and has been known to last as long as one year. However, the severity of the symptoms usually causes those infected to seek medical treatment before spontaneous resolution occurs. Following proper treatment, migration of the larvae within the skin is halted and relief of the associated itching can occur in less than 48 hours (reported for thiabendazole).

This is separate from the similar cutaneous larva currens which is caused by "Strongyloides". Larva currens is also a cause of migratory pruritic eruptions but is marked by 1) migratory speed on the order of inches per hour 2) perianal involvement due to autoinfection from stool and 3) a wide band of urticaria.

Treatment is symptomatic.

Treatment does not require a doctor's attention unless the case is severe, with most affected using a topical anti-itch cream (diphenhydramine) and a cortisone solution (hydrocortisone). Do not scratch the area, and avoid any clothing that may irritate the affected area; scratching will result in localized swelling and intense itching.

Upon exiting the water, prompt removal of swim clothing (while it is still wet) followed by a warm sea-water shower largely negates the risk of Seabather's eruption even in endemic areas. A hot freshwater shower with soap (paying particular attention to the hair and areas covered by the suit) is a somewhat less-effective alternative if uncontaminated seawater is unavailable. The contaminated swimsuit should be machine washed with laundry soap and dried in warm air.

Animals can be affected as well, and a cortisone solution for humans can be used on dogs.

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.

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.

Feeding the lawn with a nitrogen based fertilizer will help the grass recover and help prevent future attacks.

Red Thread can be treated using a fungicide that contains benomyl or carbendazim. The infection will rarely kill the grass, usually only affecting the blades and not the roots, and the lawn should recover in time.

References

1) Ryzin, Benjamin Van. “Red Thread.” "Wisconsin Horticulture", 23 June 2013, hort.uwex.edu/articles/red-thread/

2) Harmon, Philip, and Richard Latin. “Red Thread.” "Purdue Extension", Dec. 2009, www.extension.purdue.edu/extmedia/bp/bp-104-w.pdf.

3) “Red Thread.” "Plant Protection", NuTurf, nuturf.com.au/wp-content/uploads/sites/2/2015/09/Red-Thread-Info.pdf.

4) “Suppression of Soil-Borne Plant Diseases with Composts: A Review.” "Taylor & Francis", www.tandfonline.com/doi/abs/10.1080/09583150400015904

5) “Red Thread — Laetisaria Fuciformis.” "Red Thread (Laetisaria Fuciformis) - MSU Turf Diseases.net - Disease Identification and Information. A Resource Guide from the Dept. of Plant Pathology at Michigan State University", www.msuturfdiseases.net/details/_/red_thread_14/.

6) “Lawn and Turf-Red Thread.” "Pacific Northwest Pest Management Handbooks", OSU Extension Service - Extension and Experiment Station Communications, 4 Apr. 2017, pnwhandbooks.org/plantdisease/host-disease/lawn-turf-red-thread.

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

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

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

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.

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.

Whilst usually a straightforward diagnosis at times the appearance can raise concern that the rash could be due to herpes simplex; however, the latter generally has a more clustered and vesicular appearance.

In uncertain cases, a scraping of a lesion can be taken and the fluid examined under the microscope. Herpes lesions will have a positive direct fluorescent antibody test. The fluid from erythema toxicum lesions will show many eosinophils. If blood samples are taken, they may show a high level of circulating eosinophils; however, this is not usually required.

Differential diagnosis may include Herpes simplex virus, Impetigo, neonatal sepsis, Listeria and Varicella (chicken pox).

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.

In all cases of suspected NEH, a skin biopsy should be performed, because the clinical symptoms are non specific, but the histopathological findings on the biopsy are specific. The biopsy shows characteristic changes of the eccrine glands, the major sweat glands of the body.

In NEH, eccrine gland necrosis, and neutrophils surroundings the eccrine glands, are typical findings on biopsy. If the chemotherapy has recently been administered, chemotherapy induced neutropenia may be present, and, as a result, the neutrophils may be absent. But the other characteristic finding, i.e. eccrine gland necrosis, can still be seen. A vacuolar interface dermatitis also is visible in glands and ducts, along with necrosis of the lining cells.

In addition, in patients receiving chemotherapy, keratinocyte atypia can be seen.

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.

This infection affects multiple organs, including the eyes, brain, lung, and liver, and can be fatal.

It is estimated that 2—3 percent of hospitalised patients are affected by a drug eruption, and that serious drug eruptions occur in around 1 in 1000 patients.

It is self limiting condition

1.reassurence

2.steriod cream for local application

3.moisterizer lotion

Because the eruption is transient and self-limiting, no treatment is indicated.

Drug eruptions are diagnosed mainly from the medical history and clinical examination. However, they can mimic a wide range of other conditions, thus delaying diagnosis (for example, in drug-induced lupus erythematosus, or the acne-like rash caused by erlotinib). A skin biopsy, blood tests or immunological tests can also be useful.

Drug reactions have characteristic timing. The typical amount of time it takes for a rash to appear after exposure to a drug can help categorize the type of reaction. For example, Acute generalized exanthematous pustulosis usually occurs within 4 days of starting the culprit drug. Drug Reaction with Eosinophilia and Systemic Symptoms usually occurs between 15 and 40 days after exposure. Toxic epidermal necrolysis and Stevens-Johnson syndrome typically occur 7–21 days after exposure. Anaphylaxis occurs within minutes. Simple exanthematous eruptions occur between 4 and 14 days after exposure.

TEN and SJS are severe cutaneous drug reactions that involve the skin and mucous membranes. To accurately diagnose this condition, a detailed drug history is crucial. Often, several drugs may be causative and allergy testing may be helpful. Sulfa drugs are well-known to induce TEN or SJS in certain people. For example, HIV patients have an increased incidence of SJS or TEN compared to the general population and have been found to express low levels of the drug metabolizing enzyme responsible for detoxifying sulfa drugs. Genetics plays an important role in predisposing certain populations to TEN and SJS. As such, there are some FDA recommended genetic screening tests available for certain drugs and ethnic populations to prevent the occurrence of a drug eruption. The most well known example is carbamezepine (an anti-convulsant used to treat seizures) hypersensitivity associated with the presence of HLA-B*5801 genetic allele in Asian populations.

DIHS is a delayed onset drug eruption, often occurring a few weeks to 3 months after initiation of a drug. Interestingly, worsening of systemic symptoms occurs 3-4 days after cessation of the offending drug. There are genetic risk alleles that are predictive of the development of DIHS for particular drugs and ethnic populations. The most important of which is abacavir (an anti-viral used in the treatment of HIV) hypersensitivity associated with the presence of the HLA-B*5701 allele in European and African population in the United States and Australians.

AGEP is often caused by antimicrobial, anti-fungal or antimalarial drugs. Diagnosis is often carried out by patch testing. This testing should be performed within one month after resolution of the rash and patch test results are interpreted at different time points: 48 hours, 72hours and even later at 96 hours and 120 hours in order to improve the sensitivity.

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.

The treatment is (1) stop the offending drug (antibiotics), (2) symptomatic (fever), and (3) for complications (hepatitis).