Antibiotics are the primary treatment. The specific approach to their use is dependent on the individual affected and the stage of the disease. For most people with early localized infection, oral administration of doxycycline is widely recommended as the first choice, as it is effective against not only "Borrelia" bacteria but also a variety of other illnesses carried by ticks. Doxycycline is contraindicated in children younger than eight years of age and women who are pregnant or breastfeeding; alternatives to doxycycline are amoxicillin, cefuroxime axetil, and azithromycin. Individuals with early disseminated or late infection may have symptomatic cardiac disease, refractory Lyme arthritis, or neurologic symptoms like meningitis or encephalitis. Intravenous administration of ceftriaxone is recommended as the first choice in these cases; cefotaxime and doxycycline are available as alternatives.

These treatment regimens last from one to four weeks. If joint swelling persists or returns, a second round of antibiotics may be considered. Outside of that, a prolonged antibiotic regimen lasting more than 28 days is not recommended as no clinical evidence shows it to be effective. IgM and IgG antibody levels may be elevated for years even after successful treatment with antibiotics. As antibody levels are not indicative of treatment success, testing for them is not recommended.

Outdoor workers are at risk of Lyme disease if they work at sites with infected ticks. In 2010, the highest number of confirmed Lyme disease cases were reported from New Jersey, Pennsylvania, Wisconsin, New York, Massachusetts, Connecticut, Minnesota, Maryland, Virginia, New Hampshire, Delaware, and Maine. U.S. workers in the northeastern and north-central States are at highest risk of exposure to infected ticks. Ticks may also transmit other tick-borne diseases to workers in these and other regions of the country. Worksites with woods, bushes, high grass, or leaf litter are likely to have more ticks. Outdoor workers should be extra careful to protect themselves in the late spring and summer when young ticks are most active.

Both lyme disease and STARI can be treated with antibiotics, particularly doxycyclin.

Southern tick-associated rash illness (STARI) produces a similar rash pattern although it develops more quickly and is smaller. This erythema is also sometimes called erythema migrans or EM. The associated infectious agent has not been determined. Antibiotic treatment resolves the illness quickly.

In the United States, sarcoidosis has a prevalence of approximately 10 cases per 100,000 whites and 36 cases per 100,000 blacks. Heerfordt syndrome is present in 4.1–5.6% of those with sarcoidosis.

Heerfordt syndrome, also referred to as uveoparotid fever, Heerfordt–Mylius syndrome, Heerfordt–Waldenström syndrome, and Waldenström's uveoparotitis, is a rare manifestation of sarcoidosis. The symptoms include inflammation of the eye (uveitis), swelling of the parotid gland, chronic fever, and in some cases, of the facial nerves.

Autoimmune polyendocrine syndrome type 1 treatment is based on the symptoms that are presented by the affected individual, additionally there is:

- Hormone replacement

- Systemic antifungal treatment

- Immunosuppressive treatment

Harlequin syndrome is not debilitating so treatment is not normally necessary. In cases where the individual may feel socially embarrassed, contralateral sympathectomy may be considered, although compensatory flushing and sweating of other parts of the body may occur. In contralateral sympathectomy, the nerve bundles that cause the flushing in the face are interrupted. This procedure causes both sides of the face to no longer flush or sweat. Since symptoms of Harlequin syndrome do not typically impair a person’s daily life, this treatment is only recommended if a person is very uncomfortable with the flushing and sweating associated with the syndrome.

Autoimmune polyendocrine syndrome type 1 (APS-1), also known as autoimmune polyendocrinopathy-candidiasis–ectodermal dystrophy/dysplasia (APECED), autoimmune polyglandular syndrome type 1, Whitaker syndrome, or candidiasis-hypoparathyroidism–Addison's disease syndrome, is a subtype of autoimmune polyendocrine syndrome (autoimmune polyglandular syndrome) in which multiple endocrine glands dysfunction as a result of autoimmunity. It is a genetic disorder inherited in autosomal recessive fashion due to a defect in the "AIRE" gene (autoimmune regulator), which is located on chromosome 21 and normally confers immune tolerance.

In August 2016, researchers at the Instituto de Assistência dos Servidores do Estado do Rio de Janeiro used botulinum toxin as a method to block the acetylcholine release from the presynaptic neurons. Although they have seen a reduction in one sided flushing, sweating still occurs.

There have been case studies of individuals whom have experienced this syndrome after an operation. Two patients, a 37-year-old and 58-year-old female patients suffering from metastatic cancer were scheduled for placement of an intrathecal pump drug delivery system. After the intrathecal pump was placed, certain medications were given to the patients. Once the medications were administered, both patients had one sided facial flushes, closely resembling Harlequin Syndrome. Patients were given neurological exams to confirm that their nerves were still intact. An MRI was performed and showed no significant evidence of bleeding or nerve compression. After close observation for 16 hours, symptoms of the Harlequin syndrome was diminished and both patients did not have another episode.

Another case study was based on a 6-year-old male visiting an outpatient setting for one sided flushes during or after physical activity or exposed to heat. Vitals, laboratory tests, and CT scans were normal. Along with the flushes, the right pupil was 1.5 mm in size, while the left pupil was 2.5 mm in size; however, no ptosis, miosis, or enophthalmos was noted. The patient also had an MRI scan to rule out any lesion near the brain or spinal cord. No abnormalities were noted and the patient did not receive any treatments. The patient was diagnosed with idiopathic Harlequin syndrome.

Although the mechanism is still unclear, the pathophysiology of this condition, close monitoring, and reassurance are vital factors for successful management.

Since Usher syndrome results from the loss of a gene, gene therapy that adds the proper protein back ("gene replacement") may alleviate it, provided the added protein becomes functional. Recent studies of mouse models have shown one form of the disease—that associated with a mutation in myosin VIIa—can be alleviated by replacing the mutant gene using a lentivirus. However, some of the mutated genes associated with Usher syndrome encode very large proteins—most notably, the "USH2A" and "GPR98" proteins, which have roughly 6000 amino-acid residues. Gene replacement therapy for such large proteins may be difficult.

As of 2017, data on optimal treatment was limited. Therapies with hormones is the standard of care, namely adrenocorticotrophic hormone (ACTH), or oral

corticosteroids such as prednisone. Vigabatrin is also a common consideration, though there is a risk of visual field loss with long term use. The high cost of ACTH leads doctors to avoid it in the US; higher dose prednisone appears to generate equivalent outcomes.

As of 2017 data from clinical trials of the ketogenic diet for treating infantile spams was inconsistent; most trials were as a second-line therapy after failure of drug treatment, and as of 2017 it had not been explored as a first line treatment in an adequately designed clinical trial.

Anticholinergic drugs have been reported to be extremely effective in 40% of the patients with the Pisa syndrome. Patients with Pisa syndrome that is resistant to anticholinergic drugs is mostly resolved by the reduction of the administration of the antipsychotic drugs as previously mentioned. While the specific pathology underlying idiopathic Pisa syndrome is unknown, the administration of anticholinergic drugs has provided resolution in known cases.

Reducing the dosage of the antipsychotic drugs resulted in gradual improvement in the abnormal posture. In some cases, discontinuing the use of those drugs resulted in complete disappearance of the syndrome. The time it took for the improvement and the disappearance of the syndrome depended on the type of drug being administered or the specific cause of the syndrome itself.

After the first discovery and description of Marshall–Smith syndrome in 1971, research to this rare syndrome has been carried out.

- Adam, M., Hennekam, R.C.M., Butler, M.G., Raf, M., Keppen, L., Bull, M., Clericuzio, C., Burke, L., Guttacher, A., Ormond, K., & Hoyme, H.E. (2002). Marshall–Smith syndrome: An osteochondrodysplasia with connective tissue abnormalities. 23rd Annual David W. Smith Workshop on Malformations and Morphogenesis, August 7, Clemson, SC.

- Adam MP, Hennekam RC, Keppen LD, Bull MJ, Clericuzio CL, Burke LW, Guttmacher AE, Ormond KE and Hoyme HE: Marshall-Smith Syndrome: Natural history and evidence of an osteochondrodysplasia with connective tissue abnormalities. American Journal of Medical Genetics 137A:117–124, 2005.

- Baldellou Vazquez A, Ruiz-Echarri Zelaya MP, Loris Pablo C, Ferr#{225}ndez Longas A, Tamparillas Salvador M. El sIndrome de Marshall-Smith: a prop#{243}sito de una observad#{243}n personal. An Esp Pediatr 1983; 18:45-50.

- Butler, M.G. (2003). Marshall–Smith syndrome. In: The NORD Guide to Rare Disorders. (pp219–220) Lippincott, Williams & Wilkins, Philadelphia, PA.

- Charon A, Gillerot T, Van Maldergem L, Van Schaftingen MH, de Bont B, Koulischer L. The Marshall–Smith syndrome. Eur J Pediatr 1990; 150: 54-5.

- Dernedde, G., Pendeville, P., Veyckemans, F., Verellen, G. & Gillerot, Y. (1998). Anaesthetic management of a child with Marshall–Smith syndrome. Canadian Journal of Anesthesia. 45 (7): 660. Anaesthetic management of a child with Marshall-Smith syndrome

- Diab, M., Raff, M., Gunther, D.F. (2002). Osseous fragility in Marshall–Smith syndrome. Clinical Report: Osseous fragility in Marshall-Smith syndrome

- Ehresmann, T., Gillessen-Kaesbach G., Koenig R. (2005). Late diagnosis of Marshall Smith Syndrome (MSS). In: Medgen 17.

- Hassan M, Sutton T, Mage K, LimalJM, Rappaport R. The syndrome of accelerated bone maturation in the newborn infant with dysmorphism and congenital malformations: (the so-called Marshall–Smith syndrome). Pediatr Radiol 1976; 5:53-57.

- Hoyme HE and Bull MJ: The Marshall-Smith Syndrome: Natural history beyond infancy. Western Society for Pediatric Research, Carmel, California, February, 1987. Clin Res 35:68A, 1987.

- Hoyme HE and Bull MJ: The Marshall-Smith Syndrome: Natural history beyond infancy. David W. Smith Morphogenesis and Malformations Workshop. Greenville, SC, August, 1987. Proceedings of the Greenwood Genetics Center 7:152, 1988.

- Hoyme HE, Byers PH, Guttmacher AE: Marshall–Smith syndrome: Further evidence of an osteochondrodysplasia in long-term survivors. David W. Smith Morphogenesis and Malformations Workshop, Winston-Salem, NC, August, 1992. Proceedings of the Greenwood Genetic Center 12:70, 1993.

- .

- Tzu-Jou Wang (2002). Marshall–Smith syndrome in a Taiwanese patient with T-cell immunodeficiency. Am J Med Genet Part A;112 (1):107-108.

There is an association between taking aspirin for viral illnesses and the development of Reye syndrome, but no animal model of Reye syndrome has been developed in which aspirin causes the condition.

The serious symptoms of Reye syndrome appear to result from damage to cellular mitochondria, at least in the liver, and there are a number of ways that aspirin could cause or exacerbate mitochondrial damage. A potential increased risk of developing Reye syndrome is one of the main reasons that aspirin has not been recommended for use in children and teenagers, the age group for which the risk of lasting serious effects is highest.

No research has found a definitive cause of Reye syndrome, and association with aspirin has been shown through epidemiological studies. The diagnosis of "Reye Syndrome" greatly decreased in the 1980s, when genetic testing for inborn errors of metabolism was becoming available in developed countries. A retrospective study of 49 survivors of cases diagnosed as "Reye's Syndrome" showed that the majority of the surviving patients had various metabolic disorders, particularly a fatty-acid oxidation disorder medium-chain acyl-CoA dehydrogenase deficiency.

In some countries, oral mouthcare product Bonjela (not the form specifically designed for teething) has labeling cautioning against its use in children, given its salicylate content. There have been no cases of Reye syndrome following its use, and the measure is a precaution. Other medications containing salicylates are often similarly labeled as a precaution.

The Centers for Disease Control and Prevention (CDC), the U.S. Surgeon General, the American Academy of Pediatrics (AAP) and the Food and Drug Administration (FDA) recommend that aspirin and combination products containing aspirin not be given to children under 19 years of age during episodes of fever-causing illnesses. Hence, in the United States, it is advised that the opinion of a doctor or pharmacist should be obtained before anyone under 19 years of age is given any medication containing aspirin (also known on some medicine labels as acetylsalicylate, salicylate, acetylsalicylic acid, ASA, or salicylic acid).

Current advice in the United Kingdom by the Committee on Safety of Medicines is that aspirin should not be given to those under the age of 16 years, unless specifically indicated in Kawasaki disease or in the prevention of blood clot formation.

Many professionals that are likely to be involved in the treatment of those with Stickler's syndrome, include anesthesiologists, oral and maxillofacial surgeons; craniofacial surgeons; ear, nose, and throat specialists, ophthalmologists, optometrists, audiologists, speech pathologists, physical therapists and rheumatologists.

There is no medical treatment for either syndrome but there are some recommendations that can help with prevention or early identification of some of the problems. Children with either syndrome should have their hearing tested, and adults should be aware that the hearing loss may not develop until the adult years. Yearly visits to an ophthalmologist or other eye care professional who has been informed of the diagnosis of Stickler or Marshall syndrome is important for all affected individuals. Children should have the opportunity to have myopia corrected as early as possible, and treatment for cataracts or detached retinas may be more effective with early identification. Support for the joints is especially important during sports, and some recommend that contact sports should be avoided by those who have very loose joints.

It is not possible to make a generalised prognosis for development due to the variability of causes, as mentioned above, the differing types of symptoms and cause. Each case must be considered individually.

The prognosis for children with idiopathic West syndrome are mostly more positive than for those with the cryptogenic or symptomatic forms. Idiopathic cases are less likely to show signs of developmental problems before the attacks begin, the attacks can often be treated more easily and effectively and there is a lower relapse rate. Children with this form of the syndrome are less likely to go on to develop other forms of epilepsy; around two in every five children develop at the same rate as healthy children.

In other cases, however, treatment of West syndrome is relatively difficult and the results of therapy often dissatisfying; for children with symptomatic and cryptogenic West syndrome, the prognosis is generally not positive, especially when they prove resistant to therapy.

Statistically, 5 out of every 100 children with West syndrome do not survive beyond five years of age, in some cases due to the cause of the syndrome, in others for reasons related to their medication. Only less than half of all children can become entirely free from attacks with the help of medication. Statistics show that treatment produces a satisfactory result in around three out of ten cases, with only one in every 25 children's cognitive and motoric development developing more or less normally.

A large proportion (up to 90%) of children suffer severe physical and cognitive impairments, even when treatment for the attacks is successful. This is not usually because of the epileptic fits, but rather because of the causes behind them (cerebral anomalies or their location or degree of severity). Severe, frequent attacks can (further) damage the brain.

Permanent damage often associated with West syndrome in the literature include cognitive disabilities, learning difficulties and behavioural problems, cerebral palsy (up to 5 out of 10 children), psychological disorders and often autism (in around 3 out of 10 children). Once more, the cause of each individual case of West syndrome must be considered when debating cause and effect.

As many as 6 out of 10 children with West syndrome suffer from epilepsy later in life. Sometimes West syndrome turns into a focal or other generalised epilepsy. Around half of all children develop Lennox-Gastaut syndrome.

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

Even in syndromes with no known etiology, the presence of the associated symptoms with a statistically improbable correlation, normally leads the researchers to hypothesize that there exists an unknown underlying cause for all the described symptoms.

Documented cases of Reye syndrome in adults are rare. The recovery of adults with the syndrome is generally complete, with liver and brain function returning to normal within two weeks of onset. In children, however, mild to severe permanent brain damage is possible, especially in infants. Over thirty percent of the cases reported in the United States from 1981 through 1997 resulted in fatality.

Treatment for the disease itself is nonexistent, but there are options for most of the symptoms. For example, one suffering from hearing loss would be given hearing aids, and those with Hirschsprung’s disorder can be treated with a colostomy.

Virus-related cutaneous conditions are caused by two main groups of viruses–DNA and RNA types–both of which are obligatory intracellular parasites.

- Alphavirus infection

- Asymmetric periflexural exanthem of childhood (unilateral laterothoracic exanthem)

- B virus infection

- Boston exanthem disease

- Bovine papular stomatitis

- Bowenoid papulosis

- Buffalopox

- Butcher's wart

- Chikungunya fever

- Condylomata acuminata

- Congenital rubella syndrome

- Cowpox

- Cytomegalic inclusion disease

- Dengue (Break-bone fever)

- Disseminated herpes zoster

- Eczema herpeticum (Kaposi's varicelliform eruption)

- Eczema vaccinatum

- Epidermodysplasia verruciformis

- Eruptive pseudoangiomatosis

- Erythema infectiosum (fifth disease, slapped cheek disease)

- Exanthem of primary HIV infection (acute retroviral syndrome)

- Farmyard pox

- Generalized vaccinia

- Genital herpes (herpes genitalis, herpes progenitalis)

- Gianotti–Crosti syndrome (infantile papular acrodermatitis, papular acrodermatitis of childhood, papulovesicular acrolocated syndrome)

- Giant condyloma acuminatum (Buschke–Löwenstein tumor, giant condyloma of Buschke–Löwenstein tumor)

- Hand-foot-and-mouth disease

- Heck's disease (focal epithelial hyperplasia)

- Hemorrhagic fever with renal syndrome

- Hepatitis B

- Hepatitis C

- Herpangina

- Herpes gladiatorum (scrum pox)

- Herpes simplex

- Herpes zoster oticus (Ramsay–Hunt syndrome)

- Herpetic keratoconjunctivitis

- Herpetic sycosis

- Herpetic whitlow

- HIV-associated pruritus

- Human monkeypox

- Human T-lymphotropic virus 1 infection

- Human tanapox

- Immune reconstitution inflammatory syndrome (immune recovery syndrome)

- Infectious mononucleosis (glandular fever)

- Inflammatory skin lesions following zoster infection (isotopic response)

- Intrauterine herpes simplex

- Kaposi sarcoma

- Lassa fever

- Lipschütz ulcer (ulcus vulvae acutum)

- Measles (rubeola, morbilli)

- Milker's nodule

- Modified varicella-like syndrome

- Molluscum contagiosum

- Myrmecia

- Neonatal herpes simplex

- Ophthalmic zoster

- Orf (contagious pustular dermatosis, ecthyma contagiosum, infectious labial dermatitis, sheep pox)

- Orf-induced immunobullous disease

- Orolabial herpes (herpes labialis)

- Papular purpuric gloves and socks syndrome

- Pigmented wart

- Postherpetic neuralgia (zoster-associated pain)

- Post-vaccination follicular eruption

- Progressive vaccinia (vaccinia gangrenosum, vaccinia necrosum)

- Pseudocowpox

- Recurrent respiratory papillomatosis (laryngeal papillomatosis)

- Rift Valley fever

- Roseola infantum (exanthem subitum, exanthema subitum, sixth disease)

- Roseola vaccinia

- Rubella (German measles)

- Sandfly fever (Pappataci fever, phlebotomus fever)

- Sealpox

- Varicella (chickenpox)

- Variola major (smallpox)

- Verruca plana (flat wart)

- Verruca plantaris (plantar wart)

- Verruca vulgaris (wart)

- Verrucae palmares et plantares

- Viral-associated trichodysplasia (ciclosporin-induced folliculodystrophy)

- Wasting syndrome

- West Nile virus infection

- Zoster (herpes zoster, shingles)

- Zoster sine herpete

Muir–Torre was observed to occur in 14 of 50 families (28%) and in 14 of 152 individuals (9.2%) with Lynch syndrome, also known as HNPCC.

The 2 major MMR proteins involved are hMLH1 and hMSH2. Approximately 70% of tumors associated with the MTS have microsatellite instability. While germline disruption of hMLH1 and hMSH2 is evenly distributed in HNPCC, disruption of hMSH2 is seen in greater than 90% of MTS patients.

Gastrointestinal and genitourinary cancers are the most common internal malignancies. Colorectal cancer is the most common visceral neoplasm in Muir–Torre syndrome patients.