For early cases, prompt treatment is usually curative. However, the severity and treatment of Lyme disease may be complicated due to late diagnosis, failure of antibiotic treatment, and simultaneous infection with other tick-borne diseases (coinfections), including ehrlichiosis, babesiosis, and immune suppression in the patient.

It is believed that less than 5% of people have lingering symptoms of fatigue, pain, or joint and muscle aches at the time they finish treatment. These symptoms can last for more than 6 months. This condition is called post-treatment lyme disease syndrome. As of 2016 the reason for the lingering symptoms was not known; the condition is generally managed similarly to fibromyalgia or chronic fatigue syndrome.

In dogs, a serious long-term prognosis may result in glomerular disease, which is a category of kidney damage that may cause chronic kidney disease. Dogs may also experience chronic joint disease if the disease is left untreated. However, the majority of cases of Lyme disease in dogs result in a complete recovery with, and sometimes without, treatment with antibiotics. In rare cases, Lyme disease can be fatal to both humans and dogs.

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 is a condition caused in an autosomal recessive manner. Furthermore, it is due to a defect in AIRE gene (which helps to make a protein that is called the autoimmune regulator) mapped to 21q22.3 chromosome location, hence chromosome 21.

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.

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

Infection-related cutaneous conditions may be caused by bacteria, fungi, yeast, viruses, or parasites.

Harlequin syndrome is a condition characterized by asymmetric sweating and flushing on the upper thoracic region of the chest, neck, and face. Harlequin syndrome is considered an injury to the autonomic nervous system (ANS). The ANS controls some of the body's natural processes such as sweating, skin flushing, and pupil response to stimuli. Such individuals with this syndrome have an absence of sweat skin flushing unilaterally; usually on the one side of the face, arms, and chest. It is an autonomic disorder that may occur at any age. Harlequin syndrome affects fewer than 200,000 people in the United States.

Symptoms associated with Harlequin syndrome are more likely to appear when a person has been in the following conditions: exercising, warm environment, and intense emotional situation. Since one side of the body sweats and flushes appropriately to the condition, the other side of the body will have an absence of such symptoms. This syndrome has also been called the "Harlequin sign," and thought to be one of the spectrum of diseases that may cause Harlequin syndrome.

It can also be the outcome of a one sided endoscopic thoracic sympathectomy (ETS) or endoscopic sympathetic blockade (ESB) surgery.

Harlequin syndrome can also be seen as a complication of VA (veno-arterial) extracorporeal membrane oxygenation (ECMO). This involves differential hypoxemia (low oxygen levels in the blood) of the upper body in comparison to the lower body.

One possible cause of Harlequin syndrome is a lesion to the preganglionic or postganglionic cervical sympathetic fibers and parasympathetic neurons of the ciliary ganglion. It is also believed that torsion (twisting) of the thoracic spine can cause blockage of the anterior radicular artery leading to Harlequin syndrome. The sympathetic deficit on the denervated side causes the flushing of the opposite side to appear more pronounced. It is unclear whether or not the response of the undamaged side was normal or excessive, but it is believed that it could be a result of the body attempting to compensate for the damaged side and maintain homeostasis.

Since the cause and mechanism of Harlequin syndrome is still unknown, there is no way to prevent this syndrome.

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.

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.

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.

It is still unknown which bio-chemical mechanisms lead to the occurrence of West syndrome. It is conjectured that it is a malfunction of neurotransmitter function, or more precisely, a malfunction in the regulation of the GABA transmission process. Another possibility being researched is a hyper-production of the Corticotropin-releasing hormone (CRH). It is possible that more than one factor is involved. Both hypotheses are supported by the effect of certain medications used to treat West syndrome.

Cases of epilepsy have been historically divided into three different groups: symptomatic, cryptogenic, and unknown. The International League Against Epilepsy (ILAE) recommended in 2011 to abandon these terms for reasons of clarity and instead try to place individual cases into one of the following 3 groups: genetic, structural/metabolic, and unknown. The new terms are more immediately clear in their meaning, except that the structural and metabolic group includes cases that have a genetic component that does not always directly lead to the condition. Only the genetic grouping has a known direct genetic cause. "Unknown" cases may be of "unknown" genetic, structural, metabolic, or other unknown cause.

The old terminology was defined by the ILAE as follows:

- symptomatic: the epilepsy is the consequence of a known or suspected disorder of the central nervous system.

- cryptogenic: this refers to a disorder whose cause is hidden or occult. Cryptogenic epilepsies are presumed to be symptomatic.

- idiopathic: there is no underlying cause other than a possible hereditary predisposition.

The remainder of this section will refer to the older terminology.

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.

Typically, females and older patients with organic brain changes are more likely to develop Pisa syndrome. Organic brain changes are physical changes in the brain which lead to neurological dysfunction, including dementia and frontal lobe syndrome. This includes the presence of neurodegenerative illnesses such as Alzheimer's Disease and Parkinson's Disease.

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.

Pisa syndrome is predominantly caused by a prolonged administration or an overly dosed administration of antipsychotic drugs. Although antipsychotic drugs are known to be the main drugs that are concerned with this syndrome, several other drugs are reported to have caused the syndrome as well. Certain antidepressants, psychoactive drugs, and antiemetics have also been found to cause Pisa syndrome in patients.

Drugs found to have caused Pisa Syndrome:

- Atypical antipsychotic drugs- ex. clozapine, aripiprazole

- Tricyclic antidepressants- ex. clomipramine

- Psychoactive drugs

- Antiemetic drugs

- Cholinesterase inhibitors

- Galantamine

Based on the drugs that caused Pisa syndrome, it has been implicated that the syndrome may be due to a dopaminergic-cholinergic imbalance or a serotonergic or noradrenergic dysfunction. For the development of Pisa syndrome that cannot be alleviated by anticholinergic drugs, it has been considered that asymmetric brain functions or neural transmission may be the underlying mechanism. How these drugs interact with the biochemistry of the brain to cause the syndrome is unknown and a topic of current research.

Respiratory complications are often cause of death in early infancy.

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.

There is considerable research into the causes, diagnosis and treatments for FGIDs. Diet, microbiome, genetics, neuromuscular function and immunological response all interact. Heightened mast cell activation has been proposed to be a common factor among FGIDs, contributing to visceral hypersensitivity as well as epithelial, neuromuscular, and motility dysfunction.

Usher syndrome, also known as Hallgren syndrome, Usher-Hallgren syndrome, retinitis pigmentosa-dysacusis syndrome, or dystrophia retinae dysacusis syndrome, is an extremely rare genetic disorder caused by a mutation in any one of at least 11 genes resulting in a combination of hearing loss and visual impairment. It is a leading cause of deafblindness and is at present incurable.

Usher syndrome is classed into three subtypes according to onset and severity of symptoms. All three subtypes are caused by mutations in genes involved in the function of the inner ear and retina. These mutations are inherited in an autosomal recessive pattern.

Overall, the estimated prevalence of Stickler syndrome is about 1 in 10,000 people. Stickler syndrome affects 1 in 7,500 to 9,000 newborns.