Symptoms can appear ten to 30 minutes after ingestion, and include nausea, vomiting, diarrhea, abdominal pain,  tingling or burning lips, gums, tongue, face, neck, arms, legs, and toes. Shortness of breath, dry mouth, a choking feeling, confused or slurred speech, and loss of coordination are also possible. PSP in wild marine mammals
PSP has been implicated as a possible cause of sea otter mortality and morbidity in Alaska, as one of its primary prey items, the butter clam (Saxidomus gigantea) bioaccumulates saxitoxin as a chemical defense mechanism. In addition, ingestion of saxitoxin-containing mackerel has been implicated in the death of humpback whales.Additional cases where PSP was suspected as the cause of death in Mediterranean monk seals (Monachus monachus) in the Mediterranean Sea  have been questioned due to lack of additional testing to rule out other causes of mortality. Detection and treatment
In Vivo, in Vitro, analytical techniques and immunoassays can all be used in order to determine whether saxitoxin is present within shellfish or has been ingested by humans. The most common In Vivo method used is that of mouse bioassays, which provides quantitative and qualitative data regarding the relative toxicity of a suspected PSP infection. An in Vitro method of detection commonly used is that of receptor binding assays which provides similar data to that of mouse bioassays.
Incontinentia pigmenti (IP) is a rare X-linked dominant genetic disorder that affects the skin, hair, teeth, nails and central nervous system. It is named from its appearance under a microscope.The disease is characterized by skin abnormalities that begin in childhood, usually a blistering rash which heals, followed by the development of harder skin growths. The skin may develop grey or brown patches which fade with time. Other symptoms can include hair loss, dental abnormalities, eye abnormalities that can lead to vision loss and lined or pitted fingernails and toenails. Associated problems can include delayed development, intellectual disability, seizures and other neurological problems. Most males with the disease do not survive to childbirth. Incontinentia pigmenti is caused by a mutation in the IKBKG gene, which encodes the NEMO protein, which serves to protect cells against TNF-alpha-induced apoptosis. A lack of IKBKG therefore makes cells more prone to apoptosis. There is no specific treatment; individual conditions must be managed by specialists. Presentation
The skin lesions evolve through characteristic stages:
blistering (from birth to about four months of age),
a wart-like rash (for several months),
swirling macular hyperpigmentation (from about six months of age into adulthood), followed by
linear hypopigmentation.Alopecia, dental anomalies, and dystrophic nails are observed. Some patients have retinal vascular abnormalities predisposing to retinal detachment in early childhood. Cognitive delays or intellectual disability are occasionally seen.The discolored skin is caused by excessive deposits of melanin (normal skin pigment). Most newborns with IP will develop discolored skin within the first two weeks.