Cardiovascular symptoms include bradycardia, tachycardia, hypotension, hypertension, orthostatic tachycardia, exercise intolerance, and rhythm disorders. Death from the condition can occur, but is very rare.Dyspareunia and other ciguatera symptoms have developed in otherwise healthy males and females following sexual intercourse with partners suffering ciguatera poisoning, signifying that the toxin may be sexually transmitted. Diarrhea and facial rashes have been reported in breastfed infants of poisoned mothers, suggesting that ciguatera toxins migrate into breast milk.The symptoms can last from weeks to years, and in extreme cases as long as 20 years, often leading to long-term disability. Most people do recover slowly over time. Cause
Gambierdiscus toxicus is the primary dinoflagellate responsible for the production of a number of similar polyether toxins, including ciguatoxin, maitotoxin, gambieric acid and scaritoxin, as well as the long-chain alcohol palytoxin. Other dinoflagellates that may cause ciguatera include Prorocentrum spp., Ostreopsis spp., Coolia monotis, Thecadinium spp. and Amphidinium carterae. Diagnosis
Diagnosis is based on a persons symptoms together with having recently eaten fish. If a number of those who eat the same fish have symptoms the diagnosis becomes more likely. If some of the fish they had previously eaten is available this can also be tested to confirm the diagnosis. Other potential causes such as paralytic shellfish poisoning (PSP), neurotoxic shellfish poisoning (NSP), scombrotoxin fish poisoning, and pufferfish poisoning should be excluded.The reversal of hot and cold sensations is an occasional symptom of CFP that may help differentiate it from intestinal "flu". Treatment
There is no known effective treatment or antidote for ciguatera poisoning.
chronic myelogenous leukemia (CML), polycythemia vera, essential thrombocytosis, or myelofibrosis). The detection of a chloroma is considered de facto evidence these premalignant conditions have transformed into an acute leukemia requiring appropriate treatment. For example, presence of a chloroma is sufficient to indicate chronic myelogenous leukemia has entered its blast crisis phase. In Eosinophilic leukemia
At least one case of FIP1L1-PDGFRA fusion gene-induced eosinophilic leukemia presenting with myeloid sarcoma and eosinophilia has been reported. This form of myeloid sarcoma is distinguished by its highly successful treatment with imatinib (the recommended treatment for FIP1L1-PDGRGA fusion gene-induced eosinophilic leukemia) rather than more aggressive and toxic therapy. Primary chloroma
Very rarely, chloroma can occur without a known pre-existing or concomitant diagnosis of acute leukemia, acute promyelocytic leukemia or MDS/MPS; this is known as primary chloroma. Diagnosis is particularly challenging in this situation (see below). In almost all reported cases of primary chloroma, acute leukemia has developed shortly afterward (median time to development of acute leukemia 7 months, range 1–25 months). Therefore, primary chloroma could be considered an initial manifestation of acute leukemia, rather than a localized process, and could be treated as such. Where disease development or markers indicate progresses to acute promyleocytic leukemia (AML3) treatment should be tailored to this form of disease. Location and symptoms
Chloromas may occur in virtually any organ or tissue. The most common areas of involvement are the skin (also known as leukemia cutis) and the gums.