Orientia tsutsugamushi
"O. tsutsugamushi" causes a complex and dangerous infection scrub typhus. Infection starts when chiggers bite on the skin during their feeding. The bacteria are deposited at the site of feeding (inoculation), where they multiply. They cause progressive tissue damage (necrosis). Necrosis progresses to inflammation of the blood vessels called vasculitis. This in turn causes inflammation of the lymph nodes, called lymphadenopathy. Within a few days, vasculitis extends to various organs including liver, brain, kidney, meninges and the lung. The disease is responsible for nearly a quarter of all the febrile (high fever) illness in endemic areas. Mortality in severe case or due to improper treatment or misdiagnosis may be as high as 30-70%. About 6% of infected people die untreated, and 1.4% of the patients die even with medical treatment. Moreover, death rate can be as high as 13% where medical treatment is not properly handled. In cases of misdiagnosis and failure of treatment, systemic complications rapidly develop including acute respiratory distress syndrome, acute kidney failure, encephalitis, gastrointestinal bleeding, hepatitis, meningitis, myocarditis, pancreatitis, pneumonia, septic shock, sub-acute thyroiditis, and multi-organ dysfunctions. Harmful symptoms involving multiple organ failure and neurological impairment are difficult to treat, and can be lifelong debilitation or directly fatal. The central nervous system is often affected and result in various complications including cerebellitis, cranial nerve palsies, meningoencephalitis, plexopathy, transverse myelitis, neuroleptic malignant syndrome, and Guillan-Barré syndrome. Death rates due to complications can be up to 14% in brain infections, and 24% with multiple organ failure. It is the major cause of acute encephalitis syndrome in India, where viral infection Japanese encephalitis has been regarded as the main factor.
Amanita bisporigera
"Amanita bisporigera" is considered the most toxic North American "Amanita" mushroom, with little variation in toxin content between different fruit bodies. Three subtypes of amatoxin have been described: α-, β, and γ-amanitin. The principal amatoxin, α-amanitin, is readily absorbed across the intestine, and 60% of the absorbed toxin is excreted into bile and undergoes enterohepatic circulation; the kidneys clear the remaining 40%. The toxin inhibits the enzyme RNA polymerase II, thereby interfering with DNA transcription, which suppresses RNA production and protein synthesis. This causes cellular necrosis, especially in cells which are initially exposed and have rapid rates of protein synthesis. This process results in severe acute liver dysfunction and, ultimately, liver failure. Amatoxins are not broken down by boiling, freezing, or drying. Roughly 0.2 to 0.4 milligrams of α-amanitin is present in 1 gram of "A. bisporigera"; the lethal dose in humans is less than 0.1 mg/kg body weight. One mature fruit body can contain 10–12 mg of α-amanitin, enough for a lethal dose. The α-amanitin concentration in the spores is about 17% that of the fruit body tissues. "A. bisporigera" also contains the phallotoxin phallacidin, structurally related to the amatoxins but considered less poisonous because of poor absorption. Poisonings (from similar white amanitas) have also been reported in domestic animals, including dogs, cats, and cows.