What if M.S, Grand Mal seizures, meningitis and the like are all a result of the central nervous systems protective barrier being destroyed by disseminated Strongyloidiasis? Specifically Larva currens/Cutaneous strongyloidiasis maybe?
Strongyloidiasis Current Status with Emphasis in Diagnosis and Drug Research
CDC-Strongyloides -|- Larva Currens -|- Strongyloides meningitis -|- Cutaneous Larva Migrans & Larva Currens
From www.epilepsy.com <–THIS – IF YOU HAVE HAD SEIZURES
Strongyloides stercoralis is a small nematode that can parasitize the small bowel of humans. Larvae living freely in moist soil invade rapidly through contacted skin and migrate into lymphatics to reach the venous system, where they travel to the lungs, migrate up airways to the glottis, and then down the esophagus to the small intestine.
When immune function is compromised (e.g., in HIV infection or AIDS), the CNS can become involved in disseminated strongyloidiasis. CNS manifestations can be secondary to larvae infestation. More commonly, however, gut bacteria transmitted by the migrating parasite produce bacterial meningitis. Seizures can be an epiphenomenon of these complications.
Thiabendazole can be helpful if started early in the disease process, but disseminated strongyloidiasis is usually fatal.Comorbid seizure management is routine.162
Adapted from: Goldstein MA and Harden CL. Infectious states. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;83-133.
With permission from Elsevier (www.elsevier.com).
The course of Strongyloides stercoralis infection is usually asymptomatic with a low discharge of rhabditoid larva in feces. However, the deleterious effects of alcohol consumption seem to enhance the susceptibility to infection, as shown by a fivefold higher strongyloidiasis frequency in alcoholics than in nonalcoholics. Moreover, the association between S. stercoralis infection and alcoholism presents a risk for hyperinfection and severe strongyloidiasis. There are several possible mechanisms for the disruption of the host-parasite equilibrium in ethanol-addicted patients with chronic strongyloidiasis. One explanation is that chronic ethanol intake stimulates the hypothalamic-pituitary-adrenal (HPA) axis to produce excessive levels of endogenous cortisol, which in turn can lead to a deficiency in type 2 T helper cells (Th2) protective response, and also to mimic the parasite hormone ecdysone, which promotes the transformation of rhabditiform larvae to filariform larvae, leading to auto-infection. Therefore, when untreated, alcoholic patients are continuously infected by this autoinfection mechanism. Thus, the early diagnosis of strongyloidiasis and treatment can prevent serious forms of hyperinfection in ethanol abusers.
Strongyloides stercoralis Infection and Strongyloidiasis
The Strongyloides stercoralis threadworm is a soil-transmitted nematode that resides in the small intestine of human hosts. The parasitic infection takes place when filariform larvae penetrate through the skin, usually of the feet, and migrate through the bloodstream to the lungs . After ascending the respiratory tract to the oropharynx, larvae are swallowed and reach the duodenal mucosal crypts to grow into parthenogenetic females that produce embryonated-eggs. Thereafter, rhabditoid larvae hatch from the eggs and are excreted in feces. However, some larvae may transform into the filariform infective stage and penetrate the perirectal mucosa or skin, thereby reentering the circulatory system and starting the cycle again. Therefore, if not treated, because this is an auto-infection process, the host may remain in a chronic carrier state for decades .