He recovered making a near complete neurological recovery; however, he has stated that learning has been more difficult for him since contracting the disease.In 2018, a 10-year-old girl in the Spanish city of Toledo became the first person to have PAM in Spain, and was successfully treated using intravenous and intrathecal amphotericin B.

Prognosis
Since its first description in the 1960s, only seven people worldwide have been reported to have survived PAM out of 450 cases diagnosed, implying a fatality rate of about 98.5%. The survivors include four in the United States, one in Mexico and one in Spain. One of the US survivors had brain damage that is likely permanent, but there are two documented surviving cases in the United States who made a full recovery with no neurological damage; they were both treated with the same protocols. Epidemiology
The disease is rare and highly lethal: there had only been 300 cases as of 2008. Drug treatment research at Aga Khan University in Pakistan has shown that in-vitro drug susceptibility tests with some FDA approved drugs used for non-infectious diseases (digoxin and procyclidine were shown to be most effective of the drugs studied) have proved to kill Naegleria fowleri with an amoebicidal rate greater than 95%. The same source has also proposed a device for drug delivery via the transcranial route to the brain.In the US, the most common states with cases reported of PAM from N. fowleri are the southern states, with Texas and Florida having the highest prevalence.
There is now strong evidence that DDD is caused by uncontrolled AP activation.Spontaneous remissions of MPGN II are rare; approximately half of those affected with MPGN II will progress to end stage renal disease within ten years.In many cases, people with MPGN II can develop drusen caused by deposits within Bruchs membrane beneath the retinal pigment epithelium of the eye. Over time, vision can deteriorate, and subretinal neovascular membranes, macular detachment, and central serous retinopathy can develop. Type III
Type III is very rare, it is characterized by a mixture of subepithelial and subendothelial immune and/or complement deposits. These deposits elicit an immune response, causing damage to cells and structures within their vicinity. Has similar pathological findings of Type I disease.A candidate gene has been identified on chromosome 1.Complement component 3 is seen under immunofluorescence. it is associated with complement receptor 6 deficiency. Pathology
Membranoproliferative glomerulonephritis involves deposits at the intraglomerular mesangium. It is also the main hepatitis C associated nephropathy. It also is related to a number of autoimmune diseases, prominently systemic lupus erythematosus (SLE), Class IV. Also found with Sjögren syndrome, rheumatoid arthritis, inherited complement deficiencies (esp C3 deficiency), scleroderma, Celiac disease.The histomorphologic differential diagnosis includes transplant glomerulopathy and thrombotic microangiopathies. Diagnosis
The GBM is rebuilt on top of the deposits, causing a "tram tracking" appearance under the microscope. Mesangial cellularity is increased. Treatment
Primary MPGN is treated with steroids, plasma exchange and other immunosuppressive drugs. Secondary MPGN is treated by treating the associated infection, autoimmune disease or neoplasms.