What these inoculated parasites, called "sporozoites", do in the skin and lymphatics, exactly, has yet to be accurately determined. However, a percentage of sporozoites follow the bloodstream to the liver, where they invade hepatocytes. They grow and divide in the liver for 2–10 days, with each infected hepatocyte eventually harboring up to 40,000 parasites. The infected hepatocytes break down, releasing this invasive form of Plasmodium cells, called "merozoites" into the bloodstream. In the blood, the merozoites rapidly invade individual red blood cells, replicating over 24–72 hours to form 16–32 new merozoites. The infected red blood cell lyses, and the new merozoites infect new red blood cells, resulting in a cycle that continuously amplifies the number of parasites in an infected person. However, most of the P. vivax replicating merozoite biomass is now (since 2021) known to be hidden in the spleen and bone marrow (perhaps elsewhere too), thereby supporting the astute, long-standing (since 2011) but previously ignored theory that non-circulating merozoites are the source many P. vivax malarial recurrences (see “Recurrent malaria” section below). Over rounds of this red blood cell infection cycle in the bloodstream and elsewhere, a small portion of parasites do not replicate, but instead develop into early sexual stage parasites called male and female "gametocytes". These gametocytes develop in the bone marrow for 11 days, then return to the blood circulation to await uptake by the bite of another mosquito.
Non-specific interstitial pneumonia (NSIP) is a form of idiopathic interstitial pneumonia. Symptoms
Symptoms include cough, difficulty breathing, and fatigue. Causes
It has been suggested that idiopathic nonspecific interstitial pneumonia has an autoimmune mechanism, and is a possible complication of undifferentiated connective tissue disease; however, not enough research has been done at this time to find a cause. Patients with NSIP will often have other unrelated lung diseases like COPD or emphysema, along with other auto-immune disorders. Diagnosis
A full clinical diagnosis can only be made from a lung biopsy of the tissue, fully best performed by a VATS, done by a cardio-thoracic surgeon. Some pulmonologists may first attempt a bronchoscopy; however, this frequently fails to give a full or correct diagnosis.Lung biopsies performed on patients with NSIP reveal two different disease patterns – cellular and fibrosing – which are associated with different prognoses. The cellular pattern displays chronic inflammation with minimal fibrosis. The fibrosing pattern displays interstitial fibrosis with various inflammation levels. Both patterns are uniform and lack the prominent fibroblastic foci that are found in other types of idiopathic interstitial pneumonia. Treatment
Commonly used drugs include prednisone, imuran, and cellcept. For active cases of pneumonia for these patients, Levaquin is a commonly used antibiotic. Almost all patients with NSIP will be on oxygen. Prognosis
The fibrosing pattern of NSIP has a five-year survival rate of 86% to 92%, while the cellular pattern of NSIP has a 100% five-year survival rate. Patients with NSIP (whether cellular or fibrosing), have a better prognosis than those with usual interstitial pneumonia (UIP).