Balamuthia mandrillaris, an opportunistic agent of granulomatous amebic encephalitis, infects the brain via the olfactory nerve pathway.

Balamuthia mandrillaris is a free-living ameba and an opportunistic agent of lethal granulomatous amebic encephalitis (GAE) in humans and other mammals. Its supposed routes of infection have been largely assumed from what is known about Acanthamoeba spp. and Naegleria fowleri, other free-living amebae and opportunistic encephalitis agents. However, formal proof for any migratory pathway, from GAE patients or from animal models, has been lacking. Here, immunodeficient mice were infected with B. mandrillaris amebae by intranasal instillation, the most likely natural portal of entry. By means of classical and immunohistology, the amebae are shown to adhere to the nasal epithelium, progress along the olfactory nerves, traverse the cribriform plate of the ethmoid bone, and finally infect the brain. A similar invasion pathway has been described for N. fowleri. The data suggest that the olfactory nerve pathway is a likely route for natural infection of the brain by B. mandrillaris amebae.

[Studies on chemotactic behaviors of Strongyloides ratti infective larvae in vitro and migration routes of the larvae in rat head].

For the purpose of clarifying host-finding mechanisms, the infective larvae of Strongyloides ratti were run on an agarose plate which had been placed various attractants around the larvae. They were accumulated at the sites of sodium compounds, serum proteins and albumins. At 20, 30, 40 hours after infection, rats were killed and heads were separated. They were then processed for thin section specimens. Larvae were found in brains, olfactory bulbs and its nerves. These larvae seemed to move along olfactory nerves during descending from the cranial cavity. Another migration study was done by whole body autoradiography after 35S-methionine labeling for clarifying the larval pathway how to invade cranial cavity in the rats. They first crawled under subcutaneous region of rat and then accumulated at the tip of the nose. Next, they began to ascend olfactory nerves. They were in cranial cavity up to 20 hours after infection and then descending same route to nasal cavity. I don't know why they aim the cranial cavity but they had necessity to invade the cranial cavity and stay there for appropriate time to be an adult in the intestine.

A light microscopy study of the migration of Naegleria fowleri from the nasal submucosa to the central nervous system during the early stage of primary amebic meningoencephalitis in mice.

The migratory pathway of Naegleria fowleri from the nasal submucosa to the central nervous system (CNS) during the early stage of primary amebic meningoencephalitis (PAM) was investigated in mice. Twenty-one-day-old CD-1 mice were inoculated by intranasal instillation of 1 x 10(6) amebas. Animals were divided into 3 groups of 5 and, after being anesthetized, were killed at intervals of 24, 32, and 48 hr postinoculation by transcardial perfusion with formaldehyde, acetic acid, and methanol. The heads were decalcified, divided in the midsagittal plane, and the area of the cribriform plate removed and embedded in paraffin. Serial sections were cut at 8 microm and stained with a combination of celestin blue, Harris' hematoxylin, and acid fuchsin for light microscopy. Focal inflammation and amebas were observed in the submucosal nerve plexus, olfactory nerves penetrating the cribriform plate, and the olfactory bulb of the brain as early as 24 hr postinoculation. The time periods selected assured that the disease process would not obliterate soft tissue structures. Earlier studies used moribund mice in which the inflammation and the number of amebas were overwhelming. The present study provides convincing evidence that amebas gain initial access to the CNS through olfactory nerves within the cribriform plate during the early stages of PAM.