The microsporidia are a unique group of uni-cellular obligate intracellular parasites.

They are observed as free-living, mature spores of approximately 1-4m in length and
characterized by a protective chitinous exospore containing a polaroplast, posterior vacuole,
and coiled polar filament that transfers the spore contents (sporoplasm) into the host-cell
cytoplasm (reviewed in Texier et al., 2010). Existing freely in a variety of environments, spores
exhibit high resistance to extremely low temperatures (Koudela et al., 1999), dessication
(Waller, 1979), and a range of pH values (Shadduck and Polley, 1978). Consequently, spores can
remain viable for time periods ranging from months to years in various environments (Kramer,
1970) and may be considered ubiquitous.
Microsporidia infect host cells by a germination process in which the polar filament is
everted from inside the spore, and penetrates the hosts cell membrane. The spore
subsequently extrudes the sporoplasm into the host cytoplasm. The sporoplasm then
undergoes repeated division, creating multiple meronts. This is followed by sporogony,
producing sporonts, which further divide into sporoblasts. Sporoblasts subsequently develop
into mature spores that are released into the surrounding environment by host cell rupture
(Figure 1.4). Entry to host cells may be initiated from outside the host membrane or by
phagocytic uptake (Franzen et al., 2005), but ultimately it appears to depend on specific triggers
preceding germination. The germination process seems to be mediated by chemical conditions
specific to suitable hosts (reviewed in Keohane and Weiss, 1998), such as pH shifts between the
stomach and intestine or chemical changes in the phagosome (Franzen, 2004). Stimulation of
spore activation and germination by such specific conditions likely serves an adaptive function
by ensuring that infective processes are initiated only when in close proximity to a suitable
host. Given the 50-100m length of a spores polar filament (Xu and Wiess, 2005), host cell-
detection prior to germination would greatly increase the probability of successful infection.

Microsporidia adalah kelompok yang unik dari uni - selular parasit obligat intraseluler .
Mereka diamati sebagai hidup bebas , spora matang sekitar 1 - 4m panjang dan
ditandai dengan exospore chitinous pelindung yang mengandung polaroplast , posterior vakuola ,
dan melingkar filamen kutub yang mentransfer isi spora ( sporoplasm ) ke dalam sel inang
sitoplasma ( terakhir di Texier et al . , 2010). Yang ada secara bebas di berbagai lingkungan , spora
menunjukkan resistensi yang tinggi terhadap temperatur yang sangat rendah ( Koudela et al . , 1999) ,
dessication
( Waller , 1979) , dan berbagai nilai pH ( Shadduck dan Polley , 1978) . Akibatnya , spora dapat
tetap bertahan untuk jangka waktu mulai dari bulan sampai tahun di berbagai lingkungan ( Kramer ,
1970) dan dapat dianggap mana-mana .
Microsporidia menginfeksi sel inang oleh proses perkecambahan dimana filamen kutub
everted dari dalam spora , dan menembus membran sel inang . spora
kemudian Ekstrud sporoplasm ke dalam sitoplasma inang . Sporoplasm kemudian
mengalami pembelahan berulang-ulang, membuat beberapa meronts . Ini diikuti dengan sporogoni ,
memproduksi sporonts , yang selanjutnya membagi menjadi sporoblasts . Sporoblasts kemudian
mengembangkan
menjadi spora matang yang dilepaskan ke lingkungan sekitarnya oleh ruptur sel inang
( Gambar 1.4 ) . Masuk ke sel inang dapat dimulai dari luar membran host atau oleh
serapan fagositosis ( Franzen et al . , 2005) , tetapi akhirnya tampaknya tergantung pada pemicu
tertentu
sebelumnya perkecambahan . Proses perkecambahan tampaknya dimediasi oleh kondisi kimia
khusus untuk host yang cocok ( terakhir di Keohane dan Weiss , 1998) , seperti perubahan pH antara
lambung dan usus atau perubahan kimia dalam phagosome ( Franzen , 2004) . Stimulasi aktivasi spora
dan perkecambahan oleh kondisi tertentu seperti mungkin melayani fungsi adaptif
dengan memastikan bahwa proses infeksi yang dimulai hanya ketika di dekat yang cocok
tuan rumah . Mengingat panjang 50 - 100m filamen spora yang polar ( Xu dan Wiess , 2005) , sel inang
deteksi sebelum perkecambahan akan sangat meningkatkan kemungkinan infeksi sukses


Generalized life cycle schematic for microsporidian infection. 1) Infective spores (IS) detect host cells
(HC) and pierce the host membrane with a polar filament (PF). This may occur from outside the cell (a), or from
within a phagolysosome following phagocytic uptake (b). 2) Spore contents (sporoplasm, SP) are extruded into
host cell cytoplasm where merogeny occurs, producing meronts (M). 3) Spore proliferative development into
sporonts (S) may occur within (a) a parasitophorous vacuole (PV) derived from host membrane or (b) in direct
contact with host cell cytoplasm. 4) Proliferation continues and sporonts metamorphose into mature spores (MS)
that eventually fill host cytoplasm. 5) Subsequent death of host cell releases mature infective spores into the
environment. N host cell nucleus. Image Mike MacLeod, 2012.

Generalized siklus hidup skematis untuk infeksi mikrosporidia. 1) infektif spora (IS) mendeteksi
sel inang
(HC) dan menembus membran host dengan filamen polar (PF). Hal ini mungkin terjadi dari luar
sel (a), atau dari
dalam phagolysosome berikut serapan fagositosis (b). 2) Isi Spore (sporoplasm, SP) yang
diekstrusi menjadi
tuan sitoplasma sel di mana merogeny terjadi, memproduksi meronts (M). 3) Spore
pengembangan proliferatif ke
sporonts (S) dapat terjadi dalam (a) vakuola parasitophorous (PV) yang berasal dari membran
host atau (b) dalam langsung
kontak dengan sitoplasma sel inang. 4) Proliferasi terus dan sporonts bermetamorfosis menjadi
spora matang (MS)
yang akhirnya mengisi tuan sitoplasma. 5) kematian selanjutnya dari rilis sel inang dewasa spora
infektif ke dalam
lingkungan. N - inti sel inang. Gambar Mike MacLeod, 2012.



Neon tetra disease is difficult to diagnose reliably and even more difficult to treat. Despite the name, neon
tetra disease can
affect a range of other tetras besides neon tetras, and has been reported from a variety of other aquarium
fish as well.
Identification
At very low levels of infection there may be no symptoms visible at all, and it is usually the case that the
more obvious
symptoms of neon tetra disease are only apparent on heavily infected aquarium fish a few days away
from death. Infected
aquarium fish will often spend less time with their schoolmates than normal, typically hiding away under
aquarium plants and
showing no interest in fish food. The aquarium fishs colors fade, and sometimes gray or white patches on
the flanks
become apparent. In advanced cases the aquarium fish may have trouble swimming, and the fish may
develop odd
swellings or contortions indicative of damage to the musculature. Usually the aquarium fish dies within
two or three days of
the first symptoms of neon tetra disease becoming apparent.
Despite the name, neon tetra disease can affect a range of other tetras besides neons, and has been
reported from a
variety of other aquarium fish as well
Unfortunately for the aquarist several other diseases can cause similar symptoms to neon tetra disease,
including systemic
bacterial infections, chronically poor diet and/or environmental conditions, and even old age. Some
aquarists have coined
the term false neon tetra disease to refer to bacterial infections with broadly similar symptoms
Pathology
The parasite responsible for neon tetra disease is called Pleistophora hyphessobryconis. It is a single-
celled organism that
gets into its host by being consumed alongside fish food. The parasite was first identified in neon tetras,
hence the common
name, but it has also been reported from a range of other tetras as well. Less frequently, it has been
reported to affect
non-tetras including minnows, danios, goldfish, and even angelfish
Life Cycle
Pleistophora hyphessobryconis gets into the aquarium fish through accidental ingestion. Under aquarium
conditions this is
most commonly some sort of scavenging or cannibalism, the parasites inside a dead fish being
consumed by a healthy fish.
Once inside the gut the parasite spreads throughout the fishs body and eventually gets into the skeletal
muscles where it
matures. Eventually the parasites produce large numbers of spores, and when the host fish is eaten by a
predator or
consumed by a scavenger after death, the spores are then able to get into new fish
Parasites in tissues other than the muscles, for example those in the gut or kidneys, may release viable
spores into the
aquarium water in other ways as well, even before the host fish dies. This is why isolating infected
aquarium fish is so
important. In one laboratory experiment, an infected neon tetra was placed alongside a group of ten zebra
danios, and no
fewer than seven of those danios became infected