Sex organs, the gonads, are also incompletely separated and are interdependent between sexes. Egg-making organ, the vitelline gland in female does not develop in the absence of male. Male gametes, spermatozoa, are present in the oviduct. In males, there are rudimentary ovaries, oviduct, and oocytes (developing female gametes), as well as vitelline cells. Males also possess the genes for hermaphroditism in flukes. Thus, they are technically hermaphrodites. Egg
The eggs are oval-shaped, measuring 115–175 µm long and 45–47 µm wide, and ~150 µm diameter on average. They have pointed spines towards the broader base on one side, i.e. lateral spines. This is an important diagnostic tool because co-infection with S. haematobium (having a terminal-spined eggs) is common, and they are hard to distinguish. When the eggs are released into the water, a lot of them are immature and unfertilised so that they do not hatch. When the eggs are larger than 160 µm in diameter, they also fail to hatch. Larva
The miracidium (from the Greek word μειράκιον, meirakion, meaning youth) is pear-shaped, and gradually elongates as it ages. It measures about 136 μm long and 55 μm wide. The body is covered by anucleate epidermal plates separated by epidermal ridges. The epidermal cells give off numerous hair-like cilia on the body surface. There are 17–22 epidermal cells. Epidermal plate is absent only at the extreme anterior called apical papilla, or terebratorium, which contains numerous sensory organelles.
Spinocerebellar ataxia type 6 (SCA6) is a rare, late-onset, autosomal dominant disorder, which, like other types of SCA, is characterized by dysarthria, oculomotor disorders, peripheral neuropathy, and ataxia of the gait, stance, and limbs due to cerebellar dysfunction. Unlike other types, SCA 6 is not fatal. This cerebellar function is permanent and progressive, differentiating it from episodic ataxia type 2 (EA2) where said dysfunction is episodic. In some SCA6 families, some members show these classic signs of SCA6 while others show signs more similar to EA2, suggesting that there is some phenotypic overlap between the two disorders. SCA6 is caused by mutations in CACNA1A, a gene encoding a calcium channel α subunit. These mutations tend to be trinucleotide repeats of CAG, leading to the production of mutant proteins containing stretches of 20 or more consecutive glutamine residues; these proteins have an increased tendency to form intracellular agglomerations. Unlike many other polyglutamine expansion disorders expansion length is not a determining factor for the age that symptoms present. Signs and symptoms
SCA6 is typified by progressive and permanent cerebellar dysfunction. These cerebellar signs include ataxia and dysarthria, likely caused by cerebellar atrophy. Prior to diagnosis and the onset of major symptoms, patients often report a feeling of "wooziness" and momentary imbalance when turning corners or making rapid movements. The age at which symptoms first occur varies widely, from age 19 to 71, but is typically between 43 and 52.