The Myxosporidia that invade tissues are often deadly to their hosts. They may be present in a state of “diffuse infiltration” when practically every organ of the body may be infected, as in barbel disease (due to Myxobolus pfeifferi). On the other hand, the parasites may be concentrated at one spot, when cysts, either large or small, are produced. Such cysts occur on the gills of many fishes. A few additional important pathogenic forms are Myxobolus cyprini, the excitant of “pockenkrankheit” of carp, and Lentospora cerebralis, parasitic in the skeleton of Salmonidæ and Gadidæ. The skeletons of the tail, fins and skull particularly are seats of infection, and from the skull the Lentospora can spread to the semicircular canals, resulting in loss of power to maintain its balance on the part of the fish. On this account the malady is termed “drehkrankheit.” Young fish are more particularly infected. Myxobolus neurobius infects the spinal cord and nerves of trout.
Myxosporidia are divided into two sub-orders—Disporea and Polysporea—according to whether they form only two or several spores during their growth. The former include two genera limited to fishes, which are easily distinguishable by the shape of the spores: Leptotheca, Thél., with a rounded spore, and Ceratomyxa, Thél., with a very elongate spore. The larger number of genera belong to the Polysporea, which are divided into three families:
| (1) Amœboid germ with a vacuole the contents of which do not stain with iodine. |  | (a) With two polar capsules.—Myxidiidæ. |
| (b) With four polar capsules.—Chloromyxidæ. | ||
| (2) Amœboid germ with a vacuole stainable with iodine. Spores with two polar capsules.—Myxobolidæ. | ||
| For further subdivisions the differences in the spores are principally utilized. | ||
Order. Microsporidia, Balbiani.
These are the organisms discovered in the stickleback by Gluge in 1834, and in Coccus hesperidum by Leydig in 1853. They have since been found in numerous other arthropods, especially insects. They acquired particular importance when it was discovered that they were the cause of the “pébrine” disease (“gattina” of the Italians) which caused so much destruction amongst silkworms (Bombyx mori). Pasteur (1867–70) and especially Balbiani (1866) participated in the researches on Nosema bombycis, and it was the latter who classed the “pébrine bodies” or “psorospermia of the arthropoda” amongst the Sporozoa as Microsporidia (1882).[223] The complete life cycle of N. bombycis was described in 1909 by Stempell. The Microsporidia are not confined to insects and arachnoids, they are now known to occur also in crustacea, worms, bryozoa, fishes, amphibians and reptiles. Certain tumours in fishes, similar to those formed by many Myxosporidia, are produced by Microsporidia. Fantham and Porter found that Nosema apis was pathogenic to bees and other insects, and was the causal agent of the so-called “Isle of Wight” disease in bees[224] in Great Britain.
The Microsporidia, as their name implies, form minute spores which usually are oval or pear-shaped. Each spore contains a single polar capsule which is not easily visible in the fresh state (fig. 98, f) and a single amœboid germ issues from the spore (fig. 99, b).
Fig. 98.—Nosema apis. Various stages in life-cycle. a, planonts or amœbulæ from chyle stomach of bee; b, amœboid planont creeping over surface of gut epithelial cell; c, uninucleate trophozoite within epithelial cell; d, meront with nucleus divided into four, about to form four spores; e, epithelial cell crowded with spores; f, young spore; g, spore showing five nuclei, polar filament ejected, and amœbula, about to issue. × 1,500, a-e; × 2,150, f-g. (After Fantham and Porter.)
The life cycle of Nosema apis, parasitic in bees, may be taken as an example of that of a microsporidian. The infection of the host is initiated by the ingestion of spores of N. apis in food or drink contaminated with the excrement of other infected bees. Under the influence of the digestive juice of the bee the spore-coat (sporocyst) softens, the polar filament is ejected and anchors the spore to the gut epithelium, and the minute amœbula contained in the spore emerges. The amœbula is capable of active amœboid movements (fig. 98, b) and so is termed the planont or wandering form (fig. 98, a). After a short time each planont penetrates between or into the cells of the epithelium of the gut, a few only passing through into the body cavity. Within the cells the amœbulæ become more or less rounded, lose their power of movement, and after a period of growth of the trophozoite (fig. 98, c) commence to divide actively, these dividing forms being known as meronts (fig. 98, d). Various forms of fission occur, and during this phase, termed merogony, the numbers of the parasite within the host are greatly increased, with concomitant destruction of the epithelium (fig. 98, e). After a time sporogony commences. The full-grown meront becomes successively the pansporoblast and sporoblast. Nuclear multiplication and differentiation ensue and five nuclei are ultimately produced. At the same time a sporocyst is secreted, and two vacuoles are produced within. One is the polar capsule, and within it the polar filament is differentiated; the other forms the posterior vacuole (fig. 98, g). Between the two vacuoles the body cytoplasm or sporoplasm forms a girdle-like mass. Of the nuclei, one regulates the polar capsule, two control the secretion of the sporocyst, and two remain in the sporoplasm. The polar capsule and polar filament are not usually visible in the fresh condition, but can be demonstrated by the use of various chemical reagents (fig. 100). The sporoplasm ultimately becomes the amœbula (fig. 98, g) which issues from the spore after the ejection of the polar filament.