Chlamydia spp

From Fish
A section of yellowtail kingfish gill showing epitheliocystis infection.
Branchial cysts (epitheliocystis) at the base of the secondary lamellae surrounded a thickened host epithelium.

Epitheliocystis is caused by Chlamydia spp bacteria. This bacteris occurs in both freshwater and marine fish and is widespread in all cichlid species in southern Africa, Kenya and Israel, in the common carp and in the Mediterranean and Red Sea grey mullets[1].

Life cycle

Invaded epithelial cells grow gradually into a grossly hypertrophic body. Organisms are secluded within an inclusion which expands with the increase in the bacterial mass. The border of the inclusion is lined by deformed host cell organelles: a network of microtubules or microfibrils or residue of mucus droplets. Through successive binary divisions, or budding, round chlamydia-like organisms (averaging 0.7μm in diameter) form branching chains which further transform into rickettsia-like rods (1–2μm long), single or attached into chains, which finally split into cocci (0.5 × 0.3μm in size) with condensed cytoplasm, which are the presumed dispersing infective stages. The latter are released into the water with the collapse of the host cell. This stage is structurally, as well as functionally, reminiscent of the chlamydial elementary bodies[2]. Epitheliocystis from different fish host species may vary in the morphology of individual stages and demonstrate additional stages with distinct morphology and division patterns[3].


Diagnosis

Epitheliocystis is chlamydial organisms invading and causing gross hypertrophy of integumental epithelial cells, mostly of the gills; lining and respiratory cells as well as mucus and chloride cells. Infected cells grow into transparent (up to 100 × 55 μm in size) bodies with fine granular contents. Transmission electron microscopy reveals pleomorphic (round, rods and cocci) prokaryotic organisms bound with a trilaminated membrane and containing a nucleoid. Epitheliocystis organisms thus far have not been cultured in vitro.

In benign infections, tissue changes are limited to the formation of a thin capsular structure around the hypertrophic cell, the respiratory capillaries may send extensions to the surface of the infected cell. The “proliferative” condition results in massive epithelial hyperplasia which may embed the hypertrophic infected cell as well as part or all of the gill lamellae of the filament. In mullets and carp, the mere overload of the gills with hypertrophic cells caused severe erosion of the gill architecture, which interferes with the respiratory function[4].

Treatment

Applications of antibiotics have, thus far, proved to be ineffective. The proliferative condition may be mediated through immediate reduction of stocking densities.

References

  1. Paperna, I. & Alves de Matos, A.P., (1984) The developmental cycle of epitheliocystis in carp, Cyprinus carpio L. J Fish Dis 7:137–147
  2. Paperna, I., Sabnai, I. & Zachary, A., (1981) Ultrastructural studies in piscine epitheliocystis: evidence for a pleomorphic developmental cycle. J Fish Dis 4:459–472
  3. Paperna, I., Sabnai, I. & Zachary, A., (1981) Ultrastructural studies in piscine epitheliocystis: evidence for a pleomorphic developmental cycle. J Fish Dis 4:459–472
  4. Paperna, I. & Sabnai, I., (1980) Epitheliocystis disease in Fishes. In: Ahne, W. (ed.) Fish Diseases, Third COPRAQ-Session, Springer-Verlag Berlin, Heidelberg 228–234