Myxosporeans Infection Flashcards
Common parasites of cold-blooded vertebrates, particularly fishes. Primitive metazoans, most closely related to Cnidaria. Polar capsules at opposing ends of spores.
Myxosporeans.
Types of Myxosporeans.
COELOZOIC = Infect the lumina of organs.
HISTOZOIC = Less pathogenic, infect the tissue.
Causative agents of Myxosporean infection.
Myxidium spp., Myxobolus spp., Henneguya spp., Kudoa spp., Myxosoma spp., Thelohanellus spp.
Species affected by Myxosporean infection.
Mullet, catfish, carps, climbing perch, snakehead.
Life Cycle of Myxosporeans.
1.) Myxospores released by dead fish.
2.) Released myxospores are ingested by OLIGOCHAETES.
3.) Reproduction inside oligochaetes.
4.) Sporogony.
5.) Formation of ACTINOSPORES > release.
6.) Contact to surface epithelium of fish.
7.) Release of SPOROPLASM > penetration of skin.
8.) Intracellular clusters of dividing myxo. cells.
9.) Migration to final target tissue.
Clinical Signs of Myxosporean infection.
Loss of equilibrium. Skeletal deformities.
Lesions of Myxosporean infection.
White Cyst - Skin, gills, muscle, brain, heart, ovaries.
- Produces thick, MILKY EXUDATE when ruptured.
Gill Infection > Respiratory Dysfunction.
Prevention and Control of Myxosporean infection.
Isolate and destroy infected fish. Disinfect rearing facilities - LIME.
Transmission and Life Cycle of Monogeneans.
Direct Contact.
Direct Life Cycle.
- No IH required for reproduction.
- Hermaphroditic.
- Some attach eggs to host gills.
Clinical Signs of Monogenean infestations.
Pallor. Increased mucus production. Frayed fins. Opaque cornea.
Lesions of Monogenean infestations.
Hyperplasia - Epithelial Cells.
Damage - Gill Epithelium.
Diagnosis of Monogenean infestation.
Gross Examination.
Microscopic Examination = Wet Mounts.
Prevention and Control of Monogenean infestations.
Maintain optimum stocking density and adequate feeding.
5% Salt Solution = 5 mins.
Freshwater Bath = 1 hour, 3 days.
100 ppm Formalin = 1 hour, 3 days.
150 ppm Hydrogen Peroxide = 30 mins.
ENDOparasitic flatworms measuring 1 - 2.6 x 0.2 - 0.8 mm with two sucker-like attachment organs located at the anterior and ventral portions.
Characterized by complex life cycles, usually requiring at least TWO hosts.
Digeneans.
Causative agents of Digenean infections.
Bucephalus spp., Lecithochirium spp., Pseudometadena spp., Transversotrema spp., Stellantchasmus spp., Haplorchis spp., Procevorum spp., Prosoryhnchus spp., Hemiurus spp.
Species affected by Digenean infections.
Bighead carp, grass carp, milkfish, seabass, grouper, siganid, mullet.
Life Cycle of Digenean infections.
1.) VERTEBRATE Primary Host = Sexual reproduction occurs.
2.) INTERMEDIATE HOST (Aquatic Snail) = Asexual reproduction occurs.
Clinical Signs of Digenean infections.
Distended abdomen. Retarded growth. Cysts (White to Yellow, Brown to Black) - Skin, fins, gills, muscle, stomach, or intestines.
Diagnosis of Digenean infections.
Gross Examination.
Microscopic Examination = Opaque, creamy cyst - Motile metacercariae.
“Tapeworms”. Constitutes a large class of the PLATYHELMINTHES with about 8000 species.
ENDOparasitic tapeworms with ribbon-like, segmented or unsegmented bodies, 5 - 70 mm long. Anterior attachment organ called SCOLEX armed with hooks or suckers.
Do not induce severe damage, only destruction of superficial layer of the intestinal wall at the point of scolex attachment.
Cestodes.
Causative agent of Bothriocephaliasis.
Botriocephalus acheilognathi, “Asian Tapeworm”.
- Most important pathogenic cestode of cyprinid fish.
Pathogenesis of Bothriocephaliasis.
1.) Parasite attaches to the gut wall via BOTHRIA.
2.) Engulfs intestinal folds, attaches near anterior portion.
3.) Tapeworm accumulation in area = Digestive tract BLOCKAGE.
4.) Intestinal Wall DISTENTION = PERFORATION.
5.) Parasite envelopes parts of intestines > inflammatory response.
6.) Inflammation = HEMORRHAGE, NECROSIS.
Clinical Signs of Bothriocephaliasis.
Weight loss. Anemia. Mortality (Young).
Lesions of Bothriocephaliasis.
MACROSCOPIC:
1.) Intestinal Wall = Enlarged, thin-walled, occluded.
- SEVERE: Perforation, rupture of intestines.
2.) Gall Bladder = Swollen, turgid.
MICROSCOPIC:
1.) Destruction of villi intestinales.
2.) Hemorrhage, hemolysis, or VESICULATION in lamina propria.
3.) Hepatocyte atrophy.
Diagnosis of Bothriocephaliasis.
Gross Examination = SQUASH PLATE METHOD.
- Glass slides / plate = Flatten intestinal tract; worms are detected by the reflected light in low power microscopy.
Fecal Examination = Detached segments, eggs (with OPERCULUM at the apex).
Prevention and Control of Bothriocephaliasis.
IH control. Disinfection of facilities - QUICKLIME.
Smooth, cylindrical, long worms.
Nematodes.
Causative agents of Nematode infections.
Spirocamallanus spp., Raphidascaris spp., Contracaecum spp., Echinocephalus spp.
Species affected by Nematode infections.
Siganid, grouper, catfish, snakehead, goby.
Pathogenesis of Nematode infections.
1.) Entry via ingestion of PH or IH.
2.) Adult nematodes found in fish intestinal tract.
3.) Worm tracks during development.
4.) Immune cells try to “wall off” worm = GRANULOMA.
Diagnosis of Nematode infections.
Microscopic Examination = Fresh fecal sample.
Treatment of Nematode infections.
Fenbendazole = 1.14 g/lb of food, 3 days.
Levimasole = 1.8 g/lb of food once a week, 3 weeks.
