That's interesting. I had a pretty chilled out betta in a well planted tank full of cull cherry shrimp I felt too bad to cull, but who had started breeding like mad. So I took the cowards way out and thought I'd try a betta knowing he may help with population control. He'd stalk them fairly unsuccessfully while I was watching. No doubt he ate a few, but I believed most managed to evade the betta.Betta stuffed himself with baby shrimp... but then his belly swelled. He died of bloat 11 months after
I'd be surprised if it was directly shrimp related. Shrimps are nutritionally pretty good, and would be very similar to the invertebrates a Betta would eat in the wild.I'd never even considered the shrimp diet as a reason for this.
Hi all, I'd be surprised if it was directly shrimp related. Shrimps are nutritionally pretty good, and would be very similar to the invertebrates a Betta would eat in the wild.
I haven't kept a Betta for a long time, and never with shrimps, but I fed Cherry Shrimps to my Apistogramma for a time without any problem for the fish, although I did eventually run out of shrimps.
but then his belly swelled. He died of bloat 11 months after I bought him
at 7 months he swelled up and developed drospy like yours did
https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2761.2010.01202.xMycobacteriosis in fish is a chronic progressive ubiquitous disease caused by Mycobacterium marinum, M. gordonae and M. fortuitum in most cases. The aim of this study was to describe the morphology and distribution of lesions in 322 freshwater ornamental fish across 36 species. Granulomatous inflammation was diagnosed by gross examination and histopathology testing in 188 fish (58.4%); acid‐fast rods (AFR) were determined in only 96 (51.1%) fish from 19 species after Ziehl–Neelsen staining. The most often affected organs with AFR were the kidney (81.2%), digestive tract (54.1%), liver (48.2%), spleen (45.9%) and skin (21.2%); sporadically, AFR were found in the branchiae (9.4%) and gonads (4.7%). In 14 randomly selected fish originating from four different fish tanks, the distribution of mycobacterial infection was studied by culture examination of the skin, gills, muscle tissue, digestive tract, liver, spleen and kidney. In 12 fish, the species M. marinum, M. gordonae, M. fortuitum, M. triviale, and M. avium subsp. hominissuis (serotypes 6 and 8 and genotype IS901− and IS1245+) were detected; mixed infection caused by different mycobacterial species was documented in five of them.
A hexamitid flagellate infection (probably Spironucleus) in the Siamese fighting fish, Betta splendens, was reported by Ferguson and Moccia (1980). The infected fish became inappetent, had a lethargic behavior, developed a swollen abdomen, and usually died, often with a perforated stomach. The flagellates occurred in large numbers in the abdominal cavity, mesentery, liver parenchyma, spleen, and kidney, and they were closely associated with a chronic inflammatory response. Ferguson and Moccia (1980) found that nifurpirinol effectively eradicated the flagellates when administered as both a bath and a feed medication.
Additional ectoparasites infesting the skin and gills of their fish hosts are the dinoflagellates Piscinoodinium pillulare and Amyloodinium ocellatum. Trophonts of P. pillulare occur on freshwater fishes and have an attachment disc with rhizocysts that embed in the cytoplasm of the host epidermis or gill epithelium (Lom and Schubert, 1983) and possess well-developed chloroplasts. Amyloodini ocellatum trophonts possess numerous filiform rhizoids and a stomopode which apparently aids in digesting host tissue, but they lack chloroplasts (Lom and Lawler, 1973). Life cycles of these organisms are similar, with trophonts withdrawing their penetrating processes, falling to the substratum, and covering themselves with a cellulose secretion. Cellular division produces 128 free-swimming dinospores which each divide once to form a total of 256 infective swarmers. The pathogenicity of these parasites is caused by the extensive damage to gill epithelial cells by the penetrating rhizocysts or rhizoids. The primary damage to host tissue in A. ocellatum infestations results from the injection of lytic or digestive fluids through the stomopode. Paperna (1980) has suggested that the severe histopathological changes in the gills of fishes infested with A. ocellatum might be caused by the excretion of toxic substances by the parasite, as is the case with several species of free-living dinoflagellates.
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