Darn! That could be Uronema. That is almost a classic presentation - where it erupts from the muscle tissue of the fish and breaks through to the surface. Wrasses, anthias and chromis are most commonly affected. Uronema is normally a bacteria feeder, it is found in almost all aquariums, but especially in QT. It feeds on the bacteria that in turn feeds on organic material (in the first picture, there is a lot of food stuck to the filter intake - you need to keep all of that out of a QT by physical removal after every feed. If it gets trapped in the filter, it is still in contact with the water). Once the Uronema population reaches a point, it infects the fish internally, living between the cells. It consumes the tissue and eventually breaks the surface. Sorry - I have never been able to cure it once it reaches this point. Chloroquine had some promise in treating this, but that drug is currently unavailable. Here is an excerpt from my upcoming disease book on the topic:
Uronema marinum (Red band disease)
Cause
Uronema is an elongate, oval, ciliated, motile protozoan, up to 40 um in length, that can become an opportunistic pathogen in marine aquariums. Because it is so generic-looking, identification in the field is always provisional. Most professional aquarists actually mean “Uronema-like” when they say “Uronema.”
Uronema infections have been seen in six families of fishes (in roughly descending order of frequency): Pomacentridae (damselfishes, specifically of the genus Chromis); Serranidae (subfamily Anthiinae the Anthias); Syngnathidae (seahorses and seadragons); Labridae (the wrasses); Chaetodontidae (the butterflyfishes); and, occasionally, Pomacanthidae (the angelfishes). There are, no doubt, other species of fish that can be infected.
Symptoms
This moderately common protozoan disease has symptoms that include the rapid development of a red mark in the hypodermis (fat and muscle) region of the fish, often following rows of scales so that the lesion is typically elongate and angled downward as it progresses front to back along the flank of the fish. Within a day or two of the development of the primary lesion, the fish will become lethargic and stop feeding and its respiration rate will increase. Scales above the lesion can be dislodged easily due to the massive trauma to the underlying tissue. Death follows rapidly, with few fish surviving beyond three days after the primary lesion develops.
Almost universally, aquarists who do not have access to a microscope will identify this disease as a “secondary bacterial infection resulting from some injury.” In fact, “capture damage” is often cited as the original cause due to the often-linear nature of the lesion, which looks much like a bruise from being hit with a net frame, for example. The rapid onset of the lesion (often many days after capture) and the fact that it develops internally and then erupts externally both point to another cause.
Treatment
A variety of treatments have been suggested for Uronema infections, but full control is rarely seen following most of these treatments. Part of the issue seems to be that Uronema is ubiquitous (naturally occurring in marine aquariums) and re-infection is commonplace.
Bath treatments may fail because the medication used does not target the intercellular protozoans, only those living externally on the skin of the fish. Copper treatments may reduce the numbers of these ciliates, but good control is not seen until ionic copper levels reach 0.23 ppm, and this is too close to the lethal limit for many species of fish. Formalin baths of various concentrations and durations have been proposed, but this treatment is also mostly effective against external protozoans.
The most commonly used treatment is chloroquine at 15 ppm for 30 days.
Jay
