Dear Seahorsegirl:

Pete Giwojna

Dear Seahorsegirl:

Okay, I understand that the condition of your female has not shown any signs of improvement despite the medications we have been using to treat her tail problem. She is still eating well but having the same sort of clumsiness and awkwardness using her tail to cling to a convenient perch. As you put it, it is almost as if she had suffered a minor stroke affecting her tail and lost some of the prehensility and ability to control the muscles in her tail normally.

I would complete the full 10-day regimen of Seachem Metronidazole/Focus/Garlic Guard nonetheless. Even if it does not appear to be helping significantly, it is important to complete the full regimen of the medication once you begin in order to minimize potential problems with disease resistance.

And I can tell you that it is encouraging that she is showing no signs of tail rot other than the abnormal clumsiness using her tail. It’s a very good sign that there has been no whitening of the tail tip or peeling of the skin or open sores developing on her tail (ulcerative dermatitis).

I still don’t have a very good idea of exactly what is causing this problem or what to expect down the road, Seahorsegirl. When treating tail rot and other tail infections, it often requires long-term medication with broad-spectrum antibiotics lasting several weeks or even months (multiple treatment regimens) in order to resolve the problem. But this does not seem like a typical tail rot infection…

One thing that can result in nerve damage and loss of muscle control is the formation of gas emboli that occlude veins and arteries, which is often seen in seahorses during episodes of gas bubble syndrome (GBS). When that happens, it can cause problems similar to the “bends” that can afflict divers if they ascend too quickly from depth, which can include nerve damage and paralysis (almost as if they had suffered a stroke).

In seahorses, the tail in particular is vulnerable to problems with gas bubble syndrome, so it is conceivable that your female could have experienced such a development, although I think it’s very unlikely. (Male seahorses are highly vulnerable to problems with GBS, whereas females are normally quite resistant to such problems. If none of the males in your tank have experienced problems with GBS, it would be very unusual for a female seahorse to be afflicted with gas emboli.)

As you know, gas bubble syndrome is believed to be caused by gas emboli forming within the tissue of heavily vascularized portions of the seahorse’s anatomy — the placenta-like brood pouch of males, the eye, the muscular prehensile tail — and it can take several different forms depending on where the bubbles or emboli occur. When it occurs in the brood pouch of the male, chronic pouch emphysema or bloated pouch results, leading to positive buoyancy. (Chronic pouch emphysema is by far the most common form of GBS and is, of course, restricted to males only.) When it occurs in the capillary network behind the eye (choroid rete), Exopthalmus or Popeye results, and the eye(s) can become enormously swollen. When it affects the capillary network of the gas bladder (the rete mirabile), hyperinflation of the swimbladder occurs, again resulting in positive buoyancy. When it affects the tail or snout, external gas bubbles (i.e., subcutaneous emphysema) form just beneath the skin and look like raised blisters. When intravascular emboli occur deep within the tissue and occlude blood flow, generalized edema results in the affected area. Or extravascular emboli may cause gas to build up within the coelom, often resulting in positive buoyancy and swelling or bloating of the abdominal cavity (internal GBS).

Different parts of the body can thus be affected depending on how the initial gas emboli or micronuclei form, grow and spread. During an episode of GBS, bubbles may initially form in the blood (intravascular) or outside the blood (extravascular). Either way, once formed, a number of different critical insults are possible. Intravascular bubbles may stop in closed circulatory vessels and induce ischemia, blood sludging, edema, chemistry degradations, or mechanical nerve deformation. Circulating gas emboli may occlude the arterial flow or leave the circulation to lodge in tissue sites as extravascular bubbles. Extravascular bubbles may remain locally in tissue sites, assimilating gas by diffusion from adjacent supersaturated tissue and growing until a nerve ending is deformed or circulation in nearby capillaries and vessels is restricted. Or, extravascular bubbles might enter the arterial or venous flows, at which point they become intravascular bubbles. Extravascular bubbles can thus become intravascular bubbles, and vice versa, via diffusion and perfusion. This is important because it means that under certain conditions extravascular seed bubbles or micronuclei can enter the bloodstream and migrate from their birth site to other critical areas as intravascular bubbles. If untreated, the gas bubbles worsen and the condition is fatal.

For instance, the prehensile tail of the seahorse is often affected when conditions are favorable for the formation of such gas emboli because it has a rich blood supply via the dorsal aorta and caudal vein (hence plenty of carbonic anhydrase to induce the formation of intravascular gas bubbles) and because the tail is the site where seahorses tend to store their limited fat reserves (the extravascular seed nuclei or emboli that trigger GBD form most readily in adipose tissue due to the higher solubility of certain gases in lipids than in aqueous tissues). Intravascular bubbles are seen in both the arterial and venous circulation, with vastly greater numbers detected in venous flows (venous gas emboli). The far more numerous venous bubbles are believed to first form in lipid tissues draining the veins. Lipid tissue sites possess very few nerve endings, possibly masking critical insults at first, and veins, which are thinner than arteries, appear more susceptible to extravascular gas penetration.

So it is remotely possible that your female seahorse could have developed deep-seated gas emboli in the upper part of her tail or the midsection of her tail, resulting in nerve damage and loss of muscular control in the affected area, and if that’s the case, treatment with a carbonic anhydrase inhibitor such as Diamox might be helpful. But I am very hesitant to suggest resorting to your Diamox, Seahorsegirl, because it can be harmful to inhibit the enzymatic activity of a healthy seahorse and because it seems so very unlikely that your female is having problems with gas bubble syndrome. When the tail of a seahorse is affected by GBS, it normally takes the form of external GBS or tail bubbles, which appear like upraised, translucent, blisterlike gas bubbles that form just beneath the skin (i.e., subcutaneous emphysema).

If none of your male seahorses have had any problems with GBS, and your female has had no problems with tail bubbles, and there is no noticeable swelling of her tail, it seems very unlikely that she is suffering any sort of paralysis to her tail due to deep-seated gas emboli. And if that’s the case, treating her with the Diamox could actually be harmful and counterproductive.

So for now I would just continue the 10-day regimen of Metronidazole/Focus/Garlic Guard and we can go from there. None of the other medications you presently have available in your fishroom medicine chest seem likely to produce better results. The KanaPlex is a good drug, but the active ingredient is kanamycin sulfate, a broad-spectrum aminoglycoside antibiotic that is similar to the neomycin sulfate in the NeoPlex you have been using. Likewise, Furan2, which is a combination of two different nitrofuran antibiotics, has been found to be helpful in treating some cases of tail rot, but you are already treating the seahorse with furazolidone, a nitrofuran antibiotic contained in the Seachem Focus, so I don’t believe the Furan2 would produce any better results.

There are one or two other medications you do not have at this time that might be worth a try, but it may well just be that we need to repeat multiple treatment regimens of the medications we have been using in order to get your female past this issue. If we can just keep her condition from worsening, she may be able to eventually recover on her own, just as stroke patients can regain their normal function in time following a minor stroke. Or, if it is an underlying bacterial and/or parasitic infection that is causing the problems, long-term treatment with the medications we have been using may be inhibiting the growth of these organisms, keeping them in check, which can eventually allow the immune system of the seahorse to gain the upper hand and resolve the problem.

Good luck. Please keep me posted regarding any progress (or lack thereof) and we will see how things develop…

Pete Giwojna, Ocean Rider Tech Support

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